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RJR: Recommended Bibliography 30 Oct 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: 2026-10-29
CmpDate: 2026-10-28
From dietary exposure to organ injury: microbiome-mediated biotransformation of food-chain xenobiotics across the gut-liver-kidney axis.
Frontiers in microbiology, 17:1977638.
Food-chain xenobiotics reach the intestine through food additives, processing-generated chemicals, environmental contaminants, and naturally occurring toxins. Their biological effects depend not only on intake but also on microbial metabolism and host handling. Gut microorganisms can detoxify parent compounds or generate metabolites with altered biological activity, while xenobiotic exposure can reshape microbial communities and host-microbial interactions. This review synthesizes evidence on these processes across the gut-liver-kidney axis, with particular attention to metabolic dysfunction-associated steatotic liver disease and chronic kidney disease. We examine direct microbial biotransformation alongside exposure-related changes in intestinal barrier function, immune responses, and metabolic signaling. The resulting synthesis highlights compound-specific and host-specific responses, shaped by microbial enzyme capacity, dietary context, barrier integrity, and hepatic and renal clearance. Impaired organ function can, in turn, alter microbial ecology and promote metabolite accumulation, creating bidirectional interactions between exposure and disease. Although experimental studies provide mechanistic insights, human evidence establishing causal links between dietary xenobiotics, microbial transformation, and chronic liver or kidney injury remains limited. We also evaluate the potential of integrated biomarkers, dietary interventions, and microbial enzyme-targeting strategies, identifying the evidence needed for clinical translation. Future progress requires longitudinal cohorts and controlled dietary studies that combine measured exposure, microbial function, metabolite profiles, and organ-specific outcomes. This integrated perspective provides a framework for investigating individual susceptibility to dietary xenobiotics and evaluating microbiome-informed approaches to food safety and nutrition.
Additional Links: PMID-42948378
PubMed:
Citation:
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@article {pmid42948378,
year = {2026},
author = {Li, G and Xiong, Y and Yu, X and Yu, J and Xu, R},
title = {From dietary exposure to organ injury: microbiome-mediated biotransformation of food-chain xenobiotics across the gut-liver-kidney axis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1977638},
pmid = {42948378},
issn = {1664-302X},
abstract = {Food-chain xenobiotics reach the intestine through food additives, processing-generated chemicals, environmental contaminants, and naturally occurring toxins. Their biological effects depend not only on intake but also on microbial metabolism and host handling. Gut microorganisms can detoxify parent compounds or generate metabolites with altered biological activity, while xenobiotic exposure can reshape microbial communities and host-microbial interactions. This review synthesizes evidence on these processes across the gut-liver-kidney axis, with particular attention to metabolic dysfunction-associated steatotic liver disease and chronic kidney disease. We examine direct microbial biotransformation alongside exposure-related changes in intestinal barrier function, immune responses, and metabolic signaling. The resulting synthesis highlights compound-specific and host-specific responses, shaped by microbial enzyme capacity, dietary context, barrier integrity, and hepatic and renal clearance. Impaired organ function can, in turn, alter microbial ecology and promote metabolite accumulation, creating bidirectional interactions between exposure and disease. Although experimental studies provide mechanistic insights, human evidence establishing causal links between dietary xenobiotics, microbial transformation, and chronic liver or kidney injury remains limited. We also evaluate the potential of integrated biomarkers, dietary interventions, and microbial enzyme-targeting strategies, identifying the evidence needed for clinical translation. Future progress requires longitudinal cohorts and controlled dietary studies that combine measured exposure, microbial function, metabolite profiles, and organ-specific outcomes. This integrated perspective provides a framework for investigating individual susceptibility to dietary xenobiotics and evaluating microbiome-informed approaches to food safety and nutrition.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-28
High salinity selects for halotolerant gut microbiota in the mummichog Fundulus heteroclitus.
microPublication biology, 2026:.
Mummichogs (Fundulus heteroclitus) are euryhaline fish that maintain osmoregulation across a range of salinities, but how their gut microbiomes respond remains poorly understood. Using Illumina 16S amplicon and Oxford Nanopore full-length 16S sequencing, we show that salinity is associated with reproducible gut microbiome restructuring. While alpha diversity did not differ significantly between low-salinity (5 ppt) and high-salinity (50 ppt) groups, beta diversity revealed distinct shifts in microbial communities. Specifically, high-salinity microbiomes were dominated by halotolerant Vibrio and Ahrensia species while low-salinity microbiomes retained more taxonomically diverse communities. These findings suggest host-associated microbes may contribute to osmotic homeostasis under salinity stress.
Additional Links: PMID-42948380
PubMed:
Citation:
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@article {pmid42948380,
year = {2026},
author = {Bradberry, R and Hutchinson, E and Edwards, C and Wetzel, J and Shull, AY and Gordon, S},
title = {High salinity selects for halotolerant gut microbiota in the mummichog Fundulus heteroclitus.},
journal = {microPublication biology},
volume = {2026},
number = {},
pages = {},
pmid = {42948380},
issn = {2578-9430},
abstract = {Mummichogs (Fundulus heteroclitus) are euryhaline fish that maintain osmoregulation across a range of salinities, but how their gut microbiomes respond remains poorly understood. Using Illumina 16S amplicon and Oxford Nanopore full-length 16S sequencing, we show that salinity is associated with reproducible gut microbiome restructuring. While alpha diversity did not differ significantly between low-salinity (5 ppt) and high-salinity (50 ppt) groups, beta diversity revealed distinct shifts in microbial communities. Specifically, high-salinity microbiomes were dominated by halotolerant Vibrio and Ahrensia species while low-salinity microbiomes retained more taxonomically diverse communities. These findings suggest host-associated microbes may contribute to osmotic homeostasis under salinity stress.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-28
Evaluating traditional Chinese medicine modulation of the gut microbiota-bile acid axis in metabolic and inflammatory diseases: mechanistic evidence and translational priorities.
Frontiers in microbiology, 17:1977691.
Metabolic dysfunction-associated steatotic liver disease (MASLD), obesity, type 2 diabetes mellitus (T2D), and inflammatory bowel disease (IBD) are clinically distinct disorders that share perturbations in intestinal ecology, bile-acid composition, epithelial barrier function, and immune-metabolic regulation. Traditional Chinese medicine (TCM) may modify these interconnected processes, but the translational significance of reported effects remains uncertain. Changes in microbial composition are often interpreted as mechanisms without evidence of altered microbial function, bile-acid profiles or concentrations, receptor engagement, or clinical benefit. Here, we present a structured narrative review that uses the gut microbiota-bile acid axis to evaluate TCM in metabolic and inflammatory disease. We describe how microbial bile salt hydrolases, the bile acid-inducible (bai) operon, hydroxysteroid dehydrogenases, and amino-acid conjugation diversify the bile-acid pool and influence farnesoid X receptor (FXR), Takeda G protein-coupled bile acid receptor 1 (GPBAR1, also known as TGR5), and immune pathways. We then assess evidence for defined TCM constituents and formulae in MASLD, obesity/T2D, and IBD. Across these settings, the most informative studies combine a standardized intervention with longitudinal metagenomic and targeted bile-acid profiling, host-signaling measurements, and an outcome that is attenuated by microbiota depletion, fecal microbiota transplantation, or functional microbial manipulation. Only one eligible human trial, of Qushi Huayu in adults enrolled under the historical NAFLD designation, reported both clinical and microbiota-related outcomes. Evidence for obesity/T2D and IBD was predominantly preclinical or observational, and the framework is therefore a translational assessment tool rather than a clinically validated model. We therefore propose an evidence hierarchy and a minimum translational package that integrates chemical quality control, dietary and co-medication assessment, strain- and gene-resolved microbiome analysis, targeted bile-acid metabolomics, and pathway-directed validation. TCM should be considered a potential precision adjunct to standard care only when reproducible microbial-metabolic phenotypes are linked to clinically meaningful benefit.
Additional Links: PMID-42948400
PubMed:
Citation:
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@article {pmid42948400,
year = {2026},
author = {Yu, Y and Wang, J and Yuan, Q and Yu, L and Zhang, C},
title = {Evaluating traditional Chinese medicine modulation of the gut microbiota-bile acid axis in metabolic and inflammatory diseases: mechanistic evidence and translational priorities.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1977691},
pmid = {42948400},
issn = {1664-302X},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD), obesity, type 2 diabetes mellitus (T2D), and inflammatory bowel disease (IBD) are clinically distinct disorders that share perturbations in intestinal ecology, bile-acid composition, epithelial barrier function, and immune-metabolic regulation. Traditional Chinese medicine (TCM) may modify these interconnected processes, but the translational significance of reported effects remains uncertain. Changes in microbial composition are often interpreted as mechanisms without evidence of altered microbial function, bile-acid profiles or concentrations, receptor engagement, or clinical benefit. Here, we present a structured narrative review that uses the gut microbiota-bile acid axis to evaluate TCM in metabolic and inflammatory disease. We describe how microbial bile salt hydrolases, the bile acid-inducible (bai) operon, hydroxysteroid dehydrogenases, and amino-acid conjugation diversify the bile-acid pool and influence farnesoid X receptor (FXR), Takeda G protein-coupled bile acid receptor 1 (GPBAR1, also known as TGR5), and immune pathways. We then assess evidence for defined TCM constituents and formulae in MASLD, obesity/T2D, and IBD. Across these settings, the most informative studies combine a standardized intervention with longitudinal metagenomic and targeted bile-acid profiling, host-signaling measurements, and an outcome that is attenuated by microbiota depletion, fecal microbiota transplantation, or functional microbial manipulation. Only one eligible human trial, of Qushi Huayu in adults enrolled under the historical NAFLD designation, reported both clinical and microbiota-related outcomes. Evidence for obesity/T2D and IBD was predominantly preclinical or observational, and the framework is therefore a translational assessment tool rather than a clinically validated model. We therefore propose an evidence hierarchy and a minimum translational package that integrates chemical quality control, dietary and co-medication assessment, strain- and gene-resolved microbiome analysis, targeted bile-acid metabolomics, and pathway-directed validation. TCM should be considered a potential precision adjunct to standard care only when reproducible microbial-metabolic phenotypes are linked to clinically meaningful benefit.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-28
Comparison of long and short 16S rRNA gene amplicon sequencing for agricultural soil and grain microbiomes using custom Kinnex libraries.
ISME communications, 6(1):ycag282.
Bacteria are an important component of environmental microbiomes, contributing to animal, plant, and soil health. The 16S rRNA gene is used as a barcode for taxonomic classification of bacteria and analysis of bacterial diversity in environmental samples. The 16S barcode region is ~1500 bp and has nine hypervariable regions (V1-V9) that differ in their ability to distinguish various taxa. Short-read sequencing approaches enabled the targeting of subsets of these variable regions; however, long-read sequencing platforms can span all nine hypervariable regions, resulting in greater taxonomic resolution. We explored different DNA extraction procedures, DNA polymerases, and amplicon lengths to determine their effects on taxonomic resolution. We compared the full-length 16S barcode region (V1-V9) and subsets of the barcode (V3-V5 and V4-V5) using custom amplicons in the Pacific Biosciences (PacBio) Kinnex long-read sequencing platform, which has enhanced output over traditional PacBio amplicon sequencing. To capture differences in DNA quality and microbial complexity, two types of environmental DNA samples were assessed: 32 samples from agricultural soil and another 32 samples cultured from grain. The study demonstrates that custom amplicon sequencing using the PacBio Kinnex system can be implemented with relative ease, allowing for increased outputs over traditional custom amplicon sequencing. The greatest taxonomic resolution was achieved with longer amplicons; however, interactions between DNA quality, amplicon lengths, chimeric reads, community complexity, and taxonomic assignment/resolution should be considered. The samples themselves also represent unique microbiomes that are not well represented in the literature, adding to our knowledge of diverse microbes on grain and in soils.
Additional Links: PMID-42948406
PubMed:
Citation:
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@article {pmid42948406,
year = {2026},
author = {Lee, SJ and Chin, T and Gamage, NW and Bamforth, J and Dojack, L and Osuna-Caballero, S and Pozniak, C and Bett, KE and Walkowiak, S},
title = {Comparison of long and short 16S rRNA gene amplicon sequencing for agricultural soil and grain microbiomes using custom Kinnex libraries.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag282},
pmid = {42948406},
issn = {2730-6151},
abstract = {Bacteria are an important component of environmental microbiomes, contributing to animal, plant, and soil health. The 16S rRNA gene is used as a barcode for taxonomic classification of bacteria and analysis of bacterial diversity in environmental samples. The 16S barcode region is ~1500 bp and has nine hypervariable regions (V1-V9) that differ in their ability to distinguish various taxa. Short-read sequencing approaches enabled the targeting of subsets of these variable regions; however, long-read sequencing platforms can span all nine hypervariable regions, resulting in greater taxonomic resolution. We explored different DNA extraction procedures, DNA polymerases, and amplicon lengths to determine their effects on taxonomic resolution. We compared the full-length 16S barcode region (V1-V9) and subsets of the barcode (V3-V5 and V4-V5) using custom amplicons in the Pacific Biosciences (PacBio) Kinnex long-read sequencing platform, which has enhanced output over traditional PacBio amplicon sequencing. To capture differences in DNA quality and microbial complexity, two types of environmental DNA samples were assessed: 32 samples from agricultural soil and another 32 samples cultured from grain. The study demonstrates that custom amplicon sequencing using the PacBio Kinnex system can be implemented with relative ease, allowing for increased outputs over traditional custom amplicon sequencing. The greatest taxonomic resolution was achieved with longer amplicons; however, interactions between DNA quality, amplicon lengths, chimeric reads, community complexity, and taxonomic assignment/resolution should be considered. The samples themselves also represent unique microbiomes that are not well represented in the literature, adding to our knowledge of diverse microbes on grain and in soils.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-28
Fermentation of ginsenoside Rb1 by a probiotic mixture alleviates atopic dermatitis via synergistic effects of rare ginsenoside F2 and gut microbiota-derived 12-ketolithocholic acid in mice.
Journal of ginseng research, 50(6):101153.
UNLABELLED: Atopic Dermatitis (AD) is a chronic, relapsing inflammatory skin disorder with increasing global incidence. Emerging evidence highlights a strong association between AD and gut dysbiosis. In this context, compounds from Chinese herbal medicine (CHM), such as ginsenosides, have gained attention for their anti-inflammatory and immunomodulatory properties. However, the poor bioavailability of major ginsenosides limits their therapeutic effectiveness. Recent advances in probiotic-based herbal medicine fermentation suggest that, in addition to manipulation of gut dysbiosis, probiotics also show promising potential for enhancing the bioconversion of major ginsenosides into rare ginsenosides. The objective of this study was to determine whether probiotic-fermented ginsenoside Rb1 broth (Rb1FB) could alleviate 2,4-dinitrochlorobenzene (DNCB) atopic dermatitis-like disease and to investigate the associated gut-skin mechanisms. Rb1FB improved visible skin lesions and reduced dermatitis severity and significantly reduced epidermal thickening, dermal mast-cell infiltration, serum immunoglobulin E (IgE) and tumor necrosis factor-α (TNF-α) in AD mice. Rb1FB also increased gut microbial richness and diversity, enriched Bacteroides, increased fecal 12-ketolithocholic acid (12-KLCA), and enhanced systemic exposure to the rare ginsenoside F2. Therefore, the principal biological outcomes were improvements in the clinical-like, histopathological, allergic, and inflammatory features of AD, while the microbiome, metabolomic, and serum ginsenoside findings provided potential mechanistic explanations.
METHODS: Probiotic strains Lactiplantibacillus plantarum DMU22441, Lactobacillus acidophilus DMU22440, and Lactiplantibacillus plantarum DMU22439 were screened for Rb1 utilization, and their fermentation conditions for maximum release of rare ginsenosides were optimized to prepare Rb1FB. A DNCB-induced AD mouse model was established to assess the therapeutic effects of Rb1FB. 16 S ribosomal RNA (rRNA) gene sequencing, metabolomics, transcriptomics and in vitro studies were employed to explore the mechanism of action.
RESULTS: Rb1FB significantly alleviated AD symptoms in mice, reduced serum IgE and TNF-α levels, modulated the gut microbiota, and increased systemic exposure to the rare ginsenoside F2. In TNF-α-stimulated HaCaT cells, combined treatment with F2 and gut microbiota-associated 12-KLCA produced greater suppression of selected inflammatory genes than either treatment alone and was associated with reduced NUAK family kinase 2 (NUAK2).
CONCLUSION: Rb1FB modulates the gut microbiota and its metabolites, enhances rare ginsenoside absorption, and alleviates AD symptoms in mice. F2 and 12-KLCA produced an enhanced combined inhibitory effect on inflammatory responses in vitro. These findings support the therapeutic potential of probiotic-fermented ginsenoside Rb1 for AD.
Additional Links: PMID-42948585
PubMed:
Citation:
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@article {pmid42948585,
year = {2026},
author = {Yuan, D and Walayat, B and Chen, X and Xiang, D and Xing, Y and Wang, C and Li, M and Hou, B},
title = {Fermentation of ginsenoside Rb1 by a probiotic mixture alleviates atopic dermatitis via synergistic effects of rare ginsenoside F2 and gut microbiota-derived 12-ketolithocholic acid in mice.},
journal = {Journal of ginseng research},
volume = {50},
number = {6},
pages = {101153},
pmid = {42948585},
issn = {1226-8453},
abstract = {UNLABELLED: Atopic Dermatitis (AD) is a chronic, relapsing inflammatory skin disorder with increasing global incidence. Emerging evidence highlights a strong association between AD and gut dysbiosis. In this context, compounds from Chinese herbal medicine (CHM), such as ginsenosides, have gained attention for their anti-inflammatory and immunomodulatory properties. However, the poor bioavailability of major ginsenosides limits their therapeutic effectiveness. Recent advances in probiotic-based herbal medicine fermentation suggest that, in addition to manipulation of gut dysbiosis, probiotics also show promising potential for enhancing the bioconversion of major ginsenosides into rare ginsenosides. The objective of this study was to determine whether probiotic-fermented ginsenoside Rb1 broth (Rb1FB) could alleviate 2,4-dinitrochlorobenzene (DNCB) atopic dermatitis-like disease and to investigate the associated gut-skin mechanisms. Rb1FB improved visible skin lesions and reduced dermatitis severity and significantly reduced epidermal thickening, dermal mast-cell infiltration, serum immunoglobulin E (IgE) and tumor necrosis factor-α (TNF-α) in AD mice. Rb1FB also increased gut microbial richness and diversity, enriched Bacteroides, increased fecal 12-ketolithocholic acid (12-KLCA), and enhanced systemic exposure to the rare ginsenoside F2. Therefore, the principal biological outcomes were improvements in the clinical-like, histopathological, allergic, and inflammatory features of AD, while the microbiome, metabolomic, and serum ginsenoside findings provided potential mechanistic explanations.
METHODS: Probiotic strains Lactiplantibacillus plantarum DMU22441, Lactobacillus acidophilus DMU22440, and Lactiplantibacillus plantarum DMU22439 were screened for Rb1 utilization, and their fermentation conditions for maximum release of rare ginsenosides were optimized to prepare Rb1FB. A DNCB-induced AD mouse model was established to assess the therapeutic effects of Rb1FB. 16 S ribosomal RNA (rRNA) gene sequencing, metabolomics, transcriptomics and in vitro studies were employed to explore the mechanism of action.
RESULTS: Rb1FB significantly alleviated AD symptoms in mice, reduced serum IgE and TNF-α levels, modulated the gut microbiota, and increased systemic exposure to the rare ginsenoside F2. In TNF-α-stimulated HaCaT cells, combined treatment with F2 and gut microbiota-associated 12-KLCA produced greater suppression of selected inflammatory genes than either treatment alone and was associated with reduced NUAK family kinase 2 (NUAK2).
CONCLUSION: Rb1FB modulates the gut microbiota and its metabolites, enhances rare ginsenoside absorption, and alleviates AD symptoms in mice. F2 and 12-KLCA produced an enhanced combined inhibitory effect on inflammatory responses in vitro. These findings support the therapeutic potential of probiotic-fermented ginsenoside Rb1 for AD.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-28
Contrasting microbiomes in deep-sea scleractinian and octocoral species from the South Atlantic Ocean.
Sustainable microbiology, 3(4):qvag048.
Deep-sea corals (DSC) are ecologically important, yet their microbiomes' composition, structure, and host specificity remain largely unresolved in the South Atlantic, especially for octocorals. Here, we provide a comprehensive characterization of DSC microbiomes, spanning Hexacorallia (Desmophyllum pertusum, Solenosmilia variabilis) and Octocorallia (Candidella imbricata, three Malacalcyonacea species), collected at ∼710 m depth in the Campos Basin, an active oil- and gas-producing region. Abiotic characterization revealed total hydrocarbon concentrations. Seawater and sediment samples provided further environmental context. Amplicon sequencing (16S rRNA gene), combined with alpha and beta diversity analyses, differential abundance analysis, and indicator species analysis, revealed that each coral species harboured a microbial community structure distinct from the surrounding environment, with host specificity varying along a continuum. Candidella imbricata was the individually resolved coral species with the most specialized microbiome, dominated by Endozoicomonadaceae, the lowest Shannon diversity, the highest intragroup homogeneity, and the largest number of indicator amplicon sequencing variants (ASVs). Desmophyllum pertusum showed no exclusive indicators, overlapping broadly with environmental communities, but selectively enriched the potentially hydrocarbon-degrading family Halieaceae. To our knowledge, these findings establish the first microbial baseline for DSC holobionts in this region, documenting contrasting host-specificity across scleractinian and octocoral taxa.
Additional Links: PMID-42948633
PubMed:
Citation:
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@article {pmid42948633,
year = {2026},
author = {Hill, LJ and Damasceno, T and Garritano, AN and Modolon, F and Medeiros, L and Vilela, CLS and Duarte, G and Thomas, T and Peixoto, RS},
title = {Contrasting microbiomes in deep-sea scleractinian and octocoral species from the South Atlantic Ocean.},
journal = {Sustainable microbiology},
volume = {3},
number = {4},
pages = {qvag048},
pmid = {42948633},
issn = {2755-1970},
abstract = {Deep-sea corals (DSC) are ecologically important, yet their microbiomes' composition, structure, and host specificity remain largely unresolved in the South Atlantic, especially for octocorals. Here, we provide a comprehensive characterization of DSC microbiomes, spanning Hexacorallia (Desmophyllum pertusum, Solenosmilia variabilis) and Octocorallia (Candidella imbricata, three Malacalcyonacea species), collected at ∼710 m depth in the Campos Basin, an active oil- and gas-producing region. Abiotic characterization revealed total hydrocarbon concentrations. Seawater and sediment samples provided further environmental context. Amplicon sequencing (16S rRNA gene), combined with alpha and beta diversity analyses, differential abundance analysis, and indicator species analysis, revealed that each coral species harboured a microbial community structure distinct from the surrounding environment, with host specificity varying along a continuum. Candidella imbricata was the individually resolved coral species with the most specialized microbiome, dominated by Endozoicomonadaceae, the lowest Shannon diversity, the highest intragroup homogeneity, and the largest number of indicator amplicon sequencing variants (ASVs). Desmophyllum pertusum showed no exclusive indicators, overlapping broadly with environmental communities, but selectively enriched the potentially hydrocarbon-degrading family Halieaceae. To our knowledge, these findings establish the first microbial baseline for DSC holobionts in this region, documenting contrasting host-specificity across scleractinian and octocoral taxa.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-28
Investigating the Effect of Oral Probiotic Capsules on Postpartum Sleep Quality in Primiparous Women: A triple-blind randomised controlled trial.
Sultan Qaboos University medical journal, 26(1):529-537.
OBJECTIVES: Quality of sleep is an important indicator of health. Sleep disturbance and daytime fatigue is one of the most common problems in the postpartum period. Early postpartum (first 4 weeks) is when sleep is most disturbed. The gut microbiota may affect sleep quality and affect host health through the production of metabolites and compounds. This study aimed to determine the effect of oral probiotic capsule on the quality of sleep after delivery in primiparous women.
METHOD: This triple-blind randomised controlled trial study was conducted in August to November 2023 with eligible primiparous women who gave birth at Health Centers No. 2 and 3, Mashhad, Iran. The participants were randomly and equally divided into two groups: (1) the probiotic group, which received probiotic capsules (containing Lactobacillus acidophilus, Bifidobacterium bifidum, B. lactis and B. longum) and (2) the placebo group, which received placebo capsules. All participants received one capsule daily from the third day after delivery for 30 days. The Pittsburgh Sleep Quality Index questionnaire was completed before and after the study. Kolmogorov-Smirnov and Shapiro-Wilk tests, T-test and Mann-Whitney test were used for statistical analysis. A P value of less than 0.05 was considered statistically significant.
RESULTS: A total of 60 women were included in this study (n = 30 for each group). The two groups were homogeneous in terms of demographic and obstetric characteristics except for body mass index. Before the intervention, the overall score of postpartum quality of sleep in the probiotic and placebo groups was 9.66 ± 6.21 and 11.70 ± 6.68, respectively; after the intervention, the probiotic group had a score of 6.16 ± 2.75 with the score difference of -3.50 ± 5.53 and the placebo group a score of 6.60 ± 2.66 with the score difference of -5.10 ± 6.31 with a statistically significant difference in the intervention group compared to the placebo (P = 0.003).
CONCLUSION: Consumption of probiotic capsules improves the quality of sleep and maternal health in the postpartum period.
Additional Links: PMID-42948779
PubMed:
Citation:
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@article {pmid42948779,
year = {2026},
author = {Rastegar, M and Shoorab, NJ and Salari, R and Rastaghi, S},
title = {Investigating the Effect of Oral Probiotic Capsules on Postpartum Sleep Quality in Primiparous Women: A triple-blind randomised controlled trial.},
journal = {Sultan Qaboos University medical journal},
volume = {26},
number = {1},
pages = {529-537},
pmid = {42948779},
issn = {2075-0528},
mesh = {Humans ; Female ; *Probiotics/therapeutic use/administration & dosage/pharmacology ; *Postpartum Period/drug effects ; Adult ; *Sleep Quality ; Iran ; Parity ; Capsules ; Pregnancy ; Administration, Oral ; Surveys and Questionnaires ; },
abstract = {OBJECTIVES: Quality of sleep is an important indicator of health. Sleep disturbance and daytime fatigue is one of the most common problems in the postpartum period. Early postpartum (first 4 weeks) is when sleep is most disturbed. The gut microbiota may affect sleep quality and affect host health through the production of metabolites and compounds. This study aimed to determine the effect of oral probiotic capsule on the quality of sleep after delivery in primiparous women.
METHOD: This triple-blind randomised controlled trial study was conducted in August to November 2023 with eligible primiparous women who gave birth at Health Centers No. 2 and 3, Mashhad, Iran. The participants were randomly and equally divided into two groups: (1) the probiotic group, which received probiotic capsules (containing Lactobacillus acidophilus, Bifidobacterium bifidum, B. lactis and B. longum) and (2) the placebo group, which received placebo capsules. All participants received one capsule daily from the third day after delivery for 30 days. The Pittsburgh Sleep Quality Index questionnaire was completed before and after the study. Kolmogorov-Smirnov and Shapiro-Wilk tests, T-test and Mann-Whitney test were used for statistical analysis. A P value of less than 0.05 was considered statistically significant.
RESULTS: A total of 60 women were included in this study (n = 30 for each group). The two groups were homogeneous in terms of demographic and obstetric characteristics except for body mass index. Before the intervention, the overall score of postpartum quality of sleep in the probiotic and placebo groups was 9.66 ± 6.21 and 11.70 ± 6.68, respectively; after the intervention, the probiotic group had a score of 6.16 ± 2.75 with the score difference of -3.50 ± 5.53 and the placebo group a score of 6.60 ± 2.66 with the score difference of -5.10 ± 6.31 with a statistically significant difference in the intervention group compared to the placebo (P = 0.003).
CONCLUSION: Consumption of probiotic capsules improves the quality of sleep and maternal health in the postpartum period.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Probiotics/therapeutic use/administration & dosage/pharmacology
*Postpartum Period/drug effects
Adult
*Sleep Quality
Iran
Parity
Capsules
Pregnancy
Administration, Oral
Surveys and Questionnaires
RevDate: 2026-10-29
CmpDate: 2026-10-28
Integrating cure and care in Alzheimer's disease: a systems perspective for precision medicine.
Frontiers in molecular medicine, 6:1960763.
Alzheimer's disease remains a major global health challenge, with limited disease-modifying therapies and a rapidly growing societal burden. Although amyloid and tau remain central to the field, current evidence also implicates neuroinflammation, immune dysregulation, vascular dysfunction, and host-microbe interactions in disease pathogenesis. These developments support a broader systems framework, but simply combining additional disciplines or data modalities does not by itself preserve the dynamic biology or lived experience of disease. Artificial intelligence multi-omics, and digital biomarkers can help identify clinically meaningful patterns only when data and models preserve relevant structure across time, scale, context, and uncertainty. Realizing this potential will require responsible international data sharing, interoperable infrastructure, explicit evidence provenance, and ethical governance grounded in FAIR principles, context-appropriate explainability, and privacy-preserving approaches such as federated learning. Scientific progress should therefore be measured not only by disease modification, but also by patterns of cognition, behavior, function, quality of life, and caregiver burden. This Perspective argues that cure and care are not competing or merely parallel priorities; they are linked outputs of the same continuously learning research and care ecosystem.
Additional Links: PMID-42948807
PubMed:
Citation:
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@article {pmid42948807,
year = {2026},
author = {Rice, JA and Bouteiller, JC and Khachaturian, AS},
title = {Integrating cure and care in Alzheimer's disease: a systems perspective for precision medicine.},
journal = {Frontiers in molecular medicine},
volume = {6},
number = {},
pages = {1960763},
pmid = {42948807},
issn = {2674-0095},
abstract = {Alzheimer's disease remains a major global health challenge, with limited disease-modifying therapies and a rapidly growing societal burden. Although amyloid and tau remain central to the field, current evidence also implicates neuroinflammation, immune dysregulation, vascular dysfunction, and host-microbe interactions in disease pathogenesis. These developments support a broader systems framework, but simply combining additional disciplines or data modalities does not by itself preserve the dynamic biology or lived experience of disease. Artificial intelligence multi-omics, and digital biomarkers can help identify clinically meaningful patterns only when data and models preserve relevant structure across time, scale, context, and uncertainty. Realizing this potential will require responsible international data sharing, interoperable infrastructure, explicit evidence provenance, and ethical governance grounded in FAIR principles, context-appropriate explainability, and privacy-preserving approaches such as federated learning. Scientific progress should therefore be measured not only by disease modification, but also by patterns of cognition, behavior, function, quality of life, and caregiver burden. This Perspective argues that cure and care are not competing or merely parallel priorities; they are linked outputs of the same continuously learning research and care ecosystem.},
}
RevDate: 2026-10-28
Preventing Clostridioides difficile Infection and Recurrence: Practical Strategies for Clinical Practice.
The American journal of gastroenterology pii:00000434-990000000-02322 [Epub ahead of print].
Clostridioides difficile infection (CDI) is a major cause of morbidity, mortality, and healthcare utilization worldwide. Although advances in antimicrobial stewardship and infection prevention have reduced healthcare-associated disease in some settings, the incidence of community-associated CDI and the persistent burden of recurrent CDI (rCDI) continue to pose substantial clinical challenges. Because recurrent disease is fundamentally driven by persistent disruption of the intestinal microbiome and loss of colonization resistance, prevention has emerged as the central strategy for reducing long-term disease burden. This review summarizes contemporary evidence supporting prevention of both incident and rCDI, emphasizing practical approaches for gastroenterologists. Primary prevention centers on minimizing modifiable risk factors through antimicrobial stewardship, infection prevention and control, diagnostic stewardship to distinguish colonization from infection, and strategies to preserve the intestinal microbiome. For patients with CDI, we review evidence supporting extended antibiotic regimens, oral vancomycin prophylaxis during subsequent systemic antibiotic exposure, and microbiome restoration therapies, including conventional fecal microbiota transplantation and US Food and Drug Administration-approved microbiota-based therapies, which have transformed secondary prevention by restoring microbial diversity and colonization resistance. Special consideration is given to populations at particularly high risk for recurrence, including older adults, immunocompromised individuals, transplant recipients, and patients with inflammatory bowel disease. Finally, we discuss emerging preventive strategies, including precision risk stratification, microbiome- and metabolome-based biomarkers, bile acid modulation, and approaches targeting asymptomatic colonization. Together, these advances signal a paradigm shift from treating CDI episodes to implementing personalized preventive strategies that interrupt the cycle of recurrent disease and improve long-term patient outcomes.
Additional Links: PMID-42949032
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PubMed:
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@article {pmid42949032,
year = {2026},
author = {Axelrad, JE and Allegretti, JR},
title = {Preventing Clostridioides difficile Infection and Recurrence: Practical Strategies for Clinical Practice.},
journal = {The American journal of gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ajg.0000000000004239},
pmid = {42949032},
issn = {1572-0241},
abstract = {Clostridioides difficile infection (CDI) is a major cause of morbidity, mortality, and healthcare utilization worldwide. Although advances in antimicrobial stewardship and infection prevention have reduced healthcare-associated disease in some settings, the incidence of community-associated CDI and the persistent burden of recurrent CDI (rCDI) continue to pose substantial clinical challenges. Because recurrent disease is fundamentally driven by persistent disruption of the intestinal microbiome and loss of colonization resistance, prevention has emerged as the central strategy for reducing long-term disease burden. This review summarizes contemporary evidence supporting prevention of both incident and rCDI, emphasizing practical approaches for gastroenterologists. Primary prevention centers on minimizing modifiable risk factors through antimicrobial stewardship, infection prevention and control, diagnostic stewardship to distinguish colonization from infection, and strategies to preserve the intestinal microbiome. For patients with CDI, we review evidence supporting extended antibiotic regimens, oral vancomycin prophylaxis during subsequent systemic antibiotic exposure, and microbiome restoration therapies, including conventional fecal microbiota transplantation and US Food and Drug Administration-approved microbiota-based therapies, which have transformed secondary prevention by restoring microbial diversity and colonization resistance. Special consideration is given to populations at particularly high risk for recurrence, including older adults, immunocompromised individuals, transplant recipients, and patients with inflammatory bowel disease. Finally, we discuss emerging preventive strategies, including precision risk stratification, microbiome- and metabolome-based biomarkers, bile acid modulation, and approaches targeting asymptomatic colonization. Together, these advances signal a paradigm shift from treating CDI episodes to implementing personalized preventive strategies that interrupt the cycle of recurrent disease and improve long-term patient outcomes.},
}
RevDate: 2026-10-28
Tumor-Immune Microenvironment of Early-Onset Colorectal Cancer: Implications for Immune-Based Prevention and Therapy.
Cancer immunology research pii:789654 [Epub ahead of print].
Early-onset colorectal cancer (EOCRC), typically defined as colorectal cancer diagnosed before 50 years of age, is increasing in incidence worldwide and exhibits distinctive clinical, molecular, and environmental features compared with later-onset (LOCRC) disease. However, the tumor-immune microenvironment (TiME) of EOCRC and its implications for prevention and therapy remain poorly characterized. In this review, we synthesize current evidence on the TiME of EOCRC and contrast it with that of conventional LOCRC. We first discuss global features of the EOCRC immune landscape, including innate and adaptive immune composition, functional states, and spatial organization, highlighting areas where apparent age-related differences reflect true biology versus confounding by tumor site, stage, or mismatch repair (MMR) status. We then examine immunogenomic and epigenomic determinants-such as MMR deficiency distribution, microbial mutational signatures, chromosomal instability, and age-conditioned methylation programs-that shape neoantigen landscapes, antigen presentation, and immune evasion in younger patients. Next, we review microbiome-driven immunomodulation, focusing on dysbiosis, genotoxic bacteria, and early-life and young-adult exposures as joint modifiers of mucosal immunity and tumor development. Finally, we explore how these insights inform immune-based prevention (risk stratification, screening, diet and microbiome interventions, and chemoprevention) and immunotherapy strategies, including checkpoint blockade and rational combinations in the predominant microsatellite-stable EOCRC population.
Additional Links: PMID-42949048
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PubMed:
Citation:
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@article {pmid42949048,
year = {2026},
author = {Perea, J and González-Sanmartín, M and Coiras, M and Ogino, S},
title = {Tumor-Immune Microenvironment of Early-Onset Colorectal Cancer: Implications for Immune-Based Prevention and Therapy.},
journal = {Cancer immunology research},
volume = {},
number = {},
pages = {OF1-OF15},
doi = {10.1158/2326-6066.CIR-25-1508},
pmid = {42949048},
issn = {2326-6074},
support = {PI24/0729//Instituto de Salud Carlos III (ISCIII)/ ; CRP-24-1185864-01-PROF//American Cancer Society (ACS)/ ; },
abstract = {Early-onset colorectal cancer (EOCRC), typically defined as colorectal cancer diagnosed before 50 years of age, is increasing in incidence worldwide and exhibits distinctive clinical, molecular, and environmental features compared with later-onset (LOCRC) disease. However, the tumor-immune microenvironment (TiME) of EOCRC and its implications for prevention and therapy remain poorly characterized. In this review, we synthesize current evidence on the TiME of EOCRC and contrast it with that of conventional LOCRC. We first discuss global features of the EOCRC immune landscape, including innate and adaptive immune composition, functional states, and spatial organization, highlighting areas where apparent age-related differences reflect true biology versus confounding by tumor site, stage, or mismatch repair (MMR) status. We then examine immunogenomic and epigenomic determinants-such as MMR deficiency distribution, microbial mutational signatures, chromosomal instability, and age-conditioned methylation programs-that shape neoantigen landscapes, antigen presentation, and immune evasion in younger patients. Next, we review microbiome-driven immunomodulation, focusing on dysbiosis, genotoxic bacteria, and early-life and young-adult exposures as joint modifiers of mucosal immunity and tumor development. Finally, we explore how these insights inform immune-based prevention (risk stratification, screening, diet and microbiome interventions, and chemoprevention) and immunotherapy strategies, including checkpoint blockade and rational combinations in the predominant microsatellite-stable EOCRC population.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
Vogt-Koyanagi-Harada disease: Recent perspectives.
Indian journal of ophthalmology, 74(11):1592-1604.
Vogt-Koyanagi-Harada (VKH) disease is a dynamic immune-mediated stromal choroiditis induced by dysregulated T cells targeting melanocytes. This disease is a unification of varied ocular and systemic features documented over the centuries across different parts of the world. With striking ethnic and geographic variations, VKH remains one of the leading causes of noninfectious uveitis. Recent advances in the immunopathogenesis with noted key pathogenic pathways including activation of the IL-23/IL-17 axis, impaired regulatory T-cell function with reduced expression of IL-35 levels, elevated IL-6 levels, epigenetic regulation mediated by microRNAs, and emerging evidence in the gut microbiome dysbiosis pave the way for early, targeted immunomodulatory strategies. Parallel development in the multimodal imaging front has transformed the diagnostic paradigm as to early detection of choroidal inflammation, identification of subclinical activity, and objective monitoring of the disease. Treatment emphasizes early initiation of steroid-sparing immunosuppression to prevent chronic progression and late-stage changes. Targeted approaches like biologics and Janus kinase inhibitors offer promising outcomes in refractory cases. This review integrates epidemiological perspectives, evolving immunopathogenesis, newer classifications, atypical presentations, utilization of multimodal imaging, and the therapeutic advances in VKH.
Additional Links: PMID-42949075
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PubMed:
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@article {pmid42949075,
year = {2026},
author = {Fahima, F and Nepal, S and Manna, G and Fidha, PK and Dutta Majumder, P and Biswas, J},
title = {Vogt-Koyanagi-Harada disease: Recent perspectives.},
journal = {Indian journal of ophthalmology},
volume = {74},
number = {11},
pages = {1592-1604},
doi = {10.4103/IJO.IJO_941_26},
pmid = {42949075},
issn = {1998-3689},
mesh = {Humans ; *Uveomeningoencephalitic Syndrome/diagnosis/epidemiology/immunology ; *Multimodal Imaging/methods ; Fluorescein Angiography ; },
abstract = {Vogt-Koyanagi-Harada (VKH) disease is a dynamic immune-mediated stromal choroiditis induced by dysregulated T cells targeting melanocytes. This disease is a unification of varied ocular and systemic features documented over the centuries across different parts of the world. With striking ethnic and geographic variations, VKH remains one of the leading causes of noninfectious uveitis. Recent advances in the immunopathogenesis with noted key pathogenic pathways including activation of the IL-23/IL-17 axis, impaired regulatory T-cell function with reduced expression of IL-35 levels, elevated IL-6 levels, epigenetic regulation mediated by microRNAs, and emerging evidence in the gut microbiome dysbiosis pave the way for early, targeted immunomodulatory strategies. Parallel development in the multimodal imaging front has transformed the diagnostic paradigm as to early detection of choroidal inflammation, identification of subclinical activity, and objective monitoring of the disease. Treatment emphasizes early initiation of steroid-sparing immunosuppression to prevent chronic progression and late-stage changes. Targeted approaches like biologics and Janus kinase inhibitors offer promising outcomes in refractory cases. This review integrates epidemiological perspectives, evolving immunopathogenesis, newer classifications, atypical presentations, utilization of multimodal imaging, and the therapeutic advances in VKH.},
}
MeSH Terms:
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Humans
*Uveomeningoencephalitic Syndrome/diagnosis/epidemiology/immunology
*Multimodal Imaging/methods
Fluorescein Angiography
RevDate: 2026-10-29
CmpDate: 2026-10-28
Mitochondrial Reprogramming Along the Gut-Brain Axis in Chemotherapy-Induced Cognitive Impairment: A Narrative Review.
Oxidative medicine and cellular longevity, 2026(1):.
Chemotherapy-induced cognitive impairment (CICI), often referred to as "chemobrain," is a frequently persistent complication that significantly affects memory, attention, executive function, and overall quality of life among cancer survivors. Although mitochondrial dysfunction, oxidative stress, neuroinflammation, and gut microbiota dysbiosis have each been implicated in its pathogenesis, the way these processes interact to drive cognitive decline remains incompletely understood. In this narrative review, we explore the current evidence supporting mitochondrial reprogramming as a central mechanistic link connecting chemotherapy-induced alterations in the gut-brain axis to neuronal dysfunction. Here, mitochondrial reprogramming encompasses not only overt mitochondrial damage but also adaptive and maladaptive alterations in mitochondrial bioenergetics, biogenesis, mitophagy, and metabolic signaling in response to chemotherapeutic stress. We discuss how oxidative stress, impaired mitochondrial quality control, and key inflammatory and stress-response pathways, including Nrf2/Keap1, NF-κB, the AMPK-SIRT1-PGC-1α axis, and mtDNA-mediated cGAS-STING signaling, may converge to promote neuronal injury and cognitive impairment. We further examine the contribution of chemotherapy-induced gut dysbiosis and microbiota-derived metabolites, such as short-chain fatty acids (SCFAs) and lipopolysaccharide (LPS), in modulating mitochondrial function, neuroinflammation, and blood-brain barrier (BBB) integrity via the gut-brain axis. Importantly, we differentiate findings derived directly from CICI models from those extrapolated from related fields such as neurodegenerative disorders, aging, and microbiome research, while highlighting current knowledge gaps and the scarcity of clinical data. Finally, we discuss promising therapeutic strategies aimed at restoring mitochondrial homeostasis and modulating the gut microbiota and outline priority areas for future research to facilitate the translation of these mechanistic insights into effective clinical interventions for cancer survivors.
Additional Links: PMID-42949236
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@article {pmid42949236,
year = {2026},
author = {Malhotra, A and Rao, GM and Marathe, A and Rai, S and Samyuktha Rani, V and Patil, A and Upadhya, D and Chakrapani, M},
title = {Mitochondrial Reprogramming Along the Gut-Brain Axis in Chemotherapy-Induced Cognitive Impairment: A Narrative Review.},
journal = {Oxidative medicine and cellular longevity},
volume = {2026},
number = {1},
pages = {},
pmid = {42949236},
issn = {1942-0994},
mesh = {Humans ; *Mitochondria/metabolism ; Animals ; *Chemotherapy-Related Cognitive Impairment/metabolism ; *Brain/metabolism ; *Cognitive Dysfunction/chemically induced ; *Brain-Gut Axis ; },
abstract = {Chemotherapy-induced cognitive impairment (CICI), often referred to as "chemobrain," is a frequently persistent complication that significantly affects memory, attention, executive function, and overall quality of life among cancer survivors. Although mitochondrial dysfunction, oxidative stress, neuroinflammation, and gut microbiota dysbiosis have each been implicated in its pathogenesis, the way these processes interact to drive cognitive decline remains incompletely understood. In this narrative review, we explore the current evidence supporting mitochondrial reprogramming as a central mechanistic link connecting chemotherapy-induced alterations in the gut-brain axis to neuronal dysfunction. Here, mitochondrial reprogramming encompasses not only overt mitochondrial damage but also adaptive and maladaptive alterations in mitochondrial bioenergetics, biogenesis, mitophagy, and metabolic signaling in response to chemotherapeutic stress. We discuss how oxidative stress, impaired mitochondrial quality control, and key inflammatory and stress-response pathways, including Nrf2/Keap1, NF-κB, the AMPK-SIRT1-PGC-1α axis, and mtDNA-mediated cGAS-STING signaling, may converge to promote neuronal injury and cognitive impairment. We further examine the contribution of chemotherapy-induced gut dysbiosis and microbiota-derived metabolites, such as short-chain fatty acids (SCFAs) and lipopolysaccharide (LPS), in modulating mitochondrial function, neuroinflammation, and blood-brain barrier (BBB) integrity via the gut-brain axis. Importantly, we differentiate findings derived directly from CICI models from those extrapolated from related fields such as neurodegenerative disorders, aging, and microbiome research, while highlighting current knowledge gaps and the scarcity of clinical data. Finally, we discuss promising therapeutic strategies aimed at restoring mitochondrial homeostasis and modulating the gut microbiota and outline priority areas for future research to facilitate the translation of these mechanistic insights into effective clinical interventions for cancer survivors.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mitochondria/metabolism
Animals
*Chemotherapy-Related Cognitive Impairment/metabolism
*Brain/metabolism
*Cognitive Dysfunction/chemically induced
*Brain-Gut Axis
RevDate: 2026-10-28
Nutrient control enables metabolic reconstruction of Lacticaseibacillus rhamnosus GG and analysis of secretions.
mSystems [Epub ahead of print].
UNLABELLED: Lacticaseibacillus rhamnosus GG (LGG) is an important gut commensal bacterial strain that has been extensively studied in both industrial and health settings. Despite its long history of study, a high-quality genome-scale metabolic network model (GEM) for LGG has yet to be reconstructed. Only automatically generated draft models have been published, which have notoriously limited functional accuracy. Furthermore, comprehensive nutrient requirements have not been established for well-controlled in vitro studies. Here, we present the first curated GEM for LGG using a new approach for reconstruction and validation that leverages multiple automatically generated draft models, applied study literature, and high-throughput defined media experiments. In addition, our results include a series of chemically defined media, extensive single-component nutrient dropout growth data, insights from in silico and in vitro experiments into secretion products, lactate, and indole-3-carboxaldehyde, a minimal medium, and in silico characterization of LGG's nutrient requirements. Our approach for developing interdisciplinary research tools for LGG metabolism comprises a new framework that could be applied to many understudied microorganisms, particularly useful in studying bacteria within the human microbiome.
IMPORTANCE: This study provides an important foundation for understanding how the beneficial gut bacterium Lacticaseibacillus rhamnosus GG (LGG) grows and interacts with its environment. Although LGG is one of the most widely studied probiotic bacteria, used in both health and industrial applications, a reliable tool for simulating its metabolic behavior and a clear understanding of its nutritional needs is lacking. By developing the first manually curated metabolic model of LGG and validating it through extensive laboratory experiments, this study provides new understanding of LGG's requirements and capabilities for utilizing nutrients and resources to investigate its metabolism. Completely chemically defined growth media and associated single-component dropout growth effects are also presented, and pathways for production of important compounds influencing human health are explored. The methods developed in this work also provide a framework for studying other poorly characterized microbes, helping advance research on the human microbiome and its role in health and disease.
Additional Links: PMID-42949268
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PubMed:
Citation:
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@article {pmid42949268,
year = {2026},
author = {Richmond, GR and Cunha, E and Kelly, L and Dias, Ó and Chang, RL},
title = {Nutrient control enables metabolic reconstruction of Lacticaseibacillus rhamnosus GG and analysis of secretions.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0112426},
doi = {10.1128/msystems.01124-26},
pmid = {42949268},
issn = {2379-5077},
abstract = {UNLABELLED: Lacticaseibacillus rhamnosus GG (LGG) is an important gut commensal bacterial strain that has been extensively studied in both industrial and health settings. Despite its long history of study, a high-quality genome-scale metabolic network model (GEM) for LGG has yet to be reconstructed. Only automatically generated draft models have been published, which have notoriously limited functional accuracy. Furthermore, comprehensive nutrient requirements have not been established for well-controlled in vitro studies. Here, we present the first curated GEM for LGG using a new approach for reconstruction and validation that leverages multiple automatically generated draft models, applied study literature, and high-throughput defined media experiments. In addition, our results include a series of chemically defined media, extensive single-component nutrient dropout growth data, insights from in silico and in vitro experiments into secretion products, lactate, and indole-3-carboxaldehyde, a minimal medium, and in silico characterization of LGG's nutrient requirements. Our approach for developing interdisciplinary research tools for LGG metabolism comprises a new framework that could be applied to many understudied microorganisms, particularly useful in studying bacteria within the human microbiome.
IMPORTANCE: This study provides an important foundation for understanding how the beneficial gut bacterium Lacticaseibacillus rhamnosus GG (LGG) grows and interacts with its environment. Although LGG is one of the most widely studied probiotic bacteria, used in both health and industrial applications, a reliable tool for simulating its metabolic behavior and a clear understanding of its nutritional needs is lacking. By developing the first manually curated metabolic model of LGG and validating it through extensive laboratory experiments, this study provides new understanding of LGG's requirements and capabilities for utilizing nutrients and resources to investigate its metabolism. Completely chemically defined growth media and associated single-component dropout growth effects are also presented, and pathways for production of important compounds influencing human health are explored. The methods developed in this work also provide a framework for studying other poorly characterized microbes, helping advance research on the human microbiome and its role in health and disease.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
Metabolite-Guided Regulation of the Rhizosphere Microbiome by a Synthetic Microbial Consortium and Key Mixed Metabolites Suppresses Root Rot Disease in Fritillaria pallidiflora.
Journal of agricultural and food chemistry, 74(42):32870-32884.
Continuous cropping can weaken soil disease suppression, but its microbial and metabolic bases remain unclear. We compared first-planting and replant rhizospheres of Fritillaria pallidiflora at 2-, 3-, and 4-year cultivation stages sampled in different calendar years using soil analysis, sequencing, metabolomics, and pot experiments. Replant soils had a higher root rot incidence, greater Fusarium solani abundance, and lower microbial network complexity and stability. Nitrate, ammonium, and electrical conductivities were associated with community restructuring. Five metabolites were linked to disease incidence and microbial taxa. A synthetic community (SynCom) of four Bacillus strains and one Brevibacillus laterosporus strain reduced F. solani abundance and disease incidence, enriched beneficial bacteria, increased antioxidant enzyme activities, and promoted growth. All five strains were recovered from the rhizosphere after 30 days. Combining the SynCom with the five metabolites produced the strongest disease suppression and plant growth. These findings support the evaluation of metabolite-guided microbial consortia for disease management.
Additional Links: PMID-42949318
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PubMed:
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@article {pmid42949318,
year = {2026},
author = {Yang, G and Dong, J and Qin, B and Zhang, X and Xu, Y and Dong, H and Zhao, W},
title = {Metabolite-Guided Regulation of the Rhizosphere Microbiome by a Synthetic Microbial Consortium and Key Mixed Metabolites Suppresses Root Rot Disease in Fritillaria pallidiflora.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {42},
pages = {32870-32884},
doi = {10.1021/acs.jafc.6c11017},
pmid = {42949318},
issn = {1520-5118},
support = {82360743//National Natural Science Foundation of China/ ; 82660873//National Natural Science Foundation of China/ ; MSPY202413//Shihezi University/ ; },
mesh = {Rhizosphere ; *Plant Diseases/microbiology/prevention & control ; Plant Roots/microbiology/metabolism/growth & development ; *Fritillaria/microbiology/growth & development/metabolism ; Fusarium/physiology/growth & development ; Soil Microbiology ; *Microbiota ; Bacteria/genetics/isolation & purification/classification/metabolism ; *Microbial Consortia ; Brevibacillus/physiology ; Bacillus/physiology/genetics ; },
abstract = {Continuous cropping can weaken soil disease suppression, but its microbial and metabolic bases remain unclear. We compared first-planting and replant rhizospheres of Fritillaria pallidiflora at 2-, 3-, and 4-year cultivation stages sampled in different calendar years using soil analysis, sequencing, metabolomics, and pot experiments. Replant soils had a higher root rot incidence, greater Fusarium solani abundance, and lower microbial network complexity and stability. Nitrate, ammonium, and electrical conductivities were associated with community restructuring. Five metabolites were linked to disease incidence and microbial taxa. A synthetic community (SynCom) of four Bacillus strains and one Brevibacillus laterosporus strain reduced F. solani abundance and disease incidence, enriched beneficial bacteria, increased antioxidant enzyme activities, and promoted growth. All five strains were recovered from the rhizosphere after 30 days. Combining the SynCom with the five metabolites produced the strongest disease suppression and plant growth. These findings support the evaluation of metabolite-guided microbial consortia for disease management.},
}
MeSH Terms:
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Rhizosphere
*Plant Diseases/microbiology/prevention & control
Plant Roots/microbiology/metabolism/growth & development
*Fritillaria/microbiology/growth & development/metabolism
Fusarium/physiology/growth & development
Soil Microbiology
*Microbiota
Bacteria/genetics/isolation & purification/classification/metabolism
*Microbial Consortia
Brevibacillus/physiology
Bacillus/physiology/genetics
RevDate: 2026-10-28
CmpDate: 2026-10-28
Engineering the plant holobiont for enhanced abiotic stress resilience: current insights and future directions.
Plant signaling & behavior, 21(1):2752710.
Climate change has intensified abiotic stresses such as drought, heat, and salinity, posing major threats to agricultural productivity and global food security. Conventional strategies to improve crop tolerance often face limitations in efficiency, sustainability, and environmental adaptability, underscoring the need for innovative approaches. This review focuses on the plant holobiont, which views plants and their associated microbiomes as an integrated functional unit in governing stress adaptation. Abiotic stress can disrupt plant-associated microbial communities, leading to dysbiosis and reduced holobiont resilience. Beneficial microorganisms, including plant growth-promoting rhizobacteria, endophytes, and arbuscular mycorrhizal fungi, can enhance stress tolerance by improving nutrient acquisition, regulating phytohormone signaling, strengthening antioxidant defenses, maintaining osmotic balance, and modulating stress-responsive gene expression. Emerging evidence suggests that these interactions contribute to the establishment of holobiont stress adaptation through biochemical signaling, microenvironmental modification, and epigenetic regulation, enabling plants to respond more effectively to recurrent stress. Advances in microbiome engineering, particularly through the development of synthetic microbial communities (SynComs), offer promising opportunities to restore microbial functions and enhance crop resilience under changing climatic conditions. The integration of multi-omics technologies, artificial intelligence, and precision agriculture is expected to accelerate the development of microbiome-based solutions for sustainable crop production. Collectively, microbiome engineering represents a promising, environmentally sustainable strategy to enhance the holobiont's adaptive resilience and improve long-term plant performance under abiotic stress.
Additional Links: PMID-42949855
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PubMed:
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@article {pmid42949855,
year = {2026},
author = {Albert, M and Alizadeh, M and Jefferson, TA and Prismantoro, D and Hindersah, R and Joshi, RC and Harsonowati, W and Chua, KO and Permadi, N and Miranti, M and Doni, F},
title = {Engineering the plant holobiont for enhanced abiotic stress resilience: current insights and future directions.},
journal = {Plant signaling & behavior},
volume = {21},
number = {1},
pages = {2752710},
doi = {10.1080/15592324.2026.2752710},
pmid = {42949855},
issn = {1559-2324},
mesh = {*Stress, Physiological ; *Plants/microbiology/metabolism ; *Microbiota/physiology ; Symbiosis ; Adaptation, Physiological ; },
abstract = {Climate change has intensified abiotic stresses such as drought, heat, and salinity, posing major threats to agricultural productivity and global food security. Conventional strategies to improve crop tolerance often face limitations in efficiency, sustainability, and environmental adaptability, underscoring the need for innovative approaches. This review focuses on the plant holobiont, which views plants and their associated microbiomes as an integrated functional unit in governing stress adaptation. Abiotic stress can disrupt plant-associated microbial communities, leading to dysbiosis and reduced holobiont resilience. Beneficial microorganisms, including plant growth-promoting rhizobacteria, endophytes, and arbuscular mycorrhizal fungi, can enhance stress tolerance by improving nutrient acquisition, regulating phytohormone signaling, strengthening antioxidant defenses, maintaining osmotic balance, and modulating stress-responsive gene expression. Emerging evidence suggests that these interactions contribute to the establishment of holobiont stress adaptation through biochemical signaling, microenvironmental modification, and epigenetic regulation, enabling plants to respond more effectively to recurrent stress. Advances in microbiome engineering, particularly through the development of synthetic microbial communities (SynComs), offer promising opportunities to restore microbial functions and enhance crop resilience under changing climatic conditions. The integration of multi-omics technologies, artificial intelligence, and precision agriculture is expected to accelerate the development of microbiome-based solutions for sustainable crop production. Collectively, microbiome engineering represents a promising, environmentally sustainable strategy to enhance the holobiont's adaptive resilience and improve long-term plant performance under abiotic stress.},
}
MeSH Terms:
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hide MeSH Terms
*Stress, Physiological
*Plants/microbiology/metabolism
*Microbiota/physiology
Symbiosis
Adaptation, Physiological
RevDate: 2026-10-28
CmpDate: 2026-10-28
Microbiome plasticity during the early life-stage of the angelshark (Squatina squatina) in Las Teresitas (Canary Islands).
PloS one, 21(10):e0361287.
Shark microbiome studies offer acute insights into host health, immunity, and ecological interactions, yet remain poorly studied compared to other marine vertebrates. Shark-associated microbial communities, despite being species-specific, are influenced by environmental conditions and feeding ecology. In this study, we aimed to characterize shifts in the microbiome of the Critically Endangered angelshark (Squatina squatina) during the early stages of development and to assess how environmental factors contribute to the shaping of a specific microbiota. Samples from thirty-nine juvenile angelsharks were collected from Las Teresitas nursery area in the Canary Islands over one year. Skin, oral and cloacal microbiomes were analysed using 16S rRNA gene amplicon sequencing. The sizes of individuals ranged between 24 and 42 cm in length. The shark microbiome was clearly distinct from the surrounding environment, indicating a unique composition from early life stages. Dominant bacteria present in the shark microbiomes included Vibrionaceae (up to 96%), Pseudoalteromonas (up to 63%), Rhodobacteraceae (up to 57%) and Alteromonadaceae (up to 20%). Seawater had a greater influence than sediment on the external skin microbiome, especially in younger individuals. This was not expected due to the burial behaviour of the species. Notably, the abundance of Pseudoalteromonadaceae (assessed by qPCR) was positively correlated with shark growth but was independent of the skin mucus. This suggests a protective role of this phylotype in younger individuals and may help in the adaptation to habitat conditions. This is the first comprehensive microbiome study in angelsharks, highlighting the importance of environmental preservation for microbial integrity and juvenile fitness.
Additional Links: PMID-42949873
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@article {pmid42949873,
year = {2026},
author = {Bañeras, T and Jiménez-Alvarado, D and Toledo-Padilla, H and Camps-Lahora, L and Castro, JJ and Espino-Ruano, A and Guerra-Marrero, A and Couce-Montero, L and Meyers, EKM and Bañeras, L},
title = {Microbiome plasticity during the early life-stage of the angelshark (Squatina squatina) in Las Teresitas (Canary Islands).},
journal = {PloS one},
volume = {21},
number = {10},
pages = {e0361287},
pmid = {42949873},
issn = {1932-6203},
mesh = {Animals ; RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; *Sharks/microbiology/growth & development ; Spain ; *Bacteria/genetics/classification/isolation & purification ; Skin Microbiome ; Phylogeny ; },
abstract = {Shark microbiome studies offer acute insights into host health, immunity, and ecological interactions, yet remain poorly studied compared to other marine vertebrates. Shark-associated microbial communities, despite being species-specific, are influenced by environmental conditions and feeding ecology. In this study, we aimed to characterize shifts in the microbiome of the Critically Endangered angelshark (Squatina squatina) during the early stages of development and to assess how environmental factors contribute to the shaping of a specific microbiota. Samples from thirty-nine juvenile angelsharks were collected from Las Teresitas nursery area in the Canary Islands over one year. Skin, oral and cloacal microbiomes were analysed using 16S rRNA gene amplicon sequencing. The sizes of individuals ranged between 24 and 42 cm in length. The shark microbiome was clearly distinct from the surrounding environment, indicating a unique composition from early life stages. Dominant bacteria present in the shark microbiomes included Vibrionaceae (up to 96%), Pseudoalteromonas (up to 63%), Rhodobacteraceae (up to 57%) and Alteromonadaceae (up to 20%). Seawater had a greater influence than sediment on the external skin microbiome, especially in younger individuals. This was not expected due to the burial behaviour of the species. Notably, the abundance of Pseudoalteromonadaceae (assessed by qPCR) was positively correlated with shark growth but was independent of the skin mucus. This suggests a protective role of this phylotype in younger individuals and may help in the adaptation to habitat conditions. This is the first comprehensive microbiome study in angelsharks, highlighting the importance of environmental preservation for microbial integrity and juvenile fitness.},
}
MeSH Terms:
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Animals
RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
*Sharks/microbiology/growth & development
Spain
*Bacteria/genetics/classification/isolation & purification
Skin Microbiome
Phylogeny
RevDate: 2026-10-28
Multi-omics Integration Reveals L-arginine as a Key Mediator Linking Dietary Protein to Weight Change in Cats: An Exploratory Study.
Journal of animal science pii:9003920 [Epub ahead of print].
Cats exhibit an insufficient endogenous capacity for arginine synthesis, making dietary protein a core factor in nitrogen homeostasis. In this study, we investigated whether protein level-induced body weight change is mediated by host-microbiome interactions and serum metabolites. A 180-day trial was conducted on 30 cats fed three isocaloric diets with varying crude protein levels (LP: 28%, MP: 36%, HP: 46%). Fecal shotgun metagenomic sequencing, serum short-chain fatty acid analysis, untargeted metabolomics, and targeted amino acid profiling were integrated and then subjected to causal mediation analysis. The HP diet improved protein digestibility (HP: 93.29% vs. LP: 89.36%, P = 0.027) and attenuated body weight loss (HP: -3.43% vs. -14.52%, P = 0.031) without compromising fecal scores (all groups: 2.5-3.0 throughout the trial) or intestinal barrier integrity, as indicated by unchanged serum DAO, D-LA, and LPS levels. The MP group significantly enhanced humoral immunity, as evidenced by higher serum IgA, IgG, and IgM concentrations (P < 0.05 vs. LP and HP), while the HP group boosted antioxidant capacity, with significantly increased SOD and T-AOC activities (P < 0.05 vs. LP and MP). High protein increased the abundance of Phocaeicola and decreased that of Megasphaera. Serum arginine biosynthesis pathways and branched-chain amino acids were significantly enriched in MP and HP groups compared with the LP group (P < 0.05 for both comparisons). Crucially, multi-omics network and causal mediation analysis identified L-arginine as a statistically confirmed key regulatory node in the protein-weight relationship, as evidenced by a significant indirect effect (ACME = 0.208, P = 0.006) and a non-significant direct effect (ADE = 0.31, P = 0.23). These results suggested that L-arginine may serve as a key regulatory node mediating this process linking dietary protein to body weight in cats, providing a novel mechanistic target for precision nutritional interventions in feline weight management.
Additional Links: PMID-42949890
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@article {pmid42949890,
year = {2026},
author = {Wang, H and Chang, X and Han, S and Guo, J and Xia, Z and Xiong, W},
title = {Multi-omics Integration Reveals L-arginine as a Key Mediator Linking Dietary Protein to Weight Change in Cats: An Exploratory Study.},
journal = {Journal of animal science},
volume = {},
number = {},
pages = {},
doi = {10.1093/jas/skag287},
pmid = {42949890},
issn = {1525-3163},
abstract = {Cats exhibit an insufficient endogenous capacity for arginine synthesis, making dietary protein a core factor in nitrogen homeostasis. In this study, we investigated whether protein level-induced body weight change is mediated by host-microbiome interactions and serum metabolites. A 180-day trial was conducted on 30 cats fed three isocaloric diets with varying crude protein levels (LP: 28%, MP: 36%, HP: 46%). Fecal shotgun metagenomic sequencing, serum short-chain fatty acid analysis, untargeted metabolomics, and targeted amino acid profiling were integrated and then subjected to causal mediation analysis. The HP diet improved protein digestibility (HP: 93.29% vs. LP: 89.36%, P = 0.027) and attenuated body weight loss (HP: -3.43% vs. -14.52%, P = 0.031) without compromising fecal scores (all groups: 2.5-3.0 throughout the trial) or intestinal barrier integrity, as indicated by unchanged serum DAO, D-LA, and LPS levels. The MP group significantly enhanced humoral immunity, as evidenced by higher serum IgA, IgG, and IgM concentrations (P < 0.05 vs. LP and HP), while the HP group boosted antioxidant capacity, with significantly increased SOD and T-AOC activities (P < 0.05 vs. LP and MP). High protein increased the abundance of Phocaeicola and decreased that of Megasphaera. Serum arginine biosynthesis pathways and branched-chain amino acids were significantly enriched in MP and HP groups compared with the LP group (P < 0.05 for both comparisons). Crucially, multi-omics network and causal mediation analysis identified L-arginine as a statistically confirmed key regulatory node in the protein-weight relationship, as evidenced by a significant indirect effect (ACME = 0.208, P = 0.006) and a non-significant direct effect (ADE = 0.31, P = 0.23). These results suggested that L-arginine may serve as a key regulatory node mediating this process linking dietary protein to body weight in cats, providing a novel mechanistic target for precision nutritional interventions in feline weight management.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
Wdr82-COMPASS coordinates Foxp3 and TCR signaling to sustain Treg cell control of microbiota-driven intestinal inflammation.
Science advances, 12(44):eaeh9188.
Regulatory T cells (Treg cells) maintain immune tolerance, but how broadly acting epigenetic pathways are selectively used by Treg cells versus conventional T cells (Tconv cells) remains unclear. Here, we identify the COMPASS-trimethylation of histone H3 lysine 4 (H3K4me3) pathway, through its Wdr82 component, as a key epigenetic regulator that preferentially supports Treg cell development and function. Although Wdr82 deficiency broadly impairs T cell activation, T cell-specific deletion paradoxically causes progressive, microbiota-dependent intestinal inflammation and expansion of inflammatory Tconv cell programs. This pathology is prevented by microbiome depletion or transfer of wild-type Treg cells, indicating a primary defect in Treg cell-mediated tolerance. Mechanistically, Wdr82/COMPASS promotes Foxp3 induction, maintains H3K4me3 and chromatin accessibility at Treg cell-associated genes, and restrains effector programs within the Treg cell lineage. Foxp3 coordinates with COMPASS components in a T cell receptor/costimulation-dependent manner, linking antigen receptor signaling to chromatin regulation. Together, these findings reveal selective integration of a broadly active epigenetic pathway into the Foxp3-centered regulatory hierarchy that sustains Treg cell control of microbiota-driven intestinal inflammation.
Additional Links: PMID-42950054
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Citation:
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@article {pmid42950054,
year = {2026},
author = {Huang, W and Li, J and He, M and Xu, B and Rosikiewicz, W and Hao, X and Jiang, M and Bai, L and Zhang, S and Li, L and Qi, W and Choudhary, V and Jheng, MJ and Chang, TC and Janke, LJ and Pruett-Miller, SM and Kodali, K and Yuan, ZF and High, AA and Jin, H and Li, C and Feng, Y},
title = {Wdr82-COMPASS coordinates Foxp3 and TCR signaling to sustain Treg cell control of microbiota-driven intestinal inflammation.},
journal = {Science advances},
volume = {12},
number = {44},
pages = {eaeh9188},
pmid = {42950054},
issn = {2375-2548},
mesh = {*T-Lymphocytes, Regulatory/immunology/metabolism ; *Forkhead Transcription Factors/metabolism/genetics ; Animals ; *Signal Transduction ; Mice ; *Receptors, Antigen, T-Cell/metabolism ; Histones/metabolism ; Epigenesis, Genetic ; Lymphocyte Activation ; *Inflammation/metabolism/immunology ; Intestines/immunology/microbiology ; Mice, Knockout ; *Gastrointestinal Microbiome/immunology ; },
abstract = {Regulatory T cells (Treg cells) maintain immune tolerance, but how broadly acting epigenetic pathways are selectively used by Treg cells versus conventional T cells (Tconv cells) remains unclear. Here, we identify the COMPASS-trimethylation of histone H3 lysine 4 (H3K4me3) pathway, through its Wdr82 component, as a key epigenetic regulator that preferentially supports Treg cell development and function. Although Wdr82 deficiency broadly impairs T cell activation, T cell-specific deletion paradoxically causes progressive, microbiota-dependent intestinal inflammation and expansion of inflammatory Tconv cell programs. This pathology is prevented by microbiome depletion or transfer of wild-type Treg cells, indicating a primary defect in Treg cell-mediated tolerance. Mechanistically, Wdr82/COMPASS promotes Foxp3 induction, maintains H3K4me3 and chromatin accessibility at Treg cell-associated genes, and restrains effector programs within the Treg cell lineage. Foxp3 coordinates with COMPASS components in a T cell receptor/costimulation-dependent manner, linking antigen receptor signaling to chromatin regulation. Together, these findings reveal selective integration of a broadly active epigenetic pathway into the Foxp3-centered regulatory hierarchy that sustains Treg cell control of microbiota-driven intestinal inflammation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*T-Lymphocytes, Regulatory/immunology/metabolism
*Forkhead Transcription Factors/metabolism/genetics
Animals
*Signal Transduction
Mice
*Receptors, Antigen, T-Cell/metabolism
Histones/metabolism
Epigenesis, Genetic
Lymphocyte Activation
*Inflammation/metabolism/immunology
Intestines/immunology/microbiology
Mice, Knockout
*Gastrointestinal Microbiome/immunology
RevDate: 2026-10-28
Gut bacterial-derived beneficial proteins in intestinal disease.
Microbiological research, 315:128794 pii:S0944-5013(26)00358-7 [Epub ahead of print].
The human gut microbiota is a vast and intricate microbial ecosystem that plays indispensable roles in host physiology, including nutritional metabolism, immune system development, and disease prevention. While current research has extensively focused on microbiota-derived small-molecule metabolites and virulence-associated factors, the functional contribution of gut bacteria-derived proteins remains comparatively underexplored. These proteins are emerging as key molecular mediators of host-microbe and microbe-microbe interactions. In this review, we synthesize current evidence to delineate the potential links between the spatial distribution, sources and ecological niches of gut microbiota and the repertoire of proteins they produce. We systematically categorize the functions and mechanisms of diverse bacterial-derived beneficial proteins, including enzymes, surface-associated proteins, outer membrane vesicle-associated proteins, and secreted effectors, highlighting their critical roles in antimicrobial defense, metabolic homeostasis, immune modulation, and antitumor activity from multiple perspectives. Particular emphasis is also placed on their distinct molecular strategies in mediating host interactions. Collectively, this analysis underscores the translational potential of gut microbiota-derived proteins, pointing toward innovative applications in the rational design of next-generation postbiotics, engineered bacterial proteins, and potential microbiome-based biologic therapeutics.
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@article {pmid42950485,
year = {2026},
author = {Zhou, S and Tian, Q and Ullah, S and Su, D and Geng, J and Zhang, M},
title = {Gut bacterial-derived beneficial proteins in intestinal disease.},
journal = {Microbiological research},
volume = {315},
number = {},
pages = {128794},
doi = {10.1016/j.micres.2026.128794},
pmid = {42950485},
issn = {1618-0623},
abstract = {The human gut microbiota is a vast and intricate microbial ecosystem that plays indispensable roles in host physiology, including nutritional metabolism, immune system development, and disease prevention. While current research has extensively focused on microbiota-derived small-molecule metabolites and virulence-associated factors, the functional contribution of gut bacteria-derived proteins remains comparatively underexplored. These proteins are emerging as key molecular mediators of host-microbe and microbe-microbe interactions. In this review, we synthesize current evidence to delineate the potential links between the spatial distribution, sources and ecological niches of gut microbiota and the repertoire of proteins they produce. We systematically categorize the functions and mechanisms of diverse bacterial-derived beneficial proteins, including enzymes, surface-associated proteins, outer membrane vesicle-associated proteins, and secreted effectors, highlighting their critical roles in antimicrobial defense, metabolic homeostasis, immune modulation, and antitumor activity from multiple perspectives. Particular emphasis is also placed on their distinct molecular strategies in mediating host interactions. Collectively, this analysis underscores the translational potential of gut microbiota-derived proteins, pointing toward innovative applications in the rational design of next-generation postbiotics, engineered bacterial proteins, and potential microbiome-based biologic therapeutics.},
}
RevDate: 2026-10-28
NLRP3 inflammasome dysregulation in chronic bacterial infections: mechanistic insights into treatment failure and relapse.
Human immunology, 87(12):112105 pii:S0198-8859(26)00451-9 [Epub ahead of print].
Chronic and recurrent bacterial infections are a significant clinical issue despite the development of antimicrobial treatment. It is increasingly being shown that chronic host-based inflammatory dysregulation is also an integral cause of treatment failure and persistence of illness, and not just the consequence of microbial resistance. The NLRP3 inflammasome presents an important integrated platform linking tissue destruction, metabolic strain, and microbial detection to augmented inflammatory reactions. The ultimate goal of the review is to assess chronic bacterial infection as an inflammatory resolution dysfunction, and the example of persistent NLRP3 inflammasome dysregulation and the therapeutic consequences. In this review, the existing data on the canonical and non-canonical pathways of NLRP3 activation is summarized and the interplay between metabolic reprogramming, ionic flux, mitochondrial dysfunction, and impaired autophagy are all thought to contribute to the lowered activation thresholds in chronic infection. The disease-specific pathology of the prolonged IL-1β and IL-18 generation, destabilisation of the barricade and inflammatory feedback prolongation are common pathological themes in contexts like granulomatous lung disease, intracellular persistence syndromes, biofilm-associated infections and chronic airway colonisation. Inflammasome permissiveness and resolution are exacerbated by immunometabolic changes and microbiome imbalance.
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@article {pmid42950595,
year = {2026},
author = {Girdhar, J and Jangra, S and Rastogi, A and Saxena, R},
title = {NLRP3 inflammasome dysregulation in chronic bacterial infections: mechanistic insights into treatment failure and relapse.},
journal = {Human immunology},
volume = {87},
number = {12},
pages = {112105},
doi = {10.1016/j.humimm.2026.112105},
pmid = {42950595},
issn = {1879-1166},
abstract = {Chronic and recurrent bacterial infections are a significant clinical issue despite the development of antimicrobial treatment. It is increasingly being shown that chronic host-based inflammatory dysregulation is also an integral cause of treatment failure and persistence of illness, and not just the consequence of microbial resistance. The NLRP3 inflammasome presents an important integrated platform linking tissue destruction, metabolic strain, and microbial detection to augmented inflammatory reactions. The ultimate goal of the review is to assess chronic bacterial infection as an inflammatory resolution dysfunction, and the example of persistent NLRP3 inflammasome dysregulation and the therapeutic consequences. In this review, the existing data on the canonical and non-canonical pathways of NLRP3 activation is summarized and the interplay between metabolic reprogramming, ionic flux, mitochondrial dysfunction, and impaired autophagy are all thought to contribute to the lowered activation thresholds in chronic infection. The disease-specific pathology of the prolonged IL-1β and IL-18 generation, destabilisation of the barricade and inflammatory feedback prolongation are common pathological themes in contexts like granulomatous lung disease, intracellular persistence syndromes, biofilm-associated infections and chronic airway colonisation. Inflammasome permissiveness and resolution are exacerbated by immunometabolic changes and microbiome imbalance.},
}
RevDate: 2026-10-28
Divergent aging patterns of polylactic acid (PLA) and polyvinyl chloride (PVC) plastic sheets and their differential associations with soil carbon stability.
Journal of hazardous materials, 518:144021 pii:S0304-3894(26)03002-5 [Epub ahead of print].
Plastic pollution is a growing concern. Plastic particles undergo aging that changes their properties and ecological impacts, yet how different polymers age in natural settings and relate to soil carbon cycling remains unclear. We conducted a nine-month in situ experiment to compare the aging of biodegradable PLA (polylactic acid) and conventional PVC (polyvinyl chloride) sheets and to assess their associations with soil microbial communities, enzymes, and organic carbon fractions. PLA surfaces developed hydrolysis‑induced cracks and fragmentation, whereas PVC showed oxidative roughening. These aging patterns were associated with divergent functional potential of plastisphere microbial communities. PLA‑associated soils had higher β-glucosidase and peroxidase activities, together with a trend toward higher labile carbon (FPOC) indicators than PVC‑associated soils. Mineral‑associated organic carbon (MAOC) did not differ between treatments, but MAOC proportion was negatively correlated with bulk density only under PLA. Because our study lacked an unamended control, our conclusions are limited to PLA-PVC comparisons. Our findings show that the two polymers differ in aging pathways, microbial associations, and associations with labile carbon turnover that vary with soil physical properties, suggesting that the environmental implications of biodegradable plastics cannot be assumed from their label alone.
Additional Links: PMID-42950662
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@article {pmid42950662,
year = {2026},
author = {Zhang, Y and Li, C and Wang, Y and Yan, S and Zhang, X and Xu, J and Ren, K and Liu, J},
title = {Divergent aging patterns of polylactic acid (PLA) and polyvinyl chloride (PVC) plastic sheets and their differential associations with soil carbon stability.},
journal = {Journal of hazardous materials},
volume = {518},
number = {},
pages = {144021},
doi = {10.1016/j.jhazmat.2026.144021},
pmid = {42950662},
issn = {1873-3336},
abstract = {Plastic pollution is a growing concern. Plastic particles undergo aging that changes their properties and ecological impacts, yet how different polymers age in natural settings and relate to soil carbon cycling remains unclear. We conducted a nine-month in situ experiment to compare the aging of biodegradable PLA (polylactic acid) and conventional PVC (polyvinyl chloride) sheets and to assess their associations with soil microbial communities, enzymes, and organic carbon fractions. PLA surfaces developed hydrolysis‑induced cracks and fragmentation, whereas PVC showed oxidative roughening. These aging patterns were associated with divergent functional potential of plastisphere microbial communities. PLA‑associated soils had higher β-glucosidase and peroxidase activities, together with a trend toward higher labile carbon (FPOC) indicators than PVC‑associated soils. Mineral‑associated organic carbon (MAOC) did not differ between treatments, but MAOC proportion was negatively correlated with bulk density only under PLA. Because our study lacked an unamended control, our conclusions are limited to PLA-PVC comparisons. Our findings show that the two polymers differ in aging pathways, microbial associations, and associations with labile carbon turnover that vary with soil physical properties, suggesting that the environmental implications of biodegradable plastics cannot be assumed from their label alone.},
}
RevDate: 2026-10-28
Diet quality, gut microbiome diversity, and clinical disability in multiple sclerosis: A cross-sectional case-control study.
Multiple sclerosis and related disorders, 116:108007 pii:S2211-0348(26)01042-4 [Epub ahead of print].
Dietary patterns and gut microbiome composition are increasingly recognised as modifiable factors in multiple sclerosis (MS). We aimed to evaluate dietary quality, microbiome diversity, and their inter-relationships with MS status, clinical disability, and disease-modifying therapy (DMT). We compared 288 MS cases with 274 household healthy controls (HHC). Dietary intake was assessed using healthy eating index (HEI-2015), and the groups were compared and associations analysed using multivariable linear regression. Among all HEI-2015 components, only total fruit intake was significantly higher in MS (β=+0.46; 95% CI: +0.19 to +0.74; FDR q = 0.014). Higher HEI-2015 scores were positively associated with greater Shannon alpha diversity (β=+0.077/10-unit increment; 95% CI: +0.003 to +0.150; p = 0.042). The PERMANOVA revealed independent association between microbiome beta diversity and smoking (R[2]=0.011; p = 0.007), BMI (R[2]=0.007; p = 0.010), age (R[2]=0.006; p = 0.027), and MS status (R[2]=0.005; p = 0.026), but not with diet quality (R[2]=0.006; p = 0.171). The whole grains consumption was directly associated with EDSS (FDR q = 0.033). Microbial richness differed across DMT categories (p = 0.001), and mechanism-level analysis attributed this to natalizumab, anti-CD20 therapy and dimethyl fumarate. In conclusion, higher fruit intake and dietary quality positively were related to gut microbiome diversity in MS. Disease status, smoking, and BMI are the primary drivers of microbiome community composition. Therefore, dietary modification could be a potential adjunctive strategy in MS management.
Additional Links: PMID-42950771
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PubMed:
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@article {pmid42950771,
year = {2026},
author = {Ahmed, AM and Shaheen, EF and Mohamed, MT and Gaafar, AM and Farghal, M and Mazibrada, G},
title = {Diet quality, gut microbiome diversity, and clinical disability in multiple sclerosis: A cross-sectional case-control study.},
journal = {Multiple sclerosis and related disorders},
volume = {116},
number = {},
pages = {108007},
doi = {10.1016/j.msard.2026.108007},
pmid = {42950771},
issn = {2211-0356},
abstract = {Dietary patterns and gut microbiome composition are increasingly recognised as modifiable factors in multiple sclerosis (MS). We aimed to evaluate dietary quality, microbiome diversity, and their inter-relationships with MS status, clinical disability, and disease-modifying therapy (DMT). We compared 288 MS cases with 274 household healthy controls (HHC). Dietary intake was assessed using healthy eating index (HEI-2015), and the groups were compared and associations analysed using multivariable linear regression. Among all HEI-2015 components, only total fruit intake was significantly higher in MS (β=+0.46; 95% CI: +0.19 to +0.74; FDR q = 0.014). Higher HEI-2015 scores were positively associated with greater Shannon alpha diversity (β=+0.077/10-unit increment; 95% CI: +0.003 to +0.150; p = 0.042). The PERMANOVA revealed independent association between microbiome beta diversity and smoking (R[2]=0.011; p = 0.007), BMI (R[2]=0.007; p = 0.010), age (R[2]=0.006; p = 0.027), and MS status (R[2]=0.005; p = 0.026), but not with diet quality (R[2]=0.006; p = 0.171). The whole grains consumption was directly associated with EDSS (FDR q = 0.033). Microbial richness differed across DMT categories (p = 0.001), and mechanism-level analysis attributed this to natalizumab, anti-CD20 therapy and dimethyl fumarate. In conclusion, higher fruit intake and dietary quality positively were related to gut microbiome diversity in MS. Disease status, smoking, and BMI are the primary drivers of microbiome community composition. Therefore, dietary modification could be a potential adjunctive strategy in MS management.},
}
RevDate: 2026-10-28
Dermatitis and Corynebacterium bovis infection in athymic nude rats (Rattus norvegicus).
Journal of comparative pathology, 231:1-9 pii:S0021-9975(26)00123-4 [Epub ahead of print].
Corynebacterium bovis (Cb) is a bacterium that causes a flaking dermatitis characterized histologically by orthokeratosis, acanthosis, intracorneal bacterial colonies and variable dermal inflammation in immunodeficient mice. Although Cb has been shown to establish dermal colonization in rats, its impact on the skin of immunodeficient rats remains poorly defined. This case series characterizes cutaneous lesions in 22 naïve or experimentally manipulated NIH-Fox1[rnu] (nude) rats and evaluates the association between Cb infection and dermatitis over a 5-year period. Histologically, all rats had orthokeratosis and dermatitis/folliculitis, 21/22 had acanthosis, 15/22 had bacterial presence and 9/22 had transepidermal/transfollicular keratinocyte apoptosis. Additional variable findings included furunculosis, pustules, dermal oedema and perivascular dermatitis. Inflammatory infiltrates consisted of CD3-positive lymphocytes and Iba1-positive macrophages located predominantly at the dermoepidermal junction. Corynebacterium bovis was isolated from the skin of 15/22 affected rats, and in-situ hybridization confirmed intracorneal/intrafollicular colonies of Cb in 3/11 rats examined. Nude rats also developed cutaneous lesions that corresponded histologically with a lymphocytic dermatitis, the distribution of which was often independent of Cb colonies. This study documents the first spontaneous Cb infection with dermatitis in nude rats. The frequent isolation of Cb from the skin raises the question of whether alterations in the cutaneous microbiome of nude rats may contribute to the immune modulation of dermatitis, warranting further investigation.
Additional Links: PMID-42950774
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PubMed:
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@article {pmid42950774,
year = {2026},
author = {Mammone, RM and Lipman, NS and Ricart, RJ and Carrasco, SE and Ruivo, PR and Miranda, IC},
title = {Dermatitis and Corynebacterium bovis infection in athymic nude rats (Rattus norvegicus).},
journal = {Journal of comparative pathology},
volume = {231},
number = {},
pages = {1-9},
doi = {10.1016/j.jcpa.2026.10.004},
pmid = {42950774},
issn = {1532-3129},
abstract = {Corynebacterium bovis (Cb) is a bacterium that causes a flaking dermatitis characterized histologically by orthokeratosis, acanthosis, intracorneal bacterial colonies and variable dermal inflammation in immunodeficient mice. Although Cb has been shown to establish dermal colonization in rats, its impact on the skin of immunodeficient rats remains poorly defined. This case series characterizes cutaneous lesions in 22 naïve or experimentally manipulated NIH-Fox1[rnu] (nude) rats and evaluates the association between Cb infection and dermatitis over a 5-year period. Histologically, all rats had orthokeratosis and dermatitis/folliculitis, 21/22 had acanthosis, 15/22 had bacterial presence and 9/22 had transepidermal/transfollicular keratinocyte apoptosis. Additional variable findings included furunculosis, pustules, dermal oedema and perivascular dermatitis. Inflammatory infiltrates consisted of CD3-positive lymphocytes and Iba1-positive macrophages located predominantly at the dermoepidermal junction. Corynebacterium bovis was isolated from the skin of 15/22 affected rats, and in-situ hybridization confirmed intracorneal/intrafollicular colonies of Cb in 3/11 rats examined. Nude rats also developed cutaneous lesions that corresponded histologically with a lymphocytic dermatitis, the distribution of which was often independent of Cb colonies. This study documents the first spontaneous Cb infection with dermatitis in nude rats. The frequent isolation of Cb from the skin raises the question of whether alterations in the cutaneous microbiome of nude rats may contribute to the immune modulation of dermatitis, warranting further investigation.},
}
RevDate: 2026-10-28
Role of probiotics in neonatal care: From molecular mechanisms to clinical practice.
Clinical nutrition ESPEN pii:S2405-4577(26)02312-0 [Epub ahead of print].
Premature births remain a significant global health concern, contributing to high mortality rates among children under five. Preterm newborns (<37 weeks' gestation) encounter considerable health issues due to their underdeveloped organ systems and gut microbiota. These vulnerabilities result in major complications, including necrotizing enterocolitis, sepsis, and feeding intolerance, leading to higher rates of morbidity and mortality, particularly in very preterm infants. In this context, probiotic supplementation has emerged as a widely studied intervention to restore gut homeostasis. This review summarises the therapeutic potential of probiotic strains of the Lactobacillus, Bifidobacterium, and Saccharomyces genera, along with their distinct molecular mechanisms of action, including competitive pathogen exclusion, reinforcement of the intestinal epithelial barrier, and immunomodulation. However, despite promising evidence, a critical research-to-practice gap exists due to concerns regarding the safety, strain specificity, dosage and the lack of standardized dosing guidelines. Furthermore, administration of live microbial strains to critically ill neonates carry inherent safety risks. This review aims to provide a thorough and even-handed approach on the role of probiotics in preventing preterm complications and evaluate the evolving global safety guidelines, emphasizing the urgent need for standardized, strain-specific clinical protocols to ensure their safe and effective integration in neonatal intensive care.
Additional Links: PMID-42951109
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PubMed:
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@article {pmid42951109,
year = {2026},
author = {Thakur, S and Ranot, P and Chauhan, K and Thakur, S and Bala, M},
title = {Role of probiotics in neonatal care: From molecular mechanisms to clinical practice.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105215},
doi = {10.1016/j.clnesp.2026.105215},
pmid = {42951109},
issn = {2405-4577},
abstract = {Premature births remain a significant global health concern, contributing to high mortality rates among children under five. Preterm newborns (<37 weeks' gestation) encounter considerable health issues due to their underdeveloped organ systems and gut microbiota. These vulnerabilities result in major complications, including necrotizing enterocolitis, sepsis, and feeding intolerance, leading to higher rates of morbidity and mortality, particularly in very preterm infants. In this context, probiotic supplementation has emerged as a widely studied intervention to restore gut homeostasis. This review summarises the therapeutic potential of probiotic strains of the Lactobacillus, Bifidobacterium, and Saccharomyces genera, along with their distinct molecular mechanisms of action, including competitive pathogen exclusion, reinforcement of the intestinal epithelial barrier, and immunomodulation. However, despite promising evidence, a critical research-to-practice gap exists due to concerns regarding the safety, strain specificity, dosage and the lack of standardized dosing guidelines. Furthermore, administration of live microbial strains to critically ill neonates carry inherent safety risks. This review aims to provide a thorough and even-handed approach on the role of probiotics in preventing preterm complications and evaluate the evolving global safety guidelines, emphasizing the urgent need for standardized, strain-specific clinical protocols to ensure their safe and effective integration in neonatal intensive care.},
}
RevDate: 2026-10-28
Bacteroidota-derived glycine lipids differentially regulate skeletal muscle mitochondrial adaptation during Western diet feeding in male Ldlr[-/-] mice.
The Journal of physiology [Epub ahead of print].
The Western diet (WD) is associated with skeletal muscle mitochondrial dysfunction, impaired oxidative metabolism, redox imbalance and inflammation. Emerging evidence suggests that gut microbiome-derived metabolites contribute to host metabolic regulation, yet the role of Bacteroidota-derived glycine lipids in skeletal muscle remains unknown. This study tested whether two structurally related bacterial glycine lipids, lipid 654 (L654) and lipid 1256 (L1256), regulate skeletal muscle mitochondrial remodelling in WD-fed Ldlr[-/-] mice. Male Ldlr[-/-] mice were fed a normal chow or WD and administered L654, L1256 or vehicle control for 8 weeks. Skeletal muscle glycine lipid accumulation, mitochondrial respiration, mitochondrial biogenesis markers, mitophagy-associated signalling, inflammatory and antioxidant proteins and muscle fibre cross-sectional area were assessed. L1256, but not L654, accumulated in skeletal muscle. Functionally, L1256 selectively enhanced fatty acid-supported mitochondrial respiration and increased respiratory control ratio. L1256 also increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), mitochondrial transcription factor A (TFAM) and electron transport chain complexes IV and V, suggesting enhanced oxidative mitochondrial remodelling. In parallel, L1256 altered markers associated with mitochondrial quality control signalling, increased nuclear factor erythroid 2-related factor 2 (Nrf2), manganese superoxide dismutase (MnSOD) and glutathione peroxidase 4 (GPX4), suppressed nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling and preserved muscle fibre cross-sectional area. L654 upregulated mitochondrial biogenesis transcripts without altering protein abundance. These findings identify L1256 as a microbiome-derived lipid retained within skeletal muscle that enhanced oxidative metabolism and preserved mitochondrial quality signalling under metabolic stress. The data suggest that tissue retention of bacterial lipids may be an important determinant of skeletal muscle mitochondrial adaptation. KEY POINTS: Western diet contributes to skeletal muscle mitochondrial dysfunction, impaired oxidative metabolism and chronic inflammation. Microbiome-derived glycine lipids are bioactive molecules from Bacteroidota species, but their effects on skeletal muscle mitochondrial metabolism remain poorly understood. Bacteroidota-derived glycine lipids produce distinct skeletal muscle responses in Western diet-fed Ldlr[-] [/] [-] mice, where lipid 1256 accumulated in skeletal muscle and enhanced fatty acid-supported respiration, whereas lipid 654 primarily induced transcriptional responses without detectable tissue accumulation. Lipid 1256 increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), mitochondrial transcription factor A (TFAM) and complexes IV and V of the electron transport chain together with restoration of Parkin, nuclear factor erythroid 2-related factor 2 (Nrf2), manganese superoxide dismutase (MnSOD) and glutathione peroxidase 4 (GPX4) while reducing nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and interleukin 6 (IL-6) expression and preserving skeletal muscle cross-sectional area. These findings suggest that gut microbiome-derived glycine lipids are regulators of skeletal muscle mitochondrial metabolism, and that tissue retention of bacterial lipids influences mitochondrial oxidative remodelling during metabolic stress.
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@article {pmid42951697,
year = {2026},
author = {Kim, S and Noh, SG and Ji, M and Vence, T and Gao, L and Otoko, O and Nichols, FC and Blesso, CN and Kwon, OS},
title = {Bacteroidota-derived glycine lipids differentially regulate skeletal muscle mitochondrial adaptation during Western diet feeding in male Ldlr[-/-] mice.},
journal = {The Journal of physiology},
volume = {},
number = {},
pages = {},
doi = {10.1113/JP291898},
pmid = {42951697},
issn = {1469-7793},
support = {//University of Connecticut/ ; },
abstract = {The Western diet (WD) is associated with skeletal muscle mitochondrial dysfunction, impaired oxidative metabolism, redox imbalance and inflammation. Emerging evidence suggests that gut microbiome-derived metabolites contribute to host metabolic regulation, yet the role of Bacteroidota-derived glycine lipids in skeletal muscle remains unknown. This study tested whether two structurally related bacterial glycine lipids, lipid 654 (L654) and lipid 1256 (L1256), regulate skeletal muscle mitochondrial remodelling in WD-fed Ldlr[-/-] mice. Male Ldlr[-/-] mice were fed a normal chow or WD and administered L654, L1256 or vehicle control for 8 weeks. Skeletal muscle glycine lipid accumulation, mitochondrial respiration, mitochondrial biogenesis markers, mitophagy-associated signalling, inflammatory and antioxidant proteins and muscle fibre cross-sectional area were assessed. L1256, but not L654, accumulated in skeletal muscle. Functionally, L1256 selectively enhanced fatty acid-supported mitochondrial respiration and increased respiratory control ratio. L1256 also increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), mitochondrial transcription factor A (TFAM) and electron transport chain complexes IV and V, suggesting enhanced oxidative mitochondrial remodelling. In parallel, L1256 altered markers associated with mitochondrial quality control signalling, increased nuclear factor erythroid 2-related factor 2 (Nrf2), manganese superoxide dismutase (MnSOD) and glutathione peroxidase 4 (GPX4), suppressed nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling and preserved muscle fibre cross-sectional area. L654 upregulated mitochondrial biogenesis transcripts without altering protein abundance. These findings identify L1256 as a microbiome-derived lipid retained within skeletal muscle that enhanced oxidative metabolism and preserved mitochondrial quality signalling under metabolic stress. The data suggest that tissue retention of bacterial lipids may be an important determinant of skeletal muscle mitochondrial adaptation. KEY POINTS: Western diet contributes to skeletal muscle mitochondrial dysfunction, impaired oxidative metabolism and chronic inflammation. Microbiome-derived glycine lipids are bioactive molecules from Bacteroidota species, but their effects on skeletal muscle mitochondrial metabolism remain poorly understood. Bacteroidota-derived glycine lipids produce distinct skeletal muscle responses in Western diet-fed Ldlr[-] [/] [-] mice, where lipid 1256 accumulated in skeletal muscle and enhanced fatty acid-supported respiration, whereas lipid 654 primarily induced transcriptional responses without detectable tissue accumulation. Lipid 1256 increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), mitochondrial transcription factor A (TFAM) and complexes IV and V of the electron transport chain together with restoration of Parkin, nuclear factor erythroid 2-related factor 2 (Nrf2), manganese superoxide dismutase (MnSOD) and glutathione peroxidase 4 (GPX4) while reducing nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and interleukin 6 (IL-6) expression and preserving skeletal muscle cross-sectional area. These findings suggest that gut microbiome-derived glycine lipids are regulators of skeletal muscle mitochondrial metabolism, and that tissue retention of bacterial lipids influences mitochondrial oxidative remodelling during metabolic stress.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-29
Adaptive immune plasticity in MASH: Functional states, pathological consequences, and regulatory mechanisms.
Hepatology communications, 10(11):.
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease driven by both metabolic stress and immune dysregulation. A growing body of evidence suggests that adaptive immune cells exhibit significant functional plasticity during the progression and resolution of MASH. CD8+ T cells can assume various states, including pathogenic cytotoxicity, functional exhaustion, and tissue repair; CD4+ T cells exhibit enhanced Th1/Th17 programming, reduced Treg stability, and a functional shift toward Th17/Treg; and B cells undergo remodeling between regulatory, pro-inflammatory, and antibody-effect states. These functional states determine disease outcomes through distinct effector mechanisms. The cytotoxicity and inflammatory factors of pathogenic T cells promote hepatocyte damage, metabolic dysregulation, and hepatocyte stellate cell activation, while B-cell antigen presentation, cytokine, and antibody responses further amplify inflammation and fibrosis; conversely, Tregs, Bregs, and tissue-resident CD8+ T cells with reparative functions can limit inflammation or promote the resolution of fibrosis. Adaptive immune plasticity is, in turn, continuously shaped by the hepatic metabolic environment, in which glycolipid and mitochondrial metabolic reprogramming determine the metabolic basis of different functional states, while metabolite-driven epigenetic remodeling stabilizes corresponding transcriptional programs. Microbiome components and metabolic signals originating from the gut-liver axis further regulate the state of T and B cells within the liver. Consequently, the functional states of adaptive immune cells, their pathological effects, and their metabolic regulation collectively constitute a critical immunometabolic network linking metabolic dysregulation, chronic inflammation, and the progression of fibrosis, providing a unified mechanistic framework for understanding the sustained progression of MASH and tissue repair.
Additional Links: PMID-42951872
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@article {pmid42951872,
year = {2026},
author = {Yu, X and Yang, Y and Bai, L},
title = {Adaptive immune plasticity in MASH: Functional states, pathological consequences, and regulatory mechanisms.},
journal = {Hepatology communications},
volume = {10},
number = {11},
pages = {},
pmid = {42951872},
issn = {2471-254X},
mesh = {Humans ; *Adaptive Immunity ; Animals ; Cell Plasticity/immunology ; *Fatty Liver/immunology ; Liver/immunology/pathology/metabolism ; B-Lymphocytes/immunology ; },
abstract = {Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease driven by both metabolic stress and immune dysregulation. A growing body of evidence suggests that adaptive immune cells exhibit significant functional plasticity during the progression and resolution of MASH. CD8+ T cells can assume various states, including pathogenic cytotoxicity, functional exhaustion, and tissue repair; CD4+ T cells exhibit enhanced Th1/Th17 programming, reduced Treg stability, and a functional shift toward Th17/Treg; and B cells undergo remodeling between regulatory, pro-inflammatory, and antibody-effect states. These functional states determine disease outcomes through distinct effector mechanisms. The cytotoxicity and inflammatory factors of pathogenic T cells promote hepatocyte damage, metabolic dysregulation, and hepatocyte stellate cell activation, while B-cell antigen presentation, cytokine, and antibody responses further amplify inflammation and fibrosis; conversely, Tregs, Bregs, and tissue-resident CD8+ T cells with reparative functions can limit inflammation or promote the resolution of fibrosis. Adaptive immune plasticity is, in turn, continuously shaped by the hepatic metabolic environment, in which glycolipid and mitochondrial metabolic reprogramming determine the metabolic basis of different functional states, while metabolite-driven epigenetic remodeling stabilizes corresponding transcriptional programs. Microbiome components and metabolic signals originating from the gut-liver axis further regulate the state of T and B cells within the liver. Consequently, the functional states of adaptive immune cells, their pathological effects, and their metabolic regulation collectively constitute a critical immunometabolic network linking metabolic dysregulation, chronic inflammation, and the progression of fibrosis, providing a unified mechanistic framework for understanding the sustained progression of MASH and tissue repair.},
}
MeSH Terms:
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Humans
*Adaptive Immunity
Animals
Cell Plasticity/immunology
*Fatty Liver/immunology
Liver/immunology/pathology/metabolism
B-Lymphocytes/immunology
RevDate: 2026-10-29
CmpDate: 2026-10-29
Statistical inference of keystone taxa reshaping the assembly rules of forest root microbiomes.
Nature communications, 17(1):.
Root-associated fungi and bacteria play pivotal roles in terrestrial ecosystem processes. However, identifying keystone taxa driving below-ground microbial assembly remains a major challenge. Here, we present a statistical framework for identifying microbes that reorganize microbiome assembly. Using 1,270 root samples collected from a cool-temperate forest in Japan, we reconstruct assembly landscapes describing the probabilistic structure of community states. We then find that several endophytic fungi (e.g., Phialocephala and Oidiodendron) are strongly associated with the reorganization of assembly landscape topography along abundance gradients, coinciding with shifts in mycorrhizal symbiosis. Independent datasets from Europe confirm that the highlighted genera are significantly associated with changes in mycorrhizal colonization patterns. Prokaryotic communities exhibit transitions among states characterized by core taxa, Pseudomonadota, or Actinomycetota, strongly associated with abundance gradients of Candidatus Udaeobacter and several endophytic fungi. These findings provide a scalable framework for prioritizing candidate keystone taxa and linking microbiome assembly to ecosystem-scale processes.
Additional Links: PMID-42951912
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@article {pmid42951912,
year = {2026},
author = {Noguchi, M and Suzuki, K and Fujita, H and Toju, H},
title = {Statistical inference of keystone taxa reshaping the assembly rules of forest root microbiomes.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42951912},
issn = {2041-1723},
support = {JPMJFR2048//MEXT | Japan Science and Technology Agency (JST)/ ; JPMJCR23N5//MEXT | Japan Science and Technology Agency (JST)/ ; RGP0029/2019//Human Frontier Science Program (HFSP)/ ; JP23KJ1380//MEXT | Japan Society for the Promotion of Science (JSPS)/ ; 25K02036//MEXT | Japan Society for the Promotion of Science (JSPS)/ ; 24K03127//MEXT | Japan Society for the Promotion of Science (JSPS)/ ; 23K26933//MEXT | Japan Society for the Promotion of Science (JSPS)/ ; },
mesh = {*Plant Roots/microbiology ; *Forests ; *Microbiota ; Mycorrhizae/physiology ; Symbiosis ; Bacteria/classification/genetics/isolation & purification ; Fungi/classification/genetics ; Japan ; },
abstract = {Root-associated fungi and bacteria play pivotal roles in terrestrial ecosystem processes. However, identifying keystone taxa driving below-ground microbial assembly remains a major challenge. Here, we present a statistical framework for identifying microbes that reorganize microbiome assembly. Using 1,270 root samples collected from a cool-temperate forest in Japan, we reconstruct assembly landscapes describing the probabilistic structure of community states. We then find that several endophytic fungi (e.g., Phialocephala and Oidiodendron) are strongly associated with the reorganization of assembly landscape topography along abundance gradients, coinciding with shifts in mycorrhizal symbiosis. Independent datasets from Europe confirm that the highlighted genera are significantly associated with changes in mycorrhizal colonization patterns. Prokaryotic communities exhibit transitions among states characterized by core taxa, Pseudomonadota, or Actinomycetota, strongly associated with abundance gradients of Candidatus Udaeobacter and several endophytic fungi. These findings provide a scalable framework for prioritizing candidate keystone taxa and linking microbiome assembly to ecosystem-scale processes.},
}
MeSH Terms:
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*Plant Roots/microbiology
*Forests
*Microbiota
Mycorrhizae/physiology
Symbiosis
Bacteria/classification/genetics/isolation & purification
Fungi/classification/genetics
Japan
RevDate: 2026-10-29
Clostridium perfringens Delta toxin targets CD9 to drive NEC and brain injury.
Nature [Epub ahead of print].
Necrotizing enterocolitis (NEC) is the most devastating gastrointestinal emergency in preterm infants, frequently causing mortality and long-term neurodevelopmental impairment[1,2]. Although the gut microbiota has been implicated in NEC pathogenesis[3-5], the microbial factors driving NEC and the following brain pathology remain unclear. Here we identify Clostridium perfringens pathobionts containing Delta toxin in the gut microbiome of individuals with severe and fatal NEC. Clinically, infected infants show worse outcomes, including aberrant systemic inflammation, severe neurological damage and coagulopathy. We establish a mouse model in which Delta-toxin-positive C. perfringens infection, or Delta toxin exposure alone, recapitulates clinical features of NEC, including intestinal necrosis and acute cerebral injury. Mechanistically, Delta toxin preferentially targets macrophages, potently activating inflammasome signalling and pyroptosis, triggering a rapid inflammatory cascade that compromises blood-brain barrier integrity and drives neuroinflammation. Through a genome-wide CRISPR screen, we identify the tetraspanin CD9 as the host receptor for Delta toxin. Using systemic, myeloid-specific and intestinal-epithelial-specific Cd9-knockout mice, we show that systemic and myeloid Cd9 ablation protects mice against toxin-induced lethality, blood-brain barrier dysfunction and multiorgan injury, whereas epithelial Cd9 deletion shows partial protection, implicating macrophage targeting as a primary driver of C. perfringens CD9-dependent pathogenesis. Furthermore, a neutralizing anti-Delta toxin monoclonal antibody confers protection against disease progression. These findings suggest that a subset of NEC is a specific-toxin-mediated disorder and validate the Delta toxin-CD9 axis as a therapeutic target for this subset.
Additional Links: PMID-42951958
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Citation:
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@article {pmid42951958,
year = {2026},
author = {Zhang, S and Gong, X and Tian, S and Yang, Y and Tong, X and Sheng, K and Zhang, Y and Amatsu, S and Zhang, X and Yu, D and Zhao, H and Ruan, L and Sun, H and Wu, K and Dong, M and Xiong, X},
title = {Clostridium perfringens Delta toxin targets CD9 to drive NEC and brain injury.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42951958},
issn = {1476-4687},
abstract = {Necrotizing enterocolitis (NEC) is the most devastating gastrointestinal emergency in preterm infants, frequently causing mortality and long-term neurodevelopmental impairment[1,2]. Although the gut microbiota has been implicated in NEC pathogenesis[3-5], the microbial factors driving NEC and the following brain pathology remain unclear. Here we identify Clostridium perfringens pathobionts containing Delta toxin in the gut microbiome of individuals with severe and fatal NEC. Clinically, infected infants show worse outcomes, including aberrant systemic inflammation, severe neurological damage and coagulopathy. We establish a mouse model in which Delta-toxin-positive C. perfringens infection, or Delta toxin exposure alone, recapitulates clinical features of NEC, including intestinal necrosis and acute cerebral injury. Mechanistically, Delta toxin preferentially targets macrophages, potently activating inflammasome signalling and pyroptosis, triggering a rapid inflammatory cascade that compromises blood-brain barrier integrity and drives neuroinflammation. Through a genome-wide CRISPR screen, we identify the tetraspanin CD9 as the host receptor for Delta toxin. Using systemic, myeloid-specific and intestinal-epithelial-specific Cd9-knockout mice, we show that systemic and myeloid Cd9 ablation protects mice against toxin-induced lethality, blood-brain barrier dysfunction and multiorgan injury, whereas epithelial Cd9 deletion shows partial protection, implicating macrophage targeting as a primary driver of C. perfringens CD9-dependent pathogenesis. Furthermore, a neutralizing anti-Delta toxin monoclonal antibody confers protection against disease progression. These findings suggest that a subset of NEC is a specific-toxin-mediated disorder and validate the Delta toxin-CD9 axis as a therapeutic target for this subset.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Fecal Microbiota Transplantation: A Promising Therapeutic Strategy Targeting the Microbiota-Gut-Brain Axis in Anorexia Nervosa.
Brain and behavior, 16(11):.
PURPOSE: Anorexia nervosa (AN) is a complex psychiatric disorder characterized by self-starvation, body-image disturbance, and serious medical complications. Because current treatments have variable outcomes and relapse is common, the microbiota-gut-brain axis has been investigated as a possible contributor to disease persistence. This review evaluates fecal microbiota transplantation (FMT) as an experimental microbiota-directed strategy for AN.
METHODS: PubMed, Embase, Scopus, and Google Scholar were searched for relevant studies published from January 1990 to October 2025. Eligible evidence included human reports, animal studies, and mechanistic studies examining FMT or gut-microbiota alterations in AN and related pathways.
FINDINGS: Individuals with AN have been reported to show altered microbial diversity and changes in taxa associated with short-chain fatty acid production and inflammation. These findings are heterogeneous and may reflect starvation, diet, medication exposure, or illness-related physiology. Human evidence for FMT in AN is limited to small, uncontrolled studies and case reports, while most mechanistic support comes from animal models or indirect evidence from other conditions.
CONCLUSION: Evidence for FMT in AN remains preliminary and is largely based on uncontrolled human observations and preclinical studies. FMT may alter gut microbial composition and gastrointestinal or metabolic measures, but controlled efficacy data are absent and psychiatric benefits remain unconfirmed. Well-designed controlled trials are needed to establish its safety and clinical efficacy.
Additional Links: PMID-42952078
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@article {pmid42952078,
year = {2026},
author = {Kwok, SL and Xiao, YC and Cai, XB},
title = {Fecal Microbiota Transplantation: A Promising Therapeutic Strategy Targeting the Microbiota-Gut-Brain Axis in Anorexia Nervosa.},
journal = {Brain and behavior},
volume = {16},
number = {11},
pages = {},
pmid = {42952078},
issn = {2162-3279},
support = {2023//The "Talents Support" Program of the First Affiliated Hospital of Shantou University Medical College/ ; 2024//Wu Jieping Medical Foundation Special Research Funding/ ; },
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Anorexia Nervosa/therapy/microbiology ; Animals ; *Gastrointestinal Microbiome/physiology ; *Brain-Gut Axis/physiology ; *Brain ; },
abstract = {PURPOSE: Anorexia nervosa (AN) is a complex psychiatric disorder characterized by self-starvation, body-image disturbance, and serious medical complications. Because current treatments have variable outcomes and relapse is common, the microbiota-gut-brain axis has been investigated as a possible contributor to disease persistence. This review evaluates fecal microbiota transplantation (FMT) as an experimental microbiota-directed strategy for AN.
METHODS: PubMed, Embase, Scopus, and Google Scholar were searched for relevant studies published from January 1990 to October 2025. Eligible evidence included human reports, animal studies, and mechanistic studies examining FMT or gut-microbiota alterations in AN and related pathways.
FINDINGS: Individuals with AN have been reported to show altered microbial diversity and changes in taxa associated with short-chain fatty acid production and inflammation. These findings are heterogeneous and may reflect starvation, diet, medication exposure, or illness-related physiology. Human evidence for FMT in AN is limited to small, uncontrolled studies and case reports, while most mechanistic support comes from animal models or indirect evidence from other conditions.
CONCLUSION: Evidence for FMT in AN remains preliminary and is largely based on uncontrolled human observations and preclinical studies. FMT may alter gut microbial composition and gastrointestinal or metabolic measures, but controlled efficacy data are absent and psychiatric benefits remain unconfirmed. Well-designed controlled trials are needed to establish its safety and clinical efficacy.},
}
MeSH Terms:
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hide MeSH Terms
*Fecal Microbiota Transplantation/methods
Humans
*Anorexia Nervosa/therapy/microbiology
Animals
*Gastrointestinal Microbiome/physiology
*Brain-Gut Axis/physiology
*Brain
RevDate: 2026-10-29
CmpDate: 2026-10-29
The Brain-Tooth Axis as an Early Predictor of Alzheimer's Disease.
Biomolecules & therapeutics, 34(6):1322-1330.
Alzheimer's disease (AD) is typically diagnosed after irreversible neuronal loss. Recent evidence links oral health deterioration-especially tooth loss, periodontal disease, and reduced masticatory function-to accelerated cognitive decline and dementia risk. Aging also promotes structural and immunological changes in the oral cavity, accelerating periodontal breakdown, microbiome dysbiosis, and functional tooth loss. This emerging "brain-tooth axis" suggests bidirectional interactions between the oral cavity and central nervous system via inflammatory, microbial, and sensory pathways. Periodontal inflammation, oral microbiome dysbiosis, and loss of trigeminal sensory input may promote neuroinflammation, amyloid accumulation, and hippocampal dysfunction. Conversely, early neural degeneration can impair oral maintenance and chewing behavior. This perspective outlines mechanistic hypotheses, clinical implications, and a research roadmap for integrating oral health metrics into multimodal AD risk prediction. Validating this axis could establish oral assessments as accessible biomarkers for early disease detection and prevention strategies.
Additional Links: PMID-42952210
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@article {pmid42952210,
year = {2026},
author = {Hossain, MK and Lee, HY and Kim, HJ and Kim, HR},
title = {The Brain-Tooth Axis as an Early Predictor of Alzheimer's Disease.},
journal = {Biomolecules & therapeutics},
volume = {34},
number = {6},
pages = {1322-1330},
doi = {10.4062/biomolther.2026.165},
pmid = {42952210},
issn = {1976-9148},
abstract = {Alzheimer's disease (AD) is typically diagnosed after irreversible neuronal loss. Recent evidence links oral health deterioration-especially tooth loss, periodontal disease, and reduced masticatory function-to accelerated cognitive decline and dementia risk. Aging also promotes structural and immunological changes in the oral cavity, accelerating periodontal breakdown, microbiome dysbiosis, and functional tooth loss. This emerging "brain-tooth axis" suggests bidirectional interactions between the oral cavity and central nervous system via inflammatory, microbial, and sensory pathways. Periodontal inflammation, oral microbiome dysbiosis, and loss of trigeminal sensory input may promote neuroinflammation, amyloid accumulation, and hippocampal dysfunction. Conversely, early neural degeneration can impair oral maintenance and chewing behavior. This perspective outlines mechanistic hypotheses, clinical implications, and a research roadmap for integrating oral health metrics into multimodal AD risk prediction. Validating this axis could establish oral assessments as accessible biomarkers for early disease detection and prevention strategies.},
}
RevDate: 2026-10-29
BacMap 3.0: a comprehensive knowledgebase of annotated bacterial genomes.
Nucleic acids research pii:9004252 [Epub ahead of print].
BacMap 3.0 (https://bacmap.ca) is a comprehensive, freely accessible resource integrating 23 524 bacterial and archaeal species, 32 866 genomes, >100 million genes, 1756 primary metabolic pathways, and 45 284 metabolites within one interactive platform. Despite the extraordinary growth of bacterial and archaeal genome sequencing, relevant data remain distributed across numerous specialized databases, impeding comprehensive genome-to-function analysis. While existing microbial resources generally emphasize genome annotation, taxonomy, metabolic pathways, or phenotypes separately, BacMap 3.0 unifies these complementary information layers within an organism-centred framework. It resolves this fragmentation by consolidating genomic, functional, structural, metabolic, phenotypic, ecological, and phylogenetic information into richly detailed, organism-specific "BacCards". Each BacCard combines an interactive genome map with extensive annotations covering bacterium-specific taxonomy, physiology, morphology, metabolism, protein structures, pathways, and metabolites. To facilitate data exploration, BacMap 3.0 supports taxonomic and phenotype-based browsing, chemical structure searches, interactive genome visualization, as well as gene, genome, 16S RNA, and protein BLAST searches. Building on earlier releases devoted primarily to genome visualization, BacMap 3.0 increases organismal coverage by >13-fold and transforms BacMap into an integrated bacterial knowledgebase for genome-to-function investigation across multiple biological scales. By bringing diverse biological information together in a single searchable environment, BacMap 3.0 offers a powerful platform for comparative genomics, microbiome research, infectious disease investigation, and biotechnology with a goal of accelerating the interpretation of microbial diversity, biology, and function.
Additional Links: PMID-42952395
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@article {pmid42952395,
year = {2026},
author = {Kruger, R and Kyes, M and Oler, E and Saha, S and Han, S and Poelzer, J and Wakoli, J and López-Hernández, Y and LeVatte, M and Berjanskii, M and MacKay, S and Kovur, P and Fitzsimmons, CJ and Cahill, JF and Wishart, DS},
title = {BacMap 3.0: a comprehensive knowledgebase of annotated bacterial genomes.},
journal = {Nucleic acids research},
volume = {},
number = {},
pages = {},
doi = {10.1093/nar/gkag1049},
pmid = {42952395},
issn = {1362-4962},
support = {42495//Canada Foundation for Innovation/ ; //Genome Alberta/ ; //Genome Canada/ ; 100628//Canada Research Chairs Program/ ; NSERC RGPIN-2025-04867//Natural Sciences and Engineering Research Council of Canada/ ; NSERC BCPIR-590317-2024//Natural Sciences and Engineering Research Council of Canada/ ; //NSERC Gerhard Herzberg Canada Gold Medal/ ; 601838-2025//NSERC GLDSU/ ; //Climate Action Through Grazing/ ; //CAT-G/ ; //Strategic Alliance Agreement, Combining Omic Technology and Grassland Management to Enhance Soil Carbon Sequestration and Reduce Greenhouse Gas Emissions/ ; C22GRS//Genome Canada and Genome Alberta/ ; //Governments of Canada and Alberta/ ; 2023G1491R//Results Driven Agriculture Research/ ; //Governments of Canada and Saskatchewan/ ; 20240659//Agriculture Development Fund/ ; RES0066503//University of Alberta/ ; RES0066504//University of Alberta/ ; RES0066506//University of Alberta/ ; },
abstract = {BacMap 3.0 (https://bacmap.ca) is a comprehensive, freely accessible resource integrating 23 524 bacterial and archaeal species, 32 866 genomes, >100 million genes, 1756 primary metabolic pathways, and 45 284 metabolites within one interactive platform. Despite the extraordinary growth of bacterial and archaeal genome sequencing, relevant data remain distributed across numerous specialized databases, impeding comprehensive genome-to-function analysis. While existing microbial resources generally emphasize genome annotation, taxonomy, metabolic pathways, or phenotypes separately, BacMap 3.0 unifies these complementary information layers within an organism-centred framework. It resolves this fragmentation by consolidating genomic, functional, structural, metabolic, phenotypic, ecological, and phylogenetic information into richly detailed, organism-specific "BacCards". Each BacCard combines an interactive genome map with extensive annotations covering bacterium-specific taxonomy, physiology, morphology, metabolism, protein structures, pathways, and metabolites. To facilitate data exploration, BacMap 3.0 supports taxonomic and phenotype-based browsing, chemical structure searches, interactive genome visualization, as well as gene, genome, 16S RNA, and protein BLAST searches. Building on earlier releases devoted primarily to genome visualization, BacMap 3.0 increases organismal coverage by >13-fold and transforms BacMap into an integrated bacterial knowledgebase for genome-to-function investigation across multiple biological scales. By bringing diverse biological information together in a single searchable environment, BacMap 3.0 offers a powerful platform for comparative genomics, microbiome research, infectious disease investigation, and biotechnology with a goal of accelerating the interpretation of microbial diversity, biology, and function.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Paired biopsy-surface and tissue microbiome profiling reveals tissue-associated bacterial signatures in nasopharyngeal carcinoma.
Frontiers in cellular and infection microbiology, 16:1892233.
INTRODUCTION: Tumor-associated microbiota have been implicated in cancer biology, but the relationship between bacteria detected on the biopsy surface and those detected within tumor tissue remains poorly defined.
METHODS: In this study, we profiled paired biopsy-surface swabs and tissue biopsies from patients with nasopharyngeal carcinoma (NPC) and benign nasopharyngeal lymphoid hyperplasia (NLH) controls using five-region 16S rRNA gene sequencing. Matched bulk RNA-seq data were analyzed to explore associations between microbial features, Epstein-Barr virus (EBV) transcription, host pathway activity, and inferred immune-cell composition.
RESULTS: Tissue-associated microbial profiles showed stronger separation between NPC and NLH than biopsy-surface profiles in this discovery cohort. Several NPC-enriched species-level taxonomic assignments were associated with higher EBV transcript levels, proliferative and cell-cycle pathway activity, and lower inferred CD8 T-cell and plasmacytoid dendritic-cell signatures.
DISCUSSION: These findings indicate that NPC tissue contains microbial signatures that differ from biopsy-surface communities and support further validation of tissue-associated microbe-EBV-host relationships.
Additional Links: PMID-42952527
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@article {pmid42952527,
year = {2026},
author = {Shi, N and Huang, Z and Wang, X and Xie, Y and Tang, A and Xia, W},
title = {Paired biopsy-surface and tissue microbiome profiling reveals tissue-associated bacterial signatures in nasopharyngeal carcinoma.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1892233},
pmid = {42952527},
issn = {2235-2988},
mesh = {Humans ; *Microbiota/genetics ; *Nasopharyngeal Carcinoma/microbiology/pathology ; RNA, Ribosomal, 16S/genetics ; Biopsy ; *Bacteria/classification/genetics/isolation & purification ; Herpesvirus 4, Human/genetics ; Female ; Male ; *Nasopharyngeal Neoplasms/microbiology/pathology ; Middle Aged ; Epstein-Barr Virus Infections ; },
abstract = {INTRODUCTION: Tumor-associated microbiota have been implicated in cancer biology, but the relationship between bacteria detected on the biopsy surface and those detected within tumor tissue remains poorly defined.
METHODS: In this study, we profiled paired biopsy-surface swabs and tissue biopsies from patients with nasopharyngeal carcinoma (NPC) and benign nasopharyngeal lymphoid hyperplasia (NLH) controls using five-region 16S rRNA gene sequencing. Matched bulk RNA-seq data were analyzed to explore associations between microbial features, Epstein-Barr virus (EBV) transcription, host pathway activity, and inferred immune-cell composition.
RESULTS: Tissue-associated microbial profiles showed stronger separation between NPC and NLH than biopsy-surface profiles in this discovery cohort. Several NPC-enriched species-level taxonomic assignments were associated with higher EBV transcript levels, proliferative and cell-cycle pathway activity, and lower inferred CD8 T-cell and plasmacytoid dendritic-cell signatures.
DISCUSSION: These findings indicate that NPC tissue contains microbial signatures that differ from biopsy-surface communities and support further validation of tissue-associated microbe-EBV-host relationships.},
}
MeSH Terms:
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Humans
*Microbiota/genetics
*Nasopharyngeal Carcinoma/microbiology/pathology
RNA, Ribosomal, 16S/genetics
Biopsy
*Bacteria/classification/genetics/isolation & purification
Herpesvirus 4, Human/genetics
Female
Male
*Nasopharyngeal Neoplasms/microbiology/pathology
Middle Aged
Epstein-Barr Virus Infections
RevDate: 2026-10-29
CmpDate: 2026-10-29
Editorial: Legume intercropping and rotation: impacts on soil microbiomes.
Frontiers in microbiology, 17:2006730.
Additional Links: PMID-42952614
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@article {pmid42952614,
year = {2026},
author = {Tayyab, M and Pang, Z and Nizamani, MM and Zhou, Y and Muhammad, S},
title = {Editorial: Legume intercropping and rotation: impacts on soil microbiomes.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {2006730},
doi = {10.3389/fmicb.2026.2006730},
pmid = {42952614},
issn = {1664-302X},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Environment-dependent responses of soil physicochemical properties, microbial communities and functional gene profiles to protected and open-field cultivation of Stropharia rugosoannulata.
Frontiers in microbiology, 17:1912245.
The cultivation of Stropharia rugosoannulata involves substantial organic substrate input and fungal mycelial activity, which may influence soil nutrient transformation, microbial communities and functional gene profiles. However, whether these responses differ between protected and open-field cultivation settings remains unclear at the metagenomic level. In this study, four treatments were investigated: protected cultivation soil (NT), protected uncultivated soil (NK), open-field cultivation soil (ZT) and open-field uncultivated soil (ZK). Soil physicochemical properties, enzyme activities and shotgun metagenomes were analyzed to compare cultivation-associated soil responses under the two sampled cultivation settings. Protected cultivation showed more evident biochemical responses than open-field cultivation. Compared with NK, NT had significantly higher NH 4 + -N content and sucrase activity, together with lower soil salinity and electrical conductivity, whereas no significant differences in the measured soil properties were detected between ZT and ZK. Exploratory two-way ANOVA indicated setting-associated variation in several soil variables and significant interaction effects for NH 4 + -N and NO 3 - -N. Metagenomic analysis showed treatment-associated variation in specific classified genera, with Cellvibrio and Flavobacterium showing higher relative abundances in cultivated soils. However, PERMANOVA did not detect significant separation in the overall genus-level community structure. KEGG functional profiles remained broadly stable across treatments, although protected cultivation showed more evident variation in selected functional categories. Antibiotic resistance gene profiles also exhibited treatment-specific patterns. Overall, S. rugosoannulata cultivation did not induce uniform microbial community restructuring or consistent soil improvement, but was associated with context-dependent responses in soil biochemical properties, specific microbial taxa, functional potential and resistome composition. These findings provide metagenomic insights for soil health management and resistome monitoring in continuous edible mushroom cultivation systems.
Additional Links: PMID-42952710
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@article {pmid42952710,
year = {2026},
author = {Ji, W and Tang, X and Liu, X and Su, W and Chai, W and Chen, K and Ge, J and Wang, B},
title = {Environment-dependent responses of soil physicochemical properties, microbial communities and functional gene profiles to protected and open-field cultivation of Stropharia rugosoannulata.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1912245},
pmid = {42952710},
issn = {1664-302X},
abstract = {The cultivation of Stropharia rugosoannulata involves substantial organic substrate input and fungal mycelial activity, which may influence soil nutrient transformation, microbial communities and functional gene profiles. However, whether these responses differ between protected and open-field cultivation settings remains unclear at the metagenomic level. In this study, four treatments were investigated: protected cultivation soil (NT), protected uncultivated soil (NK), open-field cultivation soil (ZT) and open-field uncultivated soil (ZK). Soil physicochemical properties, enzyme activities and shotgun metagenomes were analyzed to compare cultivation-associated soil responses under the two sampled cultivation settings. Protected cultivation showed more evident biochemical responses than open-field cultivation. Compared with NK, NT had significantly higher NH 4 + -N content and sucrase activity, together with lower soil salinity and electrical conductivity, whereas no significant differences in the measured soil properties were detected between ZT and ZK. Exploratory two-way ANOVA indicated setting-associated variation in several soil variables and significant interaction effects for NH 4 + -N and NO 3 - -N. Metagenomic analysis showed treatment-associated variation in specific classified genera, with Cellvibrio and Flavobacterium showing higher relative abundances in cultivated soils. However, PERMANOVA did not detect significant separation in the overall genus-level community structure. KEGG functional profiles remained broadly stable across treatments, although protected cultivation showed more evident variation in selected functional categories. Antibiotic resistance gene profiles also exhibited treatment-specific patterns. Overall, S. rugosoannulata cultivation did not induce uniform microbial community restructuring or consistent soil improvement, but was associated with context-dependent responses in soil biochemical properties, specific microbial taxa, functional potential and resistome composition. These findings provide metagenomic insights for soil health management and resistome monitoring in continuous edible mushroom cultivation systems.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Longitudinal integrated analysis of gut microbiota and metabolites in rectal cancer patients undergoing chemoradiotherapy.
Frontiers in microbiology, 17:1934703.
BACKGROUND: Longitudinal changes in the fecal microbiome and metabolome during concurrent chemoradiotherapy (CCRT) for rectal cancer remain incompletely characterized.
METHODS: In this prospective single-center cohort, 19 patients with rectal cancer were enrolled and 17 were included in the longitudinal analysis after two prespecified sampling-window exclusions. Fecal specimens were scheduled at nine time points: R0, collected before the first dose of capecitabine and before radiotherapy, and R3 through R24 at three-fraction intervals during treatment. Twenty unmatched healthy volunteers provided one fecal specimen for a descriptive pretreatment comparison. Full-length 16S rRNA gene sequencing and untargeted metabolomics were performed. Longitudinal microbial counts were analyzed using negative-binomial generalized linear mixed models, and metabolite features were analyzed using linear mixed-effects models; participant was included as a random intercept, and P values were adjusted using the Benjamini-Hochberg false discovery rate (FDR).
RESULTS: Nineteen genera and 27 of 176 analyzed species showed significant linear time trends during CCRT (FDR < 0.05). Parvimonas micra, Peptostreptococcus stomatis, and Gemella morbillorum decreased, whereas Lachnoclostridium pacaense, Blautia hydrogenotrophica, [Eubacterium] sulci, and Coprococcus eutactus increased. Of 2,873 analyzed metabolic features, 393 changed significantly over time. In a secondary same-cohort analysis, 17 of 50 correlation-selected taxon-metabolite pairs remained significant in time-adjusted mixed-effects models, including a positive association between C. eutactus and a feature annotated as stercobilin. Among 103 significant features with KEGG identifiers, three pathways met a nominal raw-P threshold, but none remained significant after FDR correction. Pretreatment patient samples had lower Shannon diversity and differed from healthy-control samples by ANOSIM; these comparisons were descriptive because the groups were not matched for age or sex. Five species shared the same case-control direction in this cohort and GMrepo reports, but only P. stomatis and G. morbillorum also showed significant longitudinal declines during CCRT.
CONCLUSION: This small, intensively sampled cohort identifies exploratory fecal microbial and metabolic trajectories during capecitabine-based CCRT. The findings do not establish causal mechanisms, microbial functions, disease specificity, or biomarker performance and require independent confirmation in larger cohorts.
Additional Links: PMID-42952721
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Citation:
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@article {pmid42952721,
year = {2026},
author = {Wang, L and Zhang, P and Zhang, Y and Li, Y and Qu, B and Peng, L},
title = {Longitudinal integrated analysis of gut microbiota and metabolites in rectal cancer patients undergoing chemoradiotherapy.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1934703},
pmid = {42952721},
issn = {1664-302X},
abstract = {BACKGROUND: Longitudinal changes in the fecal microbiome and metabolome during concurrent chemoradiotherapy (CCRT) for rectal cancer remain incompletely characterized.
METHODS: In this prospective single-center cohort, 19 patients with rectal cancer were enrolled and 17 were included in the longitudinal analysis after two prespecified sampling-window exclusions. Fecal specimens were scheduled at nine time points: R0, collected before the first dose of capecitabine and before radiotherapy, and R3 through R24 at three-fraction intervals during treatment. Twenty unmatched healthy volunteers provided one fecal specimen for a descriptive pretreatment comparison. Full-length 16S rRNA gene sequencing and untargeted metabolomics were performed. Longitudinal microbial counts were analyzed using negative-binomial generalized linear mixed models, and metabolite features were analyzed using linear mixed-effects models; participant was included as a random intercept, and P values were adjusted using the Benjamini-Hochberg false discovery rate (FDR).
RESULTS: Nineteen genera and 27 of 176 analyzed species showed significant linear time trends during CCRT (FDR < 0.05). Parvimonas micra, Peptostreptococcus stomatis, and Gemella morbillorum decreased, whereas Lachnoclostridium pacaense, Blautia hydrogenotrophica, [Eubacterium] sulci, and Coprococcus eutactus increased. Of 2,873 analyzed metabolic features, 393 changed significantly over time. In a secondary same-cohort analysis, 17 of 50 correlation-selected taxon-metabolite pairs remained significant in time-adjusted mixed-effects models, including a positive association between C. eutactus and a feature annotated as stercobilin. Among 103 significant features with KEGG identifiers, three pathways met a nominal raw-P threshold, but none remained significant after FDR correction. Pretreatment patient samples had lower Shannon diversity and differed from healthy-control samples by ANOSIM; these comparisons were descriptive because the groups were not matched for age or sex. Five species shared the same case-control direction in this cohort and GMrepo reports, but only P. stomatis and G. morbillorum also showed significant longitudinal declines during CCRT.
CONCLUSION: This small, intensively sampled cohort identifies exploratory fecal microbial and metabolic trajectories during capecitabine-based CCRT. The findings do not establish causal mechanisms, microbial functions, disease specificity, or biomarker performance and require independent confirmation in larger cohorts.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Comprehensive artificial intelligence-assisted mental health program for university students in China (CAMPUS): study protocol for a multi-center prospective cohort with planned embedded randomized intervention trials.
Frontiers in psychology, 17:1877887.
UNLABELLED: University students face a rising prevalence of depression, anxiety, insomnia, and suicidal ideation that exceeds the capacity of conventional, resource-constrained campus support services. Although artificial intelligence (AI)-assisted screening tools have emerged, many have evaluated selected modalities or isolated prediction tasks, and their integration with prospectively evaluated intervention pathways remains limited. This protocol describes the Comprehensive Artificial Intelligence-Assisted Mental Health Program for University Students in China (CAMPUS), a multi-center research program comprising a five-year prospective cohort, eight planned embedded randomized controlled trials, and exploratory multimodal AI and multi-omics studies across seven Chinese universities. Longitudinal cohort enrolment commenced at Henan Medical University in September 2025 and is planned to expand across seven participating universities. Multidimensional screening integrates psychological self-report (PHQ-9, GAD-7, ISI, BSI-CV, and others), physiological measurements (EEG, MRI, fNIRS, HRV, eye tracking, facial-expression analysis, ERP, voice acoustics), and an exploratory biospecimen component for multi-omics profiling, potentially including genomic, transcriptomic, proteomic, metabolomic, and microbiome analyses, subject to the finalization and approval of layer-specific protocols. Students identified through cohort screening as potentially eligible for an intervention trial will undergo trial-specific eligibility assessment. Those who meet the eligibility criteria and provide trial-specific informed consent will be individually randomized in a 1:1 ratio to the intervention or its comparator within one of eight separate two-arm, multi-center, parallel-group randomized controlled trials. A Transformer-based multimodal AI framework with SHAP-based feature attribution will be developed and internally evaluated for questionnaire-defined risk stratification and exploratory treatment-response prediction. The initial Henan Medical University cohort recruitment and university-student mental-health assessment were approved by the Ethics Review Committee of Henan Medical University (XYLL-20250484), and written informed consent is obtained from participants before enrolment. Each additional participating center will obtain local ethics approval before study activation. Findings will be disseminated through peer-reviewed publications, scientific conferences, and policy briefs, providing evidence that may inform the design and prospective evaluation of youth mental-health programs in other university settings.
CLINICAL TRIAL REGISTRATION: The two clinical trials were registered in the Chinese Clinical Trial Registry (ChiCTR). The registration details and URLs are as follows: ChiCTR2500113527: https://www.chictr.org.cn/showproj.html?proj=298271; ChiCTR2500113613: https://www.chictr.org.cn/showproj.html?proj=298268.
Additional Links: PMID-42952970
PubMed:
Citation:
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@article {pmid42952970,
year = {2026},
author = {Yang, G and Liu, R and Wang, C and Zhu, R and Qin, S and Yan, J and Wang, Y and Pei, H and Liang, L and Su, Y and Wang, S and Wu, W and Ji, G and Wang, F and Wei, Y},
title = {Comprehensive artificial intelligence-assisted mental health program for university students in China (CAMPUS): study protocol for a multi-center prospective cohort with planned embedded randomized intervention trials.},
journal = {Frontiers in psychology},
volume = {17},
number = {},
pages = {1877887},
pmid = {42952970},
issn = {1664-1078},
abstract = {UNLABELLED: University students face a rising prevalence of depression, anxiety, insomnia, and suicidal ideation that exceeds the capacity of conventional, resource-constrained campus support services. Although artificial intelligence (AI)-assisted screening tools have emerged, many have evaluated selected modalities or isolated prediction tasks, and their integration with prospectively evaluated intervention pathways remains limited. This protocol describes the Comprehensive Artificial Intelligence-Assisted Mental Health Program for University Students in China (CAMPUS), a multi-center research program comprising a five-year prospective cohort, eight planned embedded randomized controlled trials, and exploratory multimodal AI and multi-omics studies across seven Chinese universities. Longitudinal cohort enrolment commenced at Henan Medical University in September 2025 and is planned to expand across seven participating universities. Multidimensional screening integrates psychological self-report (PHQ-9, GAD-7, ISI, BSI-CV, and others), physiological measurements (EEG, MRI, fNIRS, HRV, eye tracking, facial-expression analysis, ERP, voice acoustics), and an exploratory biospecimen component for multi-omics profiling, potentially including genomic, transcriptomic, proteomic, metabolomic, and microbiome analyses, subject to the finalization and approval of layer-specific protocols. Students identified through cohort screening as potentially eligible for an intervention trial will undergo trial-specific eligibility assessment. Those who meet the eligibility criteria and provide trial-specific informed consent will be individually randomized in a 1:1 ratio to the intervention or its comparator within one of eight separate two-arm, multi-center, parallel-group randomized controlled trials. A Transformer-based multimodal AI framework with SHAP-based feature attribution will be developed and internally evaluated for questionnaire-defined risk stratification and exploratory treatment-response prediction. The initial Henan Medical University cohort recruitment and university-student mental-health assessment were approved by the Ethics Review Committee of Henan Medical University (XYLL-20250484), and written informed consent is obtained from participants before enrolment. Each additional participating center will obtain local ethics approval before study activation. Findings will be disseminated through peer-reviewed publications, scientific conferences, and policy briefs, providing evidence that may inform the design and prospective evaluation of youth mental-health programs in other university settings.
CLINICAL TRIAL REGISTRATION: The two clinical trials were registered in the Chinese Clinical Trial Registry (ChiCTR). The registration details and URLs are as follows: ChiCTR2500113527: https://www.chictr.org.cn/showproj.html?proj=298271; ChiCTR2500113613: https://www.chictr.org.cn/showproj.html?proj=298268.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Exercise-related brain remodeling through bidirectional brain-body crosstalk: an integrative narrative review.
Frontiers in integrative neuroscience, 20:1954740.
Exercise is associated with favorable brain and cognitive outcomes, yet the supporting evidence spans molecular, cellular, organ, neural-circuit, imaging, and behavioral levels that differ substantially in causal strength. This narrative review develops an integrative framework across biological levels in which exercise-related brain remodeling emerges from bidirectional brain-body crosstalk rather than from a single peripheral factor or a one-way endocrine pathway. The framework links central motor commands, sensory feedback, autonomic regulation, and cerebral hemodynamics with signal generation by skeletal muscle, liver, adipose tissue, bone, the gut microbiome, and the circulating immune-vascular milieu. Metabolites, secreted factors, extracellