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RJR: Recommended Bibliography 02 Sep 2026 at 01:55 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-08-31
CmpDate: 2026-08-31
Species-specific structuring of gut bacterial and fungal communities in honey bees Apis cerana and Apis mellifera.
Antonie van Leeuwenhoek, 119(9):.
Honey bee gut microbiome studies have primarily emphasized bacteria, leaving fungal communities comparatively overlooked despite their ecological and functional importance. Whole-genome shotgun metagenomics of Apis cerana and Apis mellifera revealed fungal assemblages dominated by Ascomycota, with Basidiomycota and Microsporidia in minor proportions, alongside gut bacterial communities composed mainly of Pseudomonadota, Bacillota, and Actinomycetota. The bacterial diversity was markedly higher in A. mellifera (Shannon = 5.90; Simpson = 0.98) than in A. cerana (Shannon = 4.01; Simpson = 0.94; p > 0.05), while fungal diversity remained comparable between species (p > 0.05). Beta-diversity analyses revealed strong host-specific clustering for both bacterial (PERMANOVA R[2] = 0.7989, p > 0.05) and fungal communities (R[2] = 0.7218, p > 0.05), indicating distinct microbial organization driven by host species. Bacterial-fungal co-occurrence patterns exhibited host-specific structuring, suggesting differential inter-kingdom community organization between A. cerana and A. mellifera. Linear Discriminant Analysis Effect Size (LEfSe) identified 93 discriminatory fungal taxa (45 enriched in A. cerana, 48 in A. mellifera), highlighting yeast-dominated signatures in A. mellifera and Basidiomycota-affiliated enrichments in A. cerana. KEGG and CAZy profiling revealed host- and kingdom-specific functional differences, with bacterial communities of A. mellifera showing distinct representation of carbohydrate metabolism and nutrient-cycling functions, while fungal communities exhibited a comparatively narrower functional repertoire. Together, these findings provide a high-resolution view of honey bee bacterial and fungal microbiomes, highlighting strong host-driven divergence in taxonomy, function, and cross-kingdom interactions.
Additional Links: PMID-42671657
PubMed:
Citation:
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@article {pmid42671657,
year = {2026},
author = {Nazrin, MRR and Gouda, MNR and Kumaranag, KM and Suroshe, SS and Subramanian, S},
title = {Species-specific structuring of gut bacterial and fungal communities in honey bees Apis cerana and Apis mellifera.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {9},
pages = {},
pmid = {42671657},
issn = {1572-9699},
mesh = {Animals ; Bees/microbiology ; *Bacteria/classification/genetics/isolation & purification ; *Fungi/classification/genetics/isolation & purification ; *Gastrointestinal Microbiome ; Species Specificity ; Metagenomics ; Phylogeny ; Biodiversity ; *Mycobiome ; },
abstract = {Honey bee gut microbiome studies have primarily emphasized bacteria, leaving fungal communities comparatively overlooked despite their ecological and functional importance. Whole-genome shotgun metagenomics of Apis cerana and Apis mellifera revealed fungal assemblages dominated by Ascomycota, with Basidiomycota and Microsporidia in minor proportions, alongside gut bacterial communities composed mainly of Pseudomonadota, Bacillota, and Actinomycetota. The bacterial diversity was markedly higher in A. mellifera (Shannon = 5.90; Simpson = 0.98) than in A. cerana (Shannon = 4.01; Simpson = 0.94; p > 0.05), while fungal diversity remained comparable between species (p > 0.05). Beta-diversity analyses revealed strong host-specific clustering for both bacterial (PERMANOVA R[2] = 0.7989, p > 0.05) and fungal communities (R[2] = 0.7218, p > 0.05), indicating distinct microbial organization driven by host species. Bacterial-fungal co-occurrence patterns exhibited host-specific structuring, suggesting differential inter-kingdom community organization between A. cerana and A. mellifera. Linear Discriminant Analysis Effect Size (LEfSe) identified 93 discriminatory fungal taxa (45 enriched in A. cerana, 48 in A. mellifera), highlighting yeast-dominated signatures in A. mellifera and Basidiomycota-affiliated enrichments in A. cerana. KEGG and CAZy profiling revealed host- and kingdom-specific functional differences, with bacterial communities of A. mellifera showing distinct representation of carbohydrate metabolism and nutrient-cycling functions, while fungal communities exhibited a comparatively narrower functional repertoire. Together, these findings provide a high-resolution view of honey bee bacterial and fungal microbiomes, highlighting strong host-driven divergence in taxonomy, function, and cross-kingdom interactions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Bees/microbiology
*Bacteria/classification/genetics/isolation & purification
*Fungi/classification/genetics/isolation & purification
*Gastrointestinal Microbiome
Species Specificity
Metagenomics
Phylogeny
Biodiversity
*Mycobiome
RevDate: 2026-08-31
CmpDate: 2026-08-31
The COVID-19 pandemic influenced the temporal dynamics of antimicrobial resistance markers and bacterial community across urban wastewater treatment plants.
Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology], 57(1):.
Urban wastewater systems represent important interfaces between human activity and the environmental occurrence of antimicrobial resistance (AMR) markers. We assessed the temporal dynamics of intI1, ermB, and the 16 S rRNA gene by quantitative PCR across three wastewater systems (EPC, CJC, and JW) in Fortaleza, Brazil, from November 2021 to November 2023. Bacterial communities were additionally characterized by 16 S rRNA gene metabarcoding in 18 samples collected in December 2021 and January 2022. A synchronized decline in 16 S rRNA gene and intI1 concentrations beginning in late 2022 was observed across all three wastewater systems, suggesting a shift toward lower microbial abundance. The ermB gene showed higher and more variable concentrations during part of the pandemic period, followed by convergence toward lower levels; however, the absence of antimicrobial-consumption data precluded attribution of this pattern to changes in macrolide selective pressure. Normalized antimicrobial resistance marker abundances were comparatively stable at EPC and JW but more variable at CJC. EPC exhibited the highest ASV richness, whereas CJC and JW showed greater diversity according to Shannon and inverse Simpson indices. Beta-diversity analyses identified wastewater system as the principal factor associated with bacterial community structure, while the effect of sampling period was smaller and metric-dependent. Neither ermB nor intI1 was individually associated with community composition, although intI1 showed a limited effect after adjustment for wastewater system in one model. Physicochemical parameters were not significantly associated with normalized marker abundances in the exploratory paired analysis. Arcobacter, Acinetobacter, and other potentially relevant genera were detected, but no direct associations between these taxa and the monitored AMR markers could be established. These findings highlight the value of integrating longitudinal qPCR, microbiome profiling, and environmental characterization to improve the interpretation of targeted AMR markers in One Health wastewater surveillance.
Additional Links: PMID-42671719
PubMed:
Citation:
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@article {pmid42671719,
year = {2026},
author = {Filho, CGB and Oliveira, FAS and Rodrigues, VLM and Hissa, DC and Barros, MVH and de Farias, AA and Dantas, GT and Dos Santos, AB and Ximenes, JCM and Melo, VMM},
title = {The COVID-19 pandemic influenced the temporal dynamics of antimicrobial resistance markers and bacterial community across urban wastewater treatment plants.},
journal = {Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]},
volume = {57},
number = {1},
pages = {},
pmid = {42671719},
issn = {1678-4405},
mesh = {*Wastewater/microbiology ; Brazil/epidemiology ; *Bacteria/genetics/drug effects/classification/isolation & purification ; RNA, Ribosomal, 16S/genetics ; *COVID-19/epidemiology ; *Drug Resistance, Bacterial/genetics ; Humans ; Anti-Bacterial Agents/pharmacology ; SARS-CoV-2 ; *Microbiota ; },
abstract = {Urban wastewater systems represent important interfaces between human activity and the environmental occurrence of antimicrobial resistance (AMR) markers. We assessed the temporal dynamics of intI1, ermB, and the 16 S rRNA gene by quantitative PCR across three wastewater systems (EPC, CJC, and JW) in Fortaleza, Brazil, from November 2021 to November 2023. Bacterial communities were additionally characterized by 16 S rRNA gene metabarcoding in 18 samples collected in December 2021 and January 2022. A synchronized decline in 16 S rRNA gene and intI1 concentrations beginning in late 2022 was observed across all three wastewater systems, suggesting a shift toward lower microbial abundance. The ermB gene showed higher and more variable concentrations during part of the pandemic period, followed by convergence toward lower levels; however, the absence of antimicrobial-consumption data precluded attribution of this pattern to changes in macrolide selective pressure. Normalized antimicrobial resistance marker abundances were comparatively stable at EPC and JW but more variable at CJC. EPC exhibited the highest ASV richness, whereas CJC and JW showed greater diversity according to Shannon and inverse Simpson indices. Beta-diversity analyses identified wastewater system as the principal factor associated with bacterial community structure, while the effect of sampling period was smaller and metric-dependent. Neither ermB nor intI1 was individually associated with community composition, although intI1 showed a limited effect after adjustment for wastewater system in one model. Physicochemical parameters were not significantly associated with normalized marker abundances in the exploratory paired analysis. Arcobacter, Acinetobacter, and other potentially relevant genera were detected, but no direct associations between these taxa and the monitored AMR markers could be established. These findings highlight the value of integrating longitudinal qPCR, microbiome profiling, and environmental characterization to improve the interpretation of targeted AMR markers in One Health wastewater surveillance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Wastewater/microbiology
Brazil/epidemiology
*Bacteria/genetics/drug effects/classification/isolation & purification
RNA, Ribosomal, 16S/genetics
*COVID-19/epidemiology
*Drug Resistance, Bacterial/genetics
Humans
Anti-Bacterial Agents/pharmacology
SARS-CoV-2
*Microbiota
RevDate: 2026-08-31
CmpDate: 2026-08-31
Dietary Sulfur Compounds and Halitosis: Bridging Food Science, Microbial Metabolism, and Oral Health: A Comprehensive Review.
Molecular nutrition & food research, 70(17):e70526.
Intraoral halitosis is predominantly caused by anaerobic microbes within the tongue biofilm that break down sulfur-containing amino acids, especially cysteine and methionine, to volatile sulfur compounds (VSCs). In addition to microbial activity, there is growing evidence to suggest that dietary factors are able to influence VSC formation by affecting substrate availability, redox equilibrium, and oral ecological stability and that some of these effects are due to extraoral metabolic activity. This review integrates food chemistry, microbial ecology, and oral health to explain how dietary exposures can interact with the oral microbiome to trigger and maintain halitosis. We synthesize current evidence on tongue biofilm ecology, key microbial taxa and metabolic pathways, and the modifying roles of salivary flow, periodontal inflammation, and common beverages and condiments. Diagnostic approaches are discussed with a mechanistic viewpoint, which has focused on combined organoleptic, gas specific analysis, tongue biofilm imaging, and selective provocation testing. Comprehensively, halitosis is presented as a diet modifiable, ecology-driven disease, the diagnostics of which should be guided by phenotype, and the intervention based on microbiomes and tailored care plans should be sustainable so that evidence-based functional foods and personalized care plans can be developed.
Additional Links: PMID-42672061
PubMed:
Citation:
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hide bibtex listing
@article {pmid42672061,
year = {2026},
author = {Acheampong, R and Otu-Ayeboafo, JO},
title = {Dietary Sulfur Compounds and Halitosis: Bridging Food Science, Microbial Metabolism, and Oral Health: A Comprehensive Review.},
journal = {Molecular nutrition & food research},
volume = {70},
number = {17},
pages = {e70526},
pmid = {42672061},
issn = {1613-4133},
mesh = {*Halitosis/microbiology/etiology ; Humans ; *Oral Health ; *Sulfur Compounds/metabolism/adverse effects ; Microbiota ; Biofilms ; *Diet ; Tongue/microbiology ; },
abstract = {Intraoral halitosis is predominantly caused by anaerobic microbes within the tongue biofilm that break down sulfur-containing amino acids, especially cysteine and methionine, to volatile sulfur compounds (VSCs). In addition to microbial activity, there is growing evidence to suggest that dietary factors are able to influence VSC formation by affecting substrate availability, redox equilibrium, and oral ecological stability and that some of these effects are due to extraoral metabolic activity. This review integrates food chemistry, microbial ecology, and oral health to explain how dietary exposures can interact with the oral microbiome to trigger and maintain halitosis. We synthesize current evidence on tongue biofilm ecology, key microbial taxa and metabolic pathways, and the modifying roles of salivary flow, periodontal inflammation, and common beverages and condiments. Diagnostic approaches are discussed with a mechanistic viewpoint, which has focused on combined organoleptic, gas specific analysis, tongue biofilm imaging, and selective provocation testing. Comprehensively, halitosis is presented as a diet modifiable, ecology-driven disease, the diagnostics of which should be guided by phenotype, and the intervention based on microbiomes and tailored care plans should be sustainable so that evidence-based functional foods and personalized care plans can be developed.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Halitosis/microbiology/etiology
Humans
*Oral Health
*Sulfur Compounds/metabolism/adverse effects
Microbiota
Biofilms
*Diet
Tongue/microbiology
RevDate: 2026-08-31
CmpDate: 2026-08-31
Root-associated bacterial and fungal communities of the endangered páramo bromeliad Puya goudotiana.
PloS one, 21(8):e0357104.
Páramo, a tropical high-altitude ecosystem, is threatened by climate change and land-use change. This ecosystem hosts unique biodiversity like the endangered bromeliad Puya goudotiana. While root-associated microbiomes are essential for plant survival and stress tolerance, the microbial communities associated with this species remain uncharacterized. Oxford Nanopore amplicon sequencing was used on root endosphere and bulk soil samples of P. goudotiana, targeting the 16S rRNA gene to evaluate bacterial communities, and the 18S rRNA gene as an exploratory marker for fungal communities. We assessed the taxonomic composition, diversity, functional profiles and co-occurrence networks. Microbial communities were highly differentiated by sample type, with roots exhibiting lower alpha diversity than bulk soil. The root microbiome showed higher prevalence of acidophilic taxa such as Granulicella and Acidipila and symbionts like Bradyrhizobium, whereas bulk soils were dominated by typical páramo taxa, including Candidatus Solibacter, Candidatus Koribacter and Bryobacter. Both bulk soil and roots were characterized by a high abundance of saprotrophic fungi (e.g., Psilocybe) and potential pathogens such as Fusarium, Botrytis and Puccinia. Functional predictions indicated higher prevalence of chemoheterotrophic functions in the roots, while nitrogen and sulfur cycling functions were enriched in bulk soil. Notably, and contrary to prior expectations, co-occurrence networks were more complex in the root endosphere than in bulk soil, suggesting that rhizosphere filtering promotes structured microbial assemblages despite reducing overall diversity. These findings provide a first microbial baseline for P. goudotiana and open new perspectives for understanding plant-microbe interactions and enhancing páramo vegetation resilience under climate change.
Additional Links: PMID-42672062
PubMed:
Citation:
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@article {pmid42672062,
year = {2026},
author = {Rodríguez-Lugo, N and Patiño, LH and Cáceres, TM and Vega, L and Hantson, S and Ramírez, JD and Sanchez, A},
title = {Root-associated bacterial and fungal communities of the endangered páramo bromeliad Puya goudotiana.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0357104},
pmid = {42672062},
issn = {1932-6203},
mesh = {*Plant Roots/microbiology ; *Bromeliaceae/microbiology ; *Bacteria/genetics/classification/isolation & purification ; Soil Microbiology ; *Fungi/genetics/classification/isolation & purification ; RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; Endangered Species ; Biodiversity ; Phylogeny ; RNA, Ribosomal, 18S/genetics ; },
abstract = {Páramo, a tropical high-altitude ecosystem, is threatened by climate change and land-use change. This ecosystem hosts unique biodiversity like the endangered bromeliad Puya goudotiana. While root-associated microbiomes are essential for plant survival and stress tolerance, the microbial communities associated with this species remain uncharacterized. Oxford Nanopore amplicon sequencing was used on root endosphere and bulk soil samples of P. goudotiana, targeting the 16S rRNA gene to evaluate bacterial communities, and the 18S rRNA gene as an exploratory marker for fungal communities. We assessed the taxonomic composition, diversity, functional profiles and co-occurrence networks. Microbial communities were highly differentiated by sample type, with roots exhibiting lower alpha diversity than bulk soil. The root microbiome showed higher prevalence of acidophilic taxa such as Granulicella and Acidipila and symbionts like Bradyrhizobium, whereas bulk soils were dominated by typical páramo taxa, including Candidatus Solibacter, Candidatus Koribacter and Bryobacter. Both bulk soil and roots were characterized by a high abundance of saprotrophic fungi (e.g., Psilocybe) and potential pathogens such as Fusarium, Botrytis and Puccinia. Functional predictions indicated higher prevalence of chemoheterotrophic functions in the roots, while nitrogen and sulfur cycling functions were enriched in bulk soil. Notably, and contrary to prior expectations, co-occurrence networks were more complex in the root endosphere than in bulk soil, suggesting that rhizosphere filtering promotes structured microbial assemblages despite reducing overall diversity. These findings provide a first microbial baseline for P. goudotiana and open new perspectives for understanding plant-microbe interactions and enhancing páramo vegetation resilience under climate change.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Plant Roots/microbiology
*Bromeliaceae/microbiology
*Bacteria/genetics/classification/isolation & purification
Soil Microbiology
*Fungi/genetics/classification/isolation & purification
RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
Endangered Species
Biodiversity
Phylogeny
RNA, Ribosomal, 18S/genetics
RevDate: 2026-08-31
CmpDate: 2026-08-31
Kelp forest collapse alters the reef microbiome and associated metabolome.
Proceedings of the National Academy of Sciences of the United States of America, 123(36):e2525548123.
In many temperate regions experiencing rapid ocean warming, kelp forests are being replaced by low-lying turf algae. Yet, whether this change in biogenic habitat alters reef-level microbial structure and function, including carbon and nutrient cycling, remains largely unknown. Here, we integrated shotgun metagenomics and nontargeted metabolomics to reveal that kelp forest loss alters the composition of the reef microbial community and its associated biochemical machinery, resulting in distinct metabolomes and microbially driven elemental use/transformations on kelp- vs. turf-dominated reefs. Our results therefore suggest that microbes play a key role in shaping kelp forest ecosystem functioning. Further, they demonstrate that human-induced ocean warming has cascading effects on microbially mediated chemistry, with implications for coastal carbon storage and nutrient regeneration.
Additional Links: PMID-42673455
Publisher:
PubMed:
Citation:
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@article {pmid42673455,
year = {2026},
author = {Farrell, SP and D'Angelo, T and Yiu, DS and Kelminal Pakkir Shah, A and Stincone, P and Countway, PD and Petras, D and Brady, DC and Rasher, DB},
title = {Kelp forest collapse alters the reef microbiome and associated metabolome.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {36},
pages = {e2525548123},
doi = {10.1073/pnas.2525548123},
pmid = {42673455},
issn = {1091-6490},
support = {OIA-1489227//NSF (NSF)/ ; NA//Louise H. & David S. Ingalls Foundation/ ; 2124-390838134//Deutsche Forschungsgemeinschaft (DFG)/ ; NA//Essex Avenue Foundation/ ; NA//PADI Foundation (The PADI Foundation)/ ; },
mesh = {*Microbiota/physiology ; *Kelp/microbiology ; *Metabolome ; *Coral Reefs ; Ecosystem ; Climate Change ; },
abstract = {In many temperate regions experiencing rapid ocean warming, kelp forests are being replaced by low-lying turf algae. Yet, whether this change in biogenic habitat alters reef-level microbial structure and function, including carbon and nutrient cycling, remains largely unknown. Here, we integrated shotgun metagenomics and nontargeted metabolomics to reveal that kelp forest loss alters the composition of the reef microbial community and its associated biochemical machinery, resulting in distinct metabolomes and microbially driven elemental use/transformations on kelp- vs. turf-dominated reefs. Our results therefore suggest that microbes play a key role in shaping kelp forest ecosystem functioning. Further, they demonstrate that human-induced ocean warming has cascading effects on microbially mediated chemistry, with implications for coastal carbon storage and nutrient regeneration.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Microbiota/physiology
*Kelp/microbiology
*Metabolome
*Coral Reefs
Ecosystem
Climate Change
RevDate: 2026-08-31
Effects of different biochar application rates on CH4 emissions and Microbial Carbon Pump (MCP) mediated carbon sequestration in paddy fields: a quantitative modeling approach.
Journal of environmental management, 416:130772 pii:S0301-4797(26)02232-2 [Epub ahead of print].
Biochar amendment is a proven strategy for mitigating methane (CH4) emissions and enhancing soil carbon sequestration in rice paddies. However, the depth-dependent dynamics of microbial carbon pump (MCP)-driven recalcitrant organic carbon (ROC) formation and the underlying microbial mechanisms remain poorly characterized, particularly in the purple paddy soils of the central Sichuan Basin, China. To address this gap, we developed a novel quantitative MCP-driven ROC model and conducted a field experiment with four biochar treatments (CK, C2, C4, and C6 t ha[-1]) to investigate CH4 emissions, methane-cycling microbial community, and soil carbon fractions across a 0-80 cm profile. Biochar amendment significantly reduced CH4 emissions by 57.88-84.51% (peaking at 6 t ha[-1]) and increased methanogen and methanotroph diversity by 1.30-1.66 times. Although the concentrations of soil organic carbon (SOC), dissolved organic carbon (DOC), microbial biomass carbon (MBC), and absolute ROC decreased significantly with depth, the ROC/SOC ratio consistently increased. Crucially, our quantitative model revealed that biochar stimulated both the in vivo turnover and ex vivo modification pathways of the MCP by supplying essential labile substrates, explaining up to 92% of the variance in deep-soil carbon fractions. In conclusion, this study demonstrates that biochar serves as an effective dual-action strategy: mitigating CH4 emissions via microbiome regulation while enhancing long-term carbon sequestration through intensified MCP-driven ROC formation across the entire soil profile.
Additional Links: PMID-42673821
Publisher:
PubMed:
Citation:
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@article {pmid42673821,
year = {2026},
author = {Li, Y and Chen, H and Chen, J and Jiang, W and Liu, X and Liang, J and Zhang, K and Jiang, B and Luo, H and Xie, W and An, X and Chen, W and Yang, Z and Zhang, X},
title = {Effects of different biochar application rates on CH4 emissions and Microbial Carbon Pump (MCP) mediated carbon sequestration in paddy fields: a quantitative modeling approach.},
journal = {Journal of environmental management},
volume = {416},
number = {},
pages = {130772},
doi = {10.1016/j.jenvman.2026.130772},
pmid = {42673821},
issn = {1095-8630},
abstract = {Biochar amendment is a proven strategy for mitigating methane (CH4) emissions and enhancing soil carbon sequestration in rice paddies. However, the depth-dependent dynamics of microbial carbon pump (MCP)-driven recalcitrant organic carbon (ROC) formation and the underlying microbial mechanisms remain poorly characterized, particularly in the purple paddy soils of the central Sichuan Basin, China. To address this gap, we developed a novel quantitative MCP-driven ROC model and conducted a field experiment with four biochar treatments (CK, C2, C4, and C6 t ha[-1]) to investigate CH4 emissions, methane-cycling microbial community, and soil carbon fractions across a 0-80 cm profile. Biochar amendment significantly reduced CH4 emissions by 57.88-84.51% (peaking at 6 t ha[-1]) and increased methanogen and methanotroph diversity by 1.30-1.66 times. Although the concentrations of soil organic carbon (SOC), dissolved organic carbon (DOC), microbial biomass carbon (MBC), and absolute ROC decreased significantly with depth, the ROC/SOC ratio consistently increased. Crucially, our quantitative model revealed that biochar stimulated both the in vivo turnover and ex vivo modification pathways of the MCP by supplying essential labile substrates, explaining up to 92% of the variance in deep-soil carbon fractions. In conclusion, this study demonstrates that biochar serves as an effective dual-action strategy: mitigating CH4 emissions via microbiome regulation while enhancing long-term carbon sequestration through intensified MCP-driven ROC formation across the entire soil profile.},
}
RevDate: 2026-08-31
Association Between Ultra-Processed Foods and Clinical Relapse in Crohn's Disease: A Systematic Review and Meta-Analysis.
Journal of the Academy of Nutrition and Dietetics pii:S2212-2672(26)00553-8 [Epub ahead of print].
BACKGROUND: Higher consumption of ultra-processed foods (UPFs) has been linked to an increased risk of developing Crohn's Disease (CD) and is hypothesized to worsen activity of CD through mechanisms such as gut microbiome alterations and increased intestinal permeability.
OBJECTIVE: To assess the association between dietary intake of UPFs and clinical relapse in patients with CD.
METHODS: A comprehensive search of MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials from database inception to March 18, 2025. At the time of the search, records in the Cochrane Central Register of Controlled Trials were available through February 28, 2025. The study included prospective cohort studies and randomized controlled trials enrolling adults with CD in clinical remission, comparing higher versus lower UPF intake or no UPF, with a minimum follow-up of 6 months. Studies not meeting these criteria, including retrospective designs and non-English publications, were excluded. The primary outcome was clinical relapse within one year. Study quality was assessed using the Newcastle-Ottawa Scale, and overall certainty of evidence was evaluated using the GRADE framework. Pooled odd ratios (ORs) and 95% confidence intervals (CIs) were calculated using DerSimonian-Laird random-effects meta-analysis based on estimates and standard errors. Heterogeneity was assessed using the I[2] statistic. The publication bias was planned to assess using funnel plots and statistical tests if sufficient studies were available.
RESULTS: 1945 studies were identified through the search. After removing duplicates, and abstract screening, 13 studies were selected for full-text review and 3 prospective cohort studies involving 276 patients with CD were included in the analysis. Pooled analysis demonstrated a significant association between UPF intake and relapse in patients with CD. Patients with higher versus lower UPF intake had increased odds for clinical relapse (OR 2.27, 95% CI 1.01-5.13, p = 0.048; I[2] = 20.95%), although the certainty of the evidence was rated as very low according to the GRADE framework.
CONCLUSION: This study suggests that higher UPF intake is associated with increased odds of clinical relapse in patients with Crohn's disease in remission. However, the certainty of evidence is very low, and additional well-designed prospective studies and randomized trials are required before firm dietary recommendations can be made.
Additional Links: PMID-42674185
Publisher:
PubMed:
Citation:
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@article {pmid42674185,
year = {2026},
author = {Samnani, S and Tran, HR and Vagianos, K and Bernstein, CN and Marshall, JK and Narula, N},
title = {Association Between Ultra-Processed Foods and Clinical Relapse in Crohn's Disease: A Systematic Review and Meta-Analysis.},
journal = {Journal of the Academy of Nutrition and Dietetics},
volume = {},
number = {},
pages = {156838},
doi = {10.1016/j.jand.2026.156838},
pmid = {42674185},
issn = {2212-2672},
abstract = {BACKGROUND: Higher consumption of ultra-processed foods (UPFs) has been linked to an increased risk of developing Crohn's Disease (CD) and is hypothesized to worsen activity of CD through mechanisms such as gut microbiome alterations and increased intestinal permeability.
OBJECTIVE: To assess the association between dietary intake of UPFs and clinical relapse in patients with CD.
METHODS: A comprehensive search of MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials from database inception to March 18, 2025. At the time of the search, records in the Cochrane Central Register of Controlled Trials were available through February 28, 2025. The study included prospective cohort studies and randomized controlled trials enrolling adults with CD in clinical remission, comparing higher versus lower UPF intake or no UPF, with a minimum follow-up of 6 months. Studies not meeting these criteria, including retrospective designs and non-English publications, were excluded. The primary outcome was clinical relapse within one year. Study quality was assessed using the Newcastle-Ottawa Scale, and overall certainty of evidence was evaluated using the GRADE framework. Pooled odd ratios (ORs) and 95% confidence intervals (CIs) were calculated using DerSimonian-Laird random-effects meta-analysis based on estimates and standard errors. Heterogeneity was assessed using the I[2] statistic. The publication bias was planned to assess using funnel plots and statistical tests if sufficient studies were available.
RESULTS: 1945 studies were identified through the search. After removing duplicates, and abstract screening, 13 studies were selected for full-text review and 3 prospective cohort studies involving 276 patients with CD were included in the analysis. Pooled analysis demonstrated a significant association between UPF intake and relapse in patients with CD. Patients with higher versus lower UPF intake had increased odds for clinical relapse (OR 2.27, 95% CI 1.01-5.13, p = 0.048; I[2] = 20.95%), although the certainty of the evidence was rated as very low according to the GRADE framework.
CONCLUSION: This study suggests that higher UPF intake is associated with increased odds of clinical relapse in patients with Crohn's disease in remission. However, the certainty of evidence is very low, and additional well-designed prospective studies and randomized trials are required before firm dietary recommendations can be made.},
}
RevDate: 2026-08-31
Nano-bio interfaces as regulators of bacterial electron metabolism: from extracellular electron transfer to community-scale electron networks.
Biotechnology advances pii:S0734-9750(26)00235-1 [Epub ahead of print].
Nanomaterial-bacterium interactions are commonly interpreted through antibacterial mechanisms such as reactive oxygen species generation, photothermal effects, membrane disruption and ion toxicity. However, under nonlethal or sublethal conditions, nano-bio interfaces can also regulate bacterial electron metabolism by reshaping extracellular electron dissipation, interfacial charge transfer, charge-transfer resistance (Rct), redox buffering and biofilm-associated electron networks. Here, we propose a functional framework that views bacterial metabolism as an integrated process of electron generation, interfacial transfer and electron dissipation. Within this framework, nanomaterials are classified by their positions in bacterial electron-flow networks as electron sinks, electron relays or electron buffers. We further distinguish beneficial coupling from electron hijacking by determining whether enhanced interfacial electron transfer is coupled to NADH/NAD[+] balance, ATP production, membrane-potential maintenance and productive carbon-flux redistribution, or instead leads to futile electron loss, oxidative damage and energetic collapse. Extending this view from single cells to extracellular polymeric substances (EPS), electroactive biofilms and direct interspecies electron transfer (DIET), we discuss how nano-bio interfaces re-gate microbial electron flow at the community scale. This Review shifts the focus from how nanomaterials kill bacteria to how they reprogram microbial redox boundaries, providing a conceptual basis for antibacterial interface design, biofilm control, microbial sensing, biomanufacturing and microbiome engineering.
Additional Links: PMID-42674192
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@article {pmid42674192,
year = {2026},
author = {Ge, CA and Huang, EC and Zhang, Y},
title = {Nano-bio interfaces as regulators of bacterial electron metabolism: from extracellular electron transfer to community-scale electron networks.},
journal = {Biotechnology advances},
volume = {},
number = {},
pages = {109029},
doi = {10.1016/j.biotechadv.2026.109029},
pmid = {42674192},
issn = {1873-1899},
abstract = {Nanomaterial-bacterium interactions are commonly interpreted through antibacterial mechanisms such as reactive oxygen species generation, photothermal effects, membrane disruption and ion toxicity. However, under nonlethal or sublethal conditions, nano-bio interfaces can also regulate bacterial electron metabolism by reshaping extracellular electron dissipation, interfacial charge transfer, charge-transfer resistance (Rct), redox buffering and biofilm-associated electron networks. Here, we propose a functional framework that views bacterial metabolism as an integrated process of electron generation, interfacial transfer and electron dissipation. Within this framework, nanomaterials are classified by their positions in bacterial electron-flow networks as electron sinks, electron relays or electron buffers. We further distinguish beneficial coupling from electron hijacking by determining whether enhanced interfacial electron transfer is coupled to NADH/NAD[+] balance, ATP production, membrane-potential maintenance and productive carbon-flux redistribution, or instead leads to futile electron loss, oxidative damage and energetic collapse. Extending this view from single cells to extracellular polymeric substances (EPS), electroactive biofilms and direct interspecies electron transfer (DIET), we discuss how nano-bio interfaces re-gate microbial electron flow at the community scale. This Review shifts the focus from how nanomaterials kill bacteria to how they reprogram microbial redox boundaries, providing a conceptual basis for antibacterial interface design, biofilm control, microbial sensing, biomanufacturing and microbiome engineering.},
}
RevDate: 2026-08-31
A Call for Pan-European Prevention of Chronic Inflammatory Diseases and Allergies.
Additional Links: PMID-42674272
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PubMed:
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@article {pmid42674272,
year = {2026},
author = {Maaren, MSV and van Wijk, RG and Diamant, Z},
title = {A Call for Pan-European Prevention of Chronic Inflammatory Diseases and Allergies.},
journal = {Respiratory medicine},
volume = {},
number = {},
pages = {109136},
doi = {10.1016/j.rmed.2026.109136},
pmid = {42674272},
issn = {1532-3064},
}
RevDate: 2026-08-31
The airway microbiome in asthma.
Chest pii:S0012-3692(26)06527-X [Epub ahead of print].
TOPIC IMPORTANCE: Asthma is a heterogenous airways disease characterized by variable airflow limitation, airway inflammation and bronchial hyperresponsiveness. There is evidence to suggest that the airway microbiome plays an important role in asthma pathophysiology. Most microbiome studies have investigated the bacterial constituents of the microbiome and further studies are needed to investigate the role of the airway virome and mycobiome in asthma.
REVIEW FINDINGS: Airway microbiome dysbiosis is associated with asthma development, disease severity and inflammatory endotypes. However, it remains unclear whether dysbiosis drives inflammation or is a result of inflammation. Haemophilus and Moraxella alongside rhinovirus and respiratory syncytial virus have been shown to be associated with the development of asthma in children. In established asthma, airway microbiome dysbiosis is associated with severity and risk of exacerbation. Distinct airway microbiome profiles are observed for the different inflammatory endotypes. Asthmatic patients with eosinophilic inflammation have higher microbial diversity similar to healthy individuals while neutrophilic inflammation is associated with reduced microbial diversity, higher bacterial load and a pathogen-dominated microbiome profile suggesting an important role for dysbiosis in asthma that is currently refractory to anti-T2 biologic therapy.
SUMMARY: To understand the role of the microbiome in asthma, microbiome data must be integrated with other 'omic approaches' such as proteomics. Recent studies have used a multi-omic approach to investigate the microbiome and host interaction as well as identifying asthma endotypes and potential therapeutic targets. Antibiotics, probiotics, monoclonal antibodies, and diet could theoretically be used to therapeutically target the airway and gut microbiome in asthma.
Additional Links: PMID-42674280
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@article {pmid42674280,
year = {2026},
author = {Richardson, H and Pollock, J and Chan, R and Chalmers, JD},
title = {The airway microbiome in asthma.},
journal = {Chest},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chest.2026.08.032},
pmid = {42674280},
issn = {1931-3543},
abstract = {TOPIC IMPORTANCE: Asthma is a heterogenous airways disease characterized by variable airflow limitation, airway inflammation and bronchial hyperresponsiveness. There is evidence to suggest that the airway microbiome plays an important role in asthma pathophysiology. Most microbiome studies have investigated the bacterial constituents of the microbiome and further studies are needed to investigate the role of the airway virome and mycobiome in asthma.
REVIEW FINDINGS: Airway microbiome dysbiosis is associated with asthma development, disease severity and inflammatory endotypes. However, it remains unclear whether dysbiosis drives inflammation or is a result of inflammation. Haemophilus and Moraxella alongside rhinovirus and respiratory syncytial virus have been shown to be associated with the development of asthma in children. In established asthma, airway microbiome dysbiosis is associated with severity and risk of exacerbation. Distinct airway microbiome profiles are observed for the different inflammatory endotypes. Asthmatic patients with eosinophilic inflammation have higher microbial diversity similar to healthy individuals while neutrophilic inflammation is associated with reduced microbial diversity, higher bacterial load and a pathogen-dominated microbiome profile suggesting an important role for dysbiosis in asthma that is currently refractory to anti-T2 biologic therapy.
SUMMARY: To understand the role of the microbiome in asthma, microbiome data must be integrated with other 'omic approaches' such as proteomics. Recent studies have used a multi-omic approach to investigate the microbiome and host interaction as well as identifying asthma endotypes and potential therapeutic targets. Antibiotics, probiotics, monoclonal antibodies, and diet could theoretically be used to therapeutically target the airway and gut microbiome in asthma.},
}
RevDate: 2026-08-31
Simultaneous GC-MS Determination of Unsubstituted, Hydroxy-, Amino-, and Hydroxy-amino Short-Chain Fatty Acids Together with Amino Acids in Biological and Food Samples Following Derivatization.
Analytical biochemistry pii:S0003-2697(26)00197-1 [Epub ahead of print].
The simultaneous determination of short-chain fatty acids (SCFAs) and amino acids is of increasing interest, as these metabolite classes are important indicators of host metabolism and gut microbiota activity. They also serve as biomarkers for disease diagnosis and indicators of food composition. In this study, a gas chromatography-mass spectrometry method was developed for the simultaneous determination of both substituted (hydroxy-, amino- and hydroxy-amino-) and unsubstituted SCFAs, alongside amino acids, following derivatization and liquid-liquid extraction. Isobutyl chloroformate was employed as the derivatization reagent. The proposed method demonstrated excellent linearity, with coefficients of determination (R[2]) ranging from 0.9840 to 0.9992. Method limits of detection ranged from 0.011 to 7.2 μg/mL, while method limits of quantification ranged from 0.033 to 8.0 μg/mL. Intra-day precision (%RSD) ranged from 1.0% to 6.5% for biological samples and from 1.1% to 4.5% for eggs. Inter-day precision (%RSD) ranged from 1.0% to 5.6% for biological samples and from 2.0% to 6.7% for eggs. Matrix effects ranged from 98% to 108% for biological samples and from 96% to 113% for egg, while recoveries ranged from 90% to 111% and from 95% to 108%, respectively. To the best of our knowledge, this is the first GC-MS method enabling the simultaneous determination of substituted and unsubstituted SCFAs together with amino acids in a single analytical procedure. The proposed approach provides a reliable and versatile platform for metabolomics, microbiome research, clinical investigations, and food analysis, and can readily be extended to a broader range of target metabolites.
Additional Links: PMID-42674308
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@article {pmid42674308,
year = {2026},
author = {Katsari, KM and Stalikas, CD},
title = {Simultaneous GC-MS Determination of Unsubstituted, Hydroxy-, Amino-, and Hydroxy-amino Short-Chain Fatty Acids Together with Amino Acids in Biological and Food Samples Following Derivatization.},
journal = {Analytical biochemistry},
volume = {},
number = {},
pages = {116241},
doi = {10.1016/j.ab.2026.116241},
pmid = {42674308},
issn = {1096-0309},
abstract = {The simultaneous determination of short-chain fatty acids (SCFAs) and amino acids is of increasing interest, as these metabolite classes are important indicators of host metabolism and gut microbiota activity. They also serve as biomarkers for disease diagnosis and indicators of food composition. In this study, a gas chromatography-mass spectrometry method was developed for the simultaneous determination of both substituted (hydroxy-, amino- and hydroxy-amino-) and unsubstituted SCFAs, alongside amino acids, following derivatization and liquid-liquid extraction. Isobutyl chloroformate was employed as the derivatization reagent. The proposed method demonstrated excellent linearity, with coefficients of determination (R[2]) ranging from 0.9840 to 0.9992. Method limits of detection ranged from 0.011 to 7.2 μg/mL, while method limits of quantification ranged from 0.033 to 8.0 μg/mL. Intra-day precision (%RSD) ranged from 1.0% to 6.5% for biological samples and from 1.1% to 4.5% for eggs. Inter-day precision (%RSD) ranged from 1.0% to 5.6% for biological samples and from 2.0% to 6.7% for eggs. Matrix effects ranged from 98% to 108% for biological samples and from 96% to 113% for egg, while recoveries ranged from 90% to 111% and from 95% to 108%, respectively. To the best of our knowledge, this is the first GC-MS method enabling the simultaneous determination of substituted and unsubstituted SCFAs together with amino acids in a single analytical procedure. The proposed approach provides a reliable and versatile platform for metabolomics, microbiome research, clinical investigations, and food analysis, and can readily be extended to a broader range of target metabolites.},
}
RevDate: 2026-08-31
Effect of sucrose-free brazzein-sweetened ice cream on continuously monitored glycemic response in patients with metabolic dysfunction-associated steatotic liver disease: a randomized controlled double-blind crossover trial.
Clinical nutrition ESPEN pii:S2405-4577(26)02163-7 [Epub ahead of print].
BACKGROUND & AIMS: Reducing sugar intake is one of the key targets for improving metabolic health in metabolic dysfunction-associated steatotic liver disease (MASLD), and natural sugar substitutes remain insufficiently studied. Brazzein, a natural sweet protein 500-2000 times sweeter than sucrose, may allow replacement of sucrose while preserving sweetness, but clinical data are lacking. We aimed to evaluate postprandial glycemic responses to brazzein-sweetened ice cream, with and without inulin, compared with sucrose-sweetened ice cream in adults with MASLD, using continuous glucose monitoring (CGM).
METHODS: In this double-blind, randomized, 3-period crossover trial, 101 adults with MASLD (mean age: 54.6 y; 76% female; 44% with type 2 diabetes) consumed 100 g of ice cream sweetened with sucrose (14 g), brazzein (0.014%), or brazzein plus inulin (0.014% + 4 g) on separate days. Factory-calibrated CGM sensors were used. Principal analytic outcomes were glucose over 150 min and incremental area under the curve (iAUC). Linear mixed-effects models estimated treatment effects with adjustment for baseline glucose, period, sequence, and diabetes status. Complementary analyses evaluated whether between-formulation differences were explained by total carbohydrate content alone.
RESULTS: Compared with sucrose-sweetened, both brazzein-containing formulations produced smaller postprandial glucose excursions from 30 to 135 min (treatment × time interaction, P < 0.001). Model-adjusted iAUC was 66.3 mmol/L × min (95% CI: 54.5, 78.0) for sucrose, 31.7 (19.9, 43.6) for brazzein, and 34.3 (22.5, 46.1) for brazzein plus inulin formulations. Relative to sucrose-sweetened, iAUC was 52% lower with brazzein and 48% lower with brazzein plus inulin formulations (both P < 0.001), whereas brazzein and brazzein plus inulin formulations did not differ significantly. Complementary analyses showed that the between-formulation differences were not explained by total carbohydrate content alone. Exploratory analyses showed that formulation-related glucose trajectories differed according to diabetes status (P < 0.001). Within-stratum analyses showed lower iAUC for both brazzein-sweetened products relative to the sucrose control in participants with and without diabetes. No period, sequence, or carryover effects were observed.
CONCLUSIONS: In adults with MASLD, the tested sucrose-free brazzein-containing ice cream formulations produced substantially smaller acute CGM-derived postprandial glucose excursions and lower iAUC over 150 min than sucrose-sweetened ice cream. The similar responses observed with brazzein alone and brazzein plus inulin suggest that adding 4 g inulin did not abolish the acute glycemic advantage of the brazzein-containing formulation. Longer-term studies are needed to determine whether repeated substitution of sucrose-containing desserts with brazzein-sweetened alternatives translates into sustained metabolic, hepatic, microbiome, or behavioral benefits.
TRIAL REGISTRATION: ClinicalTrials.gov NCT06724913.
Additional Links: PMID-42674358
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PubMed:
Citation:
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@article {pmid42674358,
year = {2026},
author = {Isakov, VA and Pilipenko, VI and Goncharov, AA and Sasunova, A},
title = {Effect of sucrose-free brazzein-sweetened ice cream on continuously monitored glycemic response in patients with metabolic dysfunction-associated steatotic liver disease: a randomized controlled double-blind crossover trial.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105066},
doi = {10.1016/j.clnesp.2026.105066},
pmid = {42674358},
issn = {2405-4577},
abstract = {BACKGROUND & AIMS: Reducing sugar intake is one of the key targets for improving metabolic health in metabolic dysfunction-associated steatotic liver disease (MASLD), and natural sugar substitutes remain insufficiently studied. Brazzein, a natural sweet protein 500-2000 times sweeter than sucrose, may allow replacement of sucrose while preserving sweetness, but clinical data are lacking. We aimed to evaluate postprandial glycemic responses to brazzein-sweetened ice cream, with and without inulin, compared with sucrose-sweetened ice cream in adults with MASLD, using continuous glucose monitoring (CGM).
METHODS: In this double-blind, randomized, 3-period crossover trial, 101 adults with MASLD (mean age: 54.6 y; 76% female; 44% with type 2 diabetes) consumed 100 g of ice cream sweetened with sucrose (14 g), brazzein (0.014%), or brazzein plus inulin (0.014% + 4 g) on separate days. Factory-calibrated CGM sensors were used. Principal analytic outcomes were glucose over 150 min and incremental area under the curve (iAUC). Linear mixed-effects models estimated treatment effects with adjustment for baseline glucose, period, sequence, and diabetes status. Complementary analyses evaluated whether between-formulation differences were explained by total carbohydrate content alone.
RESULTS: Compared with sucrose-sweetened, both brazzein-containing formulations produced smaller postprandial glucose excursions from 30 to 135 min (treatment × time interaction, P < 0.001). Model-adjusted iAUC was 66.3 mmol/L × min (95% CI: 54.5, 78.0) for sucrose, 31.7 (19.9, 43.6) for brazzein, and 34.3 (22.5, 46.1) for brazzein plus inulin formulations. Relative to sucrose-sweetened, iAUC was 52% lower with brazzein and 48% lower with brazzein plus inulin formulations (both P < 0.001), whereas brazzein and brazzein plus inulin formulations did not differ significantly. Complementary analyses showed that the between-formulation differences were not explained by total carbohydrate content alone. Exploratory analyses showed that formulation-related glucose trajectories differed according to diabetes status (P < 0.001). Within-stratum analyses showed lower iAUC for both brazzein-sweetened products relative to the sucrose control in participants with and without diabetes. No period, sequence, or carryover effects were observed.
CONCLUSIONS: In adults with MASLD, the tested sucrose-free brazzein-containing ice cream formulations produced substantially smaller acute CGM-derived postprandial glucose excursions and lower iAUC over 150 min than sucrose-sweetened ice cream. The similar responses observed with brazzein alone and brazzein plus inulin suggest that adding 4 g inulin did not abolish the acute glycemic advantage of the brazzein-containing formulation. Longer-term studies are needed to determine whether repeated substitution of sucrose-containing desserts with brazzein-sweetened alternatives translates into sustained metabolic, hepatic, microbiome, or behavioral benefits.
TRIAL REGISTRATION: ClinicalTrials.gov NCT06724913.},
}
RevDate: 2026-08-31
Saccharin Revisited: Chemistry, Metabolism, Toxicology and Human Health Risk Assessment in the Era of Evidence-Based Food Safety.
Journal of applied toxicology : JAT [Epub ahead of print].
Saccharin is one of the oldest and most extensively used nonnutritive sweeteners, valued for its intense sweetness, chemical stability and negligible caloric contribution. Since its discovery in 1879, it has been widely incorporated into foods, beverages, pharmaceuticals and personal care products, while its safety has remained the subject of considerable scientific and regulatory debate. Early experimental studies linking saccharin to bladder tumour formation in rodents raised concerns regarding its carcinogenic potential; however, subsequent mechanistic investigations, epidemiological evidence and comprehensive risk assessments have demonstrated that these findings are species-specific and not directly applicable to humans. This review provides a comprehensive and critical synthesis of current knowledge on saccharin, encompassing its chemical characteristics, physicochemical properties, industrial and pharmaceutical applications, absorption, metabolism, excretion and toxicological profile. Particular emphasis is placed on evaluating evidence related to carcinogenicity, genotoxicity, metabolic effects, oxidative stress, gut microbiota interactions and other emerging health concerns through the integration of experimental, clinical and population-based studies. In addition, the review examines the scientific basis of international regulatory decisions, discusses the challenges of translating animal toxicology findings into human health risk assessment and identifies persistent knowledge gaps requiring further investigation. Current evidence consistently supports the safety of saccharin when consumed within established acceptable daily intake limits established by international regulatory agencies. Nevertheless, well-designed long-term human studies and mechanistic investigations remain necessary to better define its potential effects on metabolic health, the gut microbiome and susceptible populations. By integrating historical evidence with contemporary advances in toxicology and regulatory science, this review provides an updated framework for understanding the safety, biological effects and public health implications of saccharin consumption.
Additional Links: PMID-42674673
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@article {pmid42674673,
year = {2026},
author = {Qadir, AM and Ahmed, AMA and Zorab, MM and Omer, RA},
title = {Saccharin Revisited: Chemistry, Metabolism, Toxicology and Human Health Risk Assessment in the Era of Evidence-Based Food Safety.},
journal = {Journal of applied toxicology : JAT},
volume = {},
number = {},
pages = {},
doi = {10.1002/jat.70423},
pmid = {42674673},
issn = {1099-1263},
abstract = {Saccharin is one of the oldest and most extensively used nonnutritive sweeteners, valued for its intense sweetness, chemical stability and negligible caloric contribution. Since its discovery in 1879, it has been widely incorporated into foods, beverages, pharmaceuticals and personal care products, while its safety has remained the subject of considerable scientific and regulatory debate. Early experimental studies linking saccharin to bladder tumour formation in rodents raised concerns regarding its carcinogenic potential; however, subsequent mechanistic investigations, epidemiological evidence and comprehensive risk assessments have demonstrated that these findings are species-specific and not directly applicable to humans. This review provides a comprehensive and critical synthesis of current knowledge on saccharin, encompassing its chemical characteristics, physicochemical properties, industrial and pharmaceutical applications, absorption, metabolism, excretion and toxicological profile. Particular emphasis is placed on evaluating evidence related to carcinogenicity, genotoxicity, metabolic effects, oxidative stress, gut microbiota interactions and other emerging health concerns through the integration of experimental, clinical and population-based studies. In addition, the review examines the scientific basis of international regulatory decisions, discusses the challenges of translating animal toxicology findings into human health risk assessment and identifies persistent knowledge gaps requiring further investigation. Current evidence consistently supports the safety of saccharin when consumed within established acceptable daily intake limits established by international regulatory agencies. Nevertheless, well-designed long-term human studies and mechanistic investigations remain necessary to better define its potential effects on metabolic health, the gut microbiome and susceptible populations. By integrating historical evidence with contemporary advances in toxicology and regulatory science, this review provides an updated framework for understanding the safety, biological effects and public health implications of saccharin consumption.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-31
Intratumoral Mycobacterium abscessus promotes cytidine deaminase mutagenesis in non-small cell lung cancer.
Signal transduction and targeted therapy, 11(1):.
The intratumoral microbiota is increasingly recognized as an active component of the tumor microenvironment, yet whether it directly drives tumor mutagenesis remains unclear. Here, integrated multi-omics analysis of human non-small cell lung cancer (NSCLC) identifies Mycobacterium abscessus as a microbial determinant of APOBEC3A-associated mutagenesis. Mechanistically, the bacterial effector nucleoside diphosphate kinase (NDK) directly targets the host transcription factor IRF3 and installs a non-canonical 1-phosphohistidine modification at H263, thereby amplifying type I interferon signaling and sustaining APOBEC3A expression. This inter-kingdom phosphotransfer event links intratumoral microbial colonization to an endogenous mutational process that promotes genomic diversification. Genetic inactivation of NDK, or pharmacologic elimination using an engineered NDK-PROTAC, suppresses APOBEC3A activation and attenuates microbe driven mutagenesis. Together, these findings establish a direct microbial effector mechanism that promotes APOBEC3A-associated mutagenesis and provide a therapeutic framework to intercept microbiome driven mutagenesis in NSCLC.
Additional Links: PMID-42675040
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@article {pmid42675040,
year = {2026},
author = {Li, X and Li, MT and Ou, KP and Gao, PQ and Xiao, AH and Yang, J and Li, JN and Deng, WY and Bie, MJ and Huang, AL and Shi, XF and Long, QX},
title = {Intratumoral Mycobacterium abscessus promotes cytidine deaminase mutagenesis in non-small cell lung cancer.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {42675040},
issn = {2059-3635},
mesh = {Humans ; *Carcinoma, Non-Small-Cell Lung/genetics/microbiology/pathology ; *Cytidine Deaminase/genetics ; *Lung Neoplasms/genetics/microbiology/pathology ; *Mutagenesis/genetics ; *Mycobacterium abscessus/genetics/pathogenicity ; },
abstract = {The intratumoral microbiota is increasingly recognized as an active component of the tumor microenvironment, yet whether it directly drives tumor mutagenesis remains unclear. Here, integrated multi-omics analysis of human non-small cell lung cancer (NSCLC) identifies Mycobacterium abscessus as a microbial determinant of APOBEC3A-associated mutagenesis. Mechanistically, the bacterial effector nucleoside diphosphate kinase (NDK) directly targets the host transcription factor IRF3 and installs a non-canonical 1-phosphohistidine modification at H263, thereby amplifying type I interferon signaling and sustaining APOBEC3A expression. This inter-kingdom phosphotransfer event links intratumoral microbial colonization to an endogenous mutational process that promotes genomic diversification. Genetic inactivation of NDK, or pharmacologic elimination using an engineered NDK-PROTAC, suppresses APOBEC3A activation and attenuates microbe driven mutagenesis. Together, these findings establish a direct microbial effector mechanism that promotes APOBEC3A-associated mutagenesis and provide a therapeutic framework to intercept microbiome driven mutagenesis in NSCLC.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Carcinoma, Non-Small-Cell Lung/genetics/microbiology/pathology
*Cytidine Deaminase/genetics
*Lung Neoplasms/genetics/microbiology/pathology
*Mutagenesis/genetics
*Mycobacterium abscessus/genetics/pathogenicity
RevDate: 2026-08-31
CmpDate: 2026-09-01
Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.
Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 34(2):.
BACKGROUND: Trehalose is a promising therapeutic candidate for Alzheimer's disease (AD) that is known to induce autophagy and facilitate misfolded proteins clearance such as amyloid-β and hyperphosphorylated tau. Despite there is emerging evidence that trehalose has a wider range of molecular mechanisms and thus has a greater neuroprotective profile.
OBJECTIVE: To summarize the emerging molecular mechanisms underlying the neuroprotective effects of trehalose beyond classical autophagy and discuss its therapeutic potential in AD.
METHODS: Published evidence from preclinical studies including in-vitro and in-vivo models, along with hypothetical and emerging findings from early clinical investigations was reviewed to evaluate the molecular mechanisms, therapeutic effects, and translational challenges associated with trehalose in AD.
RESULTS: In addition to classical autophagy signalling, recent studies have demonstrated that autophagy can also regulate the stability of neuronal membrane microdomains, prevent lipid bilayers disruption by amyloid proteins, and regulate stress granules dynamics that affect the function of RNA-binding proteins. Other discoveries indicate that interactions with nutrient-sensing pathways and glucose transporter systems that simulate metabolic stress, which may activate protective mechanisms separate from the inhibition of mTOR. Trehalose could also involve in lysosomal-autophagosome fusion and modulate the microglia and astrocytes activation, suggesting an important immunometabolic function. Trehalose often connects to the gut-brain axis and show their effect in gut microbiota composition, microbial metabolite signalling and gut barrier function. These effects can influence systemic inflammation, availability of short-chain fatty acids, bile acid profiles and vagus-mediated gut-to-brain communication, all of which can influence neuroinflammation networks in AD.
CONCLUSION: Although promising results have been reported, primarily from preclinical studies, with early human investigations now beginning to emerge, opportunities remain to address, such as poor oral bioavailability, penetration into the brain and long-term safety in elderly patients. Mechanistic dissection in multi-omics approaches, microbiome-stratified models and early-phase clinical testing are the areas that need to be targeted in future research. A broader understanding of the mechanisms of action of trehalose provides a good chance to reimagine its therapeutic implications and develop novel approaches to AD.
Additional Links: PMID-42675343
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Citation:
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@article {pmid42675343,
year = {2026},
author = {Gunasekaran, SK and K, HKC and Gobinath, M and Roychowdhury, P and N, MS},
title = {Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.},
journal = {Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences},
volume = {34},
number = {2},
pages = {},
pmid = {42675343},
issn = {2008-2231},
mesh = {Humans ; *Trehalose/pharmacology/therapeutic use ; *Alzheimer Disease/drug therapy/metabolism ; Animals ; *Brain/metabolism/drug effects ; Signal Transduction/drug effects ; *Autophagy/drug effects ; *Neuroprotective Agents/pharmacology/therapeutic use ; Gastrointestinal Microbiome/drug effects ; },
abstract = {BACKGROUND: Trehalose is a promising therapeutic candidate for Alzheimer's disease (AD) that is known to induce autophagy and facilitate misfolded proteins clearance such as amyloid-β and hyperphosphorylated tau. Despite there is emerging evidence that trehalose has a wider range of molecular mechanisms and thus has a greater neuroprotective profile.
OBJECTIVE: To summarize the emerging molecular mechanisms underlying the neuroprotective effects of trehalose beyond classical autophagy and discuss its therapeutic potential in AD.
METHODS: Published evidence from preclinical studies including in-vitro and in-vivo models, along with hypothetical and emerging findings from early clinical investigations was reviewed to evaluate the molecular mechanisms, therapeutic effects, and translational challenges associated with trehalose in AD.
RESULTS: In addition to classical autophagy signalling, recent studies have demonstrated that autophagy can also regulate the stability of neuronal membrane microdomains, prevent lipid bilayers disruption by amyloid proteins, and regulate stress granules dynamics that affect the function of RNA-binding proteins. Other discoveries indicate that interactions with nutrient-sensing pathways and glucose transporter systems that simulate metabolic stress, which may activate protective mechanisms separate from the inhibition of mTOR. Trehalose could also involve in lysosomal-autophagosome fusion and modulate the microglia and astrocytes activation, suggesting an important immunometabolic function. Trehalose often connects to the gut-brain axis and show their effect in gut microbiota composition, microbial metabolite signalling and gut barrier function. These effects can influence systemic inflammation, availability of short-chain fatty acids, bile acid profiles and vagus-mediated gut-to-brain communication, all of which can influence neuroinflammation networks in AD.
CONCLUSION: Although promising results have been reported, primarily from preclinical studies, with early human investigations now beginning to emerge, opportunities remain to address, such as poor oral bioavailability, penetration into the brain and long-term safety in elderly patients. Mechanistic dissection in multi-omics approaches, microbiome-stratified models and early-phase clinical testing are the areas that need to be targeted in future research. A broader understanding of the mechanisms of action of trehalose provides a good chance to reimagine its therapeutic implications and develop novel approaches to AD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Trehalose/pharmacology/therapeutic use
*Alzheimer Disease/drug therapy/metabolism
Animals
*Brain/metabolism/drug effects
Signal Transduction/drug effects
*Autophagy/drug effects
*Neuroprotective Agents/pharmacology/therapeutic use
Gastrointestinal Microbiome/drug effects
RevDate: 2026-09-01
CmpDate: 2026-09-01
Rumen DNA virome plasticity and viral metabolic potential are associated with seasonal adaptation in grazing yak and cattle on the Qinghai-Tibet Plateau.
Journal of animal science and biotechnology, 17(1):.
BACKGROUND: As a diverse and abundant component of the rumen ecosystem, viruses interact with other microorganisms and are thought to influence microbial metabolism and host productivity. However, how the rumen virome responds to seasonal fluctuations in extreme environments remains poorly understood. Here, metagenomic analyses were used to investigate temporal dynamics of viral diversity, functional potential, and virus-host associations in the rumen virome of yak and cattle on the Qinghai-Tibet Plateau across warm and cold seasons.
RESULTS: Rumen viral communities exhibited pronounced seasonal variation in both yaks and cattle, with higher alpha diversity observed during the cold season than in the warm season. Across seasons, the yak rumen virome showed greater alpha diversity and community stability than that of cattle. In total, 27,353 temperate and 31,976 virulent viral operational taxonomic units (vOTUs) were identified, predominantly belonging to the class Caudoviricetes. These viruses were linked to microbial hosts spanning 24 bacterial and 8 archaeal phyla, with Bacteroidota and Bacillota representing the dominant lineages. Virus-host associations were more numerous in the cold season and showed distinct host-specific patterns between yaks and cattle. Cold-season virome exhibited reduced diversity of anti-defense genes and enrichment of auxiliary metabolic genes (AMGs) associated with fatty acid metabolism and hemicellulose degradation. Notably, greater divergence between yaks and cattle was observed during the cold season: the yak rumen virome was enriched in pathways related to amino acid, lipid, and energy metabolism, as well as cellulose-degrading CAZyme families, whereas the cattle rumen virome showed enrichment in general carbohydrate metabolism and replication and repair processes.
CONCLUSION: Seasonal plasticity of rumen DNA virome and pronounced interspecific divergence between yaks and cattle provide insight into their distinct microbial processes in the harsh environment of the Qinghai-Tibet Plateau. These findings suggest that the rumen DNA virome exhibits complex ecological and functional responses to seasonal variation and may be associated with host-microbiome interactions and nutrient utilization under environmental stress. This study highlights the ecological relevance of rumen viral genomes in understanding virus-microbiome interactions, microbial adaptation, and nutrient utilization in high-altitude ruminants.
Additional Links: PMID-42675508
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Citation:
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@article {pmid42675508,
year = {2026},
author = {Guo, W and Yu, Y and Wang, W and Yu, J and Zhou, M and Long, R},
title = {Rumen DNA virome plasticity and viral metabolic potential are associated with seasonal adaptation in grazing yak and cattle on the Qinghai-Tibet Plateau.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42675508},
issn = {1674-9782},
support = {32402705//National Natural Science Foundation of China/ ; XZ202502ZY0058//Science and Technology Projects of Xizang Autonomous Region, China/ ; },
abstract = {BACKGROUND: As a diverse and abundant component of the rumen ecosystem, viruses interact with other microorganisms and are thought to influence microbial metabolism and host productivity. However, how the rumen virome responds to seasonal fluctuations in extreme environments remains poorly understood. Here, metagenomic analyses were used to investigate temporal dynamics of viral diversity, functional potential, and virus-host associations in the rumen virome of yak and cattle on the Qinghai-Tibet Plateau across warm and cold seasons.
RESULTS: Rumen viral communities exhibited pronounced seasonal variation in both yaks and cattle, with higher alpha diversity observed during the cold season than in the warm season. Across seasons, the yak rumen virome showed greater alpha diversity and community stability than that of cattle. In total, 27,353 temperate and 31,976 virulent viral operational taxonomic units (vOTUs) were identified, predominantly belonging to the class Caudoviricetes. These viruses were linked to microbial hosts spanning 24 bacterial and 8 archaeal phyla, with Bacteroidota and Bacillota representing the dominant lineages. Virus-host associations were more numerous in the cold season and showed distinct host-specific patterns between yaks and cattle. Cold-season virome exhibited reduced diversity of anti-defense genes and enrichment of auxiliary metabolic genes (AMGs) associated with fatty acid metabolism and hemicellulose degradation. Notably, greater divergence between yaks and cattle was observed during the cold season: the yak rumen virome was enriched in pathways related to amino acid, lipid, and energy metabolism, as well as cellulose-degrading CAZyme families, whereas the cattle rumen virome showed enrichment in general carbohydrate metabolism and replication and repair processes.
CONCLUSION: Seasonal plasticity of rumen DNA virome and pronounced interspecific divergence between yaks and cattle provide insight into their distinct microbial processes in the harsh environment of the Qinghai-Tibet Plateau. These findings suggest that the rumen DNA virome exhibits complex ecological and functional responses to seasonal variation and may be associated with host-microbiome interactions and nutrient utilization under environmental stress. This study highlights the ecological relevance of rumen viral genomes in understanding virus-microbiome interactions, microbial adaptation, and nutrient utilization in high-altitude ruminants.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Causal relationships between oral-gut microbiome and bone neoplasm-related phenotypes: Insights from bidirectional Mendelian randomization.
Medicine, 105(35):e50422.
The human oral and gut microbiota are the 4 largest microbial communities in the body and play crucial roles in maintaining homeostasis and influencing disease. Observational studies have suggested links between these microbiota and bone neoplasm-related phenotypes, but establishing causality has been challenging due to confounding factors and reverse causality. We conducted a bidirectional, 2-sample Mendelian randomization (MR) study to investigate evidence consistent with a potential causal association between the saliva and gut microbiota and various bone neoplasm-related phenotypes. Genetic instruments for saliva and gut microbiota were sourced from large genome-wide association studies. Inverse variance weighted was the primary MR method, supplemented by 4 other MR techniques. Sensitivity analyses, including MR-Egger regression, were performed to assess pleiotropy and heterogeneity. In the forward MR analysis, Veillonella parvula from the saliva microbiota was associated with a decreased risk of bone and connective tissue neoplasms (β: -0.236, 95% CI: [-0.275, -0.197], P = 8.20E-33). MR analyses identified genetically predicted associations between several microbial taxa and bone neoplasm-related phenotypes. Reverse MR analyses showed that genetic liability to bone neoplasm-related phenotypes was associated with variation in the composition of the oral (e.g., Order Bacteroidales, Rothia mucilaginosa) and gut microbiota (e.g., Class Methanobacteria, Genus Eubacterium oxidoreducens group). Sensitivity analyses confirmed the robustness of these findings, as no statistical evidence of substantial heterogeneity or directional horizontal pleiotropy was detected. This study provides genetic evidence supporting a bidirectional causal relationship between specific saliva and gut microbiota and bone neoplasm-related phenotypes. Our findings identify several microbial taxa as potential candidates for future biomarker development and therapeutic investigation in bone neoplasm-related phenotypes. However, these genetically informed associations require further mechanistic, experimental, and prospective clinical validation before clinical application.
Additional Links: PMID-42675685
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@article {pmid42675685,
year = {2026},
author = {Zou, Q and Sun, F and Xu, W and Peng, D and Jiang, Z and Liao, H},
title = {Causal relationships between oral-gut microbiome and bone neoplasm-related phenotypes: Insights from bidirectional Mendelian randomization.},
journal = {Medicine},
volume = {105},
number = {35},
pages = {e50422},
doi = {10.1097/MD.0000000000050422},
pmid = {42675685},
issn = {1536-5964},
mesh = {Humans ; *Mendelian Randomization Analysis ; Phenotype ; *Gastrointestinal Microbiome/genetics ; *Saliva/microbiology ; *Bone Neoplasms/genetics/microbiology ; Genome-Wide Association Study ; *Mouth/microbiology ; Microbiota ; },
abstract = {The human oral and gut microbiota are the 4 largest microbial communities in the body and play crucial roles in maintaining homeostasis and influencing disease. Observational studies have suggested links between these microbiota and bone neoplasm-related phenotypes, but establishing causality has been challenging due to confounding factors and reverse causality. We conducted a bidirectional, 2-sample Mendelian randomization (MR) study to investigate evidence consistent with a potential causal association between the saliva and gut microbiota and various bone neoplasm-related phenotypes. Genetic instruments for saliva and gut microbiota were sourced from large genome-wide association studies. Inverse variance weighted was the primary MR method, supplemented by 4 other MR techniques. Sensitivity analyses, including MR-Egger regression, were performed to assess pleiotropy and heterogeneity. In the forward MR analysis, Veillonella parvula from the saliva microbiota was associated with a decreased risk of bone and connective tissue neoplasms (β: -0.236, 95% CI: [-0.275, -0.197], P = 8.20E-33). MR analyses identified genetically predicted associations between several microbial taxa and bone neoplasm-related phenotypes. Reverse MR analyses showed that genetic liability to bone neoplasm-related phenotypes was associated with variation in the composition of the oral (e.g., Order Bacteroidales, Rothia mucilaginosa) and gut microbiota (e.g., Class Methanobacteria, Genus Eubacterium oxidoreducens group). Sensitivity analyses confirmed the robustness of these findings, as no statistical evidence of substantial heterogeneity or directional horizontal pleiotropy was detected. This study provides genetic evidence supporting a bidirectional causal relationship between specific saliva and gut microbiota and bone neoplasm-related phenotypes. Our findings identify several microbial taxa as potential candidates for future biomarker development and therapeutic investigation in bone neoplasm-related phenotypes. However, these genetically informed associations require further mechanistic, experimental, and prospective clinical validation before clinical application.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Mendelian Randomization Analysis
Phenotype
*Gastrointestinal Microbiome/genetics
*Saliva/microbiology
*Bone Neoplasms/genetics/microbiology
Genome-Wide Association Study
*Mouth/microbiology
Microbiota
RevDate: 2026-09-01
CmpDate: 2026-09-01
Characterization of gut microbiota in Vietnamese children under 5 years of age with acute and persistent diarrhea: A cross-sectional study.
Medicine, 105(35):e50433.
Gut microbiota alterations have been increasingly associated with diarrheal diseases, a leading cause of morbidity and mortality in children under 5 years of age. However, explorations examining microbiota profiles across different diarrhea durations remain limited. Our study investigated microbiota alterations in Vietnamese children with diarrhea. We recruited 97 children under 5 years of age and divided them into 3 groups: healthy children (HC; n = 48), children with acute diarrhea (AD; n = 32), and children with persistent diarrhea (PD; n = 17). We collected and analyzed stool samples using 16S rRNA gene sequencing targeting the V3 to V4 region. Taxonomic classification was performed. Alpha diversity and beta diversity metrics were estimated. LEfSe analysis identified differentially abundant bacterial taxa across groups. Gut microbiota composition and diversity differed significantly among HC, AD, and PD. Alpha diversity tended to decline from HC to AD and was lowest in PD, with significant reductions observed for the Shannon index and Faith PD. Compared with HC, AD showed enrichment of Actinobacteriota and potentially pathogenic genera, including Streptococcus and Escherichia-Shigella, together with depletion of beneficial commensal taxa. PD exhibited more pronounced dysbiosis, including expansion of Proteobacteria, depletion of Bacteroidota-associated commensals, and a significantly reduced Bacteroidota-to-Firmicutes ratio. Children with AD and PD exhibited distinct gut microbiota alterations, with more pronounced microbial dysbiosis observed in PD. These findings improve our understanding of gut microbiota alterations associated with pediatric diarrhea and support future longitudinal studies incorporating comprehensive pathogen identification to clarify temporal relationships, evaluate microbiome-based biomarkers, and explore microbiota-targeted interventions.
Additional Links: PMID-42675693
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@article {pmid42675693,
year = {2026},
author = {Chung, NH and Nguyen, TA and Pham, VH and Nguyen, LT and Phan, NT and Vo, CQ and Nhu, NT},
title = {Characterization of gut microbiota in Vietnamese children under 5 years of age with acute and persistent diarrhea: A cross-sectional study.},
journal = {Medicine},
volume = {105},
number = {35},
pages = {e50433},
doi = {10.1097/MD.0000000000050433},
pmid = {42675693},
issn = {1536-5964},
mesh = {Humans ; Vietnam/epidemiology ; *Diarrhea/microbiology/epidemiology ; Child, Preschool ; *Gastrointestinal Microbiome/genetics ; Female ; Infant ; Male ; Cross-Sectional Studies ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Dysbiosis/microbiology ; Acute Disease ; Bacteria/classification/genetics ; },
abstract = {Gut microbiota alterations have been increasingly associated with diarrheal diseases, a leading cause of morbidity and mortality in children under 5 years of age. However, explorations examining microbiota profiles across different diarrhea durations remain limited. Our study investigated microbiota alterations in Vietnamese children with diarrhea. We recruited 97 children under 5 years of age and divided them into 3 groups: healthy children (HC; n = 48), children with acute diarrhea (AD; n = 32), and children with persistent diarrhea (PD; n = 17). We collected and analyzed stool samples using 16S rRNA gene sequencing targeting the V3 to V4 region. Taxonomic classification was performed. Alpha diversity and beta diversity metrics were estimated. LEfSe analysis identified differentially abundant bacterial taxa across groups. Gut microbiota composition and diversity differed significantly among HC, AD, and PD. Alpha diversity tended to decline from HC to AD and was lowest in PD, with significant reductions observed for the Shannon index and Faith PD. Compared with HC, AD showed enrichment of Actinobacteriota and potentially pathogenic genera, including Streptococcus and Escherichia-Shigella, together with depletion of beneficial commensal taxa. PD exhibited more pronounced dysbiosis, including expansion of Proteobacteria, depletion of Bacteroidota-associated commensals, and a significantly reduced Bacteroidota-to-Firmicutes ratio. Children with AD and PD exhibited distinct gut microbiota alterations, with more pronounced microbial dysbiosis observed in PD. These findings improve our understanding of gut microbiota alterations associated with pediatric diarrhea and support future longitudinal studies incorporating comprehensive pathogen identification to clarify temporal relationships, evaluate microbiome-based biomarkers, and explore microbiota-targeted interventions.},
}
MeSH Terms:
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Humans
Vietnam/epidemiology
*Diarrhea/microbiology/epidemiology
Child, Preschool
*Gastrointestinal Microbiome/genetics
Female
Infant
Male
Cross-Sectional Studies
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Dysbiosis/microbiology
Acute Disease
Bacteria/classification/genetics
RevDate: 2026-09-01
CmpDate: 2026-09-01
Healthy subjects gut microbiome modulation by Bacillus coagulans BCP92: A randomized, double-blind, placebo-controlled clinical trial.
Medicine, 105(35):e50435.
BACKGROUND: Probiotics are recognized for their ability to restore balance in the gut microbiome during dysbiosis. However, their effects on the gut microbiota of healthy individuals have rarely been investigated. This study aimed to evaluate the safety and efficacy of Bacillus coagulans (Heyndrickxia coagulans) BCP92 and its influence on microbiota composition in healthy subjects.
METHODS: In the present investigation, healthy participants (n = 48) were allocated into 2 groups and administered either Bacillus coagulans BCP92 capsules (1 billion CFU/capsule) or a placebo containing maltodextrin for 42 days. Microbiome composition and short-chain fatty acid analyses were subsequently conducted.
RESULTS: Analysis of metagenomes showed no major alterations in gut microbiome composition among participants who received B. coagulans BCP92 supplementation. However, subtle beneficial changes were observed in the treatment group, suggesting that probiotic administration may increase advantageous phyla, classes, orders, families, and some genera, while decreasing potentially harmful groups. A slight increase in short-chain fatty acids (SCFA) was also observed in the fecal samples.
CONCLUSIONS: This study implies that extended supplementation with the probiotic B. coagulans BCP92 may lead to substantial improvements in gut microbiome composition and SCFA levels.
Additional Links: PMID-42675742
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PubMed:
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@article {pmid42675742,
year = {2026},
author = {Shaikh, SS and Malek, F},
title = {Healthy subjects gut microbiome modulation by Bacillus coagulans BCP92: A randomized, double-blind, placebo-controlled clinical trial.},
journal = {Medicine},
volume = {105},
number = {35},
pages = {e50435},
doi = {10.1097/MD.0000000000050435},
pmid = {42675742},
issn = {1536-5964},
mesh = {Humans ; *Probiotics/administration & dosage ; *Bacillus coagulans/physiology ; Double-Blind Method ; *Gastrointestinal Microbiome/drug effects ; Feces/microbiology/chemistry ; Male ; Adult ; Fatty Acids, Volatile/analysis/metabolism ; Female ; Healthy Volunteers ; Young Adult ; Metagenome ; },
abstract = {BACKGROUND: Probiotics are recognized for their ability to restore balance in the gut microbiome during dysbiosis. However, their effects on the gut microbiota of healthy individuals have rarely been investigated. This study aimed to evaluate the safety and efficacy of Bacillus coagulans (Heyndrickxia coagulans) BCP92 and its influence on microbiota composition in healthy subjects.
METHODS: In the present investigation, healthy participants (n = 48) were allocated into 2 groups and administered either Bacillus coagulans BCP92 capsules (1 billion CFU/capsule) or a placebo containing maltodextrin for 42 days. Microbiome composition and short-chain fatty acid analyses were subsequently conducted.
RESULTS: Analysis of metagenomes showed no major alterations in gut microbiome composition among participants who received B. coagulans BCP92 supplementation. However, subtle beneficial changes were observed in the treatment group, suggesting that probiotic administration may increase advantageous phyla, classes, orders, families, and some genera, while decreasing potentially harmful groups. A slight increase in short-chain fatty acids (SCFA) was also observed in the fecal samples.
CONCLUSIONS: This study implies that extended supplementation with the probiotic B. coagulans BCP92 may lead to substantial improvements in gut microbiome composition and SCFA levels.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/administration & dosage
*Bacillus coagulans/physiology
Double-Blind Method
*Gastrointestinal Microbiome/drug effects
Feces/microbiology/chemistry
Male
Adult
Fatty Acids, Volatile/analysis/metabolism
Female
Healthy Volunteers
Young Adult
Metagenome
RevDate: 2026-09-01
Gut microbiome reorganization as a signal of physiological acclimation in escaped hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀).
Journal of fish biology [Epub ahead of print].
The introduction of aquaculture-derived hybrid fishes into natural marine ecosystems raises critical questions regarding their physiological capacity to acclimate to novel environments. The hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀), a widely farmed teleost in southern China, has increasingly been reported in coastal habitats following escape events. However, the gut microbiome-associated mechanisms underlying its acclimation to natural conditions remain poorly understood. Here, we compared the gut microbiomes of cultured and wild-caught individuals collected from two coastal regions using 16S rRNA gene sequencing integrated with functional prediction and microbial co-occurrence network analysis. Following their transition to natural habitats, escapees retained some dominant aquaculture-associated genera (Halomonas, Cetobacterium, Photobacterium and Vibrio) and clustered closely with local cultured counterparts rather than rearing condition. Beneath this partial taxonomic stability, however, the significant difference in intestinal microbiome between wild-caught and cultured individuals was manifested in predicted functional pathways and microbial interaction networks, characterized by shifts in immune-related processes, energy metabolism and keystone taxa. These findings indicate that hybrid groupers respond to environmental transition through functional and association-level plasticity rather than simple replacement of the gut microbial community. We propose that this dynamic microbiome rewiring may reflect microbiome-level adjustments associated with environmental transition, offering a microbial perspective on the acclimation of aquaculture-derived fishes to heterogeneous marine environments.
Additional Links: PMID-42675797
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PubMed:
Citation:
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@article {pmid42675797,
year = {2026},
author = {Song, W and Du, X and Zhang, X and Zhao, J and Ding, S},
title = {Gut microbiome reorganization as a signal of physiological acclimation in escaped hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀).},
journal = {Journal of fish biology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jfb.70631},
pmid = {42675797},
issn = {1095-8649},
support = {2022YFC2601303//National Key Research and Development Program of China/ ; 3502Z20226031//Xiamen Science and Technology Program of China/ ; },
abstract = {The introduction of aquaculture-derived hybrid fishes into natural marine ecosystems raises critical questions regarding their physiological capacity to acclimate to novel environments. The hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀), a widely farmed teleost in southern China, has increasingly been reported in coastal habitats following escape events. However, the gut microbiome-associated mechanisms underlying its acclimation to natural conditions remain poorly understood. Here, we compared the gut microbiomes of cultured and wild-caught individuals collected from two coastal regions using 16S rRNA gene sequencing integrated with functional prediction and microbial co-occurrence network analysis. Following their transition to natural habitats, escapees retained some dominant aquaculture-associated genera (Halomonas, Cetobacterium, Photobacterium and Vibrio) and clustered closely with local cultured counterparts rather than rearing condition. Beneath this partial taxonomic stability, however, the significant difference in intestinal microbiome between wild-caught and cultured individuals was manifested in predicted functional pathways and microbial interaction networks, characterized by shifts in immune-related processes, energy metabolism and keystone taxa. These findings indicate that hybrid groupers respond to environmental transition through functional and association-level plasticity rather than simple replacement of the gut microbial community. We propose that this dynamic microbiome rewiring may reflect microbiome-level adjustments associated with environmental transition, offering a microbial perspective on the acclimation of aquaculture-derived fishes to heterogeneous marine environments.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
The Oral Microbiome: A Silent Contributor to Systemic Health and Disease National Institutes of Health 2024 Workshop.
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 35(9):1490-1494.
Previously considered primarily only in the context of dental diseases, the oral microbiome is now recognized as a contributor to a variety of systemic diseases, including cancer and cardiovascular diseases. This commentary explores the evolving view of the oral cavity as a gateway to the body's broader physiologic networks, implicating oral microbiome dysbiosis in a spectrum of chronic conditions. Drawing on current evidence, we propose a re-envisioned healthcare model that integrates oral and systemic health and outline research gaps and clinical priorities to harness the oral microbiome for preventive and therapeutic gains, emphasizing cancer-relevant biomarkers and intervention opportunities.
Additional Links: PMID-42676127
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PubMed:
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@article {pmid42676127,
year = {2026},
author = {Riscuta, G and Wali, A and Mongodin, EF and Verma, M and Cardone, M and Kim, HS and McNealy, T and Mohammed, A},
title = {The Oral Microbiome: A Silent Contributor to Systemic Health and Disease National Institutes of Health 2024 Workshop.},
journal = {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
volume = {35},
number = {9},
pages = {1490-1494},
doi = {10.1158/1055-9965.EPI-25-1553},
pmid = {42676127},
issn = {1538-7755},
mesh = {Humans ; *Microbiota ; *Mouth/microbiology ; United States ; *Cardiovascular Diseases/microbiology ; *Neoplasms/microbiology/prevention & control ; National Institutes of Health (U.S.) ; *Dysbiosis ; },
abstract = {Previously considered primarily only in the context of dental diseases, the oral microbiome is now recognized as a contributor to a variety of systemic diseases, including cancer and cardiovascular diseases. This commentary explores the evolving view of the oral cavity as a gateway to the body's broader physiologic networks, implicating oral microbiome dysbiosis in a spectrum of chronic conditions. Drawing on current evidence, we propose a re-envisioned healthcare model that integrates oral and systemic health and outline research gaps and clinical priorities to harness the oral microbiome for preventive and therapeutic gains, emphasizing cancer-relevant biomarkers and intervention opportunities.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
*Mouth/microbiology
United States
*Cardiovascular Diseases/microbiology
*Neoplasms/microbiology/prevention & control
National Institutes of Health (U.S.)
*Dysbiosis
RevDate: 2026-09-01
CmpDate: 2026-09-01
An Interpretable Machine Learning Approach to Ecologically Characterize Soil Carbon and Structure From Multi-Kingdom Microbiome, Texture and Climate.
Molecular ecology, 35(17):e70535.
Soil physical structure is a critical determinant of agricultural landscape resilience, yet standard pedotransfer functions estimate soil hydraulic and structural properties using static abiotic variables, often overlooking the biological mechanisms that actively organize soil structure. This study evaluates the predictive power of multi-kingdom microbiome data (prokaryotes, fungi and microeukaryotes) for three key soil functions: soil organic carbon (SOC) stock, mean weight diameter (MWD) and macroporosity. Using a dataset of 2251 agricultural soil samples from Quebec, Canada, we benchmarked four machine learning algorithms (HGBR, RFR, XGBoost, SVR) and four data aggregation strategies. The integration of microbiome data with texture and climate variables achieved high peak predictive accuracy (R 2 range: 0.70-0.82). Methodologically, high-resolution compositional approaches (ASV-level centered log-ratio) and kingdom-balanced absolute abundances consistently outperformed taxonomic or functional aggregations. The loss of predictive power at the family level indicates that traits governing soil physical modification are phylogenetically shallow and strain-specific. Interpretability analysis using Shapley Additive Explanations (SHAP) revealed a clear functional hierarchy in soil assembly. Specific prokaryotic and fungal features drove biochemical stabilization and physical scaffolding via the microbial carbon pump and structural enmeshment dynamics. In contrast, the architectural openness of macroporosity was fundamentally constrained by abiotic physical limits (e.g., texture). Within this physical framework, specific microbial taxa, including anaerobic bacteria and microeukaryotic amoebae, functioned not as active engineers, but as high-sensitivity bio-indicators of the resulting aeration and hydrological connectivity. These results define soil physical organization as a biologically mediated hierarchy rather than a passive geological byproduct. Consequently, we propose shifting from static pedotransfer functions to a dynamic biotransfer framework that leverages multi-kingdom omic signatures to monitor soil physical resilience and crop adaptation potential.
Additional Links: PMID-42676225
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PubMed:
Citation:
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@article {pmid42676225,
year = {2026},
author = {Jeanne, T and Prunier, J and Hogue, R and Droit, A},
title = {An Interpretable Machine Learning Approach to Ecologically Characterize Soil Carbon and Structure From Multi-Kingdom Microbiome, Texture and Climate.},
journal = {Molecular ecology},
volume = {35},
number = {17},
pages = {e70535},
doi = {10.1111/mec.70535},
pmid = {42676225},
issn = {1365-294X},
support = {//Ministère de l'Agriculture, des Pêcheries et de l'Alimentation/ ; //Natural Sciences and Engineering Research Council of Canada/ ; },
mesh = {*Soil Microbiology ; *Carbon/analysis ; *Machine Learning ; *Soil/chemistry ; *Microbiota/genetics ; *Climate ; Quebec ; Fungi/classification ; },
abstract = {Soil physical structure is a critical determinant of agricultural landscape resilience, yet standard pedotransfer functions estimate soil hydraulic and structural properties using static abiotic variables, often overlooking the biological mechanisms that actively organize soil structure. This study evaluates the predictive power of multi-kingdom microbiome data (prokaryotes, fungi and microeukaryotes) for three key soil functions: soil organic carbon (SOC) stock, mean weight diameter (MWD) and macroporosity. Using a dataset of 2251 agricultural soil samples from Quebec, Canada, we benchmarked four machine learning algorithms (HGBR, RFR, XGBoost, SVR) and four data aggregation strategies. The integration of microbiome data with texture and climate variables achieved high peak predictive accuracy (R 2 range: 0.70-0.82). Methodologically, high-resolution compositional approaches (ASV-level centered log-ratio) and kingdom-balanced absolute abundances consistently outperformed taxonomic or functional aggregations. The loss of predictive power at the family level indicates that traits governing soil physical modification are phylogenetically shallow and strain-specific. Interpretability analysis using Shapley Additive Explanations (SHAP) revealed a clear functional hierarchy in soil assembly. Specific prokaryotic and fungal features drove biochemical stabilization and physical scaffolding via the microbial carbon pump and structural enmeshment dynamics. In contrast, the architectural openness of macroporosity was fundamentally constrained by abiotic physical limits (e.g., texture). Within this physical framework, specific microbial taxa, including anaerobic bacteria and microeukaryotic amoebae, functioned not as active engineers, but as high-sensitivity bio-indicators of the resulting aeration and hydrological connectivity. These results define soil physical organization as a biologically mediated hierarchy rather than a passive geological byproduct. Consequently, we propose shifting from static pedotransfer functions to a dynamic biotransfer framework that leverages multi-kingdom omic signatures to monitor soil physical resilience and crop adaptation potential.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Soil Microbiology
*Carbon/analysis
*Machine Learning
*Soil/chemistry
*Microbiota/genetics
*Climate
Quebec
Fungi/classification
RevDate: 2026-09-01
CmpDate: 2026-09-01
Predictors of impaired growth during the first year of life: findings from a longitudinal cohort study in Pakistan.
Frontiers in nutrition, 13:1912329.
BACKGROUND: This study aimed to prospectively identify sociodemographic, maternal and child-related predictors of linear growth (height-for-age-z-score, HAZ) and underweight status (weight-for-age- z-score, WAZ) at 12 months among infants from the CHAMP longitudinal cohort in Pakistan.
METHODS: We analysed data from the Child Health and Microbiome Development Study (CHAMP), a prospective cohort of 70 mother-infant dyads (72 infants, including one set of triplets) recruited within 0-28 days postpartum from rural District Swat, Pakistan, and followed at 3, 6 and 12 months, using sociodemographic, anthropometric, dietary intake and morbidity data. Weight-for-age (WAZ) and height-for-age (HAZ) z-scores were computed against the 2006 WHO Child Growth Standards. A time-staged multivariable linear regression models were fitted separately for four domains (sociodemographic, maternal, infant morbidity and infant feeding) with WAZ and HAZ at 12 months as primary outcomes. All models were adjusted for infant sex and maternal education.
RESULTS: Anthropometric assessment showed a sharp decline in WAZ between recruitment and 3-months with partial recovery thereafter, whereas HAZ improved initially but declined again at 6 and 12 months. Among all measured predictors, maternal education emerged as the most consistent upstream correlate of growth, showing positive associations with both WAZ and HAZ across sociodemographic, maternal, morbidity and feeding models. In addition, feeding practice at 6 months provided an overall statistical significance (WAZ: R [2] = 0.159, p = 0.030; HAZ: R [2] = 0.157, p = 0.032) with respect to growth. Within this model, exclusive breastfeeding for less than 6 months was associated with lower HAZ (B = -0.613, 95% CI: -1.166 to -0.060, p = 0.030), while egg and/or flesh food consumption showed a positive but borderline association with WAZ (B = 0.550, 95% CI: -0.106 to 1.205, p = 0.099).
CONCLUSION: Maternal education and infant feeding practices (specifically, not maintaining exclusive breastfeeding to 6 months and the consumption of animal-sourced foods at 6 months) were associated with infant growth during the first year of life. The exclusive breastfeeding association was attenuated after adjustment for baseline height-for-age and should be regarded as suggestive. These findings are hypothesis-generating and require confirmation in adequately powered studies.
Additional Links: PMID-42676361
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@article {pmid42676361,
year = {2026},
author = {Saidal, A and Ghani, M and Melhem, AL and Khattak, MI and Ullah, Q and Hajira, B and Shaheen, S and Tariq, K and Al Nabhani, Z and Andrews, SC and Alfheeaid, HA and Shahzad, M},
title = {Predictors of impaired growth during the first year of life: findings from a longitudinal cohort study in Pakistan.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1912329},
pmid = {42676361},
issn = {2296-861X},
abstract = {BACKGROUND: This study aimed to prospectively identify sociodemographic, maternal and child-related predictors of linear growth (height-for-age-z-score, HAZ) and underweight status (weight-for-age- z-score, WAZ) at 12 months among infants from the CHAMP longitudinal cohort in Pakistan.
METHODS: We analysed data from the Child Health and Microbiome Development Study (CHAMP), a prospective cohort of 70 mother-infant dyads (72 infants, including one set of triplets) recruited within 0-28 days postpartum from rural District Swat, Pakistan, and followed at 3, 6 and 12 months, using sociodemographic, anthropometric, dietary intake and morbidity data. Weight-for-age (WAZ) and height-for-age (HAZ) z-scores were computed against the 2006 WHO Child Growth Standards. A time-staged multivariable linear regression models were fitted separately for four domains (sociodemographic, maternal, infant morbidity and infant feeding) with WAZ and HAZ at 12 months as primary outcomes. All models were adjusted for infant sex and maternal education.
RESULTS: Anthropometric assessment showed a sharp decline in WAZ between recruitment and 3-months with partial recovery thereafter, whereas HAZ improved initially but declined again at 6 and 12 months. Among all measured predictors, maternal education emerged as the most consistent upstream correlate of growth, showing positive associations with both WAZ and HAZ across sociodemographic, maternal, morbidity and feeding models. In addition, feeding practice at 6 months provided an overall statistical significance (WAZ: R [2] = 0.159, p = 0.030; HAZ: R [2] = 0.157, p = 0.032) with respect to growth. Within this model, exclusive breastfeeding for less than 6 months was associated with lower HAZ (B = -0.613, 95% CI: -1.166 to -0.060, p = 0.030), while egg and/or flesh food consumption showed a positive but borderline association with WAZ (B = 0.550, 95% CI: -0.106 to 1.205, p = 0.099).
CONCLUSION: Maternal education and infant feeding practices (specifically, not maintaining exclusive breastfeeding to 6 months and the consumption of animal-sourced foods at 6 months) were associated with infant growth during the first year of life. The exclusive breastfeeding association was attenuated after adjustment for baseline height-for-age and should be regarded as suggestive. These findings are hypothesis-generating and require confirmation in adequately powered studies.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Spatiotemporal and tissue-specific dynamics of bacterial communities in adult female Ixodes ricinus during a four-year period.
Frontiers in cellular and infection microbiology, 16:1880365.
INTRODUCTION: The hard tick Ixodes ricinus serves as vector for life-threatening tick-borne diseases (TBDs) such as Lyme borreliosis, relapsing fever, and tick-borne encephalitis. Due to the ticks` ability to adjust to climate changes, their habitat is expanding quickly across Europe, and the incidences of TBD´s are increasing. Therefore, to better understand and control TBDs it is essential to expand the knowledge about the ticks´ microbiome, particularly the spatiotemporal and tissue-specific dynamics of I. ricinus bacterial community. This study was designed to investigate the differences in the detected bacterial communities according to the locations, where ticks had been collected, according to ticks´ tissue types and to seasonal impacts.
MATERIALS AND METHODS: A total of 723 adult female I. ricinus were collected from two locations in Bavaria over a four-year period. A defined number of individual ticks were dissected; DNA was extracted from tissue samples or complete ticks, and subsequently 16S rRNA-gene amplicon sequencing was performed.
RESULTS AND DISCUSSION: No clear impact of the seasons was detected across the complete four-year period. However, a yearly seasonal pattern was observed in spring (Sp) compared to autumn (Au). Particularly, Sp22, Sp23 and Sp24 showed no difference in effective richness. These results are consistent with previous studies. While the species richness changed between different locations, the effective richness did not. Specific tissue samples of the ticks recovered by dissection (salivary glands, midgut, exoskeleton) carried significant, distinct bacterial communities. The genus Candidatus Midichloria was most abundant and was detected in all tissue types. Borrelia spp. were not detected in any of the collected samples, besides in the mock communities, possibly due to limitations in 16S rRNA gene analysis.
Additional Links: PMID-42676372
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Citation:
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@article {pmid42676372,
year = {2026},
author = {Heuser, SL and Zenner, C and Wiesinger, A and Gänzle, M and Hiereth, S and Girl, P and Neuhaus, K and Straubinger, RK},
title = {Spatiotemporal and tissue-specific dynamics of bacterial communities in adult female Ixodes ricinus during a four-year period.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1880365},
pmid = {42676372},
issn = {2235-2988},
mesh = {Animals ; *Ixodes/microbiology ; Female ; RNA, Ribosomal, 16S/genetics ; Seasons ; *Bacteria/classification/genetics/isolation & purification ; DNA, Bacterial/genetics ; *Microbiota ; Sequence Analysis, DNA ; Spatio-Temporal Analysis ; Germany ; DNA, Ribosomal/genetics/chemistry ; },
abstract = {INTRODUCTION: The hard tick Ixodes ricinus serves as vector for life-threatening tick-borne diseases (TBDs) such as Lyme borreliosis, relapsing fever, and tick-borne encephalitis. Due to the ticks` ability to adjust to climate changes, their habitat is expanding quickly across Europe, and the incidences of TBD´s are increasing. Therefore, to better understand and control TBDs it is essential to expand the knowledge about the ticks´ microbiome, particularly the spatiotemporal and tissue-specific dynamics of I. ricinus bacterial community. This study was designed to investigate the differences in the detected bacterial communities according to the locations, where ticks had been collected, according to ticks´ tissue types and to seasonal impacts.
MATERIALS AND METHODS: A total of 723 adult female I. ricinus were collected from two locations in Bavaria over a four-year period. A defined number of individual ticks were dissected; DNA was extracted from tissue samples or complete ticks, and subsequently 16S rRNA-gene amplicon sequencing was performed.
RESULTS AND DISCUSSION: No clear impact of the seasons was detected across the complete four-year period. However, a yearly seasonal pattern was observed in spring (Sp) compared to autumn (Au). Particularly, Sp22, Sp23 and Sp24 showed no difference in effective richness. These results are consistent with previous studies. While the species richness changed between different locations, the effective richness did not. Specific tissue samples of the ticks recovered by dissection (salivary glands, midgut, exoskeleton) carried significant, distinct bacterial communities. The genus Candidatus Midichloria was most abundant and was detected in all tissue types. Borrelia spp. were not detected in any of the collected samples, besides in the mock communities, possibly due to limitations in 16S rRNA gene analysis.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Ixodes/microbiology
Female
RNA, Ribosomal, 16S/genetics
Seasons
*Bacteria/classification/genetics/isolation & purification
DNA, Bacterial/genetics
*Microbiota
Sequence Analysis, DNA
Spatio-Temporal Analysis
Germany
DNA, Ribosomal/genetics/chemistry
RevDate: 2026-09-01
CmpDate: 2026-09-01
rCCLasso: a robust framework for microbial correlation network analysis reveals age-related microbial dynamics.
Frontiers in cellular and infection microbiology, 16:1828471.
INTRODUCTION: The human gut microbiome continues to evolve beyond early adulthood, yet most microbiome aging studies focus on changes in individual taxa or overall diversity, leaving microbial interaction dynamics largely unexplored. Correlation-based microbial networks offer an interpretable framework for studying such interactions but are challenging to estimate from compositional microbiome data. Although compositionality-aware methods such as CCLasso provide principled multivariate inference, we identify a previously overlooked limitation: sensitivity to random seeds, which leads to unstable correlation estimates and irreproducible significance assessments.
METHODS: To address this issue, we propose Robust CCLasso (rCCLasso), a statistically rigorous framework that stabilizes microbial correlation estimation by integrating CCLasso outputs across multiple runs. rCCLasso aggregates sparse correlation estimates using median-based integration with positive-definite projection and combines run-specific inference through the Cauchy combination test with an additional stability criterion to control type-I error. The method is naturally parallelizable and computationally scalable.
RESULTS: Simulation studies demonstrate that rCCLasso improves inferential stability, type-I error control, and power relative to the original CCLasso. Applying rCCLasso to data from over 4,000 healthy adults in the American Gut Project (ages 18--101), we uncover age-related microbial network dynamics, characterized by marked fluctuations from early to mid-adulthood, followed by a relatively stable phase and a substantial decline in network strength in the elderly group.
DISCUSSION: Together, these results establish rCCLasso as a robust and interpretable framework for studying microbial networks in aging research.
Additional Links: PMID-42676412
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@article {pmid42676412,
year = {2026},
author = {Xie, T and Zhou, J and Wang, Y},
title = {rCCLasso: a robust framework for microbial correlation network analysis reveals age-related microbial dynamics.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1828471},
pmid = {42676412},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Aging ; *Microbial Interactions ; Computer Simulation ; *Computational Biology/methods ; },
abstract = {INTRODUCTION: The human gut microbiome continues to evolve beyond early adulthood, yet most microbiome aging studies focus on changes in individual taxa or overall diversity, leaving microbial interaction dynamics largely unexplored. Correlation-based microbial networks offer an interpretable framework for studying such interactions but are challenging to estimate from compositional microbiome data. Although compositionality-aware methods such as CCLasso provide principled multivariate inference, we identify a previously overlooked limitation: sensitivity to random seeds, which leads to unstable correlation estimates and irreproducible significance assessments.
METHODS: To address this issue, we propose Robust CCLasso (rCCLasso), a statistically rigorous framework that stabilizes microbial correlation estimation by integrating CCLasso outputs across multiple runs. rCCLasso aggregates sparse correlation estimates using median-based integration with positive-definite projection and combines run-specific inference through the Cauchy combination test with an additional stability criterion to control type-I error. The method is naturally parallelizable and computationally scalable.
RESULTS: Simulation studies demonstrate that rCCLasso improves inferential stability, type-I error control, and power relative to the original CCLasso. Applying rCCLasso to data from over 4,000 healthy adults in the American Gut Project (ages 18--101), we uncover age-related microbial network dynamics, characterized by marked fluctuations from early to mid-adulthood, followed by a relatively stable phase and a substantial decline in network strength in the elderly group.
DISCUSSION: Together, these results establish rCCLasso as a robust and interpretable framework for studying microbial networks in aging research.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
*Aging
*Microbial Interactions
Computer Simulation
*Computational Biology/methods
RevDate: 2026-09-01
CmpDate: 2026-09-01
Light governed plant-microbe interactions: the role of light in biotic stress resilience.
Physiology and molecular biology of plants : an international journal of functional plant biology, 32(9):1939-1953.
The global agricultural system is continuously facing many threats that arise from phytopathogens, which pose a serious challenge to food security worldwide. Synthetic biology approaches and advances in biotechnology have developed various methods to control these diseases, they are not yet fully effective in protecting plants from all phytopathogens. In this context, nature offers an alternative solution through plant associated microbiome. These beneficial microorganisms play a crucial role in mediating plant survival under biotic stress by influencing host immunity and metabolic responses. A better understanding of plant-microbe interactions at both genetic and metabolite levels is important. These interactions are controlled by complex regulatory networks and studying them will help us use their full potential. Consequently, research is expanding into how environmental factors, specifically light, influence plant physiology, immunity and secondary metabolism. Recent studies have suggested that light not only shapes plant immunity but also modulates the accumulation and behaviour of associated microbial community, therefore influencing the outcome of biotic stress interactions. This review focuses on the role of light as a regulatory signal in plant-microbe interactions under biotic stress. It explains how light controls secondary metabolite production and plant defence mechanisms. It also highlights how light responsive pathways can be used to develop disease-resistant and climate smart crops. The integration of photobiology with microbiome research may open new approaches for sustainable and resilient agricultural systems. This approach can help address the challenges posed by emerging phytopathogen.
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@article {pmid42676416,
year = {2026},
author = {Sharma, E and Shrivastava, V and Aeron, R and Sharma, P and Baliyan, S and Pandey, S},
title = {Light governed plant-microbe interactions: the role of light in biotic stress resilience.},
journal = {Physiology and molecular biology of plants : an international journal of functional plant biology},
volume = {32},
number = {9},
pages = {1939-1953},
pmid = {42676416},
issn = {0971-5894},
abstract = {The global agricultural system is continuously facing many threats that arise from phytopathogens, which pose a serious challenge to food security worldwide. Synthetic biology approaches and advances in biotechnology have developed various methods to control these diseases, they are not yet fully effective in protecting plants from all phytopathogens. In this context, nature offers an alternative solution through plant associated microbiome. These beneficial microorganisms play a crucial role in mediating plant survival under biotic stress by influencing host immunity and metabolic responses. A better understanding of plant-microbe interactions at both genetic and metabolite levels is important. These interactions are controlled by complex regulatory networks and studying them will help us use their full potential. Consequently, research is expanding into how environmental factors, specifically light, influence plant physiology, immunity and secondary metabolism. Recent studies have suggested that light not only shapes plant immunity but also modulates the accumulation and behaviour of associated microbial community, therefore influencing the outcome of biotic stress interactions. This review focuses on the role of light as a regulatory signal in plant-microbe interactions under biotic stress. It explains how light controls secondary metabolite production and plant defence mechanisms. It also highlights how light responsive pathways can be used to develop disease-resistant and climate smart crops. The integration of photobiology with microbiome research may open new approaches for sustainable and resilient agricultural systems. This approach can help address the challenges posed by emerging phytopathogen.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
From Mouth to Mind: Unraveling the Oral Microbiome's Role in Orofacial Pain and Neurodegeneration.
Journal of clinical practice and research, 48(4):356-367.
The human oral cavity hosts a diverse and dynamic microbiome comprising more than 700 microbial species, which plays a crucial role in maintaining oral and systemic health. Oral dysbiosis, defined as disruption of this microbial balance, has been increasingly implicated not only in periodontal disease but also in the pathogenesis of orofacial pain and neurodegenerative diseases. Key pathogens, such as Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum, have been proposed to release virulence factors, including lipopolysaccharides and gingipains, which may activate immune pathways and nociceptors, thereby driving peripheral sensitization and neuroinflammation. These organisms have also been suggested to breach mucosal and vascular barriers, enter the systemic circulation, and, in some cases, access the central nervous system. Evidence has linked oral pathogens to Alzheimer's disease, Parkinson's disease, autism spectrum disorder, and multiple sclerosis. Notably, P. gingivalis and its gingipains have been identified in postmortem brain tissue from patients with Alzheimer's disease, with proposed roles in neuroinflammation and amyloid plaque formation. Salivary microbial alterations in burning mouth syndrome and temporomandibular disorders further highlight the influence of the oral microbiome on neuropathic pain. Therefore, the oral-gut-brain axis represents a novel and promising area of investigation, offering potential diagnostic biomarkers and targeted microbial therapies for the management of chronic orofacial pain and neurological disorders.
Additional Links: PMID-42676548
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Citation:
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@article {pmid42676548,
year = {2026},
author = {Moses, S and Phulambrikar, T and Dosi, T},
title = {From Mouth to Mind: Unraveling the Oral Microbiome's Role in Orofacial Pain and Neurodegeneration.},
journal = {Journal of clinical practice and research},
volume = {48},
number = {4},
pages = {356-367},
pmid = {42676548},
issn = {2980-2156},
abstract = {The human oral cavity hosts a diverse and dynamic microbiome comprising more than 700 microbial species, which plays a crucial role in maintaining oral and systemic health. Oral dysbiosis, defined as disruption of this microbial balance, has been increasingly implicated not only in periodontal disease but also in the pathogenesis of orofacial pain and neurodegenerative diseases. Key pathogens, such as Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum, have been proposed to release virulence factors, including lipopolysaccharides and gingipains, which may activate immune pathways and nociceptors, thereby driving peripheral sensitization and neuroinflammation. These organisms have also been suggested to breach mucosal and vascular barriers, enter the systemic circulation, and, in some cases, access the central nervous system. Evidence has linked oral pathogens to Alzheimer's disease, Parkinson's disease, autism spectrum disorder, and multiple sclerosis. Notably, P. gingivalis and its gingipains have been identified in postmortem brain tissue from patients with Alzheimer's disease, with proposed roles in neuroinflammation and amyloid plaque formation. Salivary microbial alterations in burning mouth syndrome and temporomandibular disorders further highlight the influence of the oral microbiome on neuropathic pain. Therefore, the oral-gut-brain axis represents a novel and promising area of investigation, offering potential diagnostic biomarkers and targeted microbial therapies for the management of chronic orofacial pain and neurological disorders.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Disrupted terminal bilirubin catabolism links Lachnospiraceae depletion to inflammatory bowel disease.
Frontiers in microbiology, 17:1871609.
BACKGROUND: The gut microbiome mediates the reductive catabolism of bilirubin into urobilinoids, yet the bacteria and enzymes responsible for the later steps of this pathway remain largely unknown.
METHODS: Here, we combine untargeted UPLC/HRMS metabolomics with shotgun metagenomic sequencing of fecal samples from 119 participants, including patients with Crohn's disease, ulcerative colitis, and healthy controls, to map disruptions in the bilirubin catabolic pathway in inflammatory bowel disease (IBD).
RESULTS: We show that stercobilinogen and stercobilin, the terminal metabolites of this pathway, are depleted (p < 0.01) in IBD patients irrespective of disease subtype, while upstream intermediates, D-urobilinogen, remain unchanged. This metabolic bottleneck coincides with a marked reduction in members of the Lachnospiraceae family, specifically Blautia sp. SG-772 and three uncharacterized species, which show strong positive correlations with stercobilinogen and stercobilin levels.
DISCUSSION: These findings implicate Lachnospiraceae as key mediators of the yet unknown enzymatic conversion of I-urobilinogen to stercobilinogen, extending the family's known metabolic repertoire beyond short-chain fatty acid production. Given that bilirubin and its reduced metabolite stercobilinogen possess antioxidant properties, their depletion may contribute to the oxidative burden in the IBD gut. Conversely, the concurrent elevation of D-urobilin, which lacks these protective properties and has been linked to metabolic dysfunction in other contexts, may further exacerbate inflammation. Our results identify fecal bilirubin metabolites as candidate biomarkers of microbial dysbiosis in IBD and nominate specific Lachnospiraceae taxa for functional characterization of the missing stercobilinogen reductase.
Additional Links: PMID-42676636
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@article {pmid42676636,
year = {2026},
author = {Sabti, O and Lialin-Tzadikov, K and Ivanova, V and Dori-Bachash, M and Uzi-Gavrilov, S and Tik, Z and Mashiach, R and Zorea, A and Mizrahi, I and Segal, A and Moyal-Attias, K and Elinav, E and Meijler, MM},
title = {Disrupted terminal bilirubin catabolism links Lachnospiraceae depletion to inflammatory bowel disease.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1871609},
pmid = {42676636},
issn = {1664-302X},
abstract = {BACKGROUND: The gut microbiome mediates the reductive catabolism of bilirubin into urobilinoids, yet the bacteria and enzymes responsible for the later steps of this pathway remain largely unknown.
METHODS: Here, we combine untargeted UPLC/HRMS metabolomics with shotgun metagenomic sequencing of fecal samples from 119 participants, including patients with Crohn's disease, ulcerative colitis, and healthy controls, to map disruptions in the bilirubin catabolic pathway in inflammatory bowel disease (IBD).
RESULTS: We show that stercobilinogen and stercobilin, the terminal metabolites of this pathway, are depleted (p < 0.01) in IBD patients irrespective of disease subtype, while upstream intermediates, D-urobilinogen, remain unchanged. This metabolic bottleneck coincides with a marked reduction in members of the Lachnospiraceae family, specifically Blautia sp. SG-772 and three uncharacterized species, which show strong positive correlations with stercobilinogen and stercobilin levels.
DISCUSSION: These findings implicate Lachnospiraceae as key mediators of the yet unknown enzymatic conversion of I-urobilinogen to stercobilinogen, extending the family's known metabolic repertoire beyond short-chain fatty acid production. Given that bilirubin and its reduced metabolite stercobilinogen possess antioxidant properties, their depletion may contribute to the oxidative burden in the IBD gut. Conversely, the concurrent elevation of D-urobilin, which lacks these protective properties and has been linked to metabolic dysfunction in other contexts, may further exacerbate inflammation. Our results identify fecal bilirubin metabolites as candidate biomarkers of microbial dysbiosis in IBD and nominate specific Lachnospiraceae taxa for functional characterization of the missing stercobilinogen reductase.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Salivary gland microbiome of Anopheles gambiae: a mini-review of acquisition, composition, and functional significance.
Frontiers in insect science, 6:1911294.
The salivary gland (SG) is the final barrier for Plasmodium transmission to humans but remains comparatively understudied relative to the midgut microbiome. This review synthesizes current knowledge on SG microbiome acquisition routes, composition, and functional significance. Acquisition may occur via larval filter feeding, vertical (egg smearing), transstadial, or horizontal transmission during blood feeding, though their relative contributions are unknown. Compositional studies show Gram-negative genera Serratia, Elizabethkingia, Acinetobacter, Pseudomonas, and Asaia predominate; Plasmodium infection correlates with increased Serratia and decreased Elizabethkingia abundance. While immune-related genes (e.g., cecropins, defensin, GNBP, SRPN6) expressed in the SG may be modulated by resident bacteria, direct evidence of their effect on sporozoite invasion remains lacking. Gram-negative bacteria trigger Toll, Imd, and JAK-STAT pathways, but emerging evidence suggests the SG may mount a distinct, locally independent immune response compared to the systemic pathway. Paratransgenesis using Asaia shows promise, yet SG-targeted effector delivery remains untested. Ecological pressures common in West Africa, including agricultural pesticides, insecticide resistance, and larval water contamination, may influence mosquito-associated bacteria, but no studies explicitly link these to the SG microbiome. Significant knowledge gaps persist, notably the absence of field studies in high-burden regions like Nigeria and the lack of experimental manipulation to establish causality. Addressing these priorities is critical to determine whether the SG microbiome can be exploited as a transmission-blocking target.
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Citation:
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@article {pmid42676645,
year = {2026},
author = {Olafusi, CO and Afolabi, IS and Ogunlana, OO},
title = {Salivary gland microbiome of Anopheles gambiae: a mini-review of acquisition, composition, and functional significance.},
journal = {Frontiers in insect science},
volume = {6},
number = {},
pages = {1911294},
pmid = {42676645},
issn = {2673-8600},
abstract = {The salivary gland (SG) is the final barrier for Plasmodium transmission to humans but remains comparatively understudied relative to the midgut microbiome. This review synthesizes current knowledge on SG microbiome acquisition routes, composition, and functional significance. Acquisition may occur via larval filter feeding, vertical (egg smearing), transstadial, or horizontal transmission during blood feeding, though their relative contributions are unknown. Compositional studies show Gram-negative genera Serratia, Elizabethkingia, Acinetobacter, Pseudomonas, and Asaia predominate; Plasmodium infection correlates with increased Serratia and decreased Elizabethkingia abundance. While immune-related genes (e.g., cecropins, defensin, GNBP, SRPN6) expressed in the SG may be modulated by resident bacteria, direct evidence of their effect on sporozoite invasion remains lacking. Gram-negative bacteria trigger Toll, Imd, and JAK-STAT pathways, but emerging evidence suggests the SG may mount a distinct, locally independent immune response compared to the systemic pathway. Paratransgenesis using Asaia shows promise, yet SG-targeted effector delivery remains untested. Ecological pressures common in West Africa, including agricultural pesticides, insecticide resistance, and larval water contamination, may influence mosquito-associated bacteria, but no studies explicitly link these to the SG microbiome. Significant knowledge gaps persist, notably the absence of field studies in high-burden regions like Nigeria and the lack of experimental manipulation to establish causality. Addressing these priorities is critical to determine whether the SG microbiome can be exploited as a transmission-blocking target.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Drug-resistant bacterial infections in end-stage liver disease: immune imbalance and intervention advances.
Frontiers in immunology, 17:1888293.
Patients with end-stage liver disease (ESLD) face a markedly elevated risk of infections caused by multidrug-resistant (MDR) and extensively drug-resistant (XDR) bacteria. This vulnerability worsens prognosis and severely limits therapeutic options. The underlying mechanisms extend beyond hepatic synthetic and detoxification failure to encompass a complex and multifaceted state of immune dysfunction. In this review, we synthesize current evidence on how ESLD-associated immune defects drive susceptibility to drug-resistant infections. We examine key abnormalities across multiple interconnected domains: depletion and dysfunction of Kupffer cells, complement deficiency, T-cell exhaustion with regulatory T-cell expansion, disruption of the gut-liver axis, immunometabolic reprogramming driven by hyperammonemia and lactate accumulation, and upregulation of immune checkpoint molecules such as PD-1/PD-L1. These pathways collectively promote colonization, persistence, and therapeutic refractoriness of MDR pathogens. We also evaluate emerging therapeutic strategies targeting these immune defects, including checkpoint inhibitors, cytokine and cellular therapies, microbiome modulation, and metabolic interventions, while acknowledging the challenges that limit their clinical translation. By proposing an integrated framework that links distinct immune defects to MDR infection pathogenesis, we aim to guide the development of biomarker-driven, personalized immunomodulatory approaches that complement antimicrobial therapy and ultimately improve outcomes in this high-risk population.
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@article {pmid42676711,
year = {2026},
author = {Liu, J and Wu, J and Zheng, X},
title = {Drug-resistant bacterial infections in end-stage liver disease: immune imbalance and intervention advances.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1888293},
pmid = {42676711},
issn = {1664-3224},
mesh = {Humans ; *Bacterial Infections/immunology/drug therapy/microbiology ; Animals ; *End Stage Liver Disease/immunology/complications/microbiology ; *Drug Resistance, Multiple, Bacterial/immunology ; Host-Directed Therapy ; T-Cell Exhaustion ; },
abstract = {Patients with end-stage liver disease (ESLD) face a markedly elevated risk of infections caused by multidrug-resistant (MDR) and extensively drug-resistant (XDR) bacteria. This vulnerability worsens prognosis and severely limits therapeutic options. The underlying mechanisms extend beyond hepatic synthetic and detoxification failure to encompass a complex and multifaceted state of immune dysfunction. In this review, we synthesize current evidence on how ESLD-associated immune defects drive susceptibility to drug-resistant infections. We examine key abnormalities across multiple interconnected domains: depletion and dysfunction of Kupffer cells, complement deficiency, T-cell exhaustion with regulatory T-cell expansion, disruption of the gut-liver axis, immunometabolic reprogramming driven by hyperammonemia and lactate accumulation, and upregulation of immune checkpoint molecules such as PD-1/PD-L1. These pathways collectively promote colonization, persistence, and therapeutic refractoriness of MDR pathogens. We also evaluate emerging therapeutic strategies targeting these immune defects, including checkpoint inhibitors, cytokine and cellular therapies, microbiome modulation, and metabolic interventions, while acknowledging the challenges that limit their clinical translation. By proposing an integrated framework that links distinct immune defects to MDR infection pathogenesis, we aim to guide the development of biomarker-driven, personalized immunomodulatory approaches that complement antimicrobial therapy and ultimately improve outcomes in this high-risk population.},
}
MeSH Terms:
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Humans
*Bacterial Infections/immunology/drug therapy/microbiology
Animals
*End Stage Liver Disease/immunology/complications/microbiology
*Drug Resistance, Multiple, Bacterial/immunology
Host-Directed Therapy
T-Cell Exhaustion
RevDate: 2026-09-01
CmpDate: 2026-09-01
Correlation between oral microbiome characteristics and clinical phenotypes in patients with GERD and its changes after anti-reflux surgery.
Frontiers in microbiology, 17:1878947.
BACKGROUND: Gastroesophageal reflux disease is defined by the reflux of gastroduodenal material into the esophagus, leading to troublesome symptoms and complications. Although the gastrointestinal microbiome has been increasingly implicated in gastroesophageal reflux disease pathogenesis, existing research has largely centered on esophageal and intestinal microbiota. The alterations and clinical relevance of the oral microbiome in gastroesophageal reflux disease remain underexplored. Therefore, this study was designed to: (1) systematically compare the oral microbiome structure between gastroesophageal reflux disease patients and healthy controls, and to examine the correlations between differentially abundant microbial taxa and key clinical phenotypes; (2) longitudinally assess the dynamic changes in the oral microbiome after anti-reflux surgery.
METHODS: We conducted a study integrating a case-control design with a longitudinal self-controlled component. Initially, 40 patients and 20 healthy volunteers were enrolled. Following exclusions based on diagnostic confirmation, 36 gastroesophageal reflux disease patients comprised the preoperative group (Group Pre), and 17 age-, gender-, and BMI-matched healthy volunteers served as controls (Group HC). Non-stimulated whole saliva samples were collected from all participants. A subgroup of 18 patients from Group Pre subsequently underwent laparoscopic fundoplication. Their saliva samples collected 3 months postoperatively constituted the postoperative group (Group Post) for longitudinal comparison. The V3-V4 hypervariable regions of the bacterial 16S rRNA gene were amplified and sequenced using high-throughput sequencing. Sequencing data were processed and analyzed with bioinformatics pipelines to evaluate α- and β-diversity. Differential microbial features across groups were identified using Linear Discriminant Analysis Effect Size. Correlations between microbial relative abundance and clinical parameters were assessed via Spearman's rank correlation. Changes in the microbiome following surgery were evaluated using paired non-parametric statistical tests.
RESULTS: (1) Cross-sectional comparisons: no significant differences were observed in α-diversity indices (ACE, Chao1, Shannon, and Simpson; all P > 0.05) of the oral microbiome between GERD patients (Group Pre) and healthy controls (Group HC). In contrast, β-diversity analysis indicated a significant overall structural disparity between the groups (PERMANOVA, R [2] = 0.044, P = 0.003). Linear Discriminant Analysis Effect Size (LEfSe) identified discriminant taxa distinguishing the two groups, with genera like Alloprevotella and Veillonella being enriched in Group Pre, and Streptococcus enriched in Group HC. Furthermore, Spearman correlation analyses identified significant associations between specific genera and clinical parameters: the relative abundance of Veillonella showed a positive correlation with the gastroesophageal reflux disease questionaire score (r = 0.347, P = 0.038), and that of Alloprevotella correlated positively with the severity of esophagitis as graded by the Los Angeles classification (r = 0.335, P = 0.046).(2) Longitudinal analysis revealed that bacterial genera such as Veillonella, which were associated with phenotypes in cross-sectional studies, did not show significant changes in the oral microbiota between the Pre- and Post- groups. The most characteristic alteration was that the relative abundance of the pro-inflammatory genus Fusobacteriumwas succeeded by Selenomonas, a genus with potential metabolic benefits.
CONCLUSION: Our study demonstrates that gastroesophageal reflux disease is characterized by a specific oral dysbiosis, with the abundance of particular bacterial taxa correlating with clinical disease severity. Although laparoscopic anti-reflux surgery did not drastically alter the global oral microbiome architecture, it induced a targeted ecological shift. This shift was marked by the suppression of pro-inflammatory taxa, an increase in potentially beneficial commensals, and a trend toward restored α-diversity. These findings suggest that laparoscopic anti-reflux surgery may facilitate a shift of the oral microbiome toward a healthier ecological state following restoration of the anti-reflux barrier function. This observation provides a new microbiological perspective for understanding the broader physiological impact of anti-reflux surgery.
Additional Links: PMID-42676736
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@article {pmid42676736,
year = {2026},
author = {Wang, Z and Liu, Y and Han, Z and Wang, FK},
title = {Correlation between oral microbiome characteristics and clinical phenotypes in patients with GERD and its changes after anti-reflux surgery.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1878947},
pmid = {42676736},
issn = {1664-302X},
abstract = {BACKGROUND: Gastroesophageal reflux disease is defined by the reflux of gastroduodenal material into the esophagus, leading to troublesome symptoms and complications. Although the gastrointestinal microbiome has been increasingly implicated in gastroesophageal reflux disease pathogenesis, existing research has largely centered on esophageal and intestinal microbiota. The alterations and clinical relevance of the oral microbiome in gastroesophageal reflux disease remain underexplored. Therefore, this study was designed to: (1) systematically compare the oral microbiome structure between gastroesophageal reflux disease patients and healthy controls, and to examine the correlations between differentially abundant microbial taxa and key clinical phenotypes; (2) longitudinally assess the dynamic changes in the oral microbiome after anti-reflux surgery.
METHODS: We conducted a study integrating a case-control design with a longitudinal self-controlled component. Initially, 40 patients and 20 healthy volunteers were enrolled. Following exclusions based on diagnostic confirmation, 36 gastroesophageal reflux disease patients comprised the preoperative group (Group Pre), and 17 age-, gender-, and BMI-matched healthy volunteers served as controls (Group HC). Non-stimulated whole saliva samples were collected from all participants. A subgroup of 18 patients from Group Pre subsequently underwent laparoscopic fundoplication. Their saliva samples collected 3 months postoperatively constituted the postoperative group (Group Post) for longitudinal comparison. The V3-V4 hypervariable regions of the bacterial 16S rRNA gene were amplified and sequenced using high-throughput sequencing. Sequencing data were processed and analyzed with bioinformatics pipelines to evaluate α- and β-diversity. Differential microbial features across groups were identified using Linear Discriminant Analysis Effect Size. Correlations between microbial relative abundance and clinical parameters were assessed via Spearman's rank correlation. Changes in the microbiome following surgery were evaluated using paired non-parametric statistical tests.
RESULTS: (1) Cross-sectional comparisons: no significant differences were observed in α-diversity indices (ACE, Chao1, Shannon, and Simpson; all P > 0.05) of the oral microbiome between GERD patients (Group Pre) and healthy controls (Group HC). In contrast, β-diversity analysis indicated a significant overall structural disparity between the groups (PERMANOVA, R [2] = 0.044, P = 0.003). Linear Discriminant Analysis Effect Size (LEfSe) identified discriminant taxa distinguishing the two groups, with genera like Alloprevotella and Veillonella being enriched in Group Pre, and Streptococcus enriched in Group HC. Furthermore, Spearman correlation analyses identified significant associations between specific genera and clinical parameters: the relative abundance of Veillonella showed a positive correlation with the gastroesophageal reflux disease questionaire score (r = 0.347, P = 0.038), and that of Alloprevotella correlated positively with the severity of esophagitis as graded by the Los Angeles classification (r = 0.335, P = 0.046).(2) Longitudinal analysis revealed that bacterial genera such as Veillonella, which were associated with phenotypes in cross-sectional studies, did not show significant changes in the oral microbiota between the Pre- and Post- groups. The most characteristic alteration was that the relative abundance of the pro-inflammatory genus Fusobacteriumwas succeeded by Selenomonas, a genus with potential metabolic benefits.
CONCLUSION: Our study demonstrates that gastroesophageal reflux disease is characterized by a specific oral dysbiosis, with the abundance of particular bacterial taxa correlating with clinical disease severity. Although laparoscopic anti-reflux surgery did not drastically alter the global oral microbiome architecture, it induced a targeted ecological shift. This shift was marked by the suppression of pro-inflammatory taxa, an increase in potentially beneficial commensals, and a trend toward restored α-diversity. These findings suggest that laparoscopic anti-reflux surgery may facilitate a shift of the oral microbiome toward a healthier ecological state following restoration of the anti-reflux barrier function. This observation provides a new microbiological perspective for understanding the broader physiological impact of anti-reflux surgery.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Astragalus polysaccharide alleviates neuropathology and cognitive deficits by modulating gut microbiota and neuroinflammation in an Alzheimer's disease model.
Frontiers in pharmacology, 17:1830927.
BACKGROUND: Emerging evidence indicates that the neuroprotective effects of Astragalus polysaccharides (APS), an extract compound and bioactive constituent derived from traditional Chinese herbs, may be relevant to an effective prescription for delaying progression of Alzheimer's disease (AD), yet the underlying mechanisms remain to be fully elucidated. This study aimed to investigate the therapeutic efficacy of APS in alleviating cognitive impairment and neuropathology in 5×FAD transgenic mice, with a specific focus on the regulatory role of the gut-brain axis.
METHODS: Male 5×FAD mice were orally administered APS (200 mg/kg/day) for 60 days. General observations were conducted to assess the in vivo tolerance of APS. Cognitive function was evaluated using the Morris water maze (MWM). Neuropathological assessments included immunofluorescence and Western blotting for amyloid-β (Aβ) deposition, synaptic proteins, and neuroinflammatory markers. Gut microbiota composition and metabolic profiles were analyzed via 16S rRNA gene sequencing and targeted metabolomics. Furthermore, fecal microbiota transplantation (FMT) was performed to verify the causal contribution of gut microbiota to the observed therapeutic effects.
RESULTS: APS administration was well-tolerated throughout the study period, with no overt toxic effects observed. Moreover, APS administration significantly ameliorated spatial learning and memory deficits in 5×FAD mice. Mechanistically, APS treatment reduced Aβ plaque burden, restored synaptic protein expression (PSD-95 and Syntaxin), and attenuated microglia-mediated neuroinflammation by suppressing pro-inflammatory cytokines (IL-6, TNF-α) and upregulating TREM2. Microbiome analysis revealed that APS reshaped gut microbial diversity and composition, enriching beneficial taxa such as Lactobacillus. Metabolomics indicated a partial restoration of amino acid metabolism. Notably, FMT from APS-treated donors successfully reproduced the cognitive improvements and anti-inflammatory effects in recipient mice.
CONCLUSION: These findings demonstrate that APS alleviates cognitive deficits and AD-like pathology, partially through remodeling gut microbiota and modulating the gut-brain axis. APS represents a promising natural compound-based therapeutic candidate for managing cognitive decline associated with Alzheimer's disease.
Additional Links: PMID-42676794
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@article {pmid42676794,
year = {2026},
author = {Cui, X and Wei, Z and Wang, Q and Du, S and Lin, Z and Chen, Z and Zhang, J and Li, C and Tang, L and Dai, X and He, W},
title = {Astragalus polysaccharide alleviates neuropathology and cognitive deficits by modulating gut microbiota and neuroinflammation in an Alzheimer's disease model.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1830927},
pmid = {42676794},
issn = {1663-9812},
abstract = {BACKGROUND: Emerging evidence indicates that the neuroprotective effects of Astragalus polysaccharides (APS), an extract compound and bioactive constituent derived from traditional Chinese herbs, may be relevant to an effective prescription for delaying progression of Alzheimer's disease (AD), yet the underlying mechanisms remain to be fully elucidated. This study aimed to investigate the therapeutic efficacy of APS in alleviating cognitive impairment and neuropathology in 5×FAD transgenic mice, with a specific focus on the regulatory role of the gut-brain axis.
METHODS: Male 5×FAD mice were orally administered APS (200 mg/kg/day) for 60 days. General observations were conducted to assess the in vivo tolerance of APS. Cognitive function was evaluated using the Morris water maze (MWM). Neuropathological assessments included immunofluorescence and Western blotting for amyloid-β (Aβ) deposition, synaptic proteins, and neuroinflammatory markers. Gut microbiota composition and metabolic profiles were analyzed via 16S rRNA gene sequencing and targeted metabolomics. Furthermore, fecal microbiota transplantation (FMT) was performed to verify the causal contribution of gut microbiota to the observed therapeutic effects.
RESULTS: APS administration was well-tolerated throughout the study period, with no overt toxic effects observed. Moreover, APS administration significantly ameliorated spatial learning and memory deficits in 5×FAD mice. Mechanistically, APS treatment reduced Aβ plaque burden, restored synaptic protein expression (PSD-95 and Syntaxin), and attenuated microglia-mediated neuroinflammation by suppressing pro-inflammatory cytokines (IL-6, TNF-α) and upregulating TREM2. Microbiome analysis revealed that APS reshaped gut microbial diversity and composition, enriching beneficial taxa such as Lactobacillus. Metabolomics indicated a partial restoration of amino acid metabolism. Notably, FMT from APS-treated donors successfully reproduced the cognitive improvements and anti-inflammatory effects in recipient mice.
CONCLUSION: These findings demonstrate that APS alleviates cognitive deficits and AD-like pathology, partially through remodeling gut microbiota and modulating the gut-brain axis. APS represents a promising natural compound-based therapeutic candidate for managing cognitive decline associated with Alzheimer's disease.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Characterization of oral microbiome alterations in thalassemia patients using 16S rRNA gene sequencing.
Frontiers in microbiology, 17:1853312.
BACKGROUND: This study investigates the composition of the oral microbiota in thalassemia patients and compares it with healthy individuals from Saudi Arabia. Thalassemia is an inherited blood disorder characterized by reduced or absent production of globin chains, resulting in hypochromic microcytic anemia and multiple complications, such as iron overload resulting from frequent blood transfusions.
METHODS: Using 16S rRNA gene sequencing, 28 saliva samples (14 thalassemia patients and 14 healthy controls) were analyzed to assess changes in the richness and diversity of the oral microbiota.
RESULTS: Taxonomic analysis demonstrated nominal differences between the two groups, with notable variations in the abundance of several bacterial species. All taxa showing differential abundance belonged to two phyla-Firmicutes and Bacteroidota; including taxa such as Prevotella intermedia, Eubacterium sulci, and Porphyromonas gingivalis. Although several taxa showed nominal differences based on raw p-values, none remained statistically significant after Benjamini-Hochberg false discovery rate (FDR) correction. Thalassemia patients exhibited a nominal reduction in the relative abundance of bacteria such as Prevotella.
CONCLUSION: Overall, this study suggests possible alterations in the oral microbiome associated with thalassemia; however, these findings require validation in larger cohorts with comprehensive clinical and oral health data.
Additional Links: PMID-42676816
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@article {pmid42676816,
year = {2026},
author = {Alghamdi, MA and Almalki, SA and Bahieldin, A and Radhwi, O and Rather, IA},
title = {Characterization of oral microbiome alterations in thalassemia patients using 16S rRNA gene sequencing.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1853312},
pmid = {42676816},
issn = {1664-302X},
abstract = {BACKGROUND: This study investigates the composition of the oral microbiota in thalassemia patients and compares it with healthy individuals from Saudi Arabia. Thalassemia is an inherited blood disorder characterized by reduced or absent production of globin chains, resulting in hypochromic microcytic anemia and multiple complications, such as iron overload resulting from frequent blood transfusions.
METHODS: Using 16S rRNA gene sequencing, 28 saliva samples (14 thalassemia patients and 14 healthy controls) were analyzed to assess changes in the richness and diversity of the oral microbiota.
RESULTS: Taxonomic analysis demonstrated nominal differences between the two groups, with notable variations in the abundance of several bacterial species. All taxa showing differential abundance belonged to two phyla-Firmicutes and Bacteroidota; including taxa such as Prevotella intermedia, Eubacterium sulci, and Porphyromonas gingivalis. Although several taxa showed nominal differences based on raw p-values, none remained statistically significant after Benjamini-Hochberg false discovery rate (FDR) correction. Thalassemia patients exhibited a nominal reduction in the relative abundance of bacteria such as Prevotella.
CONCLUSION: Overall, this study suggests possible alterations in the oral microbiome associated with thalassemia; however, these findings require validation in larger cohorts with comprehensive clinical and oral health data.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Mechanistic evidence and assumptions in mycotoxin-gut interaction.
Frontiers in fungal biology, 7:1855881.
Mycotoxins are increasingly recognised as ecological mediators that act through a bidirectional gut-microbiota axis. Microbial metabolism governs toxin fate by driving detoxification, bioactivation, sequestration and deconjugation, whereas mycotoxin exposure reshapes microbial communities, disrupts epithelial barrier function and amplifies immune signalling. Across aflatoxin B1, ochratoxin A, fumonisin B1, deoxynivalenol and T-2 toxin, the microbiome emerges as both a determinant and a target of toxicity, with strain-level functional diversity influencing susceptibility, detoxification capacity and host outcome. A further consequence of chronic exposure may be selection for pathobionts and antibiotic-resistant populations, raising the possibility that mycotoxins contribute to microbiome instability beyond direct toxic effects. Despite these advances, most evidence remains correlative or model-specific, and causal validation in vivo is still limited. Integrating microbiology, metabolomics, epithelial biology and ecological theory is essential to understand these interactions and to better guide microbiome-informed strategies for mycotoxin exposure mitigation.
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@article {pmid42676822,
year = {2026},
author = {Garcia-Cela, E and Marcon Gasperini, A},
title = {Mechanistic evidence and assumptions in mycotoxin-gut interaction.},
journal = {Frontiers in fungal biology},
volume = {7},
number = {},
pages = {1855881},
pmid = {42676822},
issn = {2673-6128},
abstract = {Mycotoxins are increasingly recognised as ecological mediators that act through a bidirectional gut-microbiota axis. Microbial metabolism governs toxin fate by driving detoxification, bioactivation, sequestration and deconjugation, whereas mycotoxin exposure reshapes microbial communities, disrupts epithelial barrier function and amplifies immune signalling. Across aflatoxin B1, ochratoxin A, fumonisin B1, deoxynivalenol and T-2 toxin, the microbiome emerges as both a determinant and a target of toxicity, with strain-level functional diversity influencing susceptibility, detoxification capacity and host outcome. A further consequence of chronic exposure may be selection for pathobionts and antibiotic-resistant populations, raising the possibility that mycotoxins contribute to microbiome instability beyond direct toxic effects. Despite these advances, most evidence remains correlative or model-specific, and causal validation in vivo is still limited. Integrating microbiology, metabolomics, epithelial biology and ecological theory is essential to understand these interactions and to better guide microbiome-informed strategies for mycotoxin exposure mitigation.},
}
RevDate: 2026-09-01
Soil-derived, gut-dominant generalist bacteria shape the fitness of folivorous larvae.
Whether Lepidoptera harbor a conserved core gut microbiome has long remained contentious. Through large-scale microbiome profiling of folivorous larvae, their host plants, and associated soils across three climatically distinct regions of China, we identify two soil-derived generalist bacteria, Ralstonia insidiosa and Delftia sp., that colonize 97.92% of larval species examined, attaining mean relative abundances exceeding 47%, with the soil microbial reservoir as their principal source. Strikingly, these two taxa exhibit strong mutual exclusion within the larval gut yet govern host development through diametrically opposed metabolic strategies: R. insidiosa promotes larval weight gain, whereas Delftia sp. suppresses growth. This functional bifurcation, in which two widespread generalists exert opposite phenotypic effects, represents a previously undescribed phenomenon in insect-microbe symbiosis. Our findings provide broad evidence that soil microbial reservoirs can shape aboveground herbivore fitness via horizontally acquired bacteria, offering mechanistic insights for microbiome-based ecological management.
Additional Links: PMID-42676834
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@article {pmid42676834,
year = {2026},
author = {Zheng, YX and Wang, Y and Zhang, XM and Jin, Q and Zhang, Y and Wang, GF and Shao, YQ and Li, J and Sun, C and Kong, WD and Yang, CQ and Zhang, AB},
title = {Soil-derived, gut-dominant generalist bacteria shape the fitness of folivorous larvae.},
journal = {iMeta},
volume = {},
number = {},
pages = {e70169},
pmid = {42676834},
issn = {2770-596X},
abstract = {Whether Lepidoptera harbor a conserved core gut microbiome has long remained contentious. Through large-scale microbiome profiling of folivorous larvae, their host plants, and associated soils across three climatically distinct regions of China, we identify two soil-derived generalist bacteria, Ralstonia insidiosa and Delftia sp., that colonize 97.92% of larval species examined, attaining mean relative abundances exceeding 47%, with the soil microbial reservoir as their principal source. Strikingly, these two taxa exhibit strong mutual exclusion within the larval gut yet govern host development through diametrically opposed metabolic strategies: R. insidiosa promotes larval weight gain, whereas Delftia sp. suppresses growth. This functional bifurcation, in which two widespread generalists exert opposite phenotypic effects, represents a previously undescribed phenomenon in insect-microbe symbiosis. Our findings provide broad evidence that soil microbial reservoirs can shape aboveground herbivore fitness via horizontally acquired bacteria, offering mechanistic insights for microbiome-based ecological management.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Lung microbiome features associated with ICU delirium in mechanically ventilated patients: a secondary cohort analysis.
Brain, behavior, & immunity - health, 56:101335.
BACKGROUND: Delirium in mechanically ventilated intensive care unit (ICU) patients is linked to inflammatory dysregulation, but whether the pulmonary microbiome contributes to delirium risk remains unclear.
METHODS: We performed a secondary analysis of 132 mechanically ventilated adults from the MicroNAV cohort. Baseline bronchoalveolar lavage (BAL) samples collected within 12 h of intubation were profiled by 16S rRNA gene sequencing; total bacterial burden was quantified by droplet digital PCR (ddPCR; n = 125), and BAL cytokines were measured using a multiplex assay (n = 70). Concordant genus-level signals identified by four differential-abundance methods were aggregated into ecological scores and tested using logistic regression adjusted for age and Glasgow Coma Scale at intubation. Absolute abundance was estimated by multiplying relative abundance by ddPCR-derived bacterial burden.
RESULTS: Delirium was recorded in 45 patients (34.1%). Total bacterial DNA concentration was lower in patients with delirium (median 7419 vs 98,326 copies/μL, P = 0.001). A putative short-chain fatty acid (SCFA)-producing commensal score (Phocaeicola, Selenomonas, and Fretibacterium) was inversely associated with delirium in compositional analysis (OR 0.83, 95% CI 0.75-0.92, P < 0.001) and after ddPCR-anchored absolute quantification (OR 0.84, 95% CI 0.75-0.94, P = 0.002). This depletion extended to oral-core commensals (absolute OR 0.80, P < 0.001) and a pre-specified oral anaerobe score (absolute OR 0.82, P = 0.002). Opportunistic colonizers were enriched compositionally but not in absolute abundance (OR 1.10, P = 0.187). Commensal scores were positively associated with BAL IL-1β and TNF-α, whereas opportunistic-colonizer scores showed inverse associations.
CONCLUSIONS: Early pulmonary depletion of oral-derived commensals, particularly putative SCFA producers, was associated with ICU delirium. Prospective studies with standardized delirium assessment and functional metabolite measurements are needed.
Additional Links: PMID-42676966
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@article {pmid42676966,
year = {2026},
author = {Xiao, S and Lin, F and Li, Y and Zhuang, Q},
title = {Lung microbiome features associated with ICU delirium in mechanically ventilated patients: a secondary cohort analysis.},
journal = {Brain, behavior, & immunity - health},
volume = {56},
number = {},
pages = {101335},
pmid = {42676966},
issn = {2666-3546},
abstract = {BACKGROUND: Delirium in mechanically ventilated intensive care unit (ICU) patients is linked to inflammatory dysregulation, but whether the pulmonary microbiome contributes to delirium risk remains unclear.
METHODS: We performed a secondary analysis of 132 mechanically ventilated adults from the MicroNAV cohort. Baseline bronchoalveolar lavage (BAL) samples collected within 12 h of intubation were profiled by 16S rRNA gene sequencing; total bacterial burden was quantified by droplet digital PCR (ddPCR; n = 125), and BAL cytokines were measured using a multiplex assay (n = 70). Concordant genus-level signals identified by four differential-abundance methods were aggregated into ecological scores and tested using logistic regression adjusted for age and Glasgow Coma Scale at intubation. Absolute abundance was estimated by multiplying relative abundance by ddPCR-derived bacterial burden.
RESULTS: Delirium was recorded in 45 patients (34.1%). Total bacterial DNA concentration was lower in patients with delirium (median 7419 vs 98,326 copies/μL, P = 0.001). A putative short-chain fatty acid (SCFA)-producing commensal score (Phocaeicola, Selenomonas, and Fretibacterium) was inversely associated with delirium in compositional analysis (OR 0.83, 95% CI 0.75-0.92, P < 0.001) and after ddPCR-anchored absolute quantification (OR 0.84, 95% CI 0.75-0.94, P = 0.002). This depletion extended to oral-core commensals (absolute OR 0.80, P < 0.001) and a pre-specified oral anaerobe score (absolute OR 0.82, P = 0.002). Opportunistic colonizers were enriched compositionally but not in absolute abundance (OR 1.10, P = 0.187). Commensal scores were positively associated with BAL IL-1β and TNF-α, whereas opportunistic-colonizer scores showed inverse associations.
CONCLUSIONS: Early pulmonary depletion of oral-derived commensals, particularly putative SCFA producers, was associated with ICU delirium. Prospective studies with standardized delirium assessment and functional metabolite measurements are needed.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Endoscopic Prevalence of Barrett's Esophagus in a Predominantly African American and Hispanic Population.
Cureus, 18(8):e113784.
Background and aim Barrett's esophagus (BE) is a well-known premalignant disorder. Investigators have shown that the prevalence of histologically confirmed BE varies among ethnic groups in the US. However, these studies were not performed at institutions that predominantly serve US minority populations. The aim of this study was to assess the prevalence of histologically confirmed BE at an institution that serves a predominantly African American (AA) and Hispanic American patient population. Methods The Harlem Hospital endoscopy and pathology databases were searched to identify all patients who underwent esophagogastroduodenoscopy (EGD) with biopsy and had histologically confirmed BE. Histological confirmation of BE was determined by the presence of intestinal metaplasia and Alcian blue-stained goblet cells in biopsies obtained from salmon-colored esophageal mucosa. Demographic data collected included age, sex, race/ethnicity, BMI, history of gastroesophageal reflux disease, endoscopic BE length, presence of hiatal hernia, esophagitis, or esophageal ulcer, presence or absence of dysplasia, proton pump inhibitor use, active Helicobacter pylori infection, and smoking and alcohol use. Results A total of 3,012 patients underwent EGD during the study period. Esophageal biopsy was performed on salmon-colored esophageal mucosa suspicious for BE in 18 individuals. BE was histologically confirmed in eight patients: five AAs, two Hispanics, and one non-Hispanic White (nHW). The overall prevalence of BE was 0.2%, with a lower prevalence observed among AA patients (0.3%) and Hispanic patients (0.1%) than among nHW patients (3.3%, p < 0.05). Four patients had dysplasia (three with low-grade dysplasia and one with high-grade dysplasia; three AA and one Hispanic). Conclusions The prevalence of BE in our predominantly minority population was lower than that observed among nHW patients, consistent with previous literature. Investigations at the microbiome and genetic levels are needed to explain the observed disparity in BE prevalence among ethnic groups.
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@article {pmid42677001,
year = {2026},
author = {Akpoigbe, K and Culpepper-Morgan, J and Barnes, A and Kwentoh, I and Vega, KJ},
title = {Endoscopic Prevalence of Barrett's Esophagus in a Predominantly African American and Hispanic Population.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e113784},
pmid = {42677001},
issn = {2168-8184},
abstract = {Background and aim Barrett's esophagus (BE) is a well-known premalignant disorder. Investigators have shown that the prevalence of histologically confirmed BE varies among ethnic groups in the US. However, these studies were not performed at institutions that predominantly serve US minority populations. The aim of this study was to assess the prevalence of histologically confirmed BE at an institution that serves a predominantly African American (AA) and Hispanic American patient population. Methods The Harlem Hospital endoscopy and pathology databases were searched to identify all patients who underwent esophagogastroduodenoscopy (EGD) with biopsy and had histologically confirmed BE. Histological confirmation of BE was determined by the presence of intestinal metaplasia and Alcian blue-stained goblet cells in biopsies obtained from salmon-colored esophageal mucosa. Demographic data collected included age, sex, race/ethnicity, BMI, history of gastroesophageal reflux disease, endoscopic BE length, presence of hiatal hernia, esophagitis, or esophageal ulcer, presence or absence of dysplasia, proton pump inhibitor use, active Helicobacter pylori infection, and smoking and alcohol use. Results A total of 3,012 patients underwent EGD during the study period. Esophageal biopsy was performed on salmon-colored esophageal mucosa suspicious for BE in 18 individuals. BE was histologically confirmed in eight patients: five AAs, two Hispanics, and one non-Hispanic White (nHW). The overall prevalence of BE was 0.2%, with a lower prevalence observed among AA patients (0.3%) and Hispanic patients (0.1%) than among nHW patients (3.3%, p < 0.05). Four patients had dysplasia (three with low-grade dysplasia and one with high-grade dysplasia; three AA and one Hispanic). Conclusions The prevalence of BE in our predominantly minority population was lower than that observed among nHW patients, consistent with previous literature. Investigations at the microbiome and genetic levels are needed to explain the observed disparity in BE prevalence among ethnic groups.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Ecosystem retrogression enhances cross-domain microbial stability and increases the genetic potential for nutrient cycling.
mLife, 5(4):486-506.
Ecosystem retrogression drives nutrient depletion, reduced productivity, and profound reorganization of soil microbial communities. Using amplicon sequencing and genome-resolved metagenomics, we examined how cross-domain microbial networks and functional gene potential respond to long-term phosphorus and nitrogen limitation along the well-characterized Ecological Staircase chronosequence in Mendocino, California, USA. Microbial diversity and abundance declined sharply with terrace age for prokaryotes, predatory protists, and bacteriophages, whereas fungi and phototrophic protists increased in nutrient-depleted, acidic soils. These compositional shifts were accompanied by major changes in reconstructed microbial networks: relative modularity increased alongside robustness, indicating adaptive reorganization that may sustain ecosystem function under resource scarcity. Fungi emerged as central stabilizers in these restructured networks, carrying enriched genetic potential to degrade plant polymers and mobilize phosphorus and nitrogen. Despite a decline in overall phage diversity, the relative abundance of phages encoding phosphorus-mobilizing auxiliary metabolic genes increased, suggesting that viral contributions to host phosphorus metabolism may be enhanced under nutrient limitation. Together, these results demonstrate that ecosystem retrogression drives cross-domain microbial reorganization toward fewer but more interconnected lineages, characterized by greater integration of functional genetic potential. This reorganization enhances the potential for functional resilience under extreme nutrient limitation, revealing how microbial networks adapt to maintain the capacity for nutrient cycling and stability as soils age and fertility declines.
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@article {pmid42677031,
year = {2026},
author = {Ceja-Navarro, JA and Patel, D and Genco, G and Byer, A and Ning, D and Wan, KH and Celniker, SE and Zhou, J and Dijkstra, P and Hungate, BA and Pett-Ridge, J and Brodie, EL},
title = {Ecosystem retrogression enhances cross-domain microbial stability and increases the genetic potential for nutrient cycling.},
journal = {mLife},
volume = {5},
number = {4},
pages = {486-506},
pmid = {42677031},
issn = {2770-100X},
abstract = {Ecosystem retrogression drives nutrient depletion, reduced productivity, and profound reorganization of soil microbial communities. Using amplicon sequencing and genome-resolved metagenomics, we examined how cross-domain microbial networks and functional gene potential respond to long-term phosphorus and nitrogen limitation along the well-characterized Ecological Staircase chronosequence in Mendocino, California, USA. Microbial diversity and abundance declined sharply with terrace age for prokaryotes, predatory protists, and bacteriophages, whereas fungi and phototrophic protists increased in nutrient-depleted, acidic soils. These compositional shifts were accompanied by major changes in reconstructed microbial networks: relative modularity increased alongside robustness, indicating adaptive reorganization that may sustain ecosystem function under resource scarcity. Fungi emerged as central stabilizers in these restructured networks, carrying enriched genetic potential to degrade plant polymers and mobilize phosphorus and nitrogen. Despite a decline in overall phage diversity, the relative abundance of phages encoding phosphorus-mobilizing auxiliary metabolic genes increased, suggesting that viral contributions to host phosphorus metabolism may be enhanced under nutrient limitation. Together, these results demonstrate that ecosystem retrogression drives cross-domain microbial reorganization toward fewer but more interconnected lineages, characterized by greater integration of functional genetic potential. This reorganization enhances the potential for functional resilience under extreme nutrient limitation, revealing how microbial networks adapt to maintain the capacity for nutrient cycling and stability as soils age and fertility declines.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Biological and Habitual Factors That Influence Sleep and Circadian Rhythm: A Narrative Review.
Cureus, 18(8):e113792.
Sleep loss and circadian misalignment can adversely affect health. As such, a comprehensive understanding of what factors influence sleep loss and circadian misalignment benefits medical and scientific progress. While the interaction between light exposure and circadian entrainment and their relationship to circadian alignment is long-established, other factors that influence central or peripheral clocks (bodily oscillators) also contribute to circadian alignment and the potential for sleep loss. In this review, we will highlight the core factors that influence vulnerability or resilience to sleep loss and circadian misalignment, including biologic factors, such as gene haplotype, chronotype, and the gut microbiome. Furthermore, we will consider how habitual and largely modifiable variables, such as timing of meals and physical activity, can be manipulated to affect circadian and sleep cycles. Gaps in current scientific research on the effects of circadian misalignment and sleep loss will also be identified. This review will thus help inform future research and enhance the understanding of how healthy sleep and balanced circadian rhythm can improve quality of life.
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@article {pmid42677033,
year = {2026},
author = {Harmon, VJ and Davis, CJ},
title = {Biological and Habitual Factors That Influence Sleep and Circadian Rhythm: A Narrative Review.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e113792},
pmid = {42677033},
issn = {2168-8184},
abstract = {Sleep loss and circadian misalignment can adversely affect health. As such, a comprehensive understanding of what factors influence sleep loss and circadian misalignment benefits medical and scientific progress. While the interaction between light exposure and circadian entrainment and their relationship to circadian alignment is long-established, other factors that influence central or peripheral clocks (bodily oscillators) also contribute to circadian alignment and the potential for sleep loss. In this review, we will highlight the core factors that influence vulnerability or resilience to sleep loss and circadian misalignment, including biologic factors, such as gene haplotype, chronotype, and the gut microbiome. Furthermore, we will consider how habitual and largely modifiable variables, such as timing of meals and physical activity, can be manipulated to affect circadian and sleep cycles. Gaps in current scientific research on the effects of circadian misalignment and sleep loss will also be identified. This review will thus help inform future research and enhance the understanding of how healthy sleep and balanced circadian rhythm can improve quality of life.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Gut microbiota-targeted bioactive peptides as emerging axis in nutritional therapeutics: trends, challenges, and prospects.
Frontiers in nutrition, 13:1905173.
The gut microbiota is a dynamic, complex microbial ecosystem that is fundamental to human health and influences metabolism, immunity, and susceptibility to disease. There is growing evidence that bioactive peptides (BAPs) are important regulators of gut microbiota composition and function. BAPs are short protein fragments liberated through enzymatic hydrolysis or microbial fermentation in vitro and during the digestion of food proteins in vivo. The biological activities of these BAPs, beyond their antioxidant, antihypertensive, and antimicrobial effects, include maintaining gut balance and supporting overall well-being. The relationship between BAPs and gut microbiota is two-way: peptides selectively promote beneficial microbes, and the microbiota enzymatically convert peptides into bioactive metabolites such as short-chain fatty acids and altered bile acids, or further hydrolyze them into shorter BAPs. This interaction between gut microbiota and BAPs has been shown to confer significant therapeutic benefits from combined nutritional interventions in the management of chronic diseases, including obesity, diabetes, inflammatory bowel diseases, and neurological diseases. This review examines the current state of gut microbiota-targeted BAPs, including their sources, properties, and mechanisms. It underscores their contribution to microbial diversity and metabolic activity, which support immune balance and the functioning of the gut-brain axis. In addition, it addresses novel ways to increase the activity of BAPs with respect to stability and delivery. Challenges such as peptide bioavailability, microbiome diversity, and a lack of clinical evidence are also critically discussed. Future perspectives focus on leveraging omics technologies and personalized nutrition to unlock the potential of BAPs for therapeutic and functional food applications. The review indicates the promising potential of BAPs as microbiota-based, innovative, and useful agents in nutritional therapy.
Additional Links: PMID-42677167
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Citation:
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@article {pmid42677167,
year = {2026},
author = {Singh, BP and Bose, P and Je, JY},
title = {Gut microbiota-targeted bioactive peptides as emerging axis in nutritional therapeutics: trends, challenges, and prospects.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1905173},
pmid = {42677167},
issn = {2296-861X},
abstract = {The gut microbiota is a dynamic, complex microbial ecosystem that is fundamental to human health and influences metabolism, immunity, and susceptibility to disease. There is growing evidence that bioactive peptides (BAPs) are important regulators of gut microbiota composition and function. BAPs are short protein fragments liberated through enzymatic hydrolysis or microbial fermentation in vitro and during the digestion of food proteins in vivo. The biological activities of these BAPs, beyond their antioxidant, antihypertensive, and antimicrobial effects, include maintaining gut balance and supporting overall well-being. The relationship between BAPs and gut microbiota is two-way: peptides selectively promote beneficial microbes, and the microbiota enzymatically convert peptides into bioactive metabolites such as short-chain fatty acids and altered bile acids, or further hydrolyze them into shorter BAPs. This interaction between gut microbiota and BAPs has been shown to confer significant therapeutic benefits from combined nutritional interventions in the management of chronic diseases, including obesity, diabetes, inflammatory bowel diseases, and neurological diseases. This review examines the current state of gut microbiota-targeted BAPs, including their sources, properties, and mechanisms. It underscores their contribution to microbial diversity and metabolic activity, which support immune balance and the functioning of the gut-brain axis. In addition, it addresses novel ways to increase the activity of BAPs with respect to stability and delivery. Challenges such as peptide bioavailability, microbiome diversity, and a lack of clinical evidence are also critically discussed. Future perspectives focus on leveraging omics technologies and personalized nutrition to unlock the potential of BAPs for therapeutic and functional food applications. The review indicates the promising potential of BAPs as microbiota-based, innovative, and useful agents in nutritional therapy.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Gut-muscle axis in sarcopenia: from mechanisms to microbiome-based therapies.
Frontiers in nutrition, 13:1846179.
Sarcopenia is a disease characterized by reduced muscle mass and strength. In recent years, increasing evidence suggests that gut microbiota (GM) may play an important role in the pathogenesis of sarcopenia. GM is associated with muscle health by affecting muscle metabolism, regulating inflammatory responses, and promoting nutrient absorption. Despite recent rapid research progress, there are still many uncertainties regarding the causal relationship between GM and sarcopenia, key effector molecules, and individualized intervention strategies. We review the mechanisms of GM in the pathogenesis of sarcopenia with a focus on four interconnected pathways: chronic inflammation, nutrient absorption, amino acid metabolism, and GM-derived metabolites. This review aims to propose an integrated framework linking GM to muscle homeostasis to guide future research directions. Interventions targeting GM may offer a new approach for the treatment of sarcopenia, but more research is needed to clarify the causal relationship and optimize intervention measures.
Additional Links: PMID-42677176
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@article {pmid42677176,
year = {2026},
author = {Liu, Y and Lu, S and Li, L and Yin, J and Han, P and Zha, Y and Jiang, X},
title = {Gut-muscle axis in sarcopenia: from mechanisms to microbiome-based therapies.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1846179},
pmid = {42677176},
issn = {2296-861X},
abstract = {Sarcopenia is a disease characterized by reduced muscle mass and strength. In recent years, increasing evidence suggests that gut microbiota (GM) may play an important role in the pathogenesis of sarcopenia. GM is associated with muscle health by affecting muscle metabolism, regulating inflammatory responses, and promoting nutrient absorption. Despite recent rapid research progress, there are still many uncertainties regarding the causal relationship between GM and sarcopenia, key effector molecules, and individualized intervention strategies. We review the mechanisms of GM in the pathogenesis of sarcopenia with a focus on four interconnected pathways: chronic inflammation, nutrient absorption, amino acid metabolism, and GM-derived metabolites. This review aims to propose an integrated framework linking GM to muscle homeostasis to guide future research directions. Interventions targeting GM may offer a new approach for the treatment of sarcopenia, but more research is needed to clarify the causal relationship and optimize intervention measures.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
NLRP3 inflammasome pathway activation is associated with cardiac remodeling, gut microbiota dysbiosis, and dietary protein restriction in a rat heart failure model: an integrative exploratory analysis.
Frontiers in genetics, 17:1852819.
OBJECTIVE: To characterize protein expression of NLRP3 inflammasome pathway components (NLRP3, TXNIP, ASC, IL-1β, IL-18, Caspase-1) in failing myocardium alongside exploratory mRNA profiling, elucidate their correlation with gut microbiota 16S rRNA gene profiles and the metabolite trimethylamine N-oxide (TMAO), and evaluate how dietary protein restriction and probiotic intervention modulate these pathways to influence heart failure progression.
METHODS: Five groups of male SD rats were established: Control, HF, HF + Pro, LHF, and LHF + Pro, using abdominal aortic constriction. Comprehensive genomic and molecular analyses included: (1) quantitative real-time PCR (qRT-PCR) profiling of six key inflammasome genes (NLRP3, TXNIP, ASC, IL-1β, IL-18, Caspase-1); (2) Western blot protein quantification of the NLRP3 pathway; (3) gut microbiota 16S rRNA gene sequencing (V3-V4 region, Illumina NovaSeq); (4) serum biomarker enzyme-linked immunosorbent assay (IL-18, IL-1β, TNF-α, brain natriuretic peptide, TMAO); and (5) histopathological and ultrastructural analysis of myocardial tissue.
RESULTS: Serum IL-18 protein levels were significantly elevated in the LHF group compared to controls (P < 0.05) by ELISA, with the most pronounced increase observed under dietary protein restriction; however, IL-18 mRNA expression by qRT-PCR showed directionally consistent but statistically non-significant trends across groups (P = 0.929, n = 3 per group). TMAO levels were decreased in HF and HF + Pro groups but paradoxically elevated in the LHF group, a finding discussed in detail in the context of dietary substrate availability and hepatic FMO3 activity. Western blot results showed that the expression of NLRP3, TXNIP, ASC, IL-1β, and IL-18 proteins increased in all heart failure groups compared to the control group, with the most significant increase in the low-protein diet group. Pathological examination revealed increased myocardial fibrosis in heart failure groups, which was further aggravated by low-protein diet, while probiotic intervention partially improved these pathological changes.
CONCLUSION: Heart failure is associated with upregulation of NLRP3 inflammasome proteins (NLRP3-TXNIP-ASC-IL-1β/IL-18 axis) alongside gut microbiota dysbiosis; mRNA-level trends were directionally consistent but did not reach statistical significance. Low-protein diet markedly amplifies inflammasome protein expression and cardiac remodeling, while probiotic supplementation is associated with reduced NLRP3 pathway protein expression through microbiome restoration. These findings suggest NLRP3-related protein signatures as candidate biomarkers and potential therapeutic targets in heart failure, warranting further mechanistic investigation.
Additional Links: PMID-42677289
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Citation:
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@article {pmid42677289,
year = {2026},
author = {Li, X and Yang, C and Nie, M and Zhang, Y},
title = {NLRP3 inflammasome pathway activation is associated with cardiac remodeling, gut microbiota dysbiosis, and dietary protein restriction in a rat heart failure model: an integrative exploratory analysis.},
journal = {Frontiers in genetics},
volume = {17},
number = {},
pages = {1852819},
pmid = {42677289},
issn = {1664-8021},
abstract = {OBJECTIVE: To characterize protein expression of NLRP3 inflammasome pathway components (NLRP3, TXNIP, ASC, IL-1β, IL-18, Caspase-1) in failing myocardium alongside exploratory mRNA profiling, elucidate their correlation with gut microbiota 16S rRNA gene profiles and the metabolite trimethylamine N-oxide (TMAO), and evaluate how dietary protein restriction and probiotic intervention modulate these pathways to influence heart failure progression.
METHODS: Five groups of male SD rats were established: Control, HF, HF + Pro, LHF, and LHF + Pro, using abdominal aortic constriction. Comprehensive genomic and molecular analyses included: (1) quantitative real-time PCR (qRT-PCR) profiling of six key inflammasome genes (NLRP3, TXNIP, ASC, IL-1β, IL-18, Caspase-1); (2) Western blot protein quantification of the NLRP3 pathway; (3) gut microbiota 16S rRNA gene sequencing (V3-V4 region, Illumina NovaSeq); (4) serum biomarker enzyme-linked immunosorbent assay (IL-18, IL-1β, TNF-α, brain natriuretic peptide, TMAO); and (5) histopathological and ultrastructural analysis of myocardial tissue.
RESULTS: Serum IL-18 protein levels were significantly elevated in the LHF group compared to controls (P < 0.05) by ELISA, with the most pronounced increase observed under dietary protein restriction; however, IL-18 mRNA expression by qRT-PCR showed directionally consistent but statistically non-significant trends across groups (P = 0.929, n = 3 per group). TMAO levels were decreased in HF and HF + Pro groups but paradoxically elevated in the LHF group, a finding discussed in detail in the context of dietary substrate availability and hepatic FMO3 activity. Western blot results showed that the expression of NLRP3, TXNIP, ASC, IL-1β, and IL-18 proteins increased in all heart failure groups compared to the control group, with the most significant increase in the low-protein diet group. Pathological examination revealed increased myocardial fibrosis in heart failure groups, which was further aggravated by low-protein diet, while probiotic intervention partially improved these pathological changes.
CONCLUSION: Heart failure is associated with upregulation of NLRP3 inflammasome proteins (NLRP3-TXNIP-ASC-IL-1β/IL-18 axis) alongside gut microbiota dysbiosis; mRNA-level trends were directionally consistent but did not reach statistical significance. Low-protein diet markedly amplifies inflammasome protein expression and cardiac remodeling, while probiotic supplementation is associated with reduced NLRP3 pathway protein expression through microbiome restoration. These findings suggest NLRP3-related protein signatures as candidate biomarkers and potential therapeutic targets in heart failure, warranting further mechanistic investigation.},
}
RevDate: 2026-09-01
Gut microbiome in preterm infants with different weight gain outcomes.
Gut microbiology, 2:.
BACKGROUND: Inadequate in-hospital weight gain among very low birth weight (VLBW; <1500g) infants is associated with adverse outcomes. Although microbiome alterations are linked to malnutrition in older children, their association with VLBW weight gain outcomes remains unclear.
OBJECTIVE: To evaluate associations between fecal microbiome composition, functional gene pathways, and metabolomic profile, and abnormal weight gain in VLBW infants.
METHODS: Prospective cohort study of VLBW infants from birth to hospital discharge with weekly fecal sampling. Inadequate weight gain was defined at 36 weeks post-menstrual age, as growth faltering (decline in weight-for-age z-scores from birth) and growth failure (<3[rd] percentile weight-for-age). Growth faltering was categorized as mild (0.8-1.2 decline) and moderate-severe (>1.2 decline). Fecal samples underwent shotgun metagenomic sequencing with KEGG-based functional annotation; [1]H NMR-based metabolomics was performed in a subset.
RESULTS: Among 101 enrolled infants, 54% had growth faltering (28 mild; 26 moderate-severe), and 18% had growth failure. The two outcomes rarely co-occurred (n=7). Microbiome diversity and taxonomic composition changed with age but did not differ by growth outcomes. Infants with moderate-to-severe faltering had reduced abundance of the glycolysis/gluconeogenesis pathway. Infants with growth failure showed a significant lag in microbiome maturity. Metabolite concentrations measured in a subset (n=46) were not significantly different in the study groups.
CONCLUSION: Abnormal weight gain in VLBW infants was not associated with major differences in microbial compositional or fecal metabolite levels. Differences identified in pathway analysis and in microbiome maturation may help focus future efforts to investigate the gut microbiome's role in VLBW weight gain.
Additional Links: PMID-42677317
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@article {pmid42677317,
year = {2026},
author = {Daniel, SG and Matute, JD and Dhudasia, MB and Rosewood, H and Wilson, NG and Patterson, A and Hao, F and Underwood, M and Bittinger, K and Mukhopadhyay, S},
title = {Gut microbiome in preterm infants with different weight gain outcomes.},
journal = {Gut microbiology},
volume = {2},
number = {},
pages = {},
pmid = {42677317},
issn = {3051-1720},
abstract = {BACKGROUND: Inadequate in-hospital weight gain among very low birth weight (VLBW; <1500g) infants is associated with adverse outcomes. Although microbiome alterations are linked to malnutrition in older children, their association with VLBW weight gain outcomes remains unclear.
OBJECTIVE: To evaluate associations between fecal microbiome composition, functional gene pathways, and metabolomic profile, and abnormal weight gain in VLBW infants.
METHODS: Prospective cohort study of VLBW infants from birth to hospital discharge with weekly fecal sampling. Inadequate weight gain was defined at 36 weeks post-menstrual age, as growth faltering (decline in weight-for-age z-scores from birth) and growth failure (<3[rd] percentile weight-for-age). Growth faltering was categorized as mild (0.8-1.2 decline) and moderate-severe (>1.2 decline). Fecal samples underwent shotgun metagenomic sequencing with KEGG-based functional annotation; [1]H NMR-based metabolomics was performed in a subset.
RESULTS: Among 101 enrolled infants, 54% had growth faltering (28 mild; 26 moderate-severe), and 18% had growth failure. The two outcomes rarely co-occurred (n=7). Microbiome diversity and taxonomic composition changed with age but did not differ by growth outcomes. Infants with moderate-to-severe faltering had reduced abundance of the glycolysis/gluconeogenesis pathway. Infants with growth failure showed a significant lag in microbiome maturity. Metabolite concentrations measured in a subset (n=46) were not significantly different in the study groups.
CONCLUSION: Abnormal weight gain in VLBW infants was not associated with major differences in microbial compositional or fecal metabolite levels. Differences identified in pathway analysis and in microbiome maturation may help focus future efforts to investigate the gut microbiome's role in VLBW weight gain.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Contrasts in niche breadth and its drivers between soil microbes and plants in alpine grasslands.
ISME communications, 6(1):ycag193.
Niche breadth reflects the extent to which taxa or communities can tolerate environmental variations, indicating their potential to respond to environmental changes. However, it remains unclear whether micro- and macro-organisms share similar patterns of niche breadth along the same environmental gradients, and which environmental filters regulates niche breadth across different trophic levels. In this study, 180 soil samples were collected from the northeastern and central Qinghai-Tibet Plateau. By integrating microbiome sequencing with plant community surveys, we quantified niche breadth for bacteria, fungi, and plants within a multidimensional environmental space defined by principal component analysis of environmental variables. We then compared niche breadth among the three groups and identified their primary environmental drivers. The results showed that fungal communities exhibited the broadest niche breadth overall, whereas plant communities displayed the greatest variability in mean niche breadth amongst sites. Elevation was a shared determinant of niche breadth in all groups, although with contrasting response patterns. Bacterial and fungal communities exhibited broader niche breadths at higher elevations, whereas plant communities reached their maximum niche breadths at mid-elevations, suggesting contrasting adaptive strategies. A combination of abiotic (geography and environment) and biotic (community diversity and composition) factors better explained the variation in niche breadth. In particular, compared with the niche breadth of fungal communities, that of bacterial and plant communities was more strongly regulated by biotic factors such as community composition. We further confirmed that abiotic factors influenced the niche breadth of the three biological groups, both directly and indirectly, by shaping their biotic attributes. From the perspective of niche breadth, this study revealed distinct environmental adaptation patterns and the underlying mechanisms of different biological groups in alpine grassland ecosystems. Better understanding of niche breadth patterns amongst different kingdoms of life may provide improved prediction of turnover and resilience of soil ecosystems under environmental change.
Additional Links: PMID-42677325
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@article {pmid42677325,
year = {2026},
author = {Chen, L and Dong, K and Zhao, M and Yu, Z and Li, N and Kerfahi, D and Shi, Y and Jing, X and Chen, L and Chu, H and He, J and Lee, SS and Yang, T and Adams, JM},
title = {Contrasts in niche breadth and its drivers between soil microbes and plants in alpine grasslands.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag193},
pmid = {42677325},
issn = {2730-6151},
abstract = {Niche breadth reflects the extent to which taxa or communities can tolerate environmental variations, indicating their potential to respond to environmental changes. However, it remains unclear whether micro- and macro-organisms share similar patterns of niche breadth along the same environmental gradients, and which environmental filters regulates niche breadth across different trophic levels. In this study, 180 soil samples were collected from the northeastern and central Qinghai-Tibet Plateau. By integrating microbiome sequencing with plant community surveys, we quantified niche breadth for bacteria, fungi, and plants within a multidimensional environmental space defined by principal component analysis of environmental variables. We then compared niche breadth among the three groups and identified their primary environmental drivers. The results showed that fungal communities exhibited the broadest niche breadth overall, whereas plant communities displayed the greatest variability in mean niche breadth amongst sites. Elevation was a shared determinant of niche breadth in all groups, although with contrasting response patterns. Bacterial and fungal communities exhibited broader niche breadths at higher elevations, whereas plant communities reached their maximum niche breadths at mid-elevations, suggesting contrasting adaptive strategies. A combination of abiotic (geography and environment) and biotic (community diversity and composition) factors better explained the variation in niche breadth. In particular, compared with the niche breadth of fungal communities, that of bacterial and plant communities was more strongly regulated by biotic factors such as community composition. We further confirmed that abiotic factors influenced the niche breadth of the three biological groups, both directly and indirectly, by shaping their biotic attributes. From the perspective of niche breadth, this study revealed distinct environmental adaptation patterns and the underlying mechanisms of different biological groups in alpine grassland ecosystems. Better understanding of niche breadth patterns amongst different kingdoms of life may provide improved prediction of turnover and resilience of soil ecosystems under environmental change.},
}
RevDate: 2026-09-01
Metabolic shifts driven by host-microbial interactions.
The FEBS journal [Epub ahead of print].
Host-microbe interactions within the gut have been extensively reviewed in the context of host immune response. Emerging evidence, however, highlights that these inflammatory and immune outcomes are often deeply intertwined with the microbiome-derived secondary metabolites. The gut microbiota functions in concert with the host by providing an extensive repertoire of metabolic enzymes that enhance digestion and capacity to assimilate a broad spectrum of ingested food sources. This symbiotic metabolism generates a diverse array of bioactive metabolites that shape local and systemic physiology, adaptive immune responses, and neuroimmune responses. Here, we focus on microbial metabolism as a central organizing principle of host-microbiota symbiosis. Microbiota-derived metabolites, including short-chain fatty acids, secondary bile acids, tryptophan-derived indoles, sphingolipids, and gaseous byproducts, signal through downstream molecular partners like nuclear receptors, transcriptional regulators, and redox-sensitive homeostatic pathways to regulate host energy homeostasis, but also alter immune functions like gut epithelial integrity, immune tolerance, and neuroimmune crosstalk. Finally, we discuss emerging therapeutic strategies that target microbial metabolic functions-including dietary interventions, engineered probiotics, postbiotics, and receptor-directed approaches-that position microbial metabolism as a tractable axis for modulating immunometabolism homeostasis and potentially mitigating metabolic and inflammatory diseases.
Additional Links: PMID-42677452
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@article {pmid42677452,
year = {2026},
author = {Nair, T and Stuhr, NL and Weathers, BA and Curran, SP},
title = {Metabolic shifts driven by host-microbial interactions.},
journal = {The FEBS journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/febs.70704},
pmid = {42677452},
issn = {1742-4658},
support = {HF-004//Hevolution Foundation/ ; AG052374/AG/NIA NIH HHS/United States ; },
abstract = {Host-microbe interactions within the gut have been extensively reviewed in the context of host immune response. Emerging evidence, however, highlights that these inflammatory and immune outcomes are often deeply intertwined with the microbiome-derived secondary metabolites. The gut microbiota functions in concert with the host by providing an extensive repertoire of metabolic enzymes that enhance digestion and capacity to assimilate a broad spectrum of ingested food sources. This symbiotic metabolism generates a diverse array of bioactive metabolites that shape local and systemic physiology, adaptive immune responses, and neuroimmune responses. Here, we focus on microbial metabolism as a central organizing principle of host-microbiota symbiosis. Microbiota-derived metabolites, including short-chain fatty acids, secondary bile acids, tryptophan-derived indoles, sphingolipids, and gaseous byproducts, signal through downstream molecular partners like nuclear receptors, transcriptional regulators, and redox-sensitive homeostatic pathways to regulate host energy homeostasis, but also alter immune functions like gut epithelial integrity, immune tolerance, and neuroimmune crosstalk. Finally, we discuss emerging therapeutic strategies that target microbial metabolic functions-including dietary interventions, engineered probiotics, postbiotics, and receptor-directed approaches-that position microbial metabolism as a tractable axis for modulating immunometabolism homeostasis and potentially mitigating metabolic and inflammatory diseases.},
}
RevDate: 2026-09-01
Nano-boron nitride enhances soybean growth and symbiotic nitrogen fixation by modulating the rhizosphere microbiome and biogeochemical cycling.
Nanoscale [Epub ahead of print].
Nanotechnology offers promising strategies for sustainable agriculture, yet the systemic mechanisms by which nanomaterials enhance legume nitrogen fixation remain insufficiently understood. The multi-scale impacts of nano-boron nitride (nano-BN) on soybean growth, biological nitrogen fixation, and rhizosphere microbial communities were investigated. Soil addition of 50 mg kg[-1] nano-BN significantly promoted plant biomass, nodule biomass, and leghemoglobin content by 10.0%, 27.4%, and 39.4%, respectively, compared to the untreated control. Nano-BN also enhanced the NH4[+]-N and NO3[-]-N content by 24.3% and 19.9% in root tissues, while reducing these levels in rhizosphere soil. Additionally, nano-BN enriched rhizosphere-dissolved organic matter, particularly humic-like components. Metagenomic analysis revealed that nano-BN reshaped carbon and nitrogen cycling functional genes, enhancing CO2 fixation and aerobic respiration; the nitrogen fixation functional gene nifH was upregulated by 27.7%. Microbial community analysis demonstrated increased bacterial diversity and abundance of beneficial taxa, particularly Bradyrhizobium, which increased by 24.9%. Co-occurrence network analysis revealed enhanced positive interactions and greater topological complexity upon the addition of nano-BN compared to the untreated control, indicating improved community stability. Collectively, these findings demonstrate that nano-BN promotes soybean growth through integrated regulation of nutrient cycling, symbiotic nitrogen fixation, and rhizosphere microbiome assembly. Nano-BN represents an innovative nano-fertilization strategy for enhancing biological nitrogen fixation, improving nutrient use efficiency, and advancing sustainable agricultural systems.
Additional Links: PMID-42677482
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PubMed:
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@article {pmid42677482,
year = {2026},
author = {Wu, Q and Xu, X and Guo, Y and Li, H and Hao, Y and Zhang, Z and Cai, Z and White, JC and Ma, C},
title = {Nano-boron nitride enhances soybean growth and symbiotic nitrogen fixation by modulating the rhizosphere microbiome and biogeochemical cycling.},
journal = {Nanoscale},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6nr02400a},
pmid = {42677482},
issn = {2040-3372},
abstract = {Nanotechnology offers promising strategies for sustainable agriculture, yet the systemic mechanisms by which nanomaterials enhance legume nitrogen fixation remain insufficiently understood. The multi-scale impacts of nano-boron nitride (nano-BN) on soybean growth, biological nitrogen fixation, and rhizosphere microbial communities were investigated. Soil addition of 50 mg kg[-1] nano-BN significantly promoted plant biomass, nodule biomass, and leghemoglobin content by 10.0%, 27.4%, and 39.4%, respectively, compared to the untreated control. Nano-BN also enhanced the NH4[+]-N and NO3[-]-N content by 24.3% and 19.9% in root tissues, while reducing these levels in rhizosphere soil. Additionally, nano-BN enriched rhizosphere-dissolved organic matter, particularly humic-like components. Metagenomic analysis revealed that nano-BN reshaped carbon and nitrogen cycling functional genes, enhancing CO2 fixation and aerobic respiration; the nitrogen fixation functional gene nifH was upregulated by 27.7%. Microbial community analysis demonstrated increased bacterial diversity and abundance of beneficial taxa, particularly Bradyrhizobium, which increased by 24.9%. Co-occurrence network analysis revealed enhanced positive interactions and greater topological complexity upon the addition of nano-BN compared to the untreated control, indicating improved community stability. Collectively, these findings demonstrate that nano-BN promotes soybean growth through integrated regulation of nutrient cycling, symbiotic nitrogen fixation, and rhizosphere microbiome assembly. Nano-BN represents an innovative nano-fertilization strategy for enhancing biological nitrogen fixation, improving nutrient use efficiency, and advancing sustainable agricultural systems.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
From dysbiosis to precision oncology: translational role of the microbiome in gastrointestinal cancer.
Cell cycle (Georgetown, Tex.), 25(1):1-29.
Gastrointestinal (GI) cancers, including colorectal, gastric, pancreatic, hepatocellular, and esophageal malignancies, remain a leading cause of cancer-related mortality worldwide. Emerging evidence identifies the gut microbiome as a critical regulator of GI carcinogenesis, influencing tumor initiation, immune evasion, therapeutic response, and clinical outcomes through inflammation, genotoxicity, metabolic reprogramming, and epithelial barrier disruption. Importantly, biological rationale, clinical evidence, and translational opportunities differ across GI tumor types. Specific taxa, including Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, pks[+] Escherichia coli, and Helicobacter pylori, exhibit tumor-specific oncogenic roles with causal evidence ranging from associative to guideline-validated. Microbiome-based biomarkers, including composite multi-taxon models and signatures predictive of immune checkpoint inhibitor response, are evaluated using a four-tier framework (preclinical, associative, near-clinical, and validated). Microbiome-targeted therapies, including probiotics, fecal microbiota transplantation, dietary modulation, and engineered microbial therapeutics, are critically appraised according to clinical evidence and translational readiness. Advances in spatial microbiomics, single-cell analysis, multi-omics, and artificial intelligence may further accelerate microbiome-based precision oncology. This review provides a translationally stratified synthesis of microbiome-GI cancer interactions and their implications for precision oncology.
Additional Links: PMID-42677508
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@article {pmid42677508,
year = {2026},
author = {Adam, M and Venugopal, A and Almohana, A and Awadallah, M and Purohit, P and Abid, A and Jose, E and Rajendiran, A and Banka, P and Ilipilla, C and Bhuvan, F and Rai, M},
title = {From dysbiosis to precision oncology: translational role of the microbiome in gastrointestinal cancer.},
journal = {Cell cycle (Georgetown, Tex.)},
volume = {25},
number = {1},
pages = {1-29},
doi = {10.1080/15384101.2026.2725418},
pmid = {42677508},
issn = {1551-4005},
mesh = {Humans ; *Gastrointestinal Neoplasms/microbiology/therapy/pathology ; *Dysbiosis/microbiology ; *Precision Medicine ; *Gastrointestinal Microbiome ; *Translational Research, Biomedical ; Animals ; },
abstract = {Gastrointestinal (GI) cancers, including colorectal, gastric, pancreatic, hepatocellular, and esophageal malignancies, remain a leading cause of cancer-related mortality worldwide. Emerging evidence identifies the gut microbiome as a critical regulator of GI carcinogenesis, influencing tumor initiation, immune evasion, therapeutic response, and clinical outcomes through inflammation, genotoxicity, metabolic reprogramming, and epithelial barrier disruption. Importantly, biological rationale, clinical evidence, and translational opportunities differ across GI tumor types. Specific taxa, including Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, pks[+] Escherichia coli, and Helicobacter pylori, exhibit tumor-specific oncogenic roles with causal evidence ranging from associative to guideline-validated. Microbiome-based biomarkers, including composite multi-taxon models and signatures predictive of immune checkpoint inhibitor response, are evaluated using a four-tier framework (preclinical, associative, near-clinical, and validated). Microbiome-targeted therapies, including probiotics, fecal microbiota transplantation, dietary modulation, and engineered microbial therapeutics, are critically appraised according to clinical evidence and translational readiness. Advances in spatial microbiomics, single-cell analysis, multi-omics, and artificial intelligence may further accelerate microbiome-based precision oncology. This review provides a translationally stratified synthesis of microbiome-GI cancer interactions and their implications for precision oncology.},
}
MeSH Terms:
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Humans
*Gastrointestinal Neoplasms/microbiology/therapy/pathology
*Dysbiosis/microbiology
*Precision Medicine
*Gastrointestinal Microbiome
*Translational Research, Biomedical
Animals
RevDate: 2026-09-01
CmpDate: 2026-09-01
Silicon Quantum Dot Seed Priming Combined with Arbuscular Mycorrhizal Fungi Enhances Wheat Drought Tolerance through Physiological and Microbiome Regulation.
Journal of agricultural and food chemistry, 74(33):26087-26102.
Although silicon quantum dot (SiQD) seed priming and arbuscular mycorrhizal (AMF) fungal inoculation can individually alleviate drought stress, their combined effects and microbiome-associated processes remain unclear. Here, we investigated the effects of SiQD seed priming and AMF inoculation on wheat drought tolerance, plant physiology, and rhizosphere-hyphosphere bacterial communities. SiQDs increased AMF root colonization by 22.8%, and AMF inoculation enhanced shoot Si by 11.7%. Compared with either treatment, the combined treatment improved the leaf relative water content, photosynthetic rate, osmotic adjustment, and plant nitrogen and phosphorus contents under drought stress. The combined treatment also enhanced the rhizosphere microbial network stability and enriched Sphingomonas, Steroidobacter, and Limibaculum, which were positively related to nutrient acquisition and drought-related physiological traits. A core hyphosphere microbiome dominated by Sphingomonas and Steroidobacter was also detected. These findings suggest that SiQDs and AMF improve wheat drought tolerance by strengthening plant physiological performance, enhancing nutrient acquisition, and modulating rhizosphere-hyphosphere bacterial communities.
Additional Links: PMID-42677655
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@article {pmid42677655,
year = {2026},
author = {Gao, Y and Meng, Q and Liu, L and Wang, X and Shi, T and Gong, D and Wei, G and Chen, C},
title = {Silicon Quantum Dot Seed Priming Combined with Arbuscular Mycorrhizal Fungi Enhances Wheat Drought Tolerance through Physiological and Microbiome Regulation.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {33},
pages = {26087-26102},
doi = {10.1021/acs.jafc.6c07158},
pmid = {42677655},
issn = {1520-5118},
mesh = {*Triticum/microbiology/physiology/growth & development/metabolism ; Drought Resistance ; *Microbiota ; *Mycorrhizae/physiology ; *Silicon/metabolism/chemistry ; *Seeds/microbiology/growth & development/physiology/metabolism/chemistry ; *Quantum Dots/chemistry/metabolism ; Bacteria/classification/genetics/isolation & purification ; Rhizosphere ; Soil Microbiology ; Droughts ; Plant Roots/microbiology/growth & development ; Nitrogen/metabolism ; },
abstract = {Although silicon quantum dot (SiQD) seed priming and arbuscular mycorrhizal (AMF) fungal inoculation can individually alleviate drought stress, their combined effects and microbiome-associated processes remain unclear. Here, we investigated the effects of SiQD seed priming and AMF inoculation on wheat drought tolerance, plant physiology, and rhizosphere-hyphosphere bacterial communities. SiQDs increased AMF root colonization by 22.8%, and AMF inoculation enhanced shoot Si by 11.7%. Compared with either treatment, the combined treatment improved the leaf relative water content, photosynthetic rate, osmotic adjustment, and plant nitrogen and phosphorus contents under drought stress. The combined treatment also enhanced the rhizosphere microbial network stability and enriched Sphingomonas, Steroidobacter, and Limibaculum, which were positively related to nutrient acquisition and drought-related physiological traits. A core hyphosphere microbiome dominated by Sphingomonas and Steroidobacter was also detected. These findings suggest that SiQDs and AMF improve wheat drought tolerance by strengthening plant physiological performance, enhancing nutrient acquisition, and modulating rhizosphere-hyphosphere bacterial communities.},
}
MeSH Terms:
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*Triticum/microbiology/physiology/growth & development/metabolism
Drought Resistance
*Microbiota
*Mycorrhizae/physiology
*Silicon/metabolism/chemistry
*Seeds/microbiology/growth & development/physiology/metabolism/chemistry
*Quantum Dots/chemistry/metabolism
Bacteria/classification/genetics/isolation & purification
Rhizosphere
Soil Microbiology
Droughts
Plant Roots/microbiology/growth & development
Nitrogen/metabolism
RevDate: 2026-09-01
CmpDate: 2026-09-01
Ethylene Affects Soil Multifunctionality in Maize Rhizosphere by Driving Sensitive Microbial Communities.
Journal of agricultural and food chemistry, 74(33):25990-26005.
Ethylene modulates plant fitness, but its role in rhizosphere soil multifunctionality remains unclear. This study demonstrates that endogenous ethylene suppresses C- and N-cycling functions while promoting organic P mineralization in the maize rhizosphere, ultimately diminishing the overall soil multifunctionality and attenuating its phenologically driven peak at the tasseling stage. Ethylene reshaped microbial community assembly by enriching opportunistic taxa (e.g., Actinobacteria) while reducing the diversity and relative abundance of sensitive taxa. Community composition (e.g., Bacillus) and α diversity of ethylene-sensitive taxa were negatively correlated with soil multifunctionality. Inoculation with ACC deaminase-producing Bacillus pumilus and Streptomyces gardneri (opportunistic strains) significantly elevated C- and N-cycling enzyme activities and boosted maize growth. However, a direct causal link between ACC deaminase production and these effects requires further experimental validation. Collectively, these findings elucidate that ethylene drives rhizosphere biogeochemical trade-offs through the selective filtering of microbial functional guilds, providing a theoretical foundation for rhizosphere microbiome management in crop production.
Additional Links: PMID-42677665
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@article {pmid42677665,
year = {2026},
author = {Liu, X and Wang, J and Liu, Y and Liu, H and Zhang, Y and Li, Z and Zhang, M},
title = {Ethylene Affects Soil Multifunctionality in Maize Rhizosphere by Driving Sensitive Microbial Communities.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {33},
pages = {25990-26005},
doi = {10.1021/acs.jafc.6c05425},
pmid = {42677665},
issn = {1520-5118},
support = {2023M740314//China Postdoctoral Science Foundation/ ; 2024YFD2301304//National Key Research and Development Program of China/ ; },
mesh = {*Zea mays/microbiology/growth & development/metabolism ; Rhizosphere ; *Soil Microbiology ; *Ethylenes/metabolism/pharmacology ; Soil/chemistry ; *Microbiota ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Carbon-Carbon Lyases/metabolism ; Nitrogen/metabolism ; },
abstract = {Ethylene modulates plant fitness, but its role in rhizosphere soil multifunctionality remains unclear. This study demonstrates that endogenous ethylene suppresses C- and N-cycling functions while promoting organic P mineralization in the maize rhizosphere, ultimately diminishing the overall soil multifunctionality and attenuating its phenologically driven peak at the tasseling stage. Ethylene reshaped microbial community assembly by enriching opportunistic taxa (e.g., Actinobacteria) while reducing the diversity and relative abundance of sensitive taxa. Community composition (e.g., Bacillus) and α diversity of ethylene-sensitive taxa were negatively correlated with soil multifunctionality. Inoculation with ACC deaminase-producing Bacillus pumilus and Streptomyces gardneri (opportunistic strains) significantly elevated C- and N-cycling enzyme activities and boosted maize growth. However, a direct causal link between ACC deaminase production and these effects requires further experimental validation. Collectively, these findings elucidate that ethylene drives rhizosphere biogeochemical trade-offs through the selective filtering of microbial functional guilds, providing a theoretical foundation for rhizosphere microbiome management in crop production.},
}
MeSH Terms:
show MeSH Terms
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*Zea mays/microbiology/growth & development/metabolism
Rhizosphere
*Soil Microbiology
*Ethylenes/metabolism/pharmacology
Soil/chemistry
*Microbiota
*Bacteria/classification/genetics/isolation & purification/metabolism
Carbon-Carbon Lyases/metabolism
Nitrogen/metabolism
RevDate: 2026-09-01
Microbiome Insights Into Zoonotic Risk at Wildlife-Human Interfaces in a Transitioning Landscape in Thailand.
Integrative zoology [Epub ahead of print].
Land-use change is accelerating worldwide and is one of the strongest predictors of emerging zoonotic disease. These ecological transitions can disrupt host microbiomes, change pathogen carriage, and create novel opportunities for spillover at wildlife-livestock-human interfaces. Yet, little is known about how reforested landscapes influence microbiome diversity and the distribution of zoonotic bacteria in key reservoir hosts such as bats, rodents, treeshrews, and domestic dogs. We characterized the rectal microbiome of bats, rodents, and domestic dogs sampled across a land-use gradient in Nan Province, Thailand, spanning caves, forests, reforested zones, plantations, and village habitats. Full-length 16S rRNA sequencing was used to assess host- and habitat-specific patterns at the bacteria species level. Pathogen-associated taxa were identified, and their potential transmission pathways were explored using network analysis and qPCR validation targeting Salmonella spp. From 102 samples, 1816 taxa were identified, including 354 documented human pathogens. Hierarchical Modeling of Species Communities models confirmed that host species explained far more variation in pathogen occurrences than habitat type, with dogs, Menetes berdmorei, and Scotophilus heathii exhibiting particularly high pathogen diversity. Domestic dogs also displayed high network centrality and move freely across habitats, positioning them as a key bridging host. Salmonella screening detected both Salmonella enterica (serovars Newport/Typhimurium) and the reptile-associated Salmonella bongori, the latter unexpectedly in bats and rodents, with variable concordance between metabarcoding and qPCR results. Our findings demonstrate that host identity, more than habitat type, structures pathogen-associated microbiomes across a reforested landscape. Understanding these dynamics is essential to anticipate pathogen flow and strengthen One Health surveillance.
Additional Links: PMID-42677876
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@article {pmid42677876,
year = {2026},
author = {Van Leeuwen, P and Thinphovong, C and Sluydts, V and Nicolas, A and Kritiyakan, A and Kriengudom, A and Soisook, P and Chaisiri, K and Morand, S and Michaux, J},
title = {Microbiome Insights Into Zoonotic Risk at Wildlife-Human Interfaces in a Transitioning Landscape in Thailand.},
journal = {Integrative zoology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1749-4877.70167},
pmid = {42677876},
issn = {1749-4877},
support = {//Thai International Cooperation Agency/ ; ANR-24-CE35-5476//project rewild4Health/ ; 101059483//BCOMING project/ ; //European Union/ ; 40020126//FNRS/ ; },
abstract = {Land-use change is accelerating worldwide and is one of the strongest predictors of emerging zoonotic disease. These ecological transitions can disrupt host microbiomes, change pathogen carriage, and create novel opportunities for spillover at wildlife-livestock-human interfaces. Yet, little is known about how reforested landscapes influence microbiome diversity and the distribution of zoonotic bacteria in key reservoir hosts such as bats, rodents, treeshrews, and domestic dogs. We characterized the rectal microbiome of bats, rodents, and domestic dogs sampled across a land-use gradient in Nan Province, Thailand, spanning caves, forests, reforested zones, plantations, and village habitats. Full-length 16S rRNA sequencing was used to assess host- and habitat-specific patterns at the bacteria species level. Pathogen-associated taxa were identified, and their potential transmission pathways were explored using network analysis and qPCR validation targeting Salmonella spp. From 102 samples, 1816 taxa were identified, including 354 documented human pathogens. Hierarchical Modeling of Species Communities models confirmed that host species explained far more variation in pathogen occurrences than habitat type, with dogs, Menetes berdmorei, and Scotophilus heathii exhibiting particularly high pathogen diversity. Domestic dogs also displayed high network centrality and move freely across habitats, positioning them as a key bridging host. Salmonella screening detected both Salmonella enterica (serovars Newport/Typhimurium) and the reptile-associated Salmonella bongori, the latter unexpectedly in bats and rodents, with variable concordance between metabarcoding and qPCR results. Our findings demonstrate that host identity, more than habitat type, structures pathogen-associated microbiomes across a reforested landscape. Understanding these dynamics is essential to anticipate pathogen flow and strengthen One Health surveillance.},
}
RevDate: 2026-09-01
Gut microbiome-derived metabolites as prognostic biomarkers in heart failure: a systematic review and meta-analysis.
European journal of heart failure pii:8778373 [Epub ahead of print].
BACKGROUND: Growing evidence implicates gut dysbiosis in heart failure (HF) pathogenesis. This systematic review and meta-analysis synthesises prognostic associations of microbial metabolites in HF.
METHODS: Electronic databases were searched through February 2026 for studies investigating associations between gut microbial metabolites and HF outcomes. Study characteristics, baseline covariates and outcomes were extracted in duplicate. The prespecified primary outcome was all-cause mortality; the secondary outcome was major adverse cardiac events (MACE). Random-effects models were applied to pool hazard ratios. Subgroup analyses stratified cohorts by HF phenotype and aetiology; meta-regression explored potential effect modifiers. This study was preregistered on PROSPERO (CRD42025631114).
RESULTS: Twenty studies comprising 17,715 patients were included in meta-analysis; six studies were synthesised narratively. Median follow-up was 31.7 months. Elevated trimethylamine-N-oxide (TMAO) was associated with all-cause mortality in the overall population (HR 1.72, 95%CI 1.42-2.08, p=0.0002, I2 37.3%) and across HF phenotypes (HRHFrEF 2.17, 95%CI 1.68-2.81, I2 0%; HRHFpEF 1.55, 95%CI 0.92-2.61, I2 0%). Higher TMAO was also associated with MACE (HR 1.60, 95%CI 1.44-1.78, p<0.0001, I2 0%), consistent across HF phenotypes (HRHFrEF 1.43, 95%CI 1.15-1.78, I2 0%; HRHFpEF 1.76, 95%CI 1.21-2.55, I2 31.6%). Elevated phenylacetylglutamine (PAGln) was associated with mortality (HR 1.60, 95%CI 1.33-1.94, p<0.0001, I2 0%) and MACE (HR 1.65, 95%CI 1.37-1.99, p<0.0001, I2 2.1%) in the overall population. Meta-regression demonstrated no significant effect modification by baseline age, NT-proBNP, renal function or BMI.
CONCLUSION: Elevated TMAO and PAGln are consistently associated with adverse outcomes across diverse HF cohorts, highlighting their potential relevance as indicators of residual risk in HF.
Additional Links: PMID-42677938
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Citation:
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@article {pmid42677938,
year = {2026},
author = {Koeckerling, D and Reddy, RK and Guivala, SJ and Woodhead, T and Howard, JP and Ahmad, Y and Rangrez, AY and Frey, N},
title = {Gut microbiome-derived metabolites as prognostic biomarkers in heart failure: a systematic review and meta-analysis.},
journal = {European journal of heart failure},
volume = {},
number = {},
pages = {},
doi = {10.1093/ejhf/xuag283},
pmid = {42677938},
issn = {1879-0844},
abstract = {BACKGROUND: Growing evidence implicates gut dysbiosis in heart failure (HF) pathogenesis. This systematic review and meta-analysis synthesises prognostic associations of microbial metabolites in HF.
METHODS: Electronic databases were searched through February 2026 for studies investigating associations between gut microbial metabolites and HF outcomes. Study characteristics, baseline covariates and outcomes were extracted in duplicate. The prespecified primary outcome was all-cause mortality; the secondary outcome was major adverse cardiac events (MACE). Random-effects models were applied to pool hazard ratios. Subgroup analyses stratified cohorts by HF phenotype and aetiology; meta-regression explored potential effect modifiers. This study was preregistered on PROSPERO (CRD42025631114).
RESULTS: Twenty studies comprising 17,715 patients were included in meta-analysis; six studies were synthesised narratively. Median follow-up was 31.7 months. Elevated trimethylamine-N-oxide (TMAO) was associated with all-cause mortality in the overall population (HR 1.72, 95%CI 1.42-2.08, p=0.0002, I2 37.3%) and across HF phenotypes (HRHFrEF 2.17, 95%CI 1.68-2.81, I2 0%; HRHFpEF 1.55, 95%CI 0.92-2.61, I2 0%). Higher TMAO was also associated with MACE (HR 1.60, 95%CI 1.44-1.78, p<0.0001, I2 0%), consistent across HF phenotypes (HRHFrEF 1.43, 95%CI 1.15-1.78, I2 0%; HRHFpEF 1.76, 95%CI 1.21-2.55, I2 31.6%). Elevated phenylacetylglutamine (PAGln) was associated with mortality (HR 1.60, 95%CI 1.33-1.94, p<0.0001, I2 0%) and MACE (HR 1.65, 95%CI 1.37-1.99, p<0.0001, I2 2.1%) in the overall population. Meta-regression demonstrated no significant effect modification by baseline age, NT-proBNP, renal function or BMI.
CONCLUSION: Elevated TMAO and PAGln are consistently associated with adverse outcomes across diverse HF cohorts, highlighting their potential relevance as indicators of residual risk in HF.},
}
RevDate: 2026-09-01
Laryngopharyngeal Reflux Disease: Microbial Signatures and Their Associations With Clinical and Digestive Enzyme Profiles.
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery [Epub ahead of print].
OBJECTIVE: To characterize the salivary microbiome of patients with laryngopharyngeal reflux disease (LPRD) and investigate its associations with clinical presentation and salivary gastroduodenal enzymes.
STUDY DESIGN: Prospective controlled study.
SETTING: University Hospital.
METHODS: Saliva samples from patients with LPRD at the 24-hour hypopharyngeal-esophageal multichannel intraluminal impedance-pH testing and asymptomatic individuals were consecutively collected for analyzing digestive enzyme/biomarker (pepsin, elastase, bile salts, cholesterol, trypsin) and microbiome features (16S rRNA IlluminaMiSeq). Pretreatment to posttreatment symptoms and findings were evaluated with reflux symptom score and reflux sign assessment. Association between microbiome abundance, enzyme concentration, and baseline and post-treatment clinical findings were assessed.
RESULTS: Sixty-seven LPRD patients (40 females [59.7%]) and 44 controls (26 females [59.1%]) completed the evaluations. LPRD patients demonstrated significantly higher concentrations of elastase, higher salivary pH, and lower levels of cholesterol compared to controls. The comparative analysis of salivary microbiota between LPRD patients and controls demonstrated significant taxonomic-level alterations in alpha diversity (reduced Shannon index at family and genus levels in LPRD, P < .006) and beta diversity (distinct community composition by UniFrac metrics, PERMANOVA, P ≤ .005), with differential abundance of key taxa including a modulation of Streptococcus species, elevated Actinomyces and Abiotrophia, and depleted Oribacterium and Eubacterium nodatum group in LPRD patients compared to controls. Elastase, trypsin, and bile salts reported significant association with relative abundance of some bacteria.
CONCLUSION: This preliminary study supports that LPRD patients exhibit distinct microbial signatures compared to asymptomatic subjects, characterized by reduced diversity at specific taxonomic levels, subtle shifts in community membership, and differential abundance of some key genera.
Additional Links: PMID-42678000
Publisher:
PubMed:
Citation:
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@article {pmid42678000,
year = {2026},
author = {Lechien, JR and Rodrigues, PB and Vos, N and Trelcat, A and Muls, V and Aoun, J and Dequanter, D and Rodriguez, A and Hans, S and Briganti, G and Everard, A and Saussez, S},
title = {Laryngopharyngeal Reflux Disease: Microbial Signatures and Their Associations With Clinical and Digestive Enzyme Profiles.},
journal = {Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery},
volume = {},
number = {},
pages = {},
doi = {10.1002/ohn.70421},
pmid = {42678000},
issn = {1097-6817},
support = {2021//Koning Boudewijnstichting/ ; },
abstract = {OBJECTIVE: To characterize the salivary microbiome of patients with laryngopharyngeal reflux disease (LPRD) and investigate its associations with clinical presentation and salivary gastroduodenal enzymes.
STUDY DESIGN: Prospective controlled study.
SETTING: University Hospital.
METHODS: Saliva samples from patients with LPRD at the 24-hour hypopharyngeal-esophageal multichannel intraluminal impedance-pH testing and asymptomatic individuals were consecutively collected for analyzing digestive enzyme/biomarker (pepsin, elastase, bile salts, cholesterol, trypsin) and microbiome features (16S rRNA IlluminaMiSeq). Pretreatment to posttreatment symptoms and findings were evaluated with reflux symptom score and reflux sign assessment. Association between microbiome abundance, enzyme concentration, and baseline and post-treatment clinical findings were assessed.
RESULTS: Sixty-seven LPRD patients (40 females [59.7%]) and 44 controls (26 females [59.1%]) completed the evaluations. LPRD patients demonstrated significantly higher concentrations of elastase, higher salivary pH, and lower levels of cholesterol compared to controls. The comparative analysis of salivary microbiota between LPRD patients and controls demonstrated significant taxonomic-level alterations in alpha diversity (reduced Shannon index at family and genus levels in LPRD, P < .006) and beta diversity (distinct community composition by UniFrac metrics, PERMANOVA, P ≤ .005), with differential abundance of key taxa including a modulation of Streptococcus species, elevated Actinomyces and Abiotrophia, and depleted Oribacterium and Eubacterium nodatum group in LPRD patients compared to controls. Elastase, trypsin, and bile salts reported significant association with relative abundance of some bacteria.
CONCLUSION: This preliminary study supports that LPRD patients exhibit distinct microbial signatures compared to asymptomatic subjects, characterized by reduced diversity at specific taxonomic levels, subtle shifts in community membership, and differential abundance of some key genera.},
}
RevDate: 2026-09-01
Multi-kingdom gut microbiota analyses identify biomarkers of different types of pediatric short bowel syndrome.
mSystems [Epub ahead of print].
Despite recent advances in bacterial profiling across the three anatomical types of pediatric short bowel syndrome (SBS), the gut multi-kingdom remains unexplored. We characterized the four-kingdom gut microbiota using modified DNA extraction and deep shotgun metagenomic sequencing of fecal samples from 26 healthy controls and 34 pediatric SBS patients comprising three types (8 SBS I, 15 SBS II, and 11 SBS III). Overall, children with SBS exhibited a significant reduction in α-diversity compared with controls, with no difference observed among SBS types. Compared with controls, the proportion of archaea was significantly decreased in all SBS types, while bacteria, fungi, and viruses remained similar across types. Different types of SBS exhibited distinct microbial signatures: SBS I was enriched with pathogens (such as species from the Streptococcus and Klebsiella genera); SBS II was marked by a depletion of beneficial short-chain fatty acid-producing species (such as Faecalibacterium prausnitzii); and SBS III displayed loss of bile acid-metabolizing species, alongside a significant expansion of Lactobacillus species. Ecological networks were rewired in SBS, with disruption pronounced in SBS I. Functional analysis revealed that core metabolic pathways were markedly suppressed in SBS I compared with controls. Integrated correlation analyses revealed ileocecal valve loss as the primary determinant of SBS I microbial profiles, linking it to impaired secretory functions and hepatic injury. Our findings deciphered type-specific alterations in the multi-kingdom microbiota and their functional profiles, providing the basis for designing precision microbial therapies aimed at improving long-term outcomes for children with SBS.IMPORTANCEPediatric short bowel syndrome (SBS) is a primary cause of intestinal failure, yet prior research characterizing the gut microbiota has focused almost exclusively on bacteria. In this study, we characterized the multi-kingdom microbiome (including bacteria, fungi, archaea, and viruses) across the three anatomical types of pediatric SBS. We found that different SBS subtypes showed distinct microbial patterns: SBS I was enriched in pathogens, SBS II exhibited a depletion of beneficial short-chain fatty acid-producing species, and SBS III was characterized by a loss of bile acid-metabolizing microbes with an expansion of Lactobacillus. Functional analysis showed that SBS I had markedly suppressed core metabolic pathways, and integrated analyses identified the ileocecal valve as a key determinant of microbial gene profiles, with its loss linked to impaired secretion and liver injury. These findings provide a comprehensive multi-kingdom view of the pediatric SBS microbiome and highlight anatomical determinants shaping host-microbiome dysfunction.
Additional Links: PMID-42678156
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PubMed:
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@article {pmid42678156,
year = {2026},
author = {Wu, Q-Q and Li, C-Y and Chen, S-S and Xu, J and Yan, W-H and Lu, L-N and Feng, H-X and Zhou, J-A and Wang, L and Liu, N-N and Jiang, L and Wang, Y},
title = {Multi-kingdom gut microbiota analyses identify biomarkers of different types of pediatric short bowel syndrome.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0031626},
doi = {10.1128/msystems.00316-26},
pmid = {42678156},
issn = {2379-5077},
abstract = {Despite recent advances in bacterial profiling across the three anatomical types of pediatric short bowel syndrome (SBS), the gut multi-kingdom remains unexplored. We characterized the four-kingdom gut microbiota using modified DNA extraction and deep shotgun metagenomic sequencing of fecal samples from 26 healthy controls and 34 pediatric SBS patients comprising three types (8 SBS I, 15 SBS II, and 11 SBS III). Overall, children with SBS exhibited a significant reduction in α-diversity compared with controls, with no difference observed among SBS types. Compared with controls, the proportion of archaea was significantly decreased in all SBS types, while bacteria, fungi, and viruses remained similar across types. Different types of SBS exhibited distinct microbial signatures: SBS I was enriched with pathogens (such as species from the Streptococcus and Klebsiella genera); SBS II was marked by a depletion of beneficial short-chain fatty acid-producing species (such as Faecalibacterium prausnitzii); and SBS III displayed loss of bile acid-metabolizing species, alongside a significant expansion of Lactobacillus species. Ecological networks were rewired in SBS, with disruption pronounced in SBS I. Functional analysis revealed that core metabolic pathways were markedly suppressed in SBS I compared with controls. Integrated correlation analyses revealed ileocecal valve loss as the primary determinant of SBS I microbial profiles, linking it to impaired secretory functions and hepatic injury. Our findings deciphered type-specific alterations in the multi-kingdom microbiota and their functional profiles, providing the basis for designing precision microbial therapies aimed at improving long-term outcomes for children with SBS.IMPORTANCEPediatric short bowel syndrome (SBS) is a primary cause of intestinal failure, yet prior research characterizing the gut microbiota has focused almost exclusively on bacteria. In this study, we characterized the multi-kingdom microbiome (including bacteria, fungi, archaea, and viruses) across the three anatomical types of pediatric SBS. We found that different SBS subtypes showed distinct microbial patterns: SBS I was enriched in pathogens, SBS II exhibited a depletion of beneficial short-chain fatty acid-producing species, and SBS III was characterized by a loss of bile acid-metabolizing microbes with an expansion of Lactobacillus. Functional analysis showed that SBS I had markedly suppressed core metabolic pathways, and integrated analyses identified the ileocecal valve as a key determinant of microbial gene profiles, with its loss linked to impaired secretion and liver injury. These findings provide a comprehensive multi-kingdom view of the pediatric SBS microbiome and highlight anatomical determinants shaping host-microbiome dysfunction.},
}
RevDate: 2026-09-01
From trees to graphs: rethinking phylogeny in microbiome prediction.
Applied and environmental microbiology [Epub ahead of print].
Microbiome prediction models overlook phylogeny or fail to preserve evolutionary structure. In a recent Applied and Environmental Microbiology article (B. Dong, B. Wang, J. Chen, X. Xu, and Z. Z. Xu, Appl Environ Microbiol 92:e00788-26, 2026, https://doi.org/10.1128/aem.00788-26), Dong et al. present PhyloGCNE, a graph-convolutional framework that addresses these limitations by preserving evolutionary topology and learning adaptive edge-aware signal propagation. This commentary evaluates whether and when phylogenetic information improves microbiome-based prediction and considers how biological relevance and transferability can be established across contexts.
Additional Links: PMID-42678172
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PubMed:
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@article {pmid42678172,
year = {2026},
author = {Yu, Q and Bai, D and Wang, Y and Liu, Y-X},
title = {From trees to graphs: rethinking phylogeny in microbiome prediction.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0143226},
doi = {10.1128/aem.01432-26},
pmid = {42678172},
issn = {1098-5336},
abstract = {Microbiome prediction models overlook phylogeny or fail to preserve evolutionary structure. In a recent Applied and Environmental Microbiology article (B. Dong, B. Wang, J. Chen, X. Xu, and Z. Z. Xu, Appl Environ Microbiol 92:e00788-26, 2026, https://doi.org/10.1128/aem.00788-26), Dong et al. present PhyloGCNE, a graph-convolutional framework that addresses these limitations by preserving evolutionary topology and learning adaptive edge-aware signal propagation. This commentary evaluates whether and when phylogenetic information improves microbiome-based prediction and considers how biological relevance and transferability can be established across contexts.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Characterization and cellularity of myofibers during early development of Magalobrama amblycephala.
Fish physiology and biochemistry, 52(5):.
The growth and development of fish rely heavily on skeletal muscle. This study systematically characterized the morphological and developmental features of skeletal muscle in Megalobrama amblycephala during early development (0-90 days post-hatching, dph). It also determined the stage-specific contributions of hyperplasia and hypertrophy, and integrated transcriptomic and 16S rRNA sequencing analyses to preliminarily uncover the molecular regulatory network and gut microbiota adaptations associated with the rapid growth window from 15 to 20 dph. Morphological observations revealed that the length, diameter, number, and area of both red and white muscle fibers continuously increased with developmental age, and these changes were significantly synchronized with those in body length and weight. Myofiber hypertrophy predominated during juvenile growth, whereas mosaic hyperplasia was markedly enhanced at 15-20 dph, suggesting that this period represents a critical window for determining subsequent growth potential. Transcriptomic analysis revealed that upregulated KEGG pathways at 20 dph were significantly enriched in growth-related pathways, including FoxO, insulin, and AMPK signaling. Moreover, fast-twitch-specific genes (e.g., myl1, mylpfa, tnnc2.2, and tnni2a.2) and the myogenic regulatory factor myog were significantly upregulated, indicating active molecular programming toward a fast-twitch phenotype. Gut microbiota analysis showed a marked shift in microbial composition at 20 dph, with decreased Proteobacteria abundance and increased Actinobacteriota abundance. Spearman correlation analysis further revealed that 15 dph-dominant genera (such as Pseudomonas and Sphingomonas) were negatively correlated with fast-muscle genes, whereas 20 dph-enriched genera (such as Rubellimicrobium) showed positive correlations with myogenic marker genes. Functional prediction indicated enhanced metabolism of energy, amino acids, and carbohydrates at 20 dph, with reduced lipid metabolism, which closely mirrored transcriptomic trends. Collectively, the gut microbiota at 15-20 dph was highly synchronized with the activation of muscle developmental genes, constituting a key ecological factor supporting rapid growth. This study provides new insights into the multi-dimensional regulatory mechanisms of early muscle development in fish and offers a theoretical basis for strategies to enhance growth performance through microecological modulation in M. amblycephala aquaculture.
Additional Links: PMID-42678563
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@article {pmid42678563,
year = {2026},
author = {Wang, AJ and Zhang, MY and Jin, YZ and Zhu, KC and Liu, H and Gao, ZX and Wang, HL},
title = {Characterization and cellularity of myofibers during early development of Magalobrama amblycephala.},
journal = {Fish physiology and biochemistry},
volume = {52},
number = {5},
pages = {},
pmid = {42678563},
issn = {1573-5168},
support = {2022 YFF1000301//National Key Research and Development Program of China/ ; },
mesh = {Animals ; *Cyprinidae/growth & development ; RNA, Ribosomal, 16S/genetics ; Transcriptome ; Gastrointestinal Microbiome ; *Muscle Fibers, Skeletal/cytology ; Gene Expression Regulation, Developmental ; },
abstract = {The growth and development of fish rely heavily on skeletal muscle. This study systematically characterized the morphological and developmental features of skeletal muscle in Megalobrama amblycephala during early development (0-90 days post-hatching, dph). It also determined the stage-specific contributions of hyperplasia and hypertrophy, and integrated transcriptomic and 16S rRNA sequencing analyses to preliminarily uncover the molecular regulatory network and gut microbiota adaptations associated with the rapid growth window from 15 to 20 dph. Morphological observations revealed that the length, diameter, number, and area of both red and white muscle fibers continuously increased with developmental age, and these changes were significantly synchronized with those in body length and weight. Myofiber hypertrophy predominated during juvenile growth, whereas mosaic hyperplasia was markedly enhanced at 15-20 dph, suggesting that this period represents a critical window for determining subsequent growth potential. Transcriptomic analysis revealed that upregulated KEGG pathways at 20 dph were significantly enriched in growth-related pathways, including FoxO, insulin, and AMPK signaling. Moreover, fast-twitch-specific genes (e.g., myl1, mylpfa, tnnc2.2, and tnni2a.2) and the myogenic regulatory factor myog were significantly upregulated, indicating active molecular programming toward a fast-twitch phenotype. Gut microbiota analysis showed a marked shift in microbial composition at 20 dph, with decreased Proteobacteria abundance and increased Actinobacteriota abundance. Spearman correlation analysis further revealed that 15 dph-dominant genera (such as Pseudomonas and Sphingomonas) were negatively correlated with fast-muscle genes, whereas 20 dph-enriched genera (such as Rubellimicrobium) showed positive correlations with myogenic marker genes. Functional prediction indicated enhanced metabolism of energy, amino acids, and carbohydrates at 20 dph, with reduced lipid metabolism, which closely mirrored transcriptomic trends. Collectively, the gut microbiota at 15-20 dph was highly synchronized with the activation of muscle developmental genes, constituting a key ecological factor supporting rapid growth. This study provides new insights into the multi-dimensional regulatory mechanisms of early muscle development in fish and offers a theoretical basis for strategies to enhance growth performance through microecological modulation in M. amblycephala aquaculture.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Cyprinidae/growth & development
RNA, Ribosomal, 16S/genetics
Transcriptome
Gastrointestinal Microbiome
*Muscle Fibers, Skeletal/cytology
Gene Expression Regulation, Developmental
RevDate: 2026-09-01
CmpDate: 2026-09-01
Diet-driven shifts in microbiome composition and predicted metabolic functions of Mytilus coruscus larvae.
Archives of microbiology, 208(12):.
Different microalgal diets can shape the bacterial and fungal communities associated with mussel larvae. This study investigates the composition, diversity, and functional roles of bacterial and fungal communities in Mytilus coruscus planktonic larvae at the veliconcha stage, under different mixed microalgal diets. Mussel larvae were cultured under controlled conditions using two mixed diets: Isochrysis galbana + Rhinomonas reticulata (ISORHI) and I. galbana + Rhodomonas baltica (ISORHO). High-throughput sequencing revealed significant differences in the bacterial and fungal compositions between the two groups. The ISORHI group exhibited higher bacterial diversity, with Methylophaga and Marinobacter as dominant genera, while Roseovarius and Fusibacter dominated the ISORHO group. The ISORHI group also exhibited higher fungal diversity, whereas Aspergillus predominated in the ISORHO group. Functional predictions suggested that microbial communities in the ISORHI group may be more associated with carbon metabolism-related pathways, while larvae fed the ISORHI diet showed higher predicted representation of nitrogen and sulfur cycling pathways. The predicted differences suggest distinct functional potentials between the two dietary groups, though they do not represent direct measurements of metabolic activity. These findings reveal diet-induced shifts in larval microbial communities and provide a basis for future investigations into host-microbe-diet interactions in mussel aquaculture.
Additional Links: PMID-42678567
PubMed:
Citation:
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@article {pmid42678567,
year = {2026},
author = {Feng, J and Mazzei, M and Buttino, I and Li, H and Ye, Y and Yan, X},
title = {Diet-driven shifts in microbiome composition and predicted metabolic functions of Mytilus coruscus larvae.},
journal = {Archives of microbiology},
volume = {208},
number = {12},
pages = {},
pmid = {42678567},
issn = {1432-072X},
support = {42020104009//the NSFC Projects of International Cooperation and Exchanges/ ; },
mesh = {Animals ; *Mytilus/microbiology/metabolism/growth & development ; *Microbiota ; Larva/microbiology/metabolism ; *Bacteria/classification/genetics/metabolism/isolation & purification ; *Fungi/classification/genetics/isolation & purification/metabolism ; *Diet ; },
abstract = {Different microalgal diets can shape the bacterial and fungal communities associated with mussel larvae. This study investigates the composition, diversity, and functional roles of bacterial and fungal communities in Mytilus coruscus planktonic larvae at the veliconcha stage, under different mixed microalgal diets. Mussel larvae were cultured under controlled conditions using two mixed diets: Isochrysis galbana + Rhinomonas reticulata (ISORHI) and I. galbana + Rhodomonas baltica (ISORHO). High-throughput sequencing revealed significant differences in the bacterial and fungal compositions between the two groups. The ISORHI group exhibited higher bacterial diversity, with Methylophaga and Marinobacter as dominant genera, while Roseovarius and Fusibacter dominated the ISORHO group. The ISORHI group also exhibited higher fungal diversity, whereas Aspergillus predominated in the ISORHO group. Functional predictions suggested that microbial communities in the ISORHI group may be more associated with carbon metabolism-related pathways, while larvae fed the ISORHI diet showed higher predicted representation of nitrogen and sulfur cycling pathways. The predicted differences suggest distinct functional potentials between the two dietary groups, though they do not represent direct measurements of metabolic activity. These findings reveal diet-induced shifts in larval microbial communities and provide a basis for future investigations into host-microbe-diet interactions in mussel aquaculture.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Mytilus/microbiology/metabolism/growth & development
*Microbiota
Larva/microbiology/metabolism
*Bacteria/classification/genetics/metabolism/isolation & purification
*Fungi/classification/genetics/isolation & purification/metabolism
*Diet
RevDate: 2026-09-01
CmpDate: 2026-09-01
Presentations of idiopathic hemorrhagic diarrhea syndrome in dogs in relation to meteorological factors.
Journal of veterinary internal medicine, 40(5):.
BACKGROUND: Causes for idiopathic acute hemorrhagic diarrhea syndrome (AHDS) in dogs remain uncertain. Recent discoveries suggest a role for enterotoxin-producing Clostridium perfringens, but the triggers for toxin production and AHDS onset are unknown. Meteorological factors have not been examined as a possible AHDS trigger.
HYPOTHESIS/OBJECTIVES: Retrospective case-control study aiming to examine the effects of weather conditions and weather changes on the prevalence of idiopathic AHDS.
ANIMALS: Dogs (n = 412) presented with acute gastrointestinal (GI) clinical signs between January 2016 and January 2021 at a tertiary veterinary care center.
METHODS: Dogs were stratified into 3 groups: idiopathic AHDS, acute gastroenteritis, and other causes for acute GI signs. This categorization was based on the combination of patient history, physical examination, and further diagnostic evaluation (eg, laboratory and imaging diagnostics). Meteorological data were extracted for each dog based on the geocodes of their primary location and were analyzed for associations with AHDS presentations by building a random forest model and calculating odds ratios.
RESULTS: Increased wind speeds and shortwave radiation exposure, lower temperatures and sunlight intensity, and dry weather were linked to increased idiopathic AHDS presentations in dogs in the investigated geographical region.
Our explorative study provides an outlook for prospective investigations to further evaluate potential effects of meteorological factors on the gut-brain-microbiome axis and their role in the development of idiopathic AHDS. In addition to shedding more light on pathogenetic mechanisms of an idiopathic condition, understanding these environmental and weather-related effects could be important in predicting and managing this condition.
Additional Links: PMID-42679218
Publisher:
PubMed:
Citation:
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@article {pmid42679218,
year = {2026},
author = {Karnstedt, M and Asif, A and Sibanda, TZ and Heilmann, RM},
title = {Presentations of idiopathic hemorrhagic diarrhea syndrome in dogs in relation to meteorological factors.},
journal = {Journal of veterinary internal medicine},
volume = {40},
number = {5},
pages = {},
doi = {10.1093/jvimsj/aalag184},
pmid = {42679218},
issn = {1939-1676},
support = {//Open Access Publishing Fund of Leipzig University, Leipzig, SN, Germany/ ; },
mesh = {Animals ; Dogs ; *Dog Diseases/epidemiology/etiology ; Case-Control Studies ; Retrospective Studies ; *Diarrhea/veterinary/epidemiology ; Female ; Male ; *Weather ; *Gastrointestinal Hemorrhage/veterinary/epidemiology/etiology ; Meteorological Concepts ; },
abstract = {BACKGROUND: Causes for idiopathic acute hemorrhagic diarrhea syndrome (AHDS) in dogs remain uncertain. Recent discoveries suggest a role for enterotoxin-producing Clostridium perfringens, but the triggers for toxin production and AHDS onset are unknown. Meteorological factors have not been examined as a possible AHDS trigger.
HYPOTHESIS/OBJECTIVES: Retrospective case-control study aiming to examine the effects of weather conditions and weather changes on the prevalence of idiopathic AHDS.
ANIMALS: Dogs (n = 412) presented with acute gastrointestinal (GI) clinical signs between January 2016 and January 2021 at a tertiary veterinary care center.
METHODS: Dogs were stratified into 3 groups: idiopathic AHDS, acute gastroenteritis, and other causes for acute GI signs. This categorization was based on the combination of patient history, physical examination, and further diagnostic evaluation (eg, laboratory and imaging diagnostics). Meteorological data were extracted for each dog based on the geocodes of their primary location and were analyzed for associations with AHDS presentations by building a random forest model and calculating odds ratios.
RESULTS: Increased wind speeds and shortwave radiation exposure, lower temperatures and sunlight intensity, and dry weather were linked to increased idiopathic AHDS presentations in dogs in the investigated geographical region.
Our explorative study provides an outlook for prospective investigations to further evaluate potential effects of meteorological factors on the gut-brain-microbiome axis and their role in the development of idiopathic AHDS. In addition to shedding more light on pathogenetic mechanisms of an idiopathic condition, understanding these environmental and weather-related effects could be important in predicting and managing this condition.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Dogs
*Dog Diseases/epidemiology/etiology
Case-Control Studies
Retrospective Studies
*Diarrhea/veterinary/epidemiology
Female
Male
*Weather
*Gastrointestinal Hemorrhage/veterinary/epidemiology/etiology
Meteorological Concepts
RevDate: 2026-08-29
CmpDate: 2026-08-29
From Barrier Disruption and Immune Dysregulation to Targeted Therapies in Atopic Dermatitis.
Clinical reviews in allergy & immunology, 69(1):.
Atopic dermatitis (AD) is a heterogeneous inflammatory skin disorder characterized by recurrent eczematous lesions and persistent pruritus. Its pathogenesis involves epidermal barrier dysfunction, immune dysregulation, microbial dysbiosis, and altered neuroimmune signaling. Genetic defects in structural proteins, particularly filaggrin, and altered epidermal lipids increase allergen and microbial penetration, perpetuating itch, scratching, tissue injury, and inflammation. Molecular evidence further reveals AD endotypes beyond conventional clinical phenotypes, with heterogeneity in immune polarization, barrier dysfunction, microbial colonization, and pruritic pathways. This heterogeneity may underlie differences in clinical presentation and treatment response. Conventional treatments, including skin hydration, antihistamines, and topical anti-inflammatory agents, often provide incomplete or transient control. Mechanism-based therapies targeting IL-4/IL-13, OX40/OX40L, JAK, and PDE4, together with AhR agonists, have broadened treatment options. However, efficacy must be balanced against treatment-specific risks. Biologics require monitoring for ocular and injection-site reactions, whereas systemic JAK inhibitors require monitoring for infections and laboratory abnormalities and carry regulatory class warnings regarding major adverse cardiovascular events, venous thromboembolism, and malignancy; however, these warnings are largely extrapolated from studies in older patients with rheumatoid arthritis, and the magnitude of these risks in patients with AD remains uncertain. Long-term safety and real-world evidence remain limited for several emerging therapies. This review synthesizes current knowledge of barrier dysfunction, immune heterogeneity, molecular endotypes, microbiome imbalance, neuroimmune signaling, and mechanism-based therapies. Integrating clinical phenotypes with molecular endotypes, predictive biomarkers, efficacy, and individualized safety assessment may enable more precise treatment selection and durable disease control.
Additional Links: PMID-42667317
PubMed:
Citation:
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@article {pmid42667317,
year = {2026},
author = {Luo, X and Li, Y and Feng, Y and Wang, Y and Li, Z and Zhang, Y and Shen, P},
title = {From Barrier Disruption and Immune Dysregulation to Targeted Therapies in Atopic Dermatitis.},
journal = {Clinical reviews in allergy & immunology},
volume = {69},
number = {1},
pages = {},
pmid = {42667317},
issn = {1559-0267},
support = {2023138 and 202504137//Horizontal Projects/ ; },
mesh = {Humans ; *Dermatitis, Atopic/etiology/therapy/immunology/drug therapy/metabolism ; Filaggrin Proteins ; Animals ; Molecular Targeted Therapy ; Signal Transduction ; },
abstract = {Atopic dermatitis (AD) is a heterogeneous inflammatory skin disorder characterized by recurrent eczematous lesions and persistent pruritus. Its pathogenesis involves epidermal barrier dysfunction, immune dysregulation, microbial dysbiosis, and altered neuroimmune signaling. Genetic defects in structural proteins, particularly filaggrin, and altered epidermal lipids increase allergen and microbial penetration, perpetuating itch, scratching, tissue injury, and inflammation. Molecular evidence further reveals AD endotypes beyond conventional clinical phenotypes, with heterogeneity in immune polarization, barrier dysfunction, microbial colonization, and pruritic pathways. This heterogeneity may underlie differences in clinical presentation and treatment response. Conventional treatments, including skin hydration, antihistamines, and topical anti-inflammatory agents, often provide incomplete or transient control. Mechanism-based therapies targeting IL-4/IL-13, OX40/OX40L, JAK, and PDE4, together with AhR agonists, have broadened treatment options. However, efficacy must be balanced against treatment-specific risks. Biologics require monitoring for ocular and injection-site reactions, whereas systemic JAK inhibitors require monitoring for infections and laboratory abnormalities and carry regulatory class warnings regarding major adverse cardiovascular events, venous thromboembolism, and malignancy; however, these warnings are largely extrapolated from studies in older patients with rheumatoid arthritis, and the magnitude of these risks in patients with AD remains uncertain. Long-term safety and real-world evidence remain limited for several emerging therapies. This review synthesizes current knowledge of barrier dysfunction, immune heterogeneity, molecular endotypes, microbiome imbalance, neuroimmune signaling, and mechanism-based therapies. Integrating clinical phenotypes with molecular endotypes, predictive biomarkers, efficacy, and individualized safety assessment may enable more precise treatment selection and durable disease control.},
}
MeSH Terms:
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Humans
*Dermatitis, Atopic/etiology/therapy/immunology/drug therapy/metabolism
Filaggrin Proteins
Animals
Molecular Targeted Therapy
Signal Transduction
RevDate: 2026-08-29
CmpDate: 2026-08-29
From traditional retting to precision bioprocessing: microbial ecology, enzymatic selectivity, and systems biology of jute retting.
Antonie van Leeuwenhoek, 119(9):.
Jute is one of the world's most important lignocellulosic fibre crops, yet its commercial value remains highly dependent on retting, a biologically mediated fibre extraction process still largely governed by empirical practices and variable environmental conditions. Recent advances in microbial ecology, enzymology, molecular biology, and bioprocess engineering have transformed retting from a traditional post-harvest operation into a controllable lignocellulosic bioconversion process. This review synthesizes current understanding of the structural organization of jute bast fibres, selective degradation of plant cell-wall polymers, microbial succession, extracellular enzyme networks, and physicochemical factors regulating fibre liberation. It highlights the coordinated interactions among cell-wall architecture, microbial communities, enzyme specificity, and environmental conditions that collectively determine retting efficiency and fibre quality. Emerging precision retting strategies, including defined microbial consortia, enzyme-assisted retting, ribbon retting, controlled processing systems, and water-efficient technologies, are critically evaluated for their potential to improve process reproducibility, fibre quality, and environmental sustainability. The review also examines metagenomics, metatranscriptomics, metaproteomics, metabolomics, systems biology, and artificial intelligence as enabling technologies for microbiome-guided process monitoring, predictive modelling, and digital decision support. Furthermore, this review discusses the integration of precision retting within circular bioeconomy frameworks through resource recovery, pollution mitigation, climate-resilient processing, and lignocellulosic biorefineries. Key knowledge gaps, including limited understanding of microbial interactions, lack of standardized microbial consortia, insufficient process-monitoring tools, fragmented multi-omics datasets, and challenges in industrial scale-up, are identified. Overall, this review presents a systems-level framework for advancing jute retting toward standardized, predictive, and environmentally sustainable precision bioprocessing.
Additional Links: PMID-42667435
PubMed:
Citation:
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@article {pmid42667435,
year = {2026},
author = {De, P and Chakraborti, S and Bhabai, B and Nath, S and Ghosh, PK and Khatun, N and Asif, SM},
title = {From traditional retting to precision bioprocessing: microbial ecology, enzymatic selectivity, and systems biology of jute retting.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {9},
pages = {},
pmid = {42667435},
issn = {1572-9699},
mesh = {*Systems Biology/methods ; *Lignin/metabolism/chemistry ; Microbial Consortia ; Bacteria/metabolism ; },
abstract = {Jute is one of the world's most important lignocellulosic fibre crops, yet its commercial value remains highly dependent on retting, a biologically mediated fibre extraction process still largely governed by empirical practices and variable environmental conditions. Recent advances in microbial ecology, enzymology, molecular biology, and bioprocess engineering have transformed retting from a traditional post-harvest operation into a controllable lignocellulosic bioconversion process. This review synthesizes current understanding of the structural organization of jute bast fibres, selective degradation of plant cell-wall polymers, microbial succession, extracellular enzyme networks, and physicochemical factors regulating fibre liberation. It highlights the coordinated interactions among cell-wall architecture, microbial communities, enzyme specificity, and environmental conditions that collectively determine retting efficiency and fibre quality. Emerging precision retting strategies, including defined microbial consortia, enzyme-assisted retting, ribbon retting, controlled processing systems, and water-efficient technologies, are critically evaluated for their potential to improve process reproducibility, fibre quality, and environmental sustainability. The review also examines metagenomics, metatranscriptomics, metaproteomics, metabolomics, systems biology, and artificial intelligence as enabling technologies for microbiome-guided process monitoring, predictive modelling, and digital decision support. Furthermore, this review discusses the integration of precision retting within circular bioeconomy frameworks through resource recovery, pollution mitigation, climate-resilient processing, and lignocellulosic biorefineries. Key knowledge gaps, including limited understanding of microbial interactions, lack of standardized microbial consortia, insufficient process-monitoring tools, fragmented multi-omics datasets, and challenges in industrial scale-up, are identified. Overall, this review presents a systems-level framework for advancing jute retting toward standardized, predictive, and environmentally sustainable precision bioprocessing.},
}
MeSH Terms:
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*Systems Biology/methods
*Lignin/metabolism/chemistry
Microbial Consortia
Bacteria/metabolism
RevDate: 2026-08-31
CmpDate: 2026-08-29
Dietary supplementation with phlorotannin-lowered Eisenia nipponica increases caecal antioxidant activity and promotes Akkermansia in mice.
Molecular biology reports, 53(1):.
BACKGROUND: Eisenia nipponica (EN), a traditional Japanese edible brown alga, is rich in storage polysaccharides (laminaran) and polyphenols (phlorotannins) during summer. Laminaran is a water-soluble dietary fibre readily fermented in the gut, whereas the phlorotannins in EN exhibit potent antibacterial activity against Gram-positive bacteria.
METHODS AND RESULTS: To distinguish the effects of algal fibre from those of soluble polyphenols, we prepared a phlorotannin-lowered EN via 70% ethanol washing (WEN). Either EN or WEN was added at 5% (w/w) to a high-sucrose, low-fiber (NF) diet and administered to male ICR mice for 14 days. Compared with mice fed NF diet, those fed EN and WEN showed approximately four- and three-fold increase, respectively, in caecal total phenolic content (TPC) alongside increased antioxidant activities (superoxide anion radical scavenging and Fe-reducing power). 16S rDNA amplicon sequencing revealed that both EN and WEN suppressed the caecal relative abundance of Gram-positive bacteria, such as Allobaculum. While both EN and WEN increased the abundance of laminaran-degrading Bacteroides intestinalis-like bacteria, other laminaran-degrading Bacteroides uniformis-like bacteria increased in mice fed WEN but not EN. Furthermore, while laminaran- and alginate-degrading Bacteroides acidifaciens-like bacteria were suppressed by EN, Akkermansia muciniphila-like bacteria were most abundant in mice fed WEN (14%). KEGG functional predictions indicated reduced amino acid-related metabolism and increased glycan degradation (ko00511) in both EN and WEN groups.
CONCLUSION: These results suggest that phlorotannin-lowered EN may exert beneficial effects through its antioxidant properties and promotion of next-generation probiotics such as B. uniformis and A. muciniphila.
Additional Links: PMID-42667472
PubMed:
Citation:
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@article {pmid42667472,
year = {2026},
author = {Sato, M and Nakamura, M and Azuma, S and Tomoda, Y and Nakamura, A and Takaahashi, H and Kuda, T},
title = {Dietary supplementation with phlorotannin-lowered Eisenia nipponica increases caecal antioxidant activity and promotes Akkermansia in mice.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42667472},
issn = {1573-4978},
mesh = {Animals ; *Antioxidants/metabolism/pharmacology ; Mice ; *Cecum/metabolism/microbiology/drug effects ; Male ; *Akkermansia/drug effects ; Mice, Inbred ICR ; Dietary Supplements ; *Tannins/pharmacology/metabolism ; Dietary Fiber ; *Phaeophyceae/chemistry ; Gastrointestinal Microbiome/drug effects ; *Oligochaeta/chemistry ; Polyphenols/pharmacology ; RNA, Ribosomal, 16S/genetics ; Edible Seaweeds ; Kelp ; },
abstract = {BACKGROUND: Eisenia nipponica (EN), a traditional Japanese edible brown alga, is rich in storage polysaccharides (laminaran) and polyphenols (phlorotannins) during summer. Laminaran is a water-soluble dietary fibre readily fermented in the gut, whereas the phlorotannins in EN exhibit potent antibacterial activity against Gram-positive bacteria.
METHODS AND RESULTS: To distinguish the effects of algal fibre from those of soluble polyphenols, we prepared a phlorotannin-lowered EN via 70% ethanol washing (WEN). Either EN or WEN was added at 5% (w/w) to a high-sucrose, low-fiber (NF) diet and administered to male ICR mice for 14 days. Compared with mice fed NF diet, those fed EN and WEN showed approximately four- and three-fold increase, respectively, in caecal total phenolic content (TPC) alongside increased antioxidant activities (superoxide anion radical scavenging and Fe-reducing power). 16S rDNA amplicon sequencing revealed that both EN and WEN suppressed the caecal relative abundance of Gram-positive bacteria, such as Allobaculum. While both EN and WEN increased the abundance of laminaran-degrading Bacteroides intestinalis-like bacteria, other laminaran-degrading Bacteroides uniformis-like bacteria increased in mice fed WEN but not EN. Furthermore, while laminaran- and alginate-degrading Bacteroides acidifaciens-like bacteria were suppressed by EN, Akkermansia muciniphila-like bacteria were most abundant in mice fed WEN (14%). KEGG functional predictions indicated reduced amino acid-related metabolism and increased glycan degradation (ko00511) in both EN and WEN groups.
CONCLUSION: These results suggest that phlorotannin-lowered EN may exert beneficial effects through its antioxidant properties and promotion of next-generation probiotics such as B. uniformis and A. muciniphila.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Antioxidants/metabolism/pharmacology
Mice
*Cecum/metabolism/microbiology/drug effects
Male
*Akkermansia/drug effects
Mice, Inbred ICR
Dietary Supplements
*Tannins/pharmacology/metabolism
Dietary Fiber
*Phaeophyceae/chemistry
Gastrointestinal Microbiome/drug effects
*Oligochaeta/chemistry
Polyphenols/pharmacology
RNA, Ribosomal, 16S/genetics
Edible Seaweeds
Kelp
RevDate: 2026-08-29
MiR-122 regulates liver tolerance.
JHEP reports : innovation in hepatology pii:S2589-5559(26)00291-0 [Epub ahead of print].
BACKGROUND AND AIMS: The liver is an immune privileged organ, yet it needs to overcome infections. We aimed to explore the role of the liver-specific microRNA miR-122 in liver immune tolerance.
METHODS: We developed a miR-122 knockout (KO) mouse model and assessed immune, inflammatory, and fibrogenic responses from early postnatal stages. Innate and adaptive immune alterations were studied in miR-122 KO mice. Transcriptomic profiles from autoimmune hepatitis (AIH) patients were compared to these KO mice.
RESULTS: MiR-122 KO mice developed liver inflammation and fibrosis as early as two weeks of age. An inverse correlation between miR-122 expression and inflammation/fibrosis was observed in both KO mice (p<0.01in both at weeks two (n=6) and three (n=6) of KO mice age) and human AIH samples (p<0.01, n=9). KO mice shared transcriptomic and phenotypic features with human AIH. RNA sequencing identified over 5,000 differentially expressed genes between wt and KO mice, including upregulated chemokines, immune checkpoints, and pro-fibrotic markers. IRF2, a TLR3 transcription factor, was identified as a novel direct target of miR-122.
CONCLUSIONS: MiR-122 is a key regulator of liver immune tolerance, modulating inflammation and fibrosis via distinct pathways. Its absence enhances immune activation and accelerates fibrosis. These findings identify miR-122 as a promising therapeutic target for autoimmune liver diseases.
IMPACT AND IMPLICATION: The liver is an immune-privileged organ, an adaptation likely evolved to prevent robust immune responses against material absorbed from the gastrointestinal tract. This tolerance creates a sanctuary for pathogens-including bacteria, hepatitis viruses, and parasites such as Plasmodium-within the liver parenchyma, and similarly permits the development of primary liver malignancy and metastatic seeding. We found that miR-122 regulates hepatic immune tolerance, positioning miR-122 modulation as a potential therapeutic strategy for infectious, autoimmune, malignant, and metastatic liver diseases.
Additional Links: PMID-42667984
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@article {pmid42667984,
year = {2026},
author = {Gefen, M and Layani, S and Klahr, E and Shemuelian, Z and Brandi, J and Jacobs, T and Steeg, C and Adlung, L and Kilian, C and Ordan, M and Gordon, O and Abudi, N and Abramovitch, R and Nevo, Y and Elgavish, S and Benyamini, H and Monin, J and Khvalevsky, EZ and Rosenberg, N and Markezana, A and Yaish, D and Yehezkel, AS and Simerzin, A and Rivkin, M and Amran, O and Goldenberg, DS and Peled, A and Axelrod, J and Rachmilewitz, J and Huber, S and Gagliani, N and Schramm, C and Weidemann, S and Herkel, J and Carambia, A and Safadi, R and Khalaileh, A and Imam, A and Heide, D and Hetzer, J and Rose-John, S and Heikenwälder, M and Giladi, H and Galun, E},
title = {MiR-122 regulates liver tolerance.},
journal = {JHEP reports : innovation in hepatology},
volume = {},
number = {},
pages = {102020},
doi = {10.1016/j.jhepr.2026.102020},
pmid = {42667984},
issn = {2589-5559},
abstract = {BACKGROUND AND AIMS: The liver is an immune privileged organ, yet it needs to overcome infections. We aimed to explore the role of the liver-specific microRNA miR-122 in liver immune tolerance.
METHODS: We developed a miR-122 knockout (KO) mouse model and assessed immune, inflammatory, and fibrogenic responses from early postnatal stages. Innate and adaptive immune alterations were studied in miR-122 KO mice. Transcriptomic profiles from autoimmune hepatitis (AIH) patients were compared to these KO mice.
RESULTS: MiR-122 KO mice developed liver inflammation and fibrosis as early as two weeks of age. An inverse correlation between miR-122 expression and inflammation/fibrosis was observed in both KO mice (p<0.01in both at weeks two (n=6) and three (n=6) of KO mice age) and human AIH samples (p<0.01, n=9). KO mice shared transcriptomic and phenotypic features with human AIH. RNA sequencing identified over 5,000 differentially expressed genes between wt and KO mice, including upregulated chemokines, immune checkpoints, and pro-fibrotic markers. IRF2, a TLR3 transcription factor, was identified as a novel direct target of miR-122.
CONCLUSIONS: MiR-122 is a key regulator of liver immune tolerance, modulating inflammation and fibrosis via distinct pathways. Its absence enhances immune activation and accelerates fibrosis. These findings identify miR-122 as a promising therapeutic target for autoimmune liver diseases.
IMPACT AND IMPLICATION: The liver is an immune-privileged organ, an adaptation likely evolved to prevent robust immune responses against material absorbed from the gastrointestinal tract. This tolerance creates a sanctuary for pathogens-including bacteria, hepatitis viruses, and parasites such as Plasmodium-within the liver parenchyma, and similarly permits the development of primary liver malignancy and metastatic seeding. We found that miR-122 regulates hepatic immune tolerance, positioning miR-122 modulation as a potential therapeutic strategy for infectious, autoimmune, malignant, and metastatic liver diseases.},
}
RevDate: 2026-08-29
Gut microbiota and blood biomarkers as correlating factors in patients with postoperative delirium: analysis of three prospective observational studies.
Molecular psychiatry [Epub ahead of print].
Postoperative delirium is associated with both gut microbiota alterations and Tau phosphorylation; however, how these factors interact and jointly contribute to postoperative delirium remains poorly understood. This prospective observational cohort study screened 491 patients aged ≥65 years undergoing elective laminectomy or hip or knee replacement under general or spinal anesthesia at Massachusetts General Hospital (2016-2020). The study aimed to assess the correlation between plasma Tau protein levels, specific gut microbiota, and the gut microbiota-derived metabolite indole-3-propionic acid (IPA) in participants with and without postoperative delirium. Exclusion criteria included major neurological disease, smoking history, sensory impairment, and recent antibiotic use. Delirium was assessed 24-48 h postoperatively. Out of 491 screened participants, 139 had blood biomarker data, and 86 had gut microbiota data included in the final analysis. Ten percent of the participants experienced postoperative delirium. Co-occurrence network analysis demonstrated that microbial interactions differed between postoperative delirium and non-postoperative delirium groups. Significant associations among gut microbiota, IPA, and Tau biomarkers were observed only in postoperative delirium participants. Additionally, three machine learning classifiers distinguished postoperative delirium cases from non-postoperative delirium cases with Area Under the Curve values above 50%. The results suggest that plasma Tau may interact with gut microbiota, and this interaction is associated with postoperative delirium, suggesting the involvement of a gut-blood-brain axis in postoperative delirium vulnerability. These findings implicate a microbiota-Tau interaction that may represent both a potential pathogenic mechanism and a therapeutic target for postoperative delirium pending confirmative studies. Furthermore, machine learning classifiers utilizing microbiome-derived features demonstrate a potential in distinguishing patients with and without postoperative delirium.
Additional Links: PMID-42668272
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Citation:
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@article {pmid42668272,
year = {2026},
author = {Song, W and Singh, S and Xiang, W and Baldyga, K and Stevens, K and Qi, W and Matsubara, JK and Ge, C and Deng, H and Kim, JE and Marcantonio, ER and Shen, S and Xie, Z and Zhang, Y},
title = {Gut microbiota and blood biomarkers as correlating factors in patients with postoperative delirium: analysis of three prospective observational studies.},
journal = {Molecular psychiatry},
volume = {},
number = {},
pages = {},
pmid = {42668272},
issn = {1476-5578},
support = {R21 AG065606//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R21 AG081763//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R35 GM166431//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; RF1 AG070761//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R01 AG062509//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R01 AG041274//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R01 AG098122//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; },
abstract = {Postoperative delirium is associated with both gut microbiota alterations and Tau phosphorylation; however, how these factors interact and jointly contribute to postoperative delirium remains poorly understood. This prospective observational cohort study screened 491 patients aged ≥65 years undergoing elective laminectomy or hip or knee replacement under general or spinal anesthesia at Massachusetts General Hospital (2016-2020). The study aimed to assess the correlation between plasma Tau protein levels, specific gut microbiota, and the gut microbiota-derived metabolite indole-3-propionic acid (IPA) in participants with and without postoperative delirium. Exclusion criteria included major neurological disease, smoking history, sensory impairment, and recent antibiotic use. Delirium was assessed 24-48 h postoperatively. Out of 491 screened participants, 139 had blood biomarker data, and 86 had gut microbiota data included in the final analysis. Ten percent of the participants experienced postoperative delirium. Co-occurrence network analysis demonstrated that microbial interactions differed between postoperative delirium and non-postoperative delirium groups. Significant associations among gut microbiota, IPA, and Tau biomarkers were observed only in postoperative delirium participants. Additionally, three machine learning classifiers distinguished postoperative delirium cases from non-postoperative delirium cases with Area Under the Curve values above 50%. The results suggest that plasma Tau may interact with gut microbiota, and this interaction is associated with postoperative delirium, suggesting the involvement of a gut-blood-brain axis in postoperative delirium vulnerability. These findings implicate a microbiota-Tau interaction that may represent both a potential pathogenic mechanism and a therapeutic target for postoperative delirium pending confirmative studies. Furthermore, machine learning classifiers utilizing microbiome-derived features demonstrate a potential in distinguishing patients with and without postoperative delirium.},
}
RevDate: 2026-08-29
CmpDate: 2026-08-29
Baseline gut microbiome and metabolome profiles predict weight loss after a structured lifestyle intervention.
Microbiome, 14(1):.
BACKGROUND: Obesity remains a global health challenge, and responses to lifestyle-based weight-loss interventions are heterogeneous. Here, we evaluate a one-year structured lifestyle program in 50 adults with obesity (mean BMI 42 ± 7.0 kg/m[2]), integrating clinical, microbiome, and metabolomic profiling, to identify predictors of weight-loss success and metabolic improvement (ClinicalTrials.gov: NCT01344525). The intervention included a 3-month very low-calorie formula diet (approximately 850 kcal/day), a 3-month transition phase from a formula diet to a balanced diet (approximately 1000 kcal/day), and a 6-month maintenance period in which the participants followed a balanced diet (gradually increasing to a maximum of 2000 kcal/day).
RESULTS: Following the intervention, the participants exhibited marked reductions in body weight, body fat percentage, C-reactive protein, and glycated hemoglobin. Longitudinal analyses revealed that shifts in the gut microbiota composition were associated with changes in clinical and anthropometric data, as well as gut barrier function. An increased abundance of Lachnospiraceae was associated with improved gut barrier function; the relationship was mediated by fecal butyrate and propionate. Multivariate analyses revealed that serum baseline levels of diacylphosphatidylcholine C40:1 predicted postintervention BMI, indicating that this metabolite could serve as a biomarker of weight loss success. A random forest model incorporating baseline microbial and clinical features was used to predict weight loss and clinical improvements with high accuracy.
CONCLUSIONS: Our findings elucidate the interplay between the gut microbiota and host metabolism during weight loss and highlight the potential utility of baseline profiling to achieve a high success rate in personalized obesity treatment. Video Abstract.
Additional Links: PMID-42668355
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Citation:
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@article {pmid42668355,
year = {2026},
author = {Seethaler, B and Basrai, M and Delzenne, NM and Walter, J and Nguyen, NK and Bischoff, SC},
title = {Baseline gut microbiome and metabolome profiles predict weight loss after a structured lifestyle intervention.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {},
pmid = {42668355},
issn = {2049-2618},
support = {01EA1701//Bundesministerium für Bildung und Forschung/ ; },
mesh = {Humans ; *Weight Loss ; *Obesity/microbiology/diet therapy/metabolism ; *Gastrointestinal Microbiome ; *Metabolome ; Female ; Male ; Middle Aged ; Feces/microbiology/chemistry ; Life Style ; Adult ; Caloric Restriction ; Body Mass Index ; Eubacteriales/isolation & purification ; },
abstract = {BACKGROUND: Obesity remains a global health challenge, and responses to lifestyle-based weight-loss interventions are heterogeneous. Here, we evaluate a one-year structured lifestyle program in 50 adults with obesity (mean BMI 42 ± 7.0 kg/m[2]), integrating clinical, microbiome, and metabolomic profiling, to identify predictors of weight-loss success and metabolic improvement (ClinicalTrials.gov: NCT01344525). The intervention included a 3-month very low-calorie formula diet (approximately 850 kcal/day), a 3-month transition phase from a formula diet to a balanced diet (approximately 1000 kcal/day), and a 6-month maintenance period in which the participants followed a balanced diet (gradually increasing to a maximum of 2000 kcal/day).
RESULTS: Following the intervention, the participants exhibited marked reductions in body weight, body fat percentage, C-reactive protein, and glycated hemoglobin. Longitudinal analyses revealed that shifts in the gut microbiota composition were associated with changes in clinical and anthropometric data, as well as gut barrier function. An increased abundance of Lachnospiraceae was associated with improved gut barrier function; the relationship was mediated by fecal butyrate and propionate. Multivariate analyses revealed that serum baseline levels of diacylphosphatidylcholine C40:1 predicted postintervention BMI, indicating that this metabolite could serve as a biomarker of weight loss success. A random forest model incorporating baseline microbial and clinical features was used to predict weight loss and clinical improvements with high accuracy.
CONCLUSIONS: Our findings elucidate the interplay between the gut microbiota and host metabolism during weight loss and highlight the potential utility of baseline profiling to achieve a high success rate in personalized obesity treatment. Video Abstract.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Weight Loss
*Obesity/microbiology/diet therapy/metabolism
*Gastrointestinal Microbiome
*Metabolome
Female
Male
Middle Aged
Feces/microbiology/chemistry
Life Style
Adult
Caloric Restriction
Body Mass Index
Eubacteriales/isolation & purification
RevDate: 2026-08-31
CmpDate: 2026-08-30
Gut-microbiome composition, single nucleotide polymorphisms, and differentially expressed genes correlate with aggression in an ant.
iScience, 29(9):117164.
Animals frequently display aggressive behavior, for example, when competing for food. Aggression is influenced by various extrinsic and intrinsic factors such as the microbiome and genetics. However, we currently lack understanding what factors cause animals to start aggression. Here, we use an ant species to test if chemical, microbiome, genomic, and/or transcriptomic traits correlate with the start of aggression and the reactions to it, namely reacting aggressively or peacefully. We found nine bacterial operational taxonomic units, mutations in two genes, and eight differentially expressed genes, which were positively or negatively associated with the start of aggression or reactions to it. The microbiome and genetic factors are mainly linked to hormone signaling and neurological and synaptic functions, respectively. The results indicate that multiple traits, possibly acting in concert, may affect the start of aggression and reactions to it. We speculate that such traits could promote aggression and play important evolutionary roles.
Additional Links: PMID-42668591
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@article {pmid42668591,
year = {2026},
author = {Krapf, P and Cicconardi, F and Schilling, M and Aigner, GP and Klammsteiner, T and Ayasse, M and Arthofer, W and Mikheyev, AS and Steiner, FM and Schlick-Steiner, BC},
title = {Gut-microbiome composition, single nucleotide polymorphisms, and differentially expressed genes correlate with aggression in an ant.},
journal = {iScience},
volume = {29},
number = {9},
pages = {117164},
pmid = {42668591},
issn = {2589-0042},
abstract = {Animals frequently display aggressive behavior, for example, when competing for food. Aggression is influenced by various extrinsic and intrinsic factors such as the microbiome and genetics. However, we currently lack understanding what factors cause animals to start aggression. Here, we use an ant species to test if chemical, microbiome, genomic, and/or transcriptomic traits correlate with the start of aggression and the reactions to it, namely reacting aggressively or peacefully. We found nine bacterial operational taxonomic units, mutations in two genes, and eight differentially expressed genes, which were positively or negatively associated with the start of aggression or reactions to it. The microbiome and genetic factors are mainly linked to hormone signaling and neurological and synaptic functions, respectively. The results indicate that multiple traits, possibly acting in concert, may affect the start of aggression and reactions to it. We speculate that such traits could promote aggression and play important evolutionary roles.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-30
Intratumoral microbiota in the growth of CRC and lung cancer: Comprehensive insights from etiology to therapy.
iScience, 29(9):117254.
The tumor microenvironment (TME) contains a diverse intratumoral microbiota (ITM) governing cancer onset, progression, and therapeutic response. This review compares ITM profiles of colorectal and lung cancer, two anatomically distinct malignancies linked via the gut-lung axis, and summarizes microbial detection strategies ranging from cultivation and sequencing to spatial and single-cell technologies. Oral pathobionts such as Fusobacterium nucleatum, Streptococcus, and Veillonella accumulate in both cancers, promoting tumorigenesis through chronic inflammation, immune evasion, genotoxic insults, metabolic reprogramming, and facilitating colorectal cancer lung metastasis via venous drainage and systemic dissemination. Microbial signatures in stool, saliva, blood, and tumor tissue offer non-invasive tools for detection, prognosis, and prediction of immunotherapy resistance, while antibiotics, fecal microbiota transplantation, and engineered live biotherapeutics offer strategies to remodel the TME. This synthesis positions the gut-lung axis as a systemic driver of metastasis and outlines a route toward precision microbiome-based diagnostics and therapeutics.
Additional Links: PMID-42668654
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Citation:
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@article {pmid42668654,
year = {2026},
author = {Wang, Y and Li, J and Du, X and Li, W and Wang, D and Li, Y},
title = {Intratumoral microbiota in the growth of CRC and lung cancer: Comprehensive insights from etiology to therapy.},
journal = {iScience},
volume = {29},
number = {9},
pages = {117254},
pmid = {42668654},
issn = {2589-0042},
abstract = {The tumor microenvironment (TME) contains a diverse intratumoral microbiota (ITM) governing cancer onset, progression, and therapeutic response. This review compares ITM profiles of colorectal and lung cancer, two anatomically distinct malignancies linked via the gut-lung axis, and summarizes microbial detection strategies ranging from cultivation and sequencing to spatial and single-cell technologies. Oral pathobionts such as Fusobacterium nucleatum, Streptococcus, and Veillonella accumulate in both cancers, promoting tumorigenesis through chronic inflammation, immune evasion, genotoxic insults, metabolic reprogramming, and facilitating colorectal cancer lung metastasis via venous drainage and systemic dissemination. Microbial signatures in stool, saliva, blood, and tumor tissue offer non-invasive tools for detection, prognosis, and prediction of immunotherapy resistance, while antibiotics, fecal microbiota transplantation, and engineered live biotherapeutics offer strategies to remodel the TME. This synthesis positions the gut-lung axis as a systemic driver of metastasis and outlines a route toward precision microbiome-based diagnostics and therapeutics.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-30
Proximity-ligation metagenomics reveals differential plasmid and chromosomal antimicrobial resistance gene carriage in disrupted gut ecosystems.
iScience, 29(9):117312.
Distinct ecological pressures shape accumulation of antimicrobial resistance genes (ARGs) and virulence genes in the gut microbiome. In this study, we used proximity ligation shotgun metagenomics to characterize bacterial host-mobilome relationships associated with antimicrobial resistance and virulence genes in two disease cohorts with microbiome dysbiosis: recurrent Clostridioides difficile infection (rCDI) and cirrhosis. Microbiome dysbiosis in patients with rCDI is primarily driven by prolonged antibiotic exposure, whereas dysbiosis in patients with cirrhosis results from altered gut physiology. We found an increased relative abundance of chromosomally linked antibiotic resistance determinants in both disease cohorts compared with healthy controls. The rCDI cohorts additionally exhibited increased relative abundance of plasmid-mediated ARGs.
Additional Links: PMID-42668680
PubMed:
Citation:
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@article {pmid42668680,
year = {2026},
author = {Sommer, AJ and Auch, B and Khoruts, A and Bajaj, JS},
title = {Proximity-ligation metagenomics reveals differential plasmid and chromosomal antimicrobial resistance gene carriage in disrupted gut ecosystems.},
journal = {iScience},
volume = {29},
number = {9},
pages = {117312},
pmid = {42668680},
issn = {2589-0042},
abstract = {Distinct ecological pressures shape accumulation of antimicrobial resistance genes (ARGs) and virulence genes in the gut microbiome. In this study, we used proximity ligation shotgun metagenomics to characterize bacterial host-mobilome relationships associated with antimicrobial resistance and virulence genes in two disease cohorts with microbiome dysbiosis: recurrent Clostridioides difficile infection (rCDI) and cirrhosis. Microbiome dysbiosis in patients with rCDI is primarily driven by prolonged antibiotic exposure, whereas dysbiosis in patients with cirrhosis results from altered gut physiology. We found an increased relative abundance of chromosomally linked antibiotic resistance determinants in both disease cohorts compared with healthy controls. The rCDI cohorts additionally exhibited increased relative abundance of plasmid-mediated ARGs.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-30
Microbial Communities Vary by Body Region but Remain Consistent Across Color Morphs in the Solitary Ascidian Rhopalaea abdominalis.
International journal of microbiology, 2026:1675944.
Ascidians are filter-feeding marine invertebrates that display inter- and intraspecific color variation and host diverse microbiomes. Although color variation has been used as an indicator of speciation and correlated with distinct microbiome structure in some colonial species, there is limited research on microbiome variation across color morphs and body regions in solitary ascidians. To address these knowledge gaps, three color morphs (purple, orange, and intermediate shades of pink) of the solitary Belizean ascidian Rhopalaea abdominalis were collected for phylogenetic analysis using the Cytochrome Oxidase I (COI) gene and for microbial characterization via sequencing the V4 region of the 16S rRNA gene. Microbial sequences derived from the ascidian branchial sac, gut, and tunic body regions were processed using both operational taxonomic unit (OTU) and amplicon sequence variant (ASV) pipelines to determine the resolution and consistency of sequence processing methods using mothur and QIIME 2 software, respectively. COI sequencing revealed two clades that were independent of color morphs. Microbiome characterization showed no significant differences in alpha- or beta-diversity across ascidian color morphs or COI clades but distinct microbiomes within each body region. The branchial sac harbored a higher number of core members (i.e., detected across all host individuals) that included known ascidian symbionts (e.g., Endozoicomonas), whereas the gut and tunic were colonized by taxa identified in seawater and across multiple classes of marine invertebrates. Results were highly congruent between OTU- and ASV-based pipelines, yielding statistically equivalent alpha-diversity metrics, consistent beta-diversity patterns, and similar core membership profiles. These findings reinforce the validity of both methods for studying microbial symbiont communities and corroborate previous research showing distinct microbiomes by body region and overall conservation when color morphs lack genetic differentiation.
Additional Links: PMID-42668720
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@article {pmid42668720,
year = {2026},
author = {Hutchings, B and López-Legentil, S and Stefaniak, LM and Nydam, ML and Erwin, PM},
title = {Microbial Communities Vary by Body Region but Remain Consistent Across Color Morphs in the Solitary Ascidian Rhopalaea abdominalis.},
journal = {International journal of microbiology},
volume = {2026},
number = {},
pages = {1675944},
pmid = {42668720},
issn = {1687-918X},
abstract = {Ascidians are filter-feeding marine invertebrates that display inter- and intraspecific color variation and host diverse microbiomes. Although color variation has been used as an indicator of speciation and correlated with distinct microbiome structure in some colonial species, there is limited research on microbiome variation across color morphs and body regions in solitary ascidians. To address these knowledge gaps, three color morphs (purple, orange, and intermediate shades of pink) of the solitary Belizean ascidian Rhopalaea abdominalis were collected for phylogenetic analysis using the Cytochrome Oxidase I (COI) gene and for microbial characterization via sequencing the V4 region of the 16S rRNA gene. Microbial sequences derived from the ascidian branchial sac, gut, and tunic body regions were processed using both operational taxonomic unit (OTU) and amplicon sequence variant (ASV) pipelines to determine the resolution and consistency of sequence processing methods using mothur and QIIME 2 software, respectively. COI sequencing revealed two clades that were independent of color morphs. Microbiome characterization showed no significant differences in alpha- or beta-diversity across ascidian color morphs or COI clades but distinct microbiomes within each body region. The branchial sac harbored a higher number of core members (i.e., detected across all host individuals) that included known ascidian symbionts (e.g., Endozoicomonas), whereas the gut and tunic were colonized by taxa identified in seawater and across multiple classes of marine invertebrates. Results were highly congruent between OTU- and ASV-based pipelines, yielding statistically equivalent alpha-diversity metrics, consistent beta-diversity patterns, and similar core membership profiles. These findings reinforce the validity of both methods for studying microbial symbiont communities and corroborate previous research showing distinct microbiomes by body region and overall conservation when color morphs lack genetic differentiation.},
}
RevDate: 2026-08-30
Lpb. plantarum inhalation powders for the reduction of lung inflammation and S. aureus growth control in non-CF bronchiectasis.
Expert opinion on drug delivery [Epub ahead of print].
INTRODUCTION: The reduced diversity of the lung microbiome in respiratory conditions, including bronchiectasis, promotes bacterial infection and inflammation, contributing to worsening clinical outcomes. Traditional treatments often fail to address both infection and inflammation. Because of their potential dual-action, lactic acid bacteria (LAB) directly administered to the lungs could represent an innovative therapeutic approach for these diseases.
RESEARCH DESIGN AND METHODS: Two powders for inhalation containing Lpb. plantarum, lactose, l-leucine with and without raffinose, a prebiotic, were produced by spray drying and in vitro tested. The focus was on investigating their potential in vitro anti-inflammatory and anti-microbial activities against S. aureus.
RESULTS: The powders showed a fine particle fraction (<5 µm) >40% and allowed to maintain anti-inflammatory activity in vitro for both treatment and prevention. Moreover, both the powders led to a significant reduction in S. aureus growth. The stability study of the powders in capsules at different storage conditions showed the preservation of the LAB up to 90 days in refrigerated conditions (4°C/-20°C).
CONCLUSIONS: This proof-of-concept study shows that inhalable spray-dried live LABs retain biological activity and are suitable for pulmonary delivery, supporting their potential as a microbiota-modulating therapy which, however, requires further preclinical validation.
Additional Links: PMID-42669029
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@article {pmid42669029,
year = {2026},
author = {Glieca, S and Tambassi, M and Schianchi, C and Quarta, E and Bottari, B and Bancalari, E and Bianchera, A and Mazzera, L and Scaltriti, E and Ecenarro Probst, S and Aliberti, S and Fainardi, V and Sonvico, F and Buttini, F},
title = {Lpb. plantarum inhalation powders for the reduction of lung inflammation and S. aureus growth control in non-CF bronchiectasis.},
journal = {Expert opinion on drug delivery},
volume = {},
number = {},
pages = {},
doi = {10.1080/17425247.2026.2727113},
pmid = {42669029},
issn = {1744-7593},
abstract = {INTRODUCTION: The reduced diversity of the lung microbiome in respiratory conditions, including bronchiectasis, promotes bacterial infection and inflammation, contributing to worsening clinical outcomes. Traditional treatments often fail to address both infection and inflammation. Because of their potential dual-action, lactic acid bacteria (LAB) directly administered to the lungs could represent an innovative therapeutic approach for these diseases.
RESEARCH DESIGN AND METHODS: Two powders for inhalation containing Lpb. plantarum, lactose, l-leucine with and without raffinose, a prebiotic, were produced by spray drying and in vitro tested. The focus was on investigating their potential in vitro anti-inflammatory and anti-microbial activities against S. aureus.
RESULTS: The powders showed a fine particle fraction (<5 µm) >40% and allowed to maintain anti-inflammatory activity in vitro for both treatment and prevention. Moreover, both the powders led to a significant reduction in S. aureus growth. The stability study of the powders in capsules at different storage conditions showed the preservation of the LAB up to 90 days in refrigerated conditions (4°C/-20°C).
CONCLUSIONS: This proof-of-concept study shows that inhalable spray-dried live LABs retain biological activity and are suitable for pulmonary delivery, supporting their potential as a microbiota-modulating therapy which, however, requires further preclinical validation.},
}
RevDate: 2026-08-30
CmpDate: 2026-08-30
Modulating the Gut-Microbiota-Brain Axis in Alzheimer's Disease: Therapeutic Potential of Nutritional and Metabolic Factors.
CNS neuroscience & therapeutics, 32(9):e71117.
BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia among the elderly, characterized by a gradual decline in memory and cognitive function. The growing body of evidence highlighting the interaction between the gut microbiota and the central nervous system has positioned the gut microbiota as a key area of research in AD pathogenesis.
METHODS: This review critically evaluates the preclinical evidence and clinical trial outcomes, complemented by mechanistic studies and Mendelian randomization analyses, to assess the therapeutic potential of nutritional interventions targeting the gut-microbiota-brain axis in AD.
RESULTS: Dietary components and patterns regulate the composition and function of the gut microbiota, which in turn influence brain function through the gut-microbiota-brain axis via chemical/metabolic, immune-mediated, and neural pathways. Specific nutrients, microbial metabolites, and dietary patterns have been shown to exert either protective or detrimental effects on AD pathology and cognitive function. Emerging strategies, including precision nutrition, fecal microbiota transplantation, and next-generation microbiome-based therapies, offer new avenues for AD prevention and treatment.
CONCLUSIONS: Nutritional interventions targeting the gut-microbiota-brain axis represent a promising approach for the comprehensive prevention and management of AD. Further mechanistic and clinical studies are warranted to translate these findings into effective therapeutic strategies.
Additional Links: PMID-42669137
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Citation:
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@article {pmid42669137,
year = {2026},
author = {Xu, B and Li, X and Dong, S and Zhang, Z and Jin, D and Li, G and Wang, J},
title = {Modulating the Gut-Microbiota-Brain Axis in Alzheimer's Disease: Therapeutic Potential of Nutritional and Metabolic Factors.},
journal = {CNS neuroscience & therapeutics},
volume = {32},
number = {9},
pages = {e71117},
pmid = {42669137},
issn = {1755-5949},
mesh = {Humans ; *Alzheimer Disease/metabolism/diet therapy/microbiology/therapy ; *Gastrointestinal Microbiome/physiology ; Animals ; *Brain/metabolism ; *Brain-Gut Axis/physiology ; Fecal Microbiota Transplantation/methods ; },
abstract = {BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia among the elderly, characterized by a gradual decline in memory and cognitive function. The growing body of evidence highlighting the interaction between the gut microbiota and the central nervous system has positioned the gut microbiota as a key area of research in AD pathogenesis.
METHODS: This review critically evaluates the preclinical evidence and clinical trial outcomes, complemented by mechanistic studies and Mendelian randomization analyses, to assess the therapeutic potential of nutritional interventions targeting the gut-microbiota-brain axis in AD.
RESULTS: Dietary components and patterns regulate the composition and function of the gut microbiota, which in turn influence brain function through the gut-microbiota-brain axis via chemical/metabolic, immune-mediated, and neural pathways. Specific nutrients, microbial metabolites, and dietary patterns have been shown to exert either protective or detrimental effects on AD pathology and cognitive function. Emerging strategies, including precision nutrition, fecal microbiota transplantation, and next-generation microbiome-based therapies, offer new avenues for AD prevention and treatment.
CONCLUSIONS: Nutritional interventions targeting the gut-microbiota-brain axis represent a promising approach for the comprehensive prevention and management of AD. Further mechanistic and clinical studies are warranted to translate these findings into effective therapeutic strategies.},
}
MeSH Terms:
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Humans
*Alzheimer Disease/metabolism/diet therapy/microbiology/therapy
*Gastrointestinal Microbiome/physiology
Animals
*Brain/metabolism
*Brain-Gut Axis/physiology
Fecal Microbiota Transplantation/methods
RevDate: 2026-08-30
Preparation and chemical characterization of polyphenol-rich extract from Tsaoko Fructus: alleviation of ulcerative colitis in mice by modulating gut microbiota and suppressing the JNK1-cJun signaling.
Phytomedicine : international journal of phytotherapy and phytopharmacology, 161:158752 pii:S0944-7113(26)00983-9 [Epub ahead of print].
BACKGROUND: Tsaoko Fructus, a traditional Chinese medicinal herb, has long been used to alleviate gastritis and enteritis. Nevertheless, the active constituents and underlying anti-inflammatory mechanisms remain insufficiently characterized.
PURPOSE: This study aims to optimize a polyphenol-rich fraction (3CB) from Tsaoko Fructus, evaluate its effects against ulcerative colitis (UC), and reveal the underlying mechanisms of action.
METHODS: The preparation of 3CB was optimized using response surface methodology (RSM), and its major constituents were identified by LC-PDA-MS analysis. A murine UC model was established by administering dextran sulfate sodium (DSS). To evaluate the effects of 3CB on UC mice, metagenomic sequencing of the intestinal microbiome and RNA sequencing of colon tissues were conducted. The anti-inflammatory activity of 3CB and its principal constituents was further verified by quantitative real-time PCR (qPCR), Enzyme linked immunosorbent assay (ELISA), Western blotting, immunohistochemical staining, and histopathological analysis. Network pharmacology, molecular docking, and surface plasmon resonance (SPR) assays were employed to elucidate the molecular mechanisms underlying the anti-inflammatory effects of 3CB.
RESULTS: 3CB significantly alleviated UC symptoms in DSS-induced mice, reshaped the gut microbiota with reducing pathogenic Pseudomonadota and Deferribacterota while enriching beneficial Bacteroidota, and restored microbial amino sugar and nucleotide sugar metabolism pathways of intestinal flora. Additionally, 3CB preserved colonic oxidative phosphorylation, protected the mucus barrier, and suppressed inflammatory cell infiltration and the expression of cytokines. Seven major polyphenols were identified in 3CB, with epicatechin (3) and epiafzelechin (6) being the most abundant. Mechanistic investigation revealed that the anti-inflammatory effect of 3CB was partially dependent on the JNK1-modulated MAPK signaling pathway. JNK1 was identified as a direct target of 3CB, with epiafzelechin (6) exhibiting a high binding affinity (Kd = 10.4 μM).
CONCLUSION: 3CB ameliorates UC potentially through modulation of gut microbiota, protection of the mucus barrier, and JNK1-targeted anti-inflammatory effects, highlighting its potential as a protective intervention for inflammatory bowel disease (IBD).
Additional Links: PMID-42669226
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PubMed:
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@article {pmid42669226,
year = {2026},
author = {Gongpan, P and Yang, J and Fu, H and Wu, S and Zhu, X and Chen, R and Liu, L and Geng, CA},
title = {Preparation and chemical characterization of polyphenol-rich extract from Tsaoko Fructus: alleviation of ulcerative colitis in mice by modulating gut microbiota and suppressing the JNK1-cJun signaling.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {161},
number = {},
pages = {158752},
doi = {10.1016/j.phymed.2026.158752},
pmid = {42669226},
issn = {1618-095X},
abstract = {BACKGROUND: Tsaoko Fructus, a traditional Chinese medicinal herb, has long been used to alleviate gastritis and enteritis. Nevertheless, the active constituents and underlying anti-inflammatory mechanisms remain insufficiently characterized.
PURPOSE: This study aims to optimize a polyphenol-rich fraction (3CB) from Tsaoko Fructus, evaluate its effects against ulcerative colitis (UC), and reveal the underlying mechanisms of action.
METHODS: The preparation of 3CB was optimized using response surface methodology (RSM), and its major constituents were identified by LC-PDA-MS analysis. A murine UC model was established by administering dextran sulfate sodium (DSS). To evaluate the effects of 3CB on UC mice, metagenomic sequencing of the intestinal microbiome and RNA sequencing of colon tissues were conducted. The anti-inflammatory activity of 3CB and its principal constituents was further verified by quantitative real-time PCR (qPCR), Enzyme linked immunosorbent assay (ELISA), Western blotting, immunohistochemical staining, and histopathological analysis. Network pharmacology, molecular docking, and surface plasmon resonance (SPR) assays were employed to elucidate the molecular mechanisms underlying the anti-inflammatory effects of 3CB.
RESULTS: 3CB significantly alleviated UC symptoms in DSS-induced mice, reshaped the gut microbiota with reducing pathogenic Pseudomonadota and Deferribacterota while enriching beneficial Bacteroidota, and restored microbial amino sugar and nucleotide sugar metabolism pathways of intestinal flora. Additionally, 3CB preserved colonic oxidative phosphorylation, protected the mucus barrier, and suppressed inflammatory cell infiltration and the expression of cytokines. Seven major polyphenols were identified in 3CB, with epicatechin (3) and epiafzelechin (6) being the most abundant. Mechanistic investigation revealed that the anti-inflammatory effect of 3CB was partially dependent on the JNK1-modulated MAPK signaling pathway. JNK1 was identified as a direct target of 3CB, with epiafzelechin (6) exhibiting a high binding affinity (Kd = 10.4 μM).
CONCLUSION: 3CB ameliorates UC potentially through modulation of gut microbiota, protection of the mucus barrier, and JNK1-targeted anti-inflammatory effects, highlighting its potential as a protective intervention for inflammatory bowel disease (IBD).},
}
RevDate: 2026-08-30
CmpDate: 2026-08-30
Effect of a complementary feeding intervention based on iron- and zinc-biofortified pearl millet on the gut microbiota in 12-18-month-old children: a randomized trial.
Nature communications, 17(1):.
Iron supplementation studies in children under five suggest potentially adverse gut microbiota shifts. Given iron's importance during early childhood, food-based approaches may offer a more viable supplementation strategy. Using shotgun metagenomics, we examined the effects of 9 months' daily consumption of iron/zinc-biofortified pearl millet (FeZnPM; 8.70 mg/100 g iron) versus control pearl millet (CPM; 3 mg/100 g iron) on the gut microbiome in 12-18-month-old children without severe anemia (hemoglobin ≥9.0 g/dL) from Mumbai urban slums through a randomized controlled trial, the primary outcomes of which were iron status biomarkers and infant growth (ClinicalTrials.gov ID: NCT02233764). In paired (n = 81) and endpoint (n = 108) analyses, FeZnPM consumption was not associated with detectable adverse effects on developing microbiomes and exploratory analyses suggest that it may support beneficial metabolic adaptations via direct modulation of antibiotic, antioxidant, and pollutant degradation pathways. This suggests biofortified crops could provide a sustainable approach to addressing iron deficiency while maintaining healthy microbiome development in early life.
Additional Links: PMID-42669658
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@article {pmid42669658,
year = {2026},
author = {Huey, SL and Cole, NL and Pagani, I and González, A and Finkelstein, JL and Haas, JD and Udipi, SA and Ghugre, P and Potdar, RD and Knight, R and Mehta, S},
title = {Effect of a complementary feeding intervention based on iron- and zinc-biofortified pearl millet on the gut microbiota in 12-18-month-old children: a randomized trial.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42669658},
issn = {2041-1723},
support = {2021-67017-34008//United States Department of Agriculture | Agricultural Research Service (USDA Agricultural Research Service)/ ; 5T32HD087137//U.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)/ ; },
mesh = {Humans ; *Zinc/administration & dosage ; *Pennisetum/chemistry ; Infant ; *Iron ; *Gastrointestinal Microbiome/drug effects ; Female ; Male ; *Food, Fortified ; *Infant Nutritional Physiological Phenomena ; Dietary Supplements ; Feces/microbiology ; },
abstract = {Iron supplementation studies in children under five suggest potentially adverse gut microbiota shifts. Given iron's importance during early childhood, food-based approaches may offer a more viable supplementation strategy. Using shotgun metagenomics, we examined the effects of 9 months' daily consumption of iron/zinc-biofortified pearl millet (FeZnPM; 8.70 mg/100 g iron) versus control pearl millet (CPM; 3 mg/100 g iron) on the gut microbiome in 12-18-month-old children without severe anemia (hemoglobin ≥9.0 g/dL) from Mumbai urban slums through a randomized controlled trial, the primary outcomes of which were iron status biomarkers and infant growth (ClinicalTrials.gov ID: NCT02233764). In paired (n = 81) and endpoint (n = 108) analyses, FeZnPM consumption was not associated with detectable adverse effects on developing microbiomes and exploratory analyses suggest that it may support beneficial metabolic adaptations via direct modulation of antibiotic, antioxidant, and pollutant degradation pathways. This suggests biofortified crops could provide a sustainable approach to addressing iron deficiency while maintaining healthy microbiome development in early life.},
}
MeSH Terms:
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Humans
*Zinc/administration & dosage
*Pennisetum/chemistry
Infant
*Iron
*Gastrointestinal Microbiome/drug effects
Female
Male
*Food, Fortified
*Infant Nutritional Physiological Phenomena
Dietary Supplements
Feces/microbiology
RevDate: 2026-08-30
CmpDate: 2026-08-30
Multi-omics and cultivation reveal laminarin-degrading PVC bacteria in the deep sea.
Nature communications, 17(1):.
The deep sea is home to a vast and largely unexplored microbial biosphere, along with large amounts of complex organic matter (COM). However, the functional capacity of the deep-sea microbiome to metabolize organic matter across diverse regions remains poorly understood. Here, we combine 16S rRNA gene amplicon sequencing, metagenomics, and metatranscriptomics to comprehensively characterize prokaryotic communities across different years (2018 and 2022) and habitats (cold seeps, hydrothermal vents, and seamounts). Our results reveal spatio-temporal community heterogeneity driven by geochemical gradients, alongside a widespread genetic potential for organic matter metabolism. Notably, the PVC (Planctomycetota-Verrucomicrobiota-Chlamydiota) superphylum exhibits extensive polysaccharide degradation capabilities, exemplified by the isolation of Planctomycetota strain WC338 and Lentisphaerota strain WC36 via laminarin enrichment. Growth experiments and transcriptomics confirm their strict laminarin dependence and characterize the underlying catabolic machinery-specifically, the deployment of different glycoside hydrolase (GH) families, which are broadly distributed and prevalent across the PVC superphylum. Furthermore, we demonstrate that laminarin acts as an effective selective substrate for enriching and isolating the deep-sea PVC superphylum bacteria. Collectively, these findings reveal that PVC bacteria-an overlooked group in laminarin degradation-possess specialized adaptations for polysaccharide breakdown and actively participate in laminarin turnover in deep-sea environments.
Additional Links: PMID-42669679
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@article {pmid42669679,
year = {2026},
author = {Zheng, R and Wang, C and Sun, C},
title = {Multi-omics and cultivation reveal laminarin-degrading PVC bacteria in the deep sea.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42669679},
issn = {2041-1723},
mesh = {*Seawater/microbiology ; RNA, Ribosomal, 16S/genetics ; *Glucans/metabolism ; *Bacteria/genetics/metabolism/classification/isolation & purification ; Metagenomics ; Multiomics ; Microbiota/genetics ; Phylogeny ; Glycoside Hydrolases/metabolism/genetics ; },
abstract = {The deep sea is home to a vast and largely unexplored microbial biosphere, along with large amounts of complex organic matter (COM). However, the functional capacity of the deep-sea microbiome to metabolize organic matter across diverse regions remains poorly understood. Here, we combine 16S rRNA gene amplicon sequencing, metagenomics, and metatranscriptomics to comprehensively characterize prokaryotic communities across different years (2018 and 2022) and habitats (cold seeps, hydrothermal vents, and seamounts). Our results reveal spatio-temporal community heterogeneity driven by geochemical gradients, alongside a widespread genetic potential for organic matter metabolism. Notably, the PVC (Planctomycetota-Verrucomicrobiota-Chlamydiota) superphylum exhibits extensive polysaccharide degradation capabilities, exemplified by the isolation of Planctomycetota strain WC338 and Lentisphaerota strain WC36 via laminarin enrichment. Growth experiments and transcriptomics confirm their strict laminarin dependence and characterize the underlying catabolic machinery-specifically, the deployment of different glycoside hydrolase (GH) families, which are broadly distributed and prevalent across the PVC superphylum. Furthermore, we demonstrate that laminarin acts as an effective selective substrate for enriching and isolating the deep-sea PVC superphylum bacteria. Collectively, these findings reveal that PVC bacteria-an overlooked group in laminarin degradation-possess specialized adaptations for polysaccharide breakdown and actively participate in laminarin turnover in deep-sea environments.},
}
MeSH Terms:
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*Seawater/microbiology
RNA, Ribosomal, 16S/genetics
*Glucans/metabolism
*Bacteria/genetics/metabolism/classification/isolation & purification
Metagenomics
Multiomics
Microbiota/genetics
Phylogeny
Glycoside Hydrolases/metabolism/genetics
RevDate: 2026-08-30
Bacterial Profile Stability of Middle Meatus Following Endoscopic Sinus Surgery: A Prospective Pilot Study.
American journal of rhinology & allergy [Epub ahead of print].
PurposeThe aim of this study was to explore longitudinal changes in the middle meatal microbiome following endoscopic sinus surgery (ESS), accounting for relevant clinical variables in a group of patients with chronic rhinosinusitis (CRS).MethodsParticipants with CRS without nasal polyps and CRS with nasal polyps admitted for ESS were prospectively recruited. Endoscopically guided swabs were collected from 40 CRS patients at the time of surgery and during the postoperative visit, approximately 6 weeks after the surgery, from the region of the middle meatus. Bacterial communities were characterized using the 16S rRNA gene sequencing. Paired samples from 22 patients with CRS were included in the final analysis.ResultsThe overall microbial community composition, as reflected in alpha- and beta-diversity metrics and relative taxon abundances, remained generally stable after surgery. However, using advanced statistical methods, we identified subtle alterations in the microbiome. Postoperative beta diversity differed by occupational exposure and vitamin D status, whereas the Linear Model for Differential Abundance extended to a linear mixed-effect model detected modest taxonomic variation associated with age, allergy, body mass index, 25(OH)D, and extent of surgery.ConclusionDespite various factors known to modulate CRS and anatomical changes resulting from ESS, this pilot study found that the baseline microbiome structure of the middle meatus remained largely stable postoperatively. While ESS did not result in pronounced alterations of the overall bacterial landscape, selected covariates appeared to be associated with postsurgical microbiome shifts, highlighting the need for further investigation in larger cohorts.
Additional Links: PMID-42669802
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@article {pmid42669802,
year = {2026},
author = {Brociek-Piłczyńska, A and Stępińska, M and Kwiatkowska, M and Jurkiewicz, D and Trafny, E},
title = {Bacterial Profile Stability of Middle Meatus Following Endoscopic Sinus Surgery: A Prospective Pilot Study.},
journal = {American journal of rhinology & allergy},
volume = {},
number = {},
pages = {19458924261478895},
doi = {10.1177/19458924261478895},
pmid = {42669802},
issn = {1945-8932},
abstract = {PurposeThe aim of this study was to explore longitudinal changes in the middle meatal microbiome following endoscopic sinus surgery (ESS), accounting for relevant clinical variables in a group of patients with chronic rhinosinusitis (CRS).MethodsParticipants with CRS without nasal polyps and CRS with nasal polyps admitted for ESS were prospectively recruited. Endoscopically guided swabs were collected from 40 CRS patients at the time of surgery and during the postoperative visit, approximately 6 weeks after the surgery, from the region of the middle meatus. Bacterial communities were characterized using the 16S rRNA gene sequencing. Paired samples from 22 patients with CRS were included in the final analysis.ResultsThe overall microbial community composition, as reflected in alpha- and beta-diversity metrics and relative taxon abundances, remained generally stable after surgery. However, using advanced statistical methods, we identified subtle alterations in the microbiome. Postoperative beta diversity differed by occupational exposure and vitamin D status, whereas the Linear Model for Differential Abundance extended to a linear mixed-effect model detected modest taxonomic variation associated with age, allergy, body mass index, 25(OH)D, and extent of surgery.ConclusionDespite various factors known to modulate CRS and anatomical changes resulting from ESS, this pilot study found that the baseline microbiome structure of the middle meatus remained largely stable postoperatively. While ESS did not result in pronounced alterations of the overall bacterial landscape, selected covariates appeared to be associated with postsurgical microbiome shifts, highlighting the need for further investigation in larger cohorts.},
}
RevDate: 2026-08-31
Microbiome Therapies in Inflammatory Bowel Disease, Diabetes and Obesity: From Mechanistic Insights to Clinical Translation.
Cardiovascular & hematological agents in medicinal chemistry pii:CHAMC-EPUB-157878 [Epub ahead of print].
INTRODUCTION: This study aims to explore novel clinical microbiome therapeutics for Inflammatory Bowel Disease (IBD), diabetes, and obesity. Specifically, this work seeks to elucidate the efficacy, underlying mechanisms, and therapeutic potential of microbiome-based interventions for various chronic diseases by identifying recent findings from microbiome research, clinical trials, and meta-analyses.
METHODS: Literature data for the present study were collected through a structured narrative review using databases such as PubMed, Google Scholar, and clinical trial registries. We searched for evidence published between 2013 and 2024, with a particular focus on randomized controlled trials and meta-analyses of microbiome approaches for IBD, diabetes, and obesity.
RESULTS: Gut microbiome therapies with promising effects in IBD, diabetes, and obesity include probiotics, prebiotics, Fecal Microbiota Transplantation (FMT), engineered bacterial therapies, and dietary interventions. These interventions have been shown to reduce inflammation, enhance insulin sensitivity, promote weight loss, and promote metabolic health. These effects are mediated by modulation of the immune response, metabolic control via microbial metabolites, and restoration of microbial balance and homeostasis.
DISCUSSION: Microbiome-based therapies show promise in modulating inflammation and metabolism in chronic diseases; however, variable efficacy, limited large-scale clinical evidence, and mechanistic heterogeneity necessitate cautious interpretation and further validation.
CONCLUSION: Microbiome therapies, being effective and safe, pose a risk of completely overturning current treatment paradigms. Future applications need to focus on combination therapies, personalized medicine, and technological advances to realize the potential of microbiome-based interventions to promote good patient health and quality of life.
Additional Links: PMID-42670057
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PubMed:
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@article {pmid42670057,
year = {2026},
author = {B, P and J, L and G, M and V, M and Taher, A and A, MK and G, BY and E, B},
title = {Microbiome Therapies in Inflammatory Bowel Disease, Diabetes and Obesity: From Mechanistic Insights to Clinical Translation.},
journal = {Cardiovascular & hematological agents in medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715257474588260810070022},
pmid = {42670057},
issn = {1875-6182},
abstract = {INTRODUCTION: This study aims to explore novel clinical microbiome therapeutics for Inflammatory Bowel Disease (IBD), diabetes, and obesity. Specifically, this work seeks to elucidate the efficacy, underlying mechanisms, and therapeutic potential of microbiome-based interventions for various chronic diseases by identifying recent findings from microbiome research, clinical trials, and meta-analyses.
METHODS: Literature data for the present study were collected through a structured narrative review using databases such as PubMed, Google Scholar, and clinical trial registries. We searched for evidence published between 2013 and 2024, with a particular focus on randomized controlled trials and meta-analyses of microbiome approaches for IBD, diabetes, and obesity.
RESULTS: Gut microbiome therapies with promising effects in IBD, diabetes, and obesity include probiotics, prebiotics, Fecal Microbiota Transplantation (FMT), engineered bacterial therapies, and dietary interventions. These interventions have been shown to reduce inflammation, enhance insulin sensitivity, promote weight loss, and promote metabolic health. These effects are mediated by modulation of the immune response, metabolic control via microbial metabolites, and restoration of microbial balance and homeostasis.
DISCUSSION: Microbiome-based therapies show promise in modulating inflammation and metabolism in chronic diseases; however, variable efficacy, limited large-scale clinical evidence, and mechanistic heterogeneity necessitate cautious interpretation and further validation.
CONCLUSION: Microbiome therapies, being effective and safe, pose a risk of completely overturning current treatment paradigms. Future applications need to focus on combination therapies, personalized medicine, and technological advances to realize the potential of microbiome-based interventions to promote good patient health and quality of life.},
}
RevDate: 2026-08-31
Vaginal drug delivery for precision therapy in polyendocrine metabolic ovarian syndrome: emerging technologies, translational challenges and future perspectives.
Expert opinion on drug delivery [Epub ahead of print].
INTRODUCTION: Polyendocrine Metabolic Ovarian Syndrome (PMOS) is an endocrine disorder characterized by metabolic dysfunction, hormonal imbalance, inflammation, and clinical manifestations. Current treatments, systemic drugs, may provide limited benefits because of adverse effects, variable efficacy, and poor adherence, highlighting the need for personalized therapeutic strategies. Vaginal administration offers an underexplored approach that may enable localized delivery, reduce systemic exposure, and support dosing. Furthermore, the vaginal microenvironment can influence drug stability, absorption, retention, and therapeutic outcomes.
AREAS COVERED: This review examines the pathophysiological basis of PMOS and recent advances in vaginal drug delivery (VDD) systems for precision therapy. It highlights the transition from conventional approaches to nanoscale carriers, bioresponsive formulations, genetic and microbiome-informed strategies, and 3D-printed devices. The roles of artificial intelligence, machine learning, point-of-care diagnostics, and theranostic platforms in personalized therapy are discussed, together with translational and regulatory considerations. Relevant literature was identified through searches of PubMed, Scopus, Web of Science, and Google Scholar.
EXPERT OPINION: VDD represents a promising precision medicine approach for PMOS; however, clinical translation remains challenged by vaginal microenvironment variability, limited safety evidence, formulation scalability, patient acceptance, and insufficient clinical validation. Future progress will require interdisciplinary integration of biomaterial engineering, biology, drug delivery, microbiome science, and digital health.
Additional Links: PMID-42670175
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@article {pmid42670175,
year = {2026},
author = {Shah, S and Parikh, A and Garg, S and Mehta, T},
title = {Vaginal drug delivery for precision therapy in polyendocrine metabolic ovarian syndrome: emerging technologies, translational challenges and future perspectives.},
journal = {Expert opinion on drug delivery},
volume = {},
number = {},
pages = {},
doi = {10.1080/17425247.2026.2727678},
pmid = {42670175},
issn = {1744-7593},
abstract = {INTRODUCTION: Polyendocrine Metabolic Ovarian Syndrome (PMOS) is an endocrine disorder characterized by metabolic dysfunction, hormonal imbalance, inflammation, and clinical manifestations. Current treatments, systemic drugs, may provide limited benefits because of adverse effects, variable efficacy, and poor adherence, highlighting the need for personalized therapeutic strategies. Vaginal administration offers an underexplored approach that may enable localized delivery, reduce systemic exposure, and support dosing. Furthermore, the vaginal microenvironment can influence drug stability, absorption, retention, and therapeutic outcomes.
AREAS COVERED: This review examines the pathophysiological basis of PMOS and recent advances in vaginal drug delivery (VDD) systems for precision therapy. It highlights the transition from conventional approaches to nanoscale carriers, bioresponsive formulations, genetic and microbiome-informed strategies, and 3D-printed devices. The roles of artificial intelligence, machine learning, point-of-care diagnostics, and theranostic platforms in personalized therapy are discussed, together with translational and regulatory considerations. Relevant literature was identified through searches of PubMed, Scopus, Web of Science, and Google Scholar.
EXPERT OPINION: VDD represents a promising precision medicine approach for PMOS; however, clinical translation remains challenged by vaginal microenvironment variability, limited safety evidence, formulation scalability, patient acceptance, and insufficient clinical validation. Future progress will require interdisciplinary integration of biomaterial engineering, biology, drug delivery, microbiome science, and digital health.},
}
RevDate: 2026-08-31
The correlation between dietary behaviors and gut microbiota in children with autism spectrum disorder: A cross-sectional study.
Journal of pediatric gastroenterology and nutrition [Epub ahead of print].
OBJECTIVE: This study investigated the associations between dietary behaviors and gut microbiota in children with autism spectrum disorder (ASD) stratified according to symptom severity, aiming to provide evidence for targeted interventions.
METHODS: A cross-sectional study enrolled 81 children with ASD aged 3-12 years, divided into mild-to-moderate (n = 35) and severe (n = 46) groups based on Childhood Autism Rating Scale scores. Dietary behaviors were assessed using the Children's Eating Behavior Questionnaire. Gut microbiota was analyzed by 16S rRNA (16S ribosomal RNA) gene sequencing. Spearman correlation examined associations.
RESULTS: The severe ASD group showed significantly lower Enjoyment of Food scores and higher scores for both Emotional Undereating and Emotional Overeating (p < 0.05). Alpha diversity (Shannon and Simpson indices) was significantly lower in the severe group (p < 0.05). Beta diversity showed significant between-group separation (p < 0.05). The severe group exhibited decreased Firmicutes and increased Proteobacteria at the phylum level, with decreased Faecalibacterium and Dialister and a 2.8-fold increase in Klebsiella at the genus level (p < 0.05). Correlation analysis revealed severity-dependent associations: mild-to-moderate ASD showed phylum-level associations, while severe ASD showed genus-level associations.
CONCLUSION: Children with severe ASD exhibited more pronounced dietary behavior abnormalities and gut microbiota dysbiosis. The severity-dependent associations suggest stratified intervention strategies for ASD children.
Additional Links: PMID-42670304
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PubMed:
Citation:
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@article {pmid42670304,
year = {2026},
author = {Aili, A and Yimin, Z and Maiming, N and Tuhongjiang, Y and Paerhati, J and Aini, X and Kelimu, A and Maimaiti, R},
title = {The correlation between dietary behaviors and gut microbiota in children with autism spectrum disorder: A cross-sectional study.},
journal = {Journal of pediatric gastroenterology and nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpn3.70552},
pmid = {42670304},
issn = {1536-4801},
support = {//The 14th Five-Year Plan Distinctive Program of Public Health and Preventive Medicine in Higher Education Institutions of the Xinjiang Uygur Autonomous Region/ ; TSYC202301A013//Tianshan Talent Project-Medical and Health High-Level Talent Training Program/ ; },
abstract = {OBJECTIVE: This study investigated the associations between dietary behaviors and gut microbiota in children with autism spectrum disorder (ASD) stratified according to symptom severity, aiming to provide evidence for targeted interventions.
METHODS: A cross-sectional study enrolled 81 children with ASD aged 3-12 years, divided into mild-to-moderate (n = 35) and severe (n = 46) groups based on Childhood Autism Rating Scale scores. Dietary behaviors were assessed using the Children's Eating Behavior Questionnaire. Gut microbiota was analyzed by 16S rRNA (16S ribosomal RNA) gene sequencing. Spearman correlation examined associations.
RESULTS: The severe ASD group showed significantly lower Enjoyment of Food scores and higher scores for both Emotional Undereating and Emotional Overeating (p < 0.05). Alpha diversity (Shannon and Simpson indices) was significantly lower in the severe group (p < 0.05). Beta diversity showed significant between-group separation (p < 0.05). The severe group exhibited decreased Firmicutes and increased Proteobacteria at the phylum level, with decreased Faecalibacterium and Dialister and a 2.8-fold increase in Klebsiella at the genus level (p < 0.05). Correlation analysis revealed severity-dependent associations: mild-to-moderate ASD showed phylum-level associations, while severe ASD showed genus-level associations.
CONCLUSION: Children with severe ASD exhibited more pronounced dietary behavior abnormalities and gut microbiota dysbiosis. The severity-dependent associations suggest stratified intervention strategies for ASD children.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-31
Inflammatory and Immune Pathways Driving Tumor Necrosis Factor Inhibitor Resistance in Ulcerative Colitis.
Journal of inflammation research, 19:546264 pii:546264.
Ulcerative colitis (UC) is a chronic immune-mediated inflammatory disease characterized by dysregulated mucosal immunity in genetically susceptible individuals exposed to environmental and microbial triggers. Tumor necrosis factor-alpha (TNF-α) antagonists have transformed the management of moderately-to-severely active UC and remain a cornerstone of therapy, although approximately one third of patients demonstrate primary non-response and up to half experience secondary loss of response over time. Historically, treatment failure has been attributed to pharmacokinetic factors such as inadequate drug exposure or immunogenicity. Increasing evidence suggests that TNF-α resistance is frequently mediated by pharmacodynamic factors, including cytokine redundancy and non-TNF inflammatory circuits. Among the most prominent mechanisms are activation of the IL-6 signaling axis, stromal cytokines such as oncostatin M, IL-23-driven Th17 inflammation, and IL-1-mediated innate immune responses. More exploratory mechanisms include perturbations in B-cell and plasmablast biology, transcriptional signatures associated with myeloid activation, genetic susceptibility pathways such as TREM-1 signaling, and microbiome-driven metabolic dysfunction. Emerging data also suggest a role for neutrophil extracellular traps. Although biologically plausible, the clinical relevance and therapeutic implications of several of these emerging mechanisms remain to be established. Advances in transcriptomics, single-cell sequencing, and systems biology approaches have further highlighted the heterogeneity of inflammatory pathotypes in UC and the importance of precision medicine strategies. Understanding the molecular determinants of TNF-α resistance could inform more rational therapeutic sequencing, guide optimization of existing therapies, and identify novel targets for combination or next-generation treatments aimed at improving outcomes in patients with difficult-to-treat UC. In this review, we highlight key mechanisms of TNF-α non-response, identify potentially druggable therapeutic targets within this framework, and define future directions for advancing care in patients with UC who experience TNF-α non-response.
Additional Links: PMID-42670519
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@article {pmid42670519,
year = {2026},
author = {Fairweather, M and Faggiani, I and Ma, C},
title = {Inflammatory and Immune Pathways Driving Tumor Necrosis Factor Inhibitor Resistance in Ulcerative Colitis.},
journal = {Journal of inflammation research},
volume = {19},
number = {},
pages = {546264},
doi = {10.2147/JIR.S546264},
pmid = {42670519},
issn = {1178-7031},
abstract = {Ulcerative colitis (UC) is a chronic immune-mediated inflammatory disease characterized by dysregulated mucosal immunity in genetically susceptible individuals exposed to environmental and microbial triggers. Tumor necrosis factor-alpha (TNF-α) antagonists have transformed the management of moderately-to-severely active UC and remain a cornerstone of therapy, although approximately one third of patients demonstrate primary non-response and up to half experience secondary loss of response over time. Historically, treatment failure has been attributed to pharmacokinetic factors such as inadequate drug exposure or immunogenicity. Increasing evidence suggests that TNF-α resistance is frequently mediated by pharmacodynamic factors, including cytokine redundancy and non-TNF inflammatory circuits. Among the most prominent mechanisms are activation of the IL-6 signaling axis, stromal cytokines such as oncostatin M, IL-23-driven Th17 inflammation, and IL-1-mediated innate immune responses. More exploratory mechanisms include perturbations in B-cell and plasmablast biology, transcriptional signatures associated with myeloid activation, genetic susceptibility pathways such as TREM-1 signaling, and microbiome-driven metabolic dysfunction. Emerging data also suggest a role for neutrophil extracellular traps. Although biologically plausible, the clinical relevance and therapeutic implications of several of these emerging mechanisms remain to be established. Advances in transcriptomics, single-cell sequencing, and systems biology approaches have further highlighted the heterogeneity of inflammatory pathotypes in UC and the importance of precision medicine strategies. Understanding the molecular determinants of TNF-α resistance could inform more rational therapeutic sequencing, guide optimization of existing therapies, and identify novel targets for combination or next-generation treatments aimed at improving outcomes in patients with difficult-to-treat UC. In this review, we highlight key mechanisms of TNF-α non-response, identify potentially druggable therapeutic targets within this framework, and define future directions for advancing care in patients with UC who experience TNF-α non-response.},
}
RevDate: 2026-08-31
Guiding the AI revolution in periodontology and implant dentistry: Concepts, ethics, accountability, and a roadmap for sustainable adoption.
Periodontology 2000 [Epub ahead of print].
BACKGROUND: Artificial intelligence (AI) is increasingly gaining attention in the field of periodontology and implant dentistry. Currently developed models can support diagnosis, treatment planning, and maintenance monitoring. However, most of the available literature is based on retrospective and often single-modality data sets. Therefore, they lack clinical generalizability and underrepresent the multimodal nature of periodontal and peri-implant diseases.
OBJECTIVES AND METHODS: This study examines the current status of AI in the field of periodontology and implant dentistry and discusses the associated ethical and translational challenges. A narrative review search was conducted in PubMed, Embase, and Cochrane Library through February 2026. Furthermore, it explains the responsible implementation methods and proposes a roadmap for the sustainable adoption of AI in this field.
RESULTS: The use of AI showed major promise in the field of periodontology and implantology. The main applications of AI in this field include bone loss detection, detection of intrabony defects, biofilm and microbiome-related analysis, patient communication, posttreatment monitoring, implant planning, detection of the implant system, and predicting the implant prognosis. Utilizing AI in these domains improved the efficiency, consistency, and access to care to some extent. However, there are major limitations that need to be addressed to move toward a responsible and sustainable use of AI. These limitations include reliance on single modality and single-center and nonshareable data sets, incomplete integration of clinical and biological variables, limited external validation, and persistent concern regarding bias, privacy, and explainability. These factors frame AI in periodontology as a clinician-supervised, data-dependent, and ethically guided technology rather than an isolated diagnostic tool. One of the most important factors that needs to be included in the training of clinicians is that they need to gain education on critiquing the AI outputs, use it as an assistive tool, and never over-rely on the AI outputs. The current evidence also suggests moving beyond the single-modality AI toward multimodal systems that better reflect the 2018 periodontal classification and the complexity of periodontal and peri-implant decision-making.
CONCLUSION: Use of AI has substantially improved periodontology and implant dentistry research. However, a sustainable clinical translation requires responsible implementation of the AI and a stronger data set that represents the multimodal nature of the periodontal and peri-implant diseases. Moving forward, the data sets being used to train the models need to be multimodal, multicenter, and clinically verified to support the generalizability of the findings. In addition, there needs to be clear ethical safeguards and clinician oversight to make sure the results are interpreted in the correct way.
CLINICAL RELEVANCE: As AI is becoming more prevalent among periodontists and other clinicians as an assistive tool, there is a clear need for proper education on how to use AI more effectively and responsibly. AI models and their outputs can be used for strengthening diagnosis, prognosis, treatment planning, and supportive care only when the full clinical context is provided. The long-term value of this integration of AI into clinical periodontology will largely depend on the following: whether it can be validated across diverse populations and whether it is supported by a shared clinical data infrastructure. This will ensure precise and consistent patient care in the real-world application of AI in the clinical setting.
Additional Links: PMID-42670718
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PubMed:
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@article {pmid42670718,
year = {2026},
author = {Khormali, A and Soghli, N and Miguez, PA},
title = {Guiding the AI revolution in periodontology and implant dentistry: Concepts, ethics, accountability, and a roadmap for sustainable adoption.},
journal = {Periodontology 2000},
volume = {},
number = {},
pages = {},
doi = {10.1111/prd.70078},
pmid = {42670718},
issn = {1600-0757},
abstract = {BACKGROUND: Artificial intelligence (AI) is increasingly gaining attention in the field of periodontology and implant dentistry. Currently developed models can support diagnosis, treatment planning, and maintenance monitoring. However, most of the available literature is based on retrospective and often single-modality data sets. Therefore, they lack clinical generalizability and underrepresent the multimodal nature of periodontal and peri-implant diseases.
OBJECTIVES AND METHODS: This study examines the current status of AI in the field of periodontology and implant dentistry and discusses the associated ethical and translational challenges. A narrative review search was conducted in PubMed, Embase, and Cochrane Library through February 2026. Furthermore, it explains the responsible implementation methods and proposes a roadmap for the sustainable adoption of AI in this field.
RESULTS: The use of AI showed major promise in the field of periodontology and implantology. The main applications of AI in this field include bone loss detection, detection of intrabony defects, biofilm and microbiome-related analysis, patient communication, posttreatment monitoring, implant planning, detection of the implant system, and predicting the implant prognosis. Utilizing AI in these domains improved the efficiency, consistency, and access to care to some extent. However, there are major limitations that need to be addressed to move toward a responsible and sustainable use of AI. These limitations include reliance on single modality and single-center and nonshareable data sets, incomplete integration of clinical and biological variables, limited external validation, and persistent concern regarding bias, privacy, and explainability. These factors frame AI in periodontology as a clinician-supervised, data-dependent, and ethically guided technology rather than an isolated diagnostic tool. One of the most important factors that needs to be included in the training of clinicians is that they need to gain education on critiquing the AI outputs, use it as an assistive tool, and never over-rely on the AI outputs. The current evidence also suggests moving beyond the single-modality AI toward multimodal systems that better reflect the 2018 periodontal classification and the complexity of periodontal and peri-implant decision-making.
CONCLUSION: Use of AI has substantially improved periodontology and implant dentistry research. However, a sustainable clinical translation requires responsible implementation of the AI and a stronger data set that represents the multimodal nature of the periodontal and peri-implant diseases. Moving forward, the data sets being used to train the models need to be multimodal, multicenter, and clinically verified to support the generalizability of the findings. In addition, there needs to be clear ethical safeguards and clinician oversight to make sure the results are interpreted in the correct way.
CLINICAL RELEVANCE: As AI is becoming more prevalent among periodontists and other clinicians as an assistive tool, there is a clear need for proper education on how to use AI more effectively and responsibly. AI models and their outputs can be used for strengthening diagnosis, prognosis, treatment planning, and supportive care only when the full clinical context is provided. The long-term value of this integration of AI into clinical periodontology will largely depend on the following: whether it can be validated across diverse populations and whether it is supported by a shared clinical data infrastructure. This will ensure precise and consistent patient care in the real-world application of AI in the clinical setting.},
}
RevDate: 2026-08-31
The External Exposome and Food Allergy: How Environmental Exposures Shape Disease Risk.
Allergy [Epub ahead of print].
IgE-mediated food allergy is a global health issue with rising prevalence that cannot be explained by genetic change alone, strongly suggesting that environmental exposures are a key driver. The external exposome encompasses several exposures that influence the developing immune system and modify food allergy risk. Environmental exposure to food allergens in household dust is increasingly recognized as a risk factor for sensitization, whereas early oral introduction promotes tolerance. Early-life microbial exposures, especially those associated with rural and farming environments, may protect against food allergies by stimulating innate immune pathways and shaping the gut microbiome. Co-exposures to microbial adjuvants can further alter risk in a timing-dependent manner. Epidemiological birth cohort studies have linked exposure to air pollutants, such as particulate matter and nitrogen dioxide, to food sensitization and allergy. Synthetic chemicals represent an emerging risk factor by disrupting epithelial barrier integrity and immune regulation. Ultra-processed food consumption and dietary additives may further increase risk by altering gut permeability and immune function. Significant gaps remain in our understanding of the most relevant environmental exposures affecting food allergy risk. Future research using longitudinal cohort designs and exposome-wide approaches is essential for developing evidence-based strategies to prevent food allergy.
Additional Links: PMID-42670723
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PubMed:
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@article {pmid42670723,
year = {2026},
author = {Smeekens, JM and Brough, HA and Järvinen, KM and Troyer, S and Kulis, MD and Moran, TP},
title = {The External Exposome and Food Allergy: How Environmental Exposures Shape Disease Risk.},
journal = {Allergy},
volume = {},
number = {},
pages = {},
doi = {10.1111/all.70501},
pmid = {42670723},
issn = {1398-9995},
support = {R01-ES032544/ES/NIEHS NIH HHS/United States ; },
abstract = {IgE-mediated food allergy is a global health issue with rising prevalence that cannot be explained by genetic change alone, strongly suggesting that environmental exposures are a key driver. The external exposome encompasses several exposures that influence the developing immune system and modify food allergy risk. Environmental exposure to food allergens in household dust is increasingly recognized as a risk factor for sensitization, whereas early oral introduction promotes tolerance. Early-life microbial exposures, especially those associated with rural and farming environments, may protect against food allergies by stimulating innate immune pathways and shaping the gut microbiome. Co-exposures to microbial adjuvants can further alter risk in a timing-dependent manner. Epidemiological birth cohort studies have linked exposure to air pollutants, such as particulate matter and nitrogen dioxide, to food sensitization and allergy. Synthetic chemicals represent an emerging risk factor by disrupting epithelial barrier integrity and immune regulation. Ultra-processed food consumption and dietary additives may further increase risk by altering gut permeability and immune function. Significant gaps remain in our understanding of the most relevant environmental exposures affecting food allergy risk. Future research using longitudinal cohort designs and exposome-wide approaches is essential for developing evidence-based strategies to prevent food allergy.},
}
RevDate: 2026-08-31
Mapping the omics landscape for peri-implant diseases: A scoping review.
Periodontology 2000 [Epub ahead of print].
OBJECTIVES: To map omics evidence across peri-implant health, peri-implant mucositis, and peri-implantitis, and to identify recurring molecular patterns and candidate biomarker signals relevant to diagnosis, monitoring, and treatment.
MATERIALS AND METHODS: This scoping review included human studies using genomics, DNA methylation-based epigenomics, bulk and single-cell transcriptomics, non-coding RNA analyses (including miRNA, lncRNA, and circRNA), proteomics, metabolomics, and microbiome profiling. Findings were organized by clinical state (health, mucositis, peri-implantitis) and interpreted within an implant-conditioned niche shaped by microbial, host, and biomaterial-related influences.
RESULTS: Of 319 records identified, 78 studies were included. Most focused on genomics, transcriptomics, and the microbiome, with fewer studies in DNA methylation-based epigenomics, proteomics, and metabolomics. Peri-implant health was generally associated with oxygen-tolerant, biosynthetically active microbial communities and a regulated host-response baseline. Peri-implant mucositis appeared to be an intermediate plaque-induced state marked by expansion of bridge anaerobes and early innate inflammatory activation, but it was under-represented in transcriptomic, proteomic, and epigenomic datasets. Peri-implantitis was associated with stronger coupling between dysbiosis and host-destructive responses, including recurrent innate inflammatory hubs, chemokine-driven myeloid recruitment, protease activity, osteo-immune imbalance, and catabolic metabolomic profiles enriched in polyamines and short-chain fatty acids. DNA methylation studies linked disease status, and in limited cohorts, titanium particle burden, with altered methylation patterns. Non-coding RNA studies suggested additional regulatory networks related to inflammation and bone-associated signaling. Treatment studies indicated that decontamination may reduce bacterial biomass on rough titanium surfaces, but it does not consistently eliminate residual biofilm, suggesting biological improvements may reflect ecological shifts rather than complete surface decontamination.
CONCLUSIONS: Current omics evidence suggests that peri-implant disease follows a staged, implant-conditioned biological trajectory rather than a simple binary healthy/diseased model.
Additional Links: PMID-42670778
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@article {pmid42670778,
year = {2026},
author = {Ng, E and Fragkioudakis, I and Perussolo, J and Tay, JRH and Calciolari, E and Donos, N},
title = {Mapping the omics landscape for peri-implant diseases: A scoping review.},
journal = {Periodontology 2000},
volume = {},
number = {},
pages = {},
doi = {10.1111/prd.70056},
pmid = {42670778},
issn = {1600-0757},
abstract = {OBJECTIVES: To map omics evidence across peri-implant health, peri-implant mucositis, and peri-implantitis, and to identify recurring molecular patterns and candidate biomarker signals relevant to diagnosis, monitoring, and treatment.
MATERIALS AND METHODS: This scoping review included human studies using genomics, DNA methylation-based epigenomics, bulk and single-cell transcriptomics, non-coding RNA analyses (including miRNA, lncRNA, and circRNA), proteomics, metabolomics, and microbiome profiling. Findings were organized by clinical state (health, mucositis, peri-implantitis) and interpreted within an implant-conditioned niche shaped by microbial, host, and biomaterial-related influences.
RESULTS: Of 319 records identified, 78 studies were included. Most focused on genomics, transcriptomics, and the microbiome, with fewer studies in DNA methylation-based epigenomics, proteomics, and metabolomics. Peri-implant health was generally associated with oxygen-tolerant, biosynthetically active microbial communities and a regulated host-response baseline. Peri-implant mucositis appeared to be an intermediate plaque-induced state marked by expansion of bridge anaerobes and early innate inflammatory activation, but it was under-represented in transcriptomic, proteomic, and epigenomic datasets. Peri-implantitis was associated with stronger coupling between dysbiosis and host-destructive responses, including recurrent innate inflammatory hubs, chemokine-driven myeloid recruitment, protease activity, osteo-immune imbalance, and catabolic metabolomic profiles enriched in polyamines and short-chain fatty acids. DNA methylation studies linked disease status, and in limited cohorts, titanium particle burden, with altered methylation patterns. Non-coding RNA studies suggested additional regulatory networks related to inflammation and bone-associated signaling. Treatment studies indicated that decontamination may reduce bacterial biomass on rough titanium surfaces, but it does not consistently eliminate residual biofilm, suggesting biological improvements may reflect ecological shifts rather than complete surface decontamination.
CONCLUSIONS: Current omics evidence suggests that peri-implant disease follows a staged, implant-conditioned biological trajectory rather than a simple binary healthy/diseased model.},
}
RevDate: 2026-08-31
The Dysbiosis-Barrier-Immune Axis: Unraveling the Immune Consequences of Skin Microbial Imbalance.
Immunology and cell biology [Epub ahead of print].
The skin microbiota has been reframed as a dynamic and active regulator of cutaneous barrier integrity and immune programming, moving beyond its traditional view as a passive microbial community. Dysbiosis represents a complex functional and ecological imbalance that disrupts barrier integrity and may promote sustained inflammatory immune remodeling. This mechanistic axis, in which disruption of the microbiota contributes to barrier failure and immune dysregulation, underpins chronic inflammatory skin conditions. Conventional antibiotic-centered therapies often fail to restore microbial homeostasis or immune balance, highlighting their limitations. Emerging precision microbiome therapeutics focus on targeted modulation of microbial function, signaling pathways, and ecological restoration to repair barrier defects and recalibrate immune responses. This review synthesizes current evidence linking skin microbiota dysbiosis with barrier dysfunction, inflammatory immune remodeling, and emerging microbiome-directed therapeutic strategies. We propose an integrative framework linking ecological disruption, epithelial barrier injury, and immune dysregulation while highlighting unresolved mechanistic, translational, and knowledge gaps, such as detailed molecular mechanisms of host-microbiota interactions and challenges in translating findings into clinically effective personalized interventions. Future research should prioritize multi-omics integration and biomarker-driven stratification to advance precision dermatology therapeutics grounded in mechanistic insights of skin microbial ecology.
Additional Links: PMID-42670971
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PubMed:
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@article {pmid42670971,
year = {2026},
author = {Mahdy, A and Amin, I and Mohamed, HH and Hamdy, M and Abuelhaded, K and Alam-ElDein, KM and Elbakry, OM and Abdelkhalek, A and Elkhawanky, M and Elgebaly, AS and Faraag, AHI and Mohammed, OA and Doghish, AS},
title = {The Dysbiosis-Barrier-Immune Axis: Unraveling the Immune Consequences of Skin Microbial Imbalance.},
journal = {Immunology and cell biology},
volume = {},
number = {},
pages = {},
doi = {10.1111/imcb.70161},
pmid = {42670971},
issn = {1440-1711},
abstract = {The skin microbiota has been reframed as a dynamic and active regulator of cutaneous barrier integrity and immune programming, moving beyond its traditional view as a passive microbial community. Dysbiosis represents a complex functional and ecological imbalance that disrupts barrier integrity and may promote sustained inflammatory immune remodeling. This mechanistic axis, in which disruption of the microbiota contributes to barrier failure and immune dysregulation, underpins chronic inflammatory skin conditions. Conventional antibiotic-centered therapies often fail to restore microbial homeostasis or immune balance, highlighting their limitations. Emerging precision microbiome therapeutics focus on targeted modulation of microbial function, signaling pathways, and ecological restoration to repair barrier defects and recalibrate immune responses. This review synthesizes current evidence linking skin microbiota dysbiosis with barrier dysfunction, inflammatory immune remodeling, and emerging microbiome-directed therapeutic strategies. We propose an integrative framework linking ecological disruption, epithelial barrier injury, and immune dysregulation while highlighting unresolved mechanistic, translational, and knowledge gaps, such as detailed molecular mechanisms of host-microbiota interactions and challenges in translating findings into clinically effective personalized interventions. Future research should prioritize multi-omics integration and biomarker-driven stratification to advance precision dermatology therapeutics grounded in mechanistic insights of skin microbial ecology.},
}
RevDate: 2026-08-31
Laccase-mediated biotransformation potential for fluorinated compounds by geographically diverse human gut microbiota.
mBio [Epub ahead of print].
The growing prevalence of synthetic organofluorine substances in agrochemicals, food packaging, and consumer products has led to increasing gastrointestinal exposure, with potential consequences for human health. Despite the extreme stability of fluorinated compounds, several microbial pathways for their transformation are known, including those involving laccases, a type of multicopper oxidase. However, the functionality of laccases in the gut microbiome, a natural contact point between food-associated chemicals and microbial biotransformation pathways, is poorly defined. Through a multi-study analysis of 1,578 human gut metagenomes spanning a global gradient from hunter-gatherer societies to industrialized urban populations, we found that laccase-coding gene homologs are widely distributed in the human gut microbiome. We identified a significant association between both the abundance and phylogenetic diversity of laccase homologs and the degree of urbanization. As human gut microbial laccase activity has not been experimentally demonstrated, eight gut metagenome-derived laccases were heterologously expressed and screened for activity with a redox mediator system. Six of the eight laccases demonstrated activity. One of these gut microbial laccases, derived from Veillonella, and three previously characterized laccases were then tested for their capacity to deplete 11 different food-associated chemicals. The Veillonella laccase depleted the agrochemicals cyflumetofen and fluazinam, as well as the industrial chemical bisphenol AF, to a lesser extent. By linking global gut metagenomes with activity assays, this work demonstrates the untapped potential of mining human gut metagenomes for laccases and other microbial enzymes that can actively modify various agricultural and industrial chemicals.IMPORTANCEAs adverse effects of fluorinated compounds on human health are emerging, the responsible enzymes from the human gut microbiome of geographically diverse human cohorts mediating interactions with fluorinated compounds in the gastrointestinal tract remain poorly characterized. In a multi-study analysis of publicly available microbiome sequencing data, we linked the abundance, diversity, and phylogeny of laccases within the gut microbiome to the degree of urbanization of human cohorts and experimentally demonstrated the ability of these laccases to deplete a range of food-associated fluorochemicals. Another significant contribution of our study is in the integration of rural catchment areas as a quantitative metric of urbanization in gut microbiome metagenomics and enzyme activity surveys.
Additional Links: PMID-42671175
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PubMed:
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@article {pmid42671175,
year = {2026},
author = {Schärer, MR and Yu, Y and Grawe, A and Christenson, JK and Robinson, SL and Bokulich, NA},
title = {Laccase-mediated biotransformation potential for fluorinated compounds by geographically diverse human gut microbiota.},
journal = {mBio},
volume = {},
number = {},
pages = {e0102626},
doi = {10.1128/mbio.01026-26},
pmid = {42671175},
issn = {2150-7511},
abstract = {The growing prevalence of synthetic organofluorine substances in agrochemicals, food packaging, and consumer products has led to increasing gastrointestinal exposure, with potential consequences for human health. Despite the extreme stability of fluorinated compounds, several microbial pathways for their transformation are known, including those involving laccases, a type of multicopper oxidase. However, the functionality of laccases in the gut microbiome, a natural contact point between food-associated chemicals and microbial biotransformation pathways, is poorly defined. Through a multi-study analysis of 1,578 human gut metagenomes spanning a global gradient from hunter-gatherer societies to industrialized urban populations, we found that laccase-coding gene homologs are widely distributed in the human gut microbiome. We identified a significant association between both the abundance and phylogenetic diversity of laccase homologs and the degree of urbanization. As human gut microbial laccase activity has not been experimentally demonstrated, eight gut metagenome-derived laccases were heterologously expressed and screened for activity with a redox mediator system. Six of the eight laccases demonstrated activity. One of these gut microbial laccases, derived from Veillonella, and three previously characterized laccases were then tested for their capacity to deplete 11 different food-associated chemicals. The Veillonella laccase depleted the agrochemicals cyflumetofen and fluazinam, as well as the industrial chemical bisphenol AF, to a lesser extent. By linking global gut metagenomes with activity assays, this work demonstrates the untapped potential of mining human gut metagenomes for laccases and other microbial enzymes that can actively modify various agricultural and industrial chemicals.IMPORTANCEAs adverse effects of fluorinated compounds on human health are emerging, the responsible enzymes from the human gut microbiome of geographically diverse human cohorts mediating interactions with fluorinated compounds in the gastrointestinal tract remain poorly characterized. In a multi-study analysis of publicly available microbiome sequencing data, we linked the abundance, diversity, and phylogeny of laccases within the gut microbiome to the degree of urbanization of human cohorts and experimentally demonstrated the ability of these laccases to deplete a range of food-associated fluorochemicals. Another significant contribution of our study is in the integration of rural catchment areas as a quantitative metric of urbanization in gut microbiome metagenomics and enzyme activity surveys.},
}
RevDate: 2026-08-31
Growth-dependent tRNA reprogramming and codon bias link translation to metabolic state in Enterococcus faecalis.
mBio [Epub ahead of print].
Enterococcus faecalis is a gram-positive commensal bacterium of the human gut microbiome and an opportunistic pathogen responsible for many hospital-acquired infections. Despite the clinical importance of E. faecalis, how gene and protein expression are coordinated with growth remains poorly defined. Here, we profiled transcript, protein, and tRNA pool dynamics across distinct phases of E. faecalis growth. Differences in protein abundance and corresponding mRNA levels suggested growth phase-dependent posttranscriptional regulation. Growth-associated genes exhibited biased synonymous codon usage, with ribosomal and glycolytic proteins enriched in low-abundance codons read by queuosine-modifiable tRNAs. Analysis of tRNA modification and tRNA isoacceptor abundance revealed growth phase-dependent changes, particularly in anticodon stem-loop modifications that influence synonymous codon translation. Changes in queuosine levels preceded shifts in ribosomal proteins, suggesting a contribution to codon-biased translation. Collectively, these findings reveal growth phase-associated remodeling of the E. faecalis tRNA pool and support a model in which queuosine-dependent translational reprogramming shapes protein expression during bacterial growth.IMPORTANCEEnterococcus faecalis is a common cause of hospital-acquired infections. Despite its clinical importance, a comprehensive understanding of the organism's physiology and adaptation to environmental changes remains incomplete. Here, we characterized protein, transcript, and tRNA dynamics across bacterial growth phases, uncovering a role for posttranscriptional regulation marked by tRNA reprogramming and biased synonymous codon usage. These findings enhance our understanding of E. faecalis growth and support a model of translational reprogramming therein.
Additional Links: PMID-42671178
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@article {pmid42671178,
year = {2026},
author = {Mitchener, MM and Anderson, CM and Veleba, M and Teo, K and Roch, M and Chen, R and Yuan, Y and Han, I and Dziergowska, A and Pethe, K and Begley, TJ and Kline, KA and Dedon, PC},
title = {Growth-dependent tRNA reprogramming and codon bias link translation to metabolic state in Enterococcus faecalis.},
journal = {mBio},
volume = {},
number = {},
pages = {e0147426},
doi = {10.1128/mbio.01474-26},
pmid = {42671178},
issn = {2150-7511},
abstract = {Enterococcus faecalis is a gram-positive commensal bacterium of the human gut microbiome and an opportunistic pathogen responsible for many hospital-acquired infections. Despite the clinical importance of E. faecalis, how gene and protein expression are coordinated with growth remains poorly defined. Here, we profiled transcript, protein, and tRNA pool dynamics across distinct phases of E. faecalis growth. Differences in protein abundance and corresponding mRNA levels suggested growth phase-dependent posttranscriptional regulation. Growth-associated genes exhibited biased synonymous codon usage, with ribosomal and glycolytic proteins enriched in low-abundance codons read by queuosine-modifiable tRNAs. Analysis of tRNA modification and tRNA isoacceptor abundance revealed growth phase-dependent changes, particularly in anticodon stem-loop modifications that influence synonymous codon translation. Changes in queuosine levels preceded shifts in ribosomal proteins, suggesting a contribution to codon-biased translation. Collectively, these findings reveal growth phase-associated remodeling of the E. faecalis tRNA pool and support a model in which queuosine-dependent translational reprogramming shapes protein expression during bacterial growth.IMPORTANCEEnterococcus faecalis is a common cause of hospital-acquired infections. Despite its clinical importance, a comprehensive understanding of the organism's physiology and adaptation to environmental changes remains incomplete. Here, we characterized protein, transcript, and tRNA dynamics across bacterial growth phases, uncovering a role for posttranscriptional regulation marked by tRNA reprogramming and biased synonymous codon usage. These findings enhance our understanding of E. faecalis growth and support a model of translational reprogramming therein.},
}
RevDate: 2026-08-31
Longitudinal development of infant oral ecosystem: salivary metabolomic, bacteriome, and virome dynamics in early infancy.
mSystems [Epub ahead of print].
This prospective cohort study investigated the longitudinal development of the salivary bacteriome, virome, and metabolome during early infancy. We assessed the associations between oral bacteria, viruses, and metabolites from 10 mother-infant dyads, with oral samples collected at 1 and 2 years of age. Forty saliva and plaque samples underwent untargeted metabolomic analysis, and infant saliva samples underwent metagenomic sequencing. Maternal salivary and plaque metabolomic profiles remained largely stable, whereas infant profiles were clearly separated from maternal profiles and changed with age. Notably, infant dental plaque metabolism underwent more substantial changes from year 1 to year 2 than saliva, with age-dependent metabolite shifts mainly involving energy, amino acid, nucleotide, and lipid metabolic pathways. Our findings also revealed significant developmental shifts in salivary bacteriome, virome, and functional pathway profiles during early childhood. The most abundant oral bacteria in early life, comprising over 75% of total abundance, included Veillonella, Streptococcus, Rothia, Prevotella, Neisseria, and Actinomyces species. While human viruses like Roseolovirus were detected, bacteriophages constituted the majority of the virome. Comparing infants at year 1 and year 2, we identified differentially abundant bacteria, viruses, metabolic functional pathways, and specific metabolites. We observed associations between bacteria and viruses, noting that these cross-kingdom relationships attenuated as infants grew. The study results underscore the complex and dynamic development of the oral microbiome, virome, and metabolome during early childhood.IMPORTANCEThe human oral cavity undergoes substantial microbial and metabolic development during early childhood, yet the temporal changes in the infant oral ecosystem remain incompletely understood. In this study, we longitudinally profiled the salivary metabolome, bacteriome, and virome of infants at 1 and 2 years of age. We demonstrated that the infant oral metabolome undergoes substantial developmental shifts, particularly in pathways related to energy, amino acid, and lipid metabolism; whereas maternal metabolic profiles remained stable over the same period. Furthermore, our results revealed the dynamic assembly of infant salivary virome and bacteriome and their associations with the functional pathways and metabolites. These findings provide new insights into the complex and dynamic development of the oral microbiome, virome, and metabolome in early infancy.
Additional Links: PMID-42671180
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PubMed:
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@article {pmid42671180,
year = {2026},
author = {Li, T and Lu, X and Alomeir, N and Gaca, A and Sohn, M and Gill, S and Smith, B and Munger, J and Xiao, J},
title = {Longitudinal development of infant oral ecosystem: salivary metabolomic, bacteriome, and virome dynamics in early infancy.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0094626},
doi = {10.1128/msystems.00946-26},
pmid = {42671180},
issn = {2379-5077},
abstract = {This prospective cohort study investigated the longitudinal development of the salivary bacteriome, virome, and metabolome during early infancy. We assessed the associations between oral bacteria, viruses, and metabolites from 10 mother-infant dyads, with oral samples collected at 1 and 2 years of age. Forty saliva and plaque samples underwent untargeted metabolomic analysis, and infant saliva samples underwent metagenomic sequencing. Maternal salivary and plaque metabolomic profiles remained largely stable, whereas infant profiles were clearly separated from maternal profiles and changed with age. Notably, infant dental plaque metabolism underwent more substantial changes from year 1 to year 2 than saliva, with age-dependent metabolite shifts mainly involving energy, amino acid, nucleotide, and lipid metabolic pathways. Our findings also revealed significant developmental shifts in salivary bacteriome, virome, and functional pathway profiles during early childhood. The most abundant oral bacteria in early life, comprising over 75% of total abundance, included Veillonella, Streptococcus, Rothia, Prevotella, Neisseria, and Actinomyces species. While human viruses like Roseolovirus were detected, bacteriophages constituted the majority of the virome. Comparing infants at year 1 and year 2, we identified differentially abundant bacteria, viruses, metabolic functional pathways, and specific metabolites. We observed associations between bacteria and viruses, noting that these cross-kingdom relationships attenuated as infants grew. The study results underscore the complex and dynamic development of the oral microbiome, virome, and metabolome during early childhood.IMPORTANCEThe human oral cavity undergoes substantial microbial and metabolic development during early childhood, yet the temporal changes in the infant oral ecosystem remain incompletely understood. In this study, we longitudinally profiled the salivary metabolome, bacteriome, and virome of infants at 1 and 2 years of age. We demonstrated that the infant oral metabolome undergoes substantial developmental shifts, particularly in pathways related to energy, amino acid, and lipid metabolism; whereas maternal metabolic profiles remained stable over the same period. Furthermore, our results revealed the dynamic assembly of infant salivary virome and bacteriome and their associations with the functional pathways and metabolites. These findings provide new insights into the complex and dynamic development of the oral microbiome, virome, and metabolome in early infancy.},
}
RevDate: 2026-08-31
Sulfur metabolism and immune-microbial networks across oral niches in periodontal disease.
Microbiology spectrum [Epub ahead of print].
Volatile sulfur compounds (VSCs) integrate microbial metabolism with local inflammation in periodontal disease. We profiled five oral niches (saliva, tongue, subgingival, supragingival, and interdental plaque) across clinical health, gingivitis, and periodontitis by combining direct VSC measurements (subgingival and oral headspace H2S/CH3SH), functional cysteine/methionine degradation assays, 16S rRNA profiling, gingival crevicular fluid cytokines, and targeted qPCR. Subgingival H2S concentrations were significantly elevated in periodontitis after adjusting for age, sex, plaque index, and subgingival bacterial load (β = 1.24, P = 0.03), and tracked shifts in community composition and the cytokine milieu. Oral headspace CH3SH increased with disease, whereas headspace H2S showed a bimodal pattern (health and periodontitis). In cysteine assays, subgingival and tongue biofilms were the most efficient H2S producers per mg protein; this ranking was preserved after normalization to total bacteria by qPCR. Metagenome predictions indicated enhanced sulfur metabolism in disease, particularly in subgingival plaque, with relative enrichment of SAM-cycle/methionine biosynthesis pathways in health. Methionine degradation to CH3SH increased with disease severity, shifting from subgingival sites in health to interdental/supragingival plaque in disease, and occurring most frequently in saliva. Correlation networks revealed niche- and diagnosis-specific coupling among VSCs, cytokines, and taxa, including associations of Capnocytophaga, Fusobacterium, Prevotella, and Corynebacterium, with IL-1β, IL-4, IL-8, and MCP-1. Together, these data identify the subgingival crevice as a disproportionate source of sulfide and show that sulfur metabolism is spatially organized and disease-responsive. We show that subgingival H2S as a functional marker that integrates microbial dysbiosis and inflammation.IMPORTANCEWe asked how metabolism, microbes, and immunity fit together during gum disease. Using a systems approach across five oral sites, we combined sulfur metabolite measurements, functional assays, microbiome profiling, and cytokine data, and analyzed them as one network. The result is a comprehensive map showing that sulfur metabolism is spatially organized, disease-responsive, and tightly coupled to local immune signals, with the subgingival niche playing an outsized role. Further, this integrated readout turns sulfur metabolism into a useful window on dysbiosis and inflammation and offers a path toward simple monitoring of periodontal disease, such as point-of-care sensors detecting subgingival hydrogen sulfide or methanethiol, or functional assays in which a methionine rinse is followed by measurement of oral headspace gases to assess microbial sulfur metabolism.
Additional Links: PMID-42671210
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PubMed:
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@article {pmid42671210,
year = {2026},
author = {Stephen, AS and Nagala, V and Fattah, B and Dhadwal, N and Gonzales-Marin, C and Gillam, DG and Bradshaw, DJ and Burnett, GR and Allaker, RP},
title = {Sulfur metabolism and immune-microbial networks across oral niches in periodontal disease.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0300825},
doi = {10.1128/spectrum.03008-25},
pmid = {42671210},
issn = {2165-0497},
abstract = {Volatile sulfur compounds (VSCs) integrate microbial metabolism with local inflammation in periodontal disease. We profiled five oral niches (saliva, tongue, subgingival, supragingival, and interdental plaque) across clinical health, gingivitis, and periodontitis by combining direct VSC measurements (subgingival and oral headspace H2S/CH3SH), functional cysteine/methionine degradation assays, 16S rRNA profiling, gingival crevicular fluid cytokines, and targeted qPCR. Subgingival H2S concentrations were significantly elevated in periodontitis after adjusting for age, sex, plaque index, and subgingival bacterial load (β = 1.24, P = 0.03), and tracked shifts in community composition and the cytokine milieu. Oral headspace CH3SH increased with disease, whereas headspace H2S showed a bimodal pattern (health and periodontitis). In cysteine assays, subgingival and tongue biofilms were the most efficient H2S producers per mg protein; this ranking was preserved after normalization to total bacteria by qPCR. Metagenome predictions indicated enhanced sulfur metabolism in disease, particularly in subgingival plaque, with relative enrichment of SAM-cycle/methionine biosynthesis pathways in health. Methionine degradation to CH3SH increased with disease severity, shifting from subgingival sites in health to interdental/supragingival plaque in disease, and occurring most frequently in saliva. Correlation networks revealed niche- and diagnosis-specific coupling among VSCs, cytokines, and taxa, including associations of Capnocytophaga, Fusobacterium, Prevotella, and Corynebacterium, with IL-1β, IL-4, IL-8, and MCP-1. Together, these data identify the subgingival crevice as a disproportionate source of sulfide and show that sulfur metabolism is spatially organized and disease-responsive. We show that subgingival H2S as a functional marker that integrates microbial dysbiosis and inflammation.IMPORTANCEWe asked how metabolism, microbes, and immunity fit together during gum disease. Using a systems approach across five oral sites, we combined sulfur metabolite measurements, functional assays, microbiome profiling, and cytokine data, and analyzed them as one network. The result is a comprehensive map showing that sulfur metabolism is spatially organized, disease-responsive, and tightly coupled to local immune signals, with the subgingival niche playing an outsized role. Further, this integrated readout turns sulfur metabolism into a useful window on dysbiosis and inflammation and offers a path toward simple monitoring of periodontal disease, such as point-of-care sensors detecting subgingival hydrogen sulfide or methanethiol, or functional assays in which a methionine rinse is followed by measurement of oral headspace gases to assess microbial sulfur metabolism.},
}
RevDate: 2026-08-31
Architectural confinement and seasonal forcing shape cross-domain pathogen-associated assemblages in complex built environments.
Microbiology spectrum [Epub ahead of print].
Airborne microbial pathogens in built environments (BEs) may pose health threats, yet the ecological mechanisms governing their assembly and persistence across interconnected architectural spaces are less studied. Here, we conducted a year-long, multi-spatial investigation across a university building complex, sampling the exhaust outlets of three indoor environments and adjacent outdoor inlets. By integrating the 16S rRNA gene and ITS sequencing from 437 paired bacterial-fungal samples, we characterized the spatiotemporal dynamics of airborne opportunistic pathogen-containing genera. Our study showed that spatial filtering emerged as the dominant determinant of pathogen community structure, with confined elevator environments serving as reservoirs of potential pathogens, with limited but continuous microbial influx from surrounding spaces. Some potential pathogens exhibited distinct seasonal dynamics, as exemplified by pathogen-associated fungal genera such as Fusarium, which peaked in autumn and winter, possibly driven by enhanced aerosol persistence and dispersal under cooler, drier conditions. In contrast, the bacterial counterparts exhibited greater temporal resilience, with key taxa such as Listeria actively transcribed during winter, predisposing them to increased relative abundance in spring. Cross-domain ecological networks further revealed dynamic associations among potential pathogens, centered on the skeletal structure mediated by the keystone fungal genus Aspergillus, suggesting that coordinated microbial associations may reinforce their persistence across seasons. Together, our findings suggest that the dynamics of pathogen-containing genera within BEs arise from the coupled effects of spatial filtering, climatic modulation, and microbial associations. These results provide a foundation for transitioning from static environmental control toward predictive pathogen management in BEs.IMPORTANCEBuilt environments (BEs) are the primary settings of human microbial exposure, yet the ecological principles governing the persistence of airborne pathogens across interconnected indoor spaces remain poorly resolved. By integrating bacterial and fungal community dynamics across spatial environments over four seasons, this year-long study demonstrates that the ecology of airborne pathogen-associated taxa is not static but is instead mediated by a complex interplay of spatial, climatic, and biological forces. Our findings identify enclosed, high-transit elevator spaces as critical hotspots for the accumulation of potential pathogens and highlight the role of seasonal ecological reorganization in driving airborne health risks. More broadly, this work establishes a system-level ecological framework for understanding the dynamics of airborne pathogen-associated taxa in BEs and provides a conceptual basis for developing more adaptive strategies for indoor microbial risk management.
Additional Links: PMID-42671214
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PubMed:
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@article {pmid42671214,
year = {2026},
author = {Qi, S and Zhang, S and Hu, Y and Sun, M and Xing, Z and Bao, S and Song, Y and Sun, L and Tong, X},
title = {Architectural confinement and seasonal forcing shape cross-domain pathogen-associated assemblages in complex built environments.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0191526},
doi = {10.1128/spectrum.01915-26},
pmid = {42671214},
issn = {2165-0497},
abstract = {Airborne microbial pathogens in built environments (BEs) may pose health threats, yet the ecological mechanisms governing their assembly and persistence across interconnected architectural spaces are less studied. Here, we conducted a year-long, multi-spatial investigation across a university building complex, sampling the exhaust outlets of three indoor environments and adjacent outdoor inlets. By integrating the 16S rRNA gene and ITS sequencing from 437 paired bacterial-fungal samples, we characterized the spatiotemporal dynamics of airborne opportunistic pathogen-containing genera. Our study showed that spatial filtering emerged as the dominant determinant of pathogen community structure, with confined elevator environments serving as reservoirs of potential pathogens, with limited but continuous microbial influx from surrounding spaces. Some potential pathogens exhibited distinct seasonal dynamics, as exemplified by pathogen-associated fungal genera such as Fusarium, which peaked in autumn and winter, possibly driven by enhanced aerosol persistence and dispersal under cooler, drier conditions. In contrast, the bacterial counterparts exhibited greater temporal resilience, with key taxa such as Listeria actively transcribed during winter, predisposing them to increased relative abundance in spring. Cross-domain ecological networks further revealed dynamic associations among potential pathogens, centered on the skeletal structure mediated by the keystone fungal genus Aspergillus, suggesting that coordinated microbial associations may reinforce their persistence across seasons. Together, our findings suggest that the dynamics of pathogen-containing genera within BEs arise from the coupled effects of spatial filtering, climatic modulation, and microbial associations. These results provide a foundation for transitioning from static environmental control toward predictive pathogen management in BEs.IMPORTANCEBuilt environments (BEs) are the primary settings of human microbial exposure, yet the ecological principles governing the persistence of airborne pathogens across interconnected indoor spaces remain poorly resolved. By integrating bacterial and fungal community dynamics across spatial environments over four seasons, this year-long study demonstrates that the ecology of airborne pathogen-associated taxa is not static but is instead mediated by a complex interplay of spatial, climatic, and biological forces. Our findings identify enclosed, high-transit elevator spaces as critical hotspots for the accumulation of potential pathogens and highlight the role of seasonal ecological reorganization in driving airborne health risks. More broadly, this work establishes a system-level ecological framework for understanding the dynamics of airborne pathogen-associated taxa in BEs and provides a conceptual basis for developing more adaptive strategies for indoor microbial risk management.},
}
RevDate: 2026-08-31
Manipulation of rhizosphere microbiome by Microbacterium sp. GB16_1_BI to promote plant growth.
Journal of applied microbiology pii:8776680 [Epub ahead of print].
AIM: The bioinoculant properties of a newly identified ammonium releasing novel strain of Actinomycetota- Microbacterium bengalense sp. nov. GB16_1_BI (Accession number: SRX9280401) on the microbiome structure of rice rhizosphere was assessed.
METHODS AND RESULT: GB16_1_BI may inhibit most bacteria present in the rice rhizosphere as well as encouraged the growth of rare bacteria specific to the waterlogged rice rhizosphere. The genome sequence as well as untargeted metabolome analyses of GB16_1_BI showed abundance of secondary metabolites with probable antimicrobial activity. Amplicon sequencing of the 16S rRNA V3-V4 region from the rhizosphere of the black rice showed inhibition of most bacteria by GB16_1_BI. Phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) analysis showed increased abundance in the marker genes for nitrogen cycling (nifH, nrfA and nrt) but not for nifD or nifK which was also reflected in the ANOSIM analysis in the OTUs of the N-fixing bacteria. Higher abundance of the nitrogen fixing methanotrophs-Methylosinus and Methylocystis in inoculated plants also led to study of the marker genes for methane metabolism.
CONCLUSION: Microbes dwelling in the rhizosphere contributes to the biogeochemical cycle by transforming unavailable minerals and by retaining nutrients for its growth which get released after death for plant adsorption. However, not all microbes contribute positively to plant growth. Microbes compete with plants for nutrients, cause disease or produce harmful greenhouse gases. Hence, GB16_1_BI could influence plant growth predominantly by suppressing microbes and encouraged niche-specific microbes specifically involved in nitrogen cycling.
Additional Links: PMID-42671215
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PubMed:
Citation:
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@article {pmid42671215,
year = {2026},
author = {Nag, P and Govindannagari, R and Prasad, K and Mounika, T and Chandran, LP and Das, S and Prasad Babu, MBB and Sundaram, RM},
title = {Manipulation of rhizosphere microbiome by Microbacterium sp. GB16_1_BI to promote plant growth.},
journal = {Journal of applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jambio/lxag221},
pmid = {42671215},
issn = {1365-2672},
abstract = {AIM: The bioinoculant properties of a newly identified ammonium releasing novel strain of Actinomycetota- Microbacterium bengalense sp. nov. GB16_1_BI (Accession number: SRX9280401) on the microbiome structure of rice rhizosphere was assessed.
METHODS AND RESULT: GB16_1_BI may inhibit most bacteria present in the rice rhizosphere as well as encouraged the growth of rare bacteria specific to the waterlogged rice rhizosphere. The genome sequence as well as untargeted metabolome analyses of GB16_1_BI showed abundance of secondary metabolites with probable antimicrobial activity. Amplicon sequencing of the 16S rRNA V3-V4 region from the rhizosphere of the black rice showed inhibition of most bacteria by GB16_1_BI. Phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) analysis showed increased abundance in the marker genes for nitrogen cycling (nifH, nrfA and nrt) but not for nifD or nifK which was also reflected in the ANOSIM analysis in the OTUs of the N-fixing bacteria. Higher abundance of the nitrogen fixing methanotrophs-Methylosinus and Methylocystis in inoculated plants also led to study of the marker genes for methane metabolism.
CONCLUSION: Microbes dwelling in the rhizosphere contributes to the biogeochemical cycle by transforming unavailable minerals and by retaining nutrients for its growth which get released after death for plant adsorption. However, not all microbes contribute positively to plant growth. Microbes compete with plants for nutrients, cause disease or produce harmful greenhouse gases. Hence, GB16_1_BI could influence plant growth predominantly by suppressing microbes and encouraged niche-specific microbes specifically involved in nitrogen cycling.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-31
The oral microbiome and dental health during pregnancy: Impact on maternal and foetal health outcomes.
The Malaysian journal of pathology, 48(2):241-255.
Hormonal and immune system changes during pregnancy may disrupt the resident oral microbiota causing dysbiosis that may render these women prone to gum health disease, such as gingivitis and periodontitis. This may in turn lead to systemic disorders, such as maternal gestational diabetes mellitus and hypertension, preterm birth, and low birth weight infants. Emerging evidence has associated dysbiosis of the oral microbiota during pregnancy with an imbalance and a preponderance of pathogenic bacteria such as Porphyromonas gingivalis and Fusobacterium nucleatum that may cause both placental and systemic inflammation. To mitigate the consequential adverse effects originating from poor oral health, some strategies have been proposed which include the use of probiotics, antimicrobial agents, laser therapy, and nanotechnology aimed at regulating a healthier oral microbiota to promote better overall health and pregnancy outcomes. This paper also highlights the importance of routine maternal oral health examination and management as a crucial inclusive component of antenatal care, which could positively impact on both the maternal and neonatal health outcomes. Advances and further research in this area will unravel the molecular mechanisms underlying the oral dysbiosis, systemic interactions and the fundamental basis for newer therapies to curb oral health related disorders in pregnancy.
Additional Links: PMID-42671231
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Citation:
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@article {pmid42671231,
year = {2026},
author = {Pan, SW and Wong, KK and Lim, QW and Soo, E and Cheah, FC},
title = {The oral microbiome and dental health during pregnancy: Impact on maternal and foetal health outcomes.},
journal = {The Malaysian journal of pathology},
volume = {48},
number = {2},
pages = {241-255},
pmid = {42671231},
issn = {0126-8635},
mesh = {Humans ; Female ; Pregnancy ; *Microbiota/physiology ; *Oral Health ; Pregnancy Outcome ; *Pregnancy Complications/microbiology ; *Mouth/microbiology ; *Dysbiosis/microbiology ; },
abstract = {Hormonal and immune system changes during pregnancy may disrupt the resident oral microbiota causing dysbiosis that may render these women prone to gum health disease, such as gingivitis and periodontitis. This may in turn lead to systemic disorders, such as maternal gestational diabetes mellitus and hypertension, preterm birth, and low birth weight infants. Emerging evidence has associated dysbiosis of the oral microbiota during pregnancy with an imbalance and a preponderance of pathogenic bacteria such as Porphyromonas gingivalis and Fusobacterium nucleatum that may cause both placental and systemic inflammation. To mitigate the consequential adverse effects originating from poor oral health, some strategies have been proposed which include the use of probiotics, antimicrobial agents, laser therapy, and nanotechnology aimed at regulating a healthier oral microbiota to promote better overall health and pregnancy outcomes. This paper also highlights the importance of routine maternal oral health examination and management as a crucial inclusive component of antenatal care, which could positively impact on both the maternal and neonatal health outcomes. Advances and further research in this area will unravel the molecular mechanisms underlying the oral dysbiosis, systemic interactions and the fundamental basis for newer therapies to curb oral health related disorders in pregnancy.},
}
MeSH Terms:
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Humans
Female
Pregnancy
*Microbiota/physiology
*Oral Health
Pregnancy Outcome
*Pregnancy Complications/microbiology
*Mouth/microbiology
*Dysbiosis/microbiology
RevDate: 2026-08-31
Dietary nucleotide-rich yeast extract regulates growth performance, microbiota composition and inflammatory response to lipopolysaccharide challenge in weanling pigs.
Journal of animal science pii:8776795 [Epub ahead of print].
A total of 128 weanling pigs (initial body weight, 7.5 ± 0.79 kg) were used to evaluate the effects of nucleotide (NUCL) supplementation to an adequate or low crude protein (CP) diet on growth performance, nutrient digestibility, gut microbiota composition, metabolic and inflammatory response to lipopolysaccharide (LPS) challenge. Pigs were randomly assigned to 4 dietary treatments (n = 8 replicates) in a 2 × 2 factorial arrangement of dietary CP level [adequate protein (AD) or low protein (LP)] and NUCL supplementation (0 or 9 g/kg) for a 42-d trial. The experimental diets were AD without NUCL (AD0), AD with NUCL (AD9), LP without NUCL (LOW0), and LP with NUCL (LOW9). Fecal samples were collected on d 39, 40 and 41 to determine the apparent total tract digestibility (ATTD) of nutrients. On d 42, fresh fecal samples were collected for microbiome analysis, and two pigs per pen were intraperitoneally injected with either saline or LPS (LPS; 25 µg/kg BW). Rectal temperature (RT) was recorded post-challenge, and blood samples were collected for serum analysis. Pigs fed AD diets had higher overall ADG (P < 0.01), G:F and final BW (P < 0.001) compared to LP pigs. Nucleotide supplementation increased (P < 0.05) ADG from d 28-42, final BW, and overall G:F. A significant (P < 0.01) NUCL × CP interaction was observed for d 0 to 14 ADFI which was higher in pigs fed AD9 compared to AD0, but was not different between LOW9 and LOW0 pigs. Nucleotide supplementation also increased (P < 0.01) ATTD of dry matter (DM) and gross energy (GE), while feeding low CP diets tended (P = 0.07) to increase ATTD of nitrogen compared to AD. Low CP diets had lower (P < 0.05) RT at 0 and 4 h compared to AD, while NUCL supplementation decreased (P < 0.05) RT at 4 h post-challenge compared to unsupplemented diets. A NUCL × CP (P < 0.001) interaction was found with serum tumor necrosis factor-alpha (TNF-α) which was lower in LOW9 pigs compared to LOW0, but not different in AD pigs regardless of NUCL supplementation. Both alpha and beta diversities were affected (P < 0.05) by dietary CP level, but not NUCL supplementation. Differential abundance analysis also showed that significant shifts in microbial community structure were primarily associated with dietary CP level. Collectively, these findings suggest that NUCL supplementation influences feed intake during the early post-weaning period, supports immune resilience, and modulates inflammatory responses in a dietary CP-dependent manner.
Additional Links: PMID-42671356
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PubMed:
Citation:
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@article {pmid42671356,
year = {2026},
author = {Lawal, AS and Oladele, P and Johnson, TA and Adeola, O and Ajuwon, KM},
title = {Dietary nucleotide-rich yeast extract regulates growth performance, microbiota composition and inflammatory response to lipopolysaccharide challenge in weanling pigs.},
journal = {Journal of animal science},
volume = {},
number = {},
pages = {},
doi = {10.1093/jas/skag271},
pmid = {42671356},
issn = {1525-3163},
abstract = {A total of 128 weanling pigs (initial body weight, 7.5 ± 0.79 kg) were used to evaluate the effects of nucleotide (NUCL) supplementation to an adequate or low crude protein (CP) diet on growth performance, nutrient digestibility, gut microbiota composition, metabolic and inflammatory response to lipopolysaccharide (LPS) challenge. Pigs were randomly assigned to 4 dietary treatments (n = 8 replicates) in a 2 × 2 factorial arrangement of dietary CP level [adequate protein (AD) or low protein (LP)] and NUCL supplementation (0 or 9 g/kg) for a 42-d trial. The experimental diets were AD without NUCL (AD0), AD with NUCL (AD9), LP without NUCL (LOW0), and LP with NUCL (LOW9). Fecal samples were collected on d 39, 40 and 41 to determine the apparent total tract digestibility (ATTD) of nutrients. On d 42, fresh fecal samples were collected for microbiome analysis, and two pigs per pen were intraperitoneally injected with either saline or LPS (LPS; 25 µg/kg BW). Rectal temperature (RT) was recorded post-challenge, and blood samples were collected for serum analysis. Pigs fed AD diets had higher overall ADG (P < 0.01), G:F and final BW (P < 0.001) compared to LP pigs. Nucleotide supplementation increased (P < 0.05) ADG from d 28-42, final BW, and overall G:F. A significant (P < 0.01) NUCL × CP interaction was observed for d 0 to 14 ADFI which was higher in pigs fed AD9 compared to AD0, but was not different between LOW9 and LOW0 pigs. Nucleotide supplementation also increased (P < 0.01) ATTD of dry matter (DM) and gross energy (GE), while feeding low CP diets tended (P = 0.07) to increase ATTD of nitrogen compared to AD. Low CP diets had lower (P < 0.05) RT at 0 and 4 h compared to AD, while NUCL supplementation decreased (P < 0.05) RT at 4 h post-challenge compared to unsupplemented diets. A NUCL × CP (P < 0.001) interaction was found with serum tumor necrosis factor-alpha (TNF-α) which was lower in LOW9 pigs compared to LOW0, but not different in AD pigs regardless of NUCL supplementation. Both alpha and beta diversities were affected (P < 0.05) by dietary CP level, but not NUCL supplementation. Differential abundance analysis also showed that significant shifts in microbial community structure were primarily associated with dietary CP level. Collectively, these findings suggest that NUCL supplementation influences feed intake during the early post-weaning period, supports immune resilience, and modulates inflammatory responses in a dietary CP-dependent manner.},
}
RevDate: 2026-08-31
Lactobacillus Fermentum MCC2760 Mitigates Oxidized Oil-Induced Metabolic Dysfunction and Gut-liver axis Perturbations: A Two-Generation Study in rats.
Probiotics and antimicrobial proteins [Epub ahead of print].
Dietary intake of oxidized oil is increasingly recognized as a key contributor to metabolic dysfunction. In this study, we evaluated the protective effects of Lactobacillus fermentum MCC2760 (LF) against oxidized oil-induced metabolic dysfunction across two generations in rats. Female Wistar rats were fed AIN-76 diets containing native or thermally oxidized sunflower oil (SFO) and canola oil (CNO), with or without LF supplementation (10[9] CFU/day), and the F2 generation was maintained on corresponding diets. Biochemical parameters including lipid profile, oxidative stress (OS) markers (lipid peroxides, protein carbonyls), antioxidant defense enzymes (catalase, SOD, GR, GPx, GST), inflammatory mediators (PGE2, LTB4, TNF-α, MCP-1, IL-1β, IL-6), transcription factors (NF-κB, Nrf2), organ function enzymes (SGOT, SGPT, CK-MB, CK-NAC, ALP) and fecal microbiome were assessed. Consumption of oxidized oils, irrespective of fatty acid composition, significantly disrupted lipid homeostasis, increased OS, reduced antioxidant enzyme activities and Nrf2 activity, and enhanced NF-κB activity, leading to elevated inflammatory mediators. Oxidized oil intake also increased serum markers of hepatic and cardiac injury, and induced gut dysbiosis. However, daily administration of LF significantly attenuated these metabolic disturbances by improving lipid homeostasis, antioxidant defenses, and inflammatory balance, NF-κB/Nrf2 activities, and gut microbial composition. These protective effects were consistently observed in both F1-mothers and F2 offspring, supporting metabolic resilience across generations. Overall, these findings support the potential of probiotic LF as a functional dietary strategy for mitigating oxidized oil-induced metabolic dysfunction by improving lipid homeostasis, modulating NF-κB/Nrf2 activities, and promoting gut microbial balance, with findings consistent with the involvement of the gut-liver axis.
Additional Links: PMID-42671524
PubMed:
Citation:
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@article {pmid42671524,
year = {2026},
author = {Keremane, VR and Kamala, HG and Komatwar, K and Somashekher, SK and Talahalli, RR},
title = {Lactobacillus Fermentum MCC2760 Mitigates Oxidized Oil-Induced Metabolic Dysfunction and Gut-liver axis Perturbations: A Two-Generation Study in rats.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42671524},
issn = {1867-1314},
abstract = {Dietary intake of oxidized oil is increasingly recognized as a key contributor to metabolic dysfunction. In this study, we evaluated the protective effects of Lactobacillus fermentum MCC2760 (LF) against oxidized oil-induced metabolic dysfunction across two generations in rats. Female Wistar rats were fed AIN-76 diets containing native or thermally oxidized sunflower oil (SFO) and canola oil (CNO), with or without LF supplementation (10[9] CFU/day), and the F2 generation was maintained on corresponding diets. Biochemical parameters including lipid profile, oxidative stress (OS) markers (lipid peroxides, protein carbonyls), antioxidant defense enzymes (catalase, SOD, GR, GPx, GST), inflammatory mediators (PGE2, LTB4, TNF-α, MCP-1, IL-1β, IL-6), transcription factors (NF-κB, Nrf2), organ function enzymes (SGOT, SGPT, CK-MB, CK-NAC, ALP) and fecal microbiome were assessed. Consumption of oxidized oils, irrespective of fatty acid composition, significantly disrupted lipid homeostasis, increased OS, reduced antioxidant enzyme activities and Nrf2 activity, and enhanced NF-κB activity, leading to elevated inflammatory mediators. Oxidized oil intake also increased serum markers of hepatic and cardiac injury, and induced gut dysbiosis. However, daily administration of LF significantly attenuated these metabolic disturbances by improving lipid homeostasis, antioxidant defenses, and inflammatory balance, NF-κB/Nrf2 activities, and gut microbial composition. These protective effects were consistently observed in both F1-mothers and F2 offspring, supporting metabolic resilience across generations. Overall, these findings support the potential of probiotic LF as a functional dietary strategy for mitigating oxidized oil-induced metabolic dysfunction by improving lipid homeostasis, modulating NF-κB/Nrf2 activities, and promoting gut microbial balance, with findings consistent with the involvement of the gut-liver axis.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-31
Body mass index-associated gut microbial taxa and functional pathways in women with benign and malignant breast disease.
Breast cancer research and treatment, 219(2):.
PURPOSE: Obesity is an established risk factor for breast cancer and is associated with alterations in gut microbial composition. We evaluated associations among body mass index (BMI), breast density, gut microbial diversity and composition and microbial functional pathways in women undergoing surgery for benign, high-risk/non-invasive, and invasive breast disease.
METHODS: Preoperative stool samples were collected from 131 women (median age 59) with benign (n = 23), high-risk/non-invasive (n = 47), or malignant (n = 61) disease. Shallow shotgun metagenomic sequencing was performed. Taxonomic profiling used Sourmash 4.2.4 (GTDBv207 reference database); functional profiling employed HUMAnN 3.6 with gene families mapped to MetaCyc pathways.
RESULTS: α-diversity differed across diagnosis groups and inversely correlated with increasing BMI (Inverse Simpson p = 0.025). β-diversity differed by diagnosis group and BMI. No significant differences in diversity were observed based on age, menopausal status or mammographic breast density. BMI was also associated with enrichment of Dorea, Blautia, and Streptococcus species. Functional pathway profiling showed greater relative abundance of genes involved in NAD biosynthesis, folate metabolism, and aromatic amino acid metabolism pathways with higher BMI. Cross-referencing the most significant taxonomic and functional pathway findings suggested enrichment of Blautia species, via tryptophan metabolism, might link to NAD biosynthesis.
CONCLUSION: In this study of women with benign, high-risk/non-invasive, and invasive breast disease, BMI was associated with distinct differences in gut microbial taxonomy and functional pathway profiles. These hypothesis-generating findings provide a rationale for future study to determine how the obesity-associated microbiome contributes to breast cancer development.
CLINICAL TRIAL NUMBER: Not applicable.
Additional Links: PMID-42671637
PubMed:
Citation:
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@article {pmid42671637,
year = {2026},
author = {Sample, JW and Johnson, S and Hoskin, TL and Redaelli, M and Walther-Antonio, MR and Chen, J and Degnim, AC and Hieken, TJ},
title = {Body mass index-associated gut microbial taxa and functional pathways in women with benign and malignant breast disease.},
journal = {Breast cancer research and treatment},
volume = {219},
number = {2},
pages = {},
pmid = {42671637},
issn = {1573-7217},
support = {UL1TR002377/TR/NCATS NIH HHS/United States ; },
mesh = {Humans ; Female ; *Breast Neoplasms/pathology/microbiology/etiology ; *Body Mass Index ; Middle Aged ; *Gastrointestinal Microbiome ; *Obesity/complications/microbiology ; Aged ; Adult ; Metagenomics/methods ; Metagenome ; },
abstract = {PURPOSE: Obesity is an established risk factor for breast cancer and is associated with alterations in gut microbial composition. We evaluated associations among body mass index (BMI), breast density, gut microbial diversity and composition and microbial functional pathways in women undergoing surgery for benign, high-risk/non-invasive, and invasive breast disease.
METHODS: Preoperative stool samples were collected from 131 women (median age 59) with benign (n = 23), high-risk/non-invasive (n = 47), or malignant (n = 61) disease. Shallow shotgun metagenomic sequencing was performed. Taxonomic profiling used Sourmash 4.2.4 (GTDBv207 reference database); functional profiling employed HUMAnN 3.6 with gene families mapped to MetaCyc pathways.
RESULTS: α-diversity differed across diagnosis groups and inversely correlated with increasing BMI (Inverse Simpson p = 0.025). β-diversity differed by diagnosis group and BMI. No significant differences in diversity were observed based on age, menopausal status or mammographic breast density. BMI was also associated with enrichment of Dorea, Blautia, and Streptococcus species. Functional pathway profiling showed greater relative abundance of genes involved in NAD biosynthesis, folate metabolism, and aromatic amino acid metabolism pathways with higher BMI. Cross-referencing the most significant taxonomic and functional pathway findings suggested enrichment of Blautia species, via tryptophan metabolism, might link to NAD biosynthesis.
CONCLUSION: In this study of women with benign, high-risk/non-invasive, and invasive breast disease, BMI was associated with distinct differences in gut microbial taxonomy and functional pathway profiles. These hypothesis-generating findings provide a rationale for future study to determine how the obesity-associated microbiome contributes to breast cancer development.
CLINICAL TRIAL NUMBER: Not applicable.},
}
MeSH Terms:
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Humans
Female
*Breast Neoplasms/pathology/microbiology/etiology
*Body Mass Index
Middle Aged
*Gastrointestinal Microbiome
*Obesity/complications/microbiology
Aged
Adult
Metagenomics/methods
Metagenome
RevDate: 2026-08-30
CmpDate: 2026-08-29
Gut Microbiomes of Two Bamboo Locusts Reveal Divergent Metabolic Potentials.
Ecology and evolution, 16(9):e74143.
The yellow-spined bamboo locust (Ceracris kiangsu) and the green-spined bamboo locust (Ceracris nigricornis) are two common bamboo-feeding forestry pests in China. C. kiangsu has stronger migratory capacity and causes greater damage, yet comparative studies of their gut microbiota are lacking. Here, we profiled the gut microbial communities of female C. kiangsu from six geographic populations using 16S rRNA gene amplicon sequencing (Illumina MiSeq) and compared these data with publicly available gut microbiome datasets of female C. nigricornis from NCBI. At the phylum level, the gut microbiota of both species was dominated by Firmicutes and Proteobacteria. At the genus level, dominant taxa included Klebsiella and Achromobacter. Despite these similarities, the two species differed significantly in microbial diversity. Alpha-diversity indices showed highly significant differences in richness and diversity (p < 0.01), and beta-diversity analyses (PCoA) revealed clear separation of community structure between species (PERMANOVA, p < 0.001). Functional prediction using PICRUSt2 indicated that, at KEGG Level 2, pathways related to carbohydrate and lipid metabolism were significantly enriched in C. kiangsu compared with C. nigricornis. At KEGG Level 3, C. kiangsu also showed higher predicted abundances of starch and sucrose metabolism, glycolysis/gluconeogenesis, the pentose phosphate pathway, and pyruvate metabolism. Collectively, these results reveal distinct gut microbial communities and predicted functional profiles between the two species. The enrichment of predicted carbohydrate- and lipid-related pathways in C. kiangsu generates a testable hypothesis that its gut microbiota may be associated with host energy metabolism, but direct links to flight performance or ecological fitness require further experimental validation.
Additional Links: PMID-42666504
PubMed:
Citation:
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@article {pmid42666504,
year = {2026},
author = {Liao, HY and Ren, YS and Cheng, X and Huang, HT and Jin, MZ and Zeng, Y and Zhu, DH},
title = {Gut Microbiomes of Two Bamboo Locusts Reveal Divergent Metabolic Potentials.},
journal = {Ecology and evolution},
volume = {16},
number = {9},
pages = {e74143},
pmid = {42666504},
issn = {2045-7758},
abstract = {The yellow-spined bamboo locust (Ceracris kiangsu) and the green-spined bamboo locust (Ceracris nigricornis) are two common bamboo-feeding forestry pests in China. C. kiangsu has stronger migratory capacity and causes greater damage, yet comparative studies of their gut microbiota are lacking. Here, we profiled the gut microbial communities of female C. kiangsu from six geographic populations using 16S rRNA gene amplicon sequencing (Illumina MiSeq) and compared these data with publicly available gut microbiome datasets of female C. nigricornis from NCBI. At the phylum level, the gut microbiota of both species was dominated by Firmicutes and Proteobacteria. At the genus level, dominant taxa included Klebsiella and Achromobacter. Despite these similarities, the two species differed significantly in microbial diversity. Alpha-diversity indices showed highly significant differences in richness and diversity (p < 0.01), and beta-diversity analyses (PCoA) revealed clear separation of community structure between species (PERMANOVA, p < 0.001). Functional prediction using PICRUSt2 indicated that, at KEGG Level 2, pathways related to carbohydrate and lipid metabolism were significantly enriched in C. kiangsu compared with C. nigricornis. At KEGG Level 3, C. kiangsu also showed higher predicted abundances of starch and sucrose metabolism, glycolysis/gluconeogenesis, the pentose phosphate pathway, and pyruvate metabolism. Collectively, these results reveal distinct gut microbial communities and predicted functional profiles between the two species. The enrichment of predicted carbohydrate- and lipid-related pathways in C. kiangsu generates a testable hypothesis that its gut microbiota may be associated with host energy metabolism, but direct links to flight performance or ecological fitness require further experimental validation.},
}
RevDate: 2026-08-30
CmpDate: 2026-08-29
Multicohort external validation of Anaeroglobus as a candidate salivary biomarker for childhood caries.
Frontiers in cellular and infection microbiology, 16:1850479.
OBJECTIVE: To evaluate the cross-cohort reproducibility of Anaeroglobus as a candidate salivary microbiome signal for childhood caries and to place this signal within plaque community, functional, and host-response contexts.
METHODS: Public pediatric salivary 16S rRNA cohorts were analyzed using a discovery-primary external validation-second validation framework. Genus-level features were assessed after CLR transformation and covariate adjustment, with plaque microbiome, plaque transcriptome, and deep-caries dental pulp single-cell datasets used as supporting evidence layers.
RESULTS: In the discovery cohort, Lactobacillus was associated with caries status and Anaeroglobus with total caries burden. In the primary external cohort, Anaeroglobus and Lactobacillus remained positively associated with caries [OR = 3.452 (95% CI: 1.851-6.449) and OR = 2.118 (95% CI: 1.049-4.282), respectively]. In the second validation cohort, Anaeroglobus remained directionally consistent [OR = 3.009 (95% CI: 1.241-7.312)]. The primary external microbiome model showed moderate discrimination (AUC = 0.782; approximate 95% CI: 0.703-0.861). Exploratory pooled-effect synthesis supported positive directional consistency, while the supporting plaque and multi-omics layers indicated broader community restructuring, carbohydrate/oxidative-stress adaptation, and host immune-stromal remodeling.
CONCLUSIONS: Anaeroglobus represents a directionally reproducible candidate salivary risk-related signal rather than a direct mechanistic or immediately diagnostic biomarker. The 36-sample second validation cohort should be interpreted as supportive age-extrapolation evidence, and the pooled synthesis should be interpreted as exploratory; further prospective, paired saliva-plaque, and multimodal validation is required.
Additional Links: PMID-42666505
PubMed:
Citation:
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@article {pmid42666505,
year = {2026},
author = {Wang, J and Tao, Y and Meng, HD and Zhu, XF and Xu, XM and Mi, DW},
title = {Multicohort external validation of Anaeroglobus as a candidate salivary biomarker for childhood caries.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1850479},
pmid = {42666505},
issn = {2235-2988},
mesh = {Humans ; *Dental Caries/microbiology/diagnosis ; *Saliva/microbiology ; *Biomarkers/analysis ; Microbiota ; RNA, Ribosomal, 16S/genetics ; Child ; Dental Plaque/microbiology ; Female ; Cohort Studies ; Male ; Reproducibility of Results ; *Bacteria, Anaerobic/genetics/isolation & purification/classification ; Child, Preschool ; Lactobacillus/isolation & purification/genetics ; },
abstract = {OBJECTIVE: To evaluate the cross-cohort reproducibility of Anaeroglobus as a candidate salivary microbiome signal for childhood caries and to place this signal within plaque community, functional, and host-response contexts.
METHODS: Public pediatric salivary 16S rRNA cohorts were analyzed using a discovery-primary external validation-second validation framework. Genus-level features were assessed after CLR transformation and covariate adjustment, with plaque microbiome, plaque transcriptome, and deep-caries dental pulp single-cell datasets used as supporting evidence layers.
RESULTS: In the discovery cohort, Lactobacillus was associated with caries status and Anaeroglobus with total caries burden. In the primary external cohort, Anaeroglobus and Lactobacillus remained positively associated with caries [OR = 3.452 (95% CI: 1.851-6.449) and OR = 2.118 (95% CI: 1.049-4.282), respectively]. In the second validation cohort, Anaeroglobus remained directionally consistent [OR = 3.009 (95% CI: 1.241-7.312)]. The primary external microbiome model showed moderate discrimination (AUC = 0.782; approximate 95% CI: 0.703-0.861). Exploratory pooled-effect synthesis supported positive directional consistency, while the supporting plaque and multi-omics layers indicated broader community restructuring, carbohydrate/oxidative-stress adaptation, and host immune-stromal remodeling.
CONCLUSIONS: Anaeroglobus represents a directionally reproducible candidate salivary risk-related signal rather than a direct mechanistic or immediately diagnostic biomarker. The 36-sample second validation cohort should be interpreted as supportive age-extrapolation evidence, and the pooled synthesis should be interpreted as exploratory; further prospective, paired saliva-plaque, and multimodal validation is required.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dental Caries/microbiology/diagnosis
*Saliva/microbiology
*Biomarkers/analysis
Microbiota
RNA, Ribosomal, 16S/genetics
Child
Dental Plaque/microbiology
Female
Cohort Studies
Male
Reproducibility of Results
*Bacteria, Anaerobic/genetics/isolation & purification/classification
Child, Preschool
Lactobacillus/isolation & purification/genetics
RevDate: 2026-08-30
CmpDate: 2026-08-29
Purple Potato and Its Polyphenols Modulate Cecal Fermentation in Rats.
Preventive nutrition and food science, 31(4):.
This study investigated the effects of the purple potato (PP) cultivar (cv.) 'Shadow-Queen,' rich in polyphenols and resistant starch (RS), on cecal fermentation in rats. It compared such effects with those obtained with a white potato (WP) cv. 'Toyoshiro,' and polyphenol-removed (decolorized purple potato, DPP) 'Shadow-Queen' potatoes. Seven-week-old male Fischer rats were fed diets containing WP, PP, or DPP. Compared to the cecal microbial composition of the control (CON), WP, and DPP groups, the PP group exhibited higher or lower relative abundances of the phyla Firmicutes or Bacteroidetes, respectively. Unclassified Clostridiales and Lactobacillus were more abundant in the PP than in the CON group. Compared to the other three, cecal succinate and immunoglobulin A (IgA) levels were elevated in the PP group. Compared to the CON group, cecal acetate, n-butyrate, and total short-chain fatty acid (SCFA) concentrations were enhanced in the PP, WP, and DPP groups; total SCFAs were higher in PP than in the WP or DPP groups. These results suggest that potato RS altered the cecal microbiota profile and increased SCFA production; the polyphenols in 'Shadow-Queen' potatoes further modulated the microbiota composition, thereby enhancing SCFA and IgA biosynthesis. Therefore, PPs may exert superior physiological effects compared to WPs due to the combined influence of RS and polyphenols.
Additional Links: PMID-42666652
PubMed:
Citation:
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@article {pmid42666652,
year = {2026},
author = {Chiba, M and Kilua, A and Nagata, R and Shimada, K and Tani, M and Han, KH and Fukushima, M},
title = {Purple Potato and Its Polyphenols Modulate Cecal Fermentation in Rats.},
journal = {Preventive nutrition and food science},
volume = {31},
number = {4},
pages = {},
pmid = {42666652},
issn = {2287-1098},
abstract = {This study investigated the effects of the purple potato (PP) cultivar (cv.) 'Shadow-Queen,' rich in polyphenols and resistant starch (RS), on cecal fermentation in rats. It compared such effects with those obtained with a white potato (WP) cv. 'Toyoshiro,' and polyphenol-removed (decolorized purple potato, DPP) 'Shadow-Queen' potatoes. Seven-week-old male Fischer rats were fed diets containing WP, PP, or DPP. Compared to the cecal microbial composition of the control (CON), WP, and DPP groups, the PP group exhibited higher or lower relative abundances of the phyla Firmicutes or Bacteroidetes, respectively. Unclassified Clostridiales and Lactobacillus were more abundant in the PP than in the CON group. Compared to the other three, cecal succinate and immunoglobulin A (IgA) levels were elevated in the PP group. Compared to the CON group, cecal acetate, n-butyrate, and total short-chain fatty acid (SCFA) concentrations were enhanced in the PP, WP, and DPP groups; total SCFAs were higher in PP than in the WP or DPP groups. These results suggest that potato RS altered the cecal microbiota profile and increased SCFA production; the polyphenols in 'Shadow-Queen' potatoes further modulated the microbiota composition, thereby enhancing SCFA and IgA biosynthesis. Therefore, PPs may exert superior physiological effects compared to WPs due to the combined influence of RS and polyphenols.},
}
RevDate: 2026-08-30
CmpDate: 2026-08-29
Amino Acid Metabolism in Health and Disease.
MedComm, 7(9):e70930.
Metabolic reprogramming is a central feature of many human diseases, and therapies that target altered metabolic dependencies are moving from concept to clinical testing. Amino acid homeostasis links essential and nonessential amino acid supply with branched-chain amino acid (BCAA) catabolism, one-carbon metabolism, mechanistic target of rapamycin complex 1 (mTORC1)/general control nonderepressible 2 (GCN2) nutrient sensing, glutathione-dependent redox control, epigenetic regulation, and the gut microbiota-amino acid axis. When this network is disturbed, amino acid flux can contribute to disease initiation and progression rather than simply mirroring established pathology. This review synthesizes how amino acid metabolism supports the nervous, cardiovascular, digestive, metabolic-endocrine, immune, skeletal, urinary and reproductive systems, as well as malignant and inherited metabolic disorders. We also examine how pathway-level disturbances converge on excitotoxicity, endothelial dysfunction, insulin resistance, inflammation, fibrosis, immune escape, toxic metabolite accumulation, and impaired fertility. Rather than catalog isolated findings, we emphasize unifying principles and unresolved controversies, including the context-dependent effects of BCAA signaling, the causal versus biomarker status of circulating amino acid signatures, host-gut microbiome crosstalk, and the therapeutic window of dietary, enzymatic, transporter-targeted, and microbiota-based interventions. Finally, we assess clinical translation, drawing lessons from late-stage trial failures and emerging strategies with realistic potential for precision metabolic therapy.
Additional Links: PMID-42666691
PubMed:
Citation:
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@article {pmid42666691,
year = {2026},
author = {Su, Z and Liu, J and Deng, X and Luo, Y and Xue, H and Wang, L and Xing, L and Wu, T},
title = {Amino Acid Metabolism in Health and Disease.},
journal = {MedComm},
volume = {7},
number = {9},
pages = {e70930},
pmid = {42666691},
issn = {2688-2663},
abstract = {Metabolic reprogramming is a central feature of many human diseases, and therapies that target altered metabolic dependencies are moving from concept to clinical testing. Amino acid homeostasis links essential and nonessential amino acid supply with branched-chain amino acid (BCAA) catabolism, one-carbon metabolism, mechanistic target of rapamycin complex 1 (mTORC1)/general control nonderepressible 2 (GCN2) nutrient sensing, glutathione-dependent redox control, epigenetic regulation, and the gut microbiota-amino acid axis. When this network is disturbed, amino acid flux can contribute to disease initiation and progression rather than simply mirroring established pathology. This review synthesizes how amino acid metabolism supports the nervous, cardiovascular, digestive, metabolic-endocrine, immune, skeletal, urinary and reproductive systems, as well as malignant and inherited metabolic disorders. We also examine how pathway-level disturbances converge on excitotoxicity, endothelial dysfunction, insulin resistance, inflammation, fibrosis, immune escape, toxic metabolite accumulation, and impaired fertility. Rather than catalog isolated findings, we emphasize unifying principles and unresolved controversies, including the context-dependent effects of BCAA signaling, the causal versus biomarker status of circulating amino acid signatures, host-gut microbiome crosstalk, and the therapeutic window of dietary, enzymatic, transporter-targeted, and microbiota-based interventions. Finally, we assess clinical translation, drawing lessons from late-stage trial failures and emerging strategies with realistic potential for precision metabolic therapy.},
}
RevDate: 2026-08-30
CmpDate: 2026-08-29
The lung microbiome and asthma: from inflammatory phenotype differentiation to microbe-based immunomodulatory strategies.
Frontiers in immunology, 17:1901065.
As a complex airway inflammatory disease, the pathogenesis of asthma is closely associated with dynamic changes in the lung microbiome and immune regulation. Asthmatic patients with distinct inflammatory phenotypes exhibit significant alterations in the diversity and dominant microbiota of their lung microbiome, particularly characterized by the colonization of bacteria such as Haemophilus influenzae, Moraxella catarrhalis, and Tropheryma whipplei. The microbial community modulates the differentiation of CD4[+] T-cell subsets and activates or inhibits inflammatory pathways, thereby exerting interactive effects on the eosinophilic and neutrophilic inflammatory phenotypes of asthma. Microbial products, such as lipopolysaccharide (LPS), exosomes, and bacterial lysates, play crucial roles in activating or suppressing host immune cells, mediating the initiation and progression of airway inflammation. Current studies have primarily elucidated the mechanisms by which the lung microbiome modulates asthma immune regulation and explored immunomodulatory strategies targeting microorganisms and their products, including the potential of bacterial lysates, probiotic therapy, and microbial exosome therapy in asthma. Unlike previous reviews focusing on the gut-lung axis, this review establishes correspondences between specific bacterial species and distinct asthma endotypes, and critically evaluates the methodological heterogeneity in this field. These reflections provide a theoretical basis for standardizing microbiome research, elucidating microbiota-driven differential progression of asthma subtypes, and advancing microbiome-based precision prevention strategies.
Additional Links: PMID-42666767
PubMed:
Citation:
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@article {pmid42666767,
year = {2026},
author = {Ren, S and Li, H and Dong, Z and Fang, M},
title = {The lung microbiome and asthma: from inflammatory phenotype differentiation to microbe-based immunomodulatory strategies.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1901065},
pmid = {42666767},
issn = {1664-3224},
mesh = {Humans ; *Asthma/immunology/microbiology/therapy ; *Microbiota/immunology ; Animals ; *Lung/microbiology/immunology ; Phenotype ; *Immunomodulation ; Probiotics/therapeutic use ; },
abstract = {As a complex airway inflammatory disease, the pathogenesis of asthma is closely associated with dynamic changes in the lung microbiome and immune regulation. Asthmatic patients with distinct inflammatory phenotypes exhibit significant alterations in the diversity and dominant microbiota of their lung microbiome, particularly characterized by the colonization of bacteria such as Haemophilus influenzae, Moraxella catarrhalis, and Tropheryma whipplei. The microbial community modulates the differentiation of CD4[+] T-cell subsets and activates or inhibits inflammatory pathways, thereby exerting interactive effects on the eosinophilic and neutrophilic inflammatory phenotypes of asthma. Microbial products, such as lipopolysaccharide (LPS), exosomes, and bacterial lysates, play crucial roles in activating or suppressing host immune cells, mediating the initiation and progression of airway inflammation. Current studies have primarily elucidated the mechanisms by which the lung microbiome modulates asthma immune regulation and explored immunomodulatory strategies targeting microorganisms and their products, including the potential of bacterial lysates, probiotic therapy, and microbial exosome therapy in asthma. Unlike previous reviews focusing on the gut-lung axis, this review establishes correspondences between specific bacterial species and distinct asthma endotypes, and critically evaluates the methodological heterogeneity in this field. These reflections provide a theoretical basis for standardizing microbiome research, elucidating microbiota-driven differential progression of asthma subtypes, and advancing microbiome-based precision prevention strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Asthma/immunology/microbiology/therapy
*Microbiota/immunology
Animals
*Lung/microbiology/immunology
Phenotype
*Immunomodulation
Probiotics/therapeutic use
RevDate: 2026-08-30
CmpDate: 2026-08-29
Comparative analysis of microbiota in the ocular surface of patients with atopic keratoconjunctivitis and Stevens-Johnson Syndrome with severe ocular complications.
Frontiers in immunology, 17:1887091.
INTRODUCTION: The interplay between host immunity and the microbiome is increasingly recognized as an important factor in ocular surface diseases. Although cutaneous and intestinal dysbiosis have been implicated in atopic dermatitis (AD), the role of the ocular microbiome in its severe ophthalmic manifestation, atopic keratoconjunctivitis (AKC), remains incompletely understood.
METHODS: We performed 16S rRNA gene sequencing to characterize the ocular and fecal microbiota of patients with AD and severe AKC, AD without severe ocular involvement, Stevens-Johnson syndrome (SJS) with severe ocular complications (SOC), and healthy controls. Microbial community composition was compared using principal coordinate analysis (PCoA) and taxonomic profiling.
RESULTS: Ocular microbiota composition differed among the study groups. PCoA demonstrated that SJS samples clustered separately from healthy controls, whereas AKC samples occupied an intermediate position between the healthy control and SJS groups. Taxonomic analysis revealed enrichment of Corynebacterium 1 (a SILVA genus-level taxonomic assignment) in SJS, while AKC samples exhibited increased relative abundances of both Corynebacterium 1 and Staphylococcus. In contrast, AD patients without severe ocular involvement maintained an ocular microbial community broadly similar to that of healthy controls, including the presence of Neisseria. Analysis of paired fecal samples did not reveal disease-associated clustering or major compositional differences among the study groups.
DISCUSSION: These findings suggest that, using genus-level 16S rRNA sequencing, disease-associated microbial alterations are more readily detected on the ocular surface than in the fecal microbiome in this cohort. The results support a potential contribution of the local ocular microenvironment to microbial signatures associated with immune-mediated ocular surface inflammation and provide a framework for future studies investigating the role of the ocular microbiome in disease pathogenesis.
Additional Links: PMID-42666841
PubMed:
Citation:
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@article {pmid42666841,
year = {2026},
author = {Ueta, M and Tse, KM and Nanri, H and Nishigaki, H and Takai, Y and Sanada, TJ and Kawashima, H and Hosomi, K and Miyano, T and Ishii, T and Sotozono, C and Kunisawa, J},
title = {Comparative analysis of microbiota in the ocular surface of patients with atopic keratoconjunctivitis and Stevens-Johnson Syndrome with severe ocular complications.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1887091},
pmid = {42666841},
issn = {1664-3224},
mesh = {Humans ; *Microbiota ; Female ; Male ; *Stevens-Johnson Syndrome/microbiology/complications/immunology ; Adult ; RNA, Ribosomal, 16S/genetics ; *Keratoconjunctivitis/microbiology ; Dermatitis, Atopic/microbiology ; Young Adult ; Feces/microbiology ; Bacteria/genetics/classification ; Adolescent ; Middle Aged ; Skin Microbiome ; },
abstract = {INTRODUCTION: The interplay between host immunity and the microbiome is increasingly recognized as an important factor in ocular surface diseases. Although cutaneous and intestinal dysbiosis have been implicated in atopic dermatitis (AD), the role of the ocular microbiome in its severe ophthalmic manifestation, atopic keratoconjunctivitis (AKC), remains incompletely understood.
METHODS: We performed 16S rRNA gene sequencing to characterize the ocular and fecal microbiota of patients with AD and severe AKC, AD without severe ocular involvement, Stevens-Johnson syndrome (SJS) with severe ocular complications (SOC), and healthy controls. Microbial community composition was compared using principal coordinate analysis (PCoA) and taxonomic profiling.
RESULTS: Ocular microbiota composition differed among the study groups. PCoA demonstrated that SJS samples clustered separately from healthy controls, whereas AKC samples occupied an intermediate position between the healthy control and SJS groups. Taxonomic analysis revealed enrichment of Corynebacterium 1 (a SILVA genus-level taxonomic assignment) in SJS, while AKC samples exhibited increased relative abundances of both Corynebacterium 1 and Staphylococcus. In contrast, AD patients without severe ocular involvement maintained an ocular microbial community broadly similar to that of healthy controls, including the presence of Neisseria. Analysis of paired fecal samples did not reveal disease-associated clustering or major compositional differences among the study groups.
DISCUSSION: These findings suggest that, using genus-level 16S rRNA sequencing, disease-associated microbial alterations are more readily detected on the ocular surface than in the fecal microbiome in this cohort. The results support a potential contribution of the local ocular microenvironment to microbial signatures associated with immune-mediated ocular surface inflammation and provide a framework for future studies investigating the role of the ocular microbiome in disease pathogenesis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
Female
Male
*Stevens-Johnson Syndrome/microbiology/complications/immunology
Adult
RNA, Ribosomal, 16S/genetics
*Keratoconjunctivitis/microbiology
Dermatitis, Atopic/microbiology
Young Adult
Feces/microbiology
Bacteria/genetics/classification
Adolescent
Middle Aged
Skin Microbiome
RevDate: 2026-08-30
CmpDate: 2026-08-29
Genetic dissection of the eggplant rhizosphere microbiome enables microbiome-assisted breeding.
Horticulture research, 13(9):uhag163.
Rhizosphere microbiome critically influences plant growth and health, yet the genetic mechanisms underlying host regulation of microbiome composition remain unclear. Here, we analyzed whole-genome genotype and 16S rhizosphere microbiome data from 432 globally sourced eggplant accessions (Solanum melongena L.). Eggplant population structure corresponded to geographic origins, with rhizosphere microbiomes varying significantly among subpopulations. Host genetics explains 9%-39% of the variation in individual microbial taxa abundance, with core taxa more affected by host genetic variation. Microbial genome-wide association studies (mGWAS) identified 1235 significant genetic variants associated with 46 core microbial taxa, revealing key regulatory loci including chr10:7799021 near MYB113 (associated with Stenotrophomonas, P = 2.16 × 10[-15]) and chr10:19786889 near BLH9 (associated with Mycobacterium, P = 1.24 × 10[-12]), as well as a chromosome 5 locus with specific regulatory effects on Rhizobiales. These microbiome-associated genetic variants were enriched in secondary metabolic pathways, including anthocyanin biosynthesis, benzoxazinoid biosynthesis, and brassinosteroid biosynthesis, indicating that hosts regulate microbial communities through complex metabolic networks. Notably, genetic loci controlling microbial community structure underwent strong directional selection across eggplant subpopulations from different geographic origins, providing evidence for host-microbe coadaptive evolution. This study elucidates genetic regulatory patterns of eggplant rhizosphere microbiomes, enriching the theoretical framework of plant-microbe coevolution, with broad implications for microbiome-assisted crop improvement and sustainable agriculture.
Additional Links: PMID-42666968
PubMed:
Citation:
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@article {pmid42666968,
year = {2026},
author = {Li, Y and Li, W and Gan, G and Wang, X and Wu, Y and Xu, Y and Jousset, A and Wang, Y and Shen, Q and Jiang, G and Wei, Z},
title = {Genetic dissection of the eggplant rhizosphere microbiome enables microbiome-assisted breeding.},
journal = {Horticulture research},
volume = {13},
number = {9},
pages = {uhag163},
pmid = {42666968},
issn = {2662-6810},
abstract = {Rhizosphere microbiome critically influences plant growth and health, yet the genetic mechanisms underlying host regulation of microbiome composition remain unclear. Here, we analyzed whole-genome genotype and 16S rhizosphere microbiome data from 432 globally sourced eggplant accessions (Solanum melongena L.). Eggplant population structure corresponded to geographic origins, with rhizosphere microbiomes varying significantly among subpopulations. Host genetics explains 9%-39% of the variation in individual microbial taxa abundance, with core taxa more affected by host genetic variation. Microbial genome-wide association studies (mGWAS) identified 1235 significant genetic variants associated with 46 core microbial taxa, revealing key regulatory loci including chr10:7799021 near MYB113 (associated with Stenotrophomonas, P = 2.16 × 10[-15]) and chr10:19786889 near BLH9 (associated with Mycobacterium, P = 1.24 × 10[-12]), as well as a chromosome 5 locus with specific regulatory effects on Rhizobiales. These microbiome-associated genetic variants were enriched in secondary metabolic pathways, including anthocyanin biosynthesis, benzoxazinoid biosynthesis, and brassinosteroid biosynthesis, indicating that hosts regulate microbial communities through complex metabolic networks. Notably, genetic loci controlling microbial community structure underwent strong directional selection across eggplant subpopulations from different geographic origins, providing evidence for host-microbe coadaptive evolution. This study elucidates genetic regulatory patterns of eggplant rhizosphere microbiomes, enriching the theoretical framework of plant-microbe coevolution, with broad implications for microbiome-assisted crop improvement and sustainable agriculture.},
}
RevDate: 2026-08-30
CmpDate: 2026-08-29
Vaginal high-intensity focused ultrasound in women with genitourinary syndrome of menopause: a prospective exploratory study.
Sexual medicine, 14(5):qfag077.
INTRODUCTION: Energy-based therapies for genitourinary syndrome of menopause (GSM) remain controversial, and evidence for vaginal high-intensity focused ultrasound (HIFU) is limited. The aim of this study was to evaluate the safety and exploratory efficacy of vaginal HIFU in women with GSM.
METHODS: In this prospective, single-arm, exploratory study, women with GSM underwent vaginal HIFU and were followed for 24 weeks. Women with prior gynecologic surgery or treated malignancy were eligible if ≥6 months had elapsed and clinical stability was confirmed. Patient-reported outcomes included visual analog scale (VAS) scores for GSM symptoms, the Vulvovaginal Symptoms Questionnaire (VSQ), the Female Sexual Function Index (FSFI), and the International Consultation on Incontinence Questionnaire-Short Form (ICIQ-SF). Objective measures included the Vaginal Health Index (VHI), vaginal pressure, pelvic organ prolapse quantification, vaginal pH, and vaginal microbiome profiling. The primary endpoint was the percent change from baseline to 12 weeks in the VAS score of the participant-identified most bothersome GSM symptom.
RESULTS: Eighteen women comprised the full analysis set. The primary endpoint showed a reduction in symptom severity (mean percent change -67.7%; 95% confidence interval [CI], -87.6% to -47.7%). Individual VAS scores decreased over time and were generally maintained throughout follow-up. The VSQ improved at 24 weeks (-40.4%; 95% CI, -64.6% to -16.2%), and the ICIQ-SF improved at 12 weeks (-29.0%; 95% CI, -54.6% to -3.4%), although this improvement was not sustained at 24 weeks. Total FSFI scores did not change. Improvements were observed in VHI and vaginal pressure, while vaginal pH and microbiome composition remained stable. No Grade ≥3 adverse events occurred.
DISCUSSION: In this exploratory study, vaginal HIFU was associated with improvements in the most bothersome GSM symptom and selected objective measures without serious adverse events. However, given its single-arm design and small sample size, no definitive conclusions regarding its efficacy or safety can be drawn, and further studies are needed to elucidate the mechanisms of action, optimize treatment parameters, characterize the safety profile, and determine the clinical utility of vaginal HIFU.
Additional Links: PMID-42667009
PubMed:
Citation:
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@article {pmid42667009,
year = {2026},
author = {Nagata, C and Morikawa, A and Takahashi, S and Matsuno, K and Nagae, S and Odajima, S and Nakajima, K and Noguchi, D and Kawabata, A and Nishikawa, T and Takenaka, M and Yanagida, S and Yanaihara, N and Okamoto, A},
title = {Vaginal high-intensity focused ultrasound in women with genitourinary syndrome of menopause: a prospective exploratory study.},
journal = {Sexual medicine},
volume = {14},
number = {5},
pages = {qfag077},
pmid = {42667009},
issn = {2050-1161},
abstract = {INTRODUCTION: Energy-based therapies for genitourinary syndrome of menopause (GSM) remain controversial, and evidence for vaginal high-intensity focused ultrasound (HIFU) is limited. The aim of this study was to evaluate the safety and exploratory efficacy of vaginal HIFU in women with GSM.
METHODS: In this prospective, single-arm, exploratory study, women with GSM underwent vaginal HIFU and were followed for 24 weeks. Women with prior gynecologic surgery or treated malignancy were eligible if ≥6 months had elapsed and clinical stability was confirmed. Patient-reported outcomes included visual analog scale (VAS) scores for GSM symptoms, the Vulvovaginal Symptoms Questionnaire (VSQ), the Female Sexual Function Index (FSFI), and the International Consultation on Incontinence Questionnaire-Short Form (ICIQ-SF). Objective measures included the Vaginal Health Index (VHI), vaginal pressure, pelvic organ prolapse quantification, vaginal pH, and vaginal microbiome profiling. The primary endpoint was the percent change from baseline to 12 weeks in the VAS score of the participant-identified most bothersome GSM symptom.
RESULTS: Eighteen women comprised the full analysis set. The primary endpoint showed a reduction in symptom severity (mean percent change -67.7%; 95% confidence interval [CI], -87.6% to -47.7%). Individual VAS scores decreased over time and were generally maintained throughout follow-up. The VSQ improved at 24 weeks (-40.4%; 95% CI, -64.6% to -16.2%), and the ICIQ-SF improved at 12 weeks (-29.0%; 95% CI, -54.6% to -3.4%), although this improvement was not sustained at 24 weeks. Total FSFI scores did not change. Improvements were observed in VHI and vaginal pressure, while vaginal pH and microbiome composition remained stable. No Grade ≥3 adverse events occurred.
DISCUSSION: In this exploratory study, vaginal HIFU was associated with improvements in the most bothersome GSM symptom and selected objective measures without serious adverse events. However, given its single-arm design and small sample size, no definitive conclusions regarding its efficacy or safety can be drawn, and further studies are needed to elucidate the mechanisms of action, optimize treatment parameters, characterize the safety profile, and determine the clinical utility of vaginal HIFU.},
}
RevDate: 2026-08-29
CmpDate: 2026-08-29
Efficacy of Compound Acid Chemical Peeling in Patients with Moderate Acne: A Prospective Study with Comprehensive Facial Evaluation.
Journal of visualized experiments : JoVE.
Compound acid chemical peeling is widely used to treat acne vulgaris (AV), but the biological mechanisms underlying its clinical effects remain incompletely understood. We hypothesized that compound acid chemical peeling would improve acne severity and would be associated with changes in the skin microbiome and a reduction in local inflammatory responses in patients with moderate AV. This study aimed to investigate the clinical, microbiological, and inflammatory effects of compound acid peeling in this population. We carried out a prospective, split‑face, randomized trial enrolling 30 patients with moderate AV. One hemiface received compound acid peeling twice weekly for 3 weeks (6 total sessions), followed by a 9‑week observation period. The contralateral hemiface received no treatment for the first 3 weeks and then underwent the same peeling protocol for 3 weeks, with a 6‑week follow‑up. Outcome measures included the Global Acne Grading System (GAGS), patient self‑assessment, standardized facial imaging, skin biopsy with immunohistochemistry, bacterial DNA extraction, PCR amplification, and 16S rRNA gene sequencing. Patients showed a statistically significant improvement in GAGS scores (P < 0.001). Facial imaging analysis revealed reductions in redness and porphyrin readings. Immunohistochemical staining for interleukin (IL)-1α, IL-6, IL-17, transforming growth factor-β (TGF-β), and toll-like receptor 2 (TLR2) was reduced. Skin microbiome alpha diversity decreased, with a notable decrease in the relative abundance of Staphylococcus (P < 0.05). Throughout the study, no adverse events were reported. Compound acid peeling was effective and well-tolerated during the observation period and was associated with changes in the skin microbiome and local inflammatory marker staining.
Additional Links: PMID-42667203
Publisher:
PubMed:
Citation:
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@article {pmid42667203,
year = {2026},
author = {Shi, M and Wang, R and Peng, G and Chen, Y and Pan, X and Chen, T and Chen, J},
title = {Efficacy of Compound Acid Chemical Peeling in Patients with Moderate Acne: A Prospective Study with Comprehensive Facial Evaluation.},
journal = {Journal of visualized experiments : JoVE},
volume = {},
number = {234},
pages = {},
doi = {10.3791/72116},
pmid = {42667203},
issn = {1940-087X},
mesh = {Humans ; *Acne Vulgaris/microbiology/therapy/pathology/drug therapy ; Prospective Studies ; Female ; *Chemexfoliation/methods ; Male ; Young Adult ; Adult ; Face ; Skin Microbiome ; Adolescent ; },
abstract = {Compound acid chemical peeling is widely used to treat acne vulgaris (AV), but the biological mechanisms underlying its clinical effects remain incompletely understood. We hypothesized that compound acid chemical peeling would improve acne severity and would be associated with changes in the skin microbiome and a reduction in local inflammatory responses in patients with moderate AV. This study aimed to investigate the clinical, microbiological, and inflammatory effects of compound acid peeling in this population. We carried out a prospective, split‑face, randomized trial enrolling 30 patients with moderate AV. One hemiface received compound acid peeling twice weekly for 3 weeks (6 total sessions), followed by a 9‑week observation period. The contralateral hemiface received no treatment for the first 3 weeks and then underwent the same peeling protocol for 3 weeks, with a 6‑week follow‑up. Outcome measures included the Global Acne Grading System (GAGS), patient self‑assessment, standardized facial imaging, skin biopsy with immunohistochemistry, bacterial DNA extraction, PCR amplification, and 16S rRNA gene sequencing. Patients showed a statistically significant improvement in GAGS scores (P < 0.001). Facial imaging analysis revealed reductions in redness and porphyrin readings. Immunohistochemical staining for interleukin (IL)-1α, IL-6, IL-17, transforming growth factor-β (TGF-β), and toll-like receptor 2 (TLR2) was reduced. Skin microbiome alpha diversity decreased, with a notable decrease in the relative abundance of Staphylococcus (P < 0.05). Throughout the study, no adverse events were reported. Compound acid peeling was effective and well-tolerated during the observation period and was associated with changes in the skin microbiome and local inflammatory marker staining.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Acne Vulgaris/microbiology/therapy/pathology/drug therapy
Prospective Studies
Female
*Chemexfoliation/methods
Male
Young Adult
Adult
Face
Skin Microbiome
Adolescent
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RJR Experience and Expertise
Researcher
Robbins holds BS, MS, and PhD degrees in the life sciences. He served as a tenured faculty member in the Zoology and Biological Science departments at Michigan State University. He is currently exploring the intersection between genomics, microbial ecology, and biodiversity — an area that promises to transform our understanding of the biosphere.
Educator
Robbins has extensive experience in college-level education: At MSU he taught introductory biology, genetics, and population genetics. At JHU, he was an instructor for a special course on biological database design. At FHCRC, he team-taught a graduate-level course on the history of genetics. At Bellevue College he taught medical informatics.
Administrator
Robbins has been involved in science administration at both the federal and the institutional levels. At NSF he was a program officer for database activities in the life sciences, at DOE he was a program officer for information infrastructure in the human genome project. At the Fred Hutchinson Cancer Research Center, he served as a vice president for fifteen years.
Technologist
Robbins has been involved with information technology since writing his first Fortran program as a college student. At NSF he was the first program officer for database activities in the life sciences. At JHU he held an appointment in the CS department and served as director of the informatics core for the Genome Data Base. At the FHCRC he was VP for Information Technology.
Publisher
While still at Michigan State, Robbins started his first publishing venture, founding a small company that addressed the short-run publishing needs of instructors in very large undergraduate classes. For more than 20 years, Robbins has been operating The Electronic Scholarly Publishing Project, a web site dedicated to the digital publishing of critical works in science, especially classical genetics.
Speaker
Robbins is well-known for his speaking abilities and is often called upon to provide keynote or plenary addresses at international meetings. For example, in July, 2012, he gave a well-received keynote address at the Global Biodiversity Informatics Congress, sponsored by GBIF and held in Copenhagen. The slides from that talk can be seen HERE.
Facilitator
Robbins is a skilled meeting facilitator. He prefers a participatory approach, with part of the meeting involving dynamic breakout groups, created by the participants in real time: (1) individuals propose breakout groups; (2) everyone signs up for one (or more) groups; (3) the groups with the most interested parties then meet, with reports from each group presented and discussed in a subsequent plenary session.
Designer
Robbins has been engaged with photography and design since the 1960s, when he worked for a professional photography laboratory. He now prefers digital photography and tools for their precision and reproducibility. He designed his first web site more than 20 years ago and he personally designed and implemented this web site. He engages in graphic design as a hobby.
RJR Picks from Around the Web (updated 11 MAY 2018 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.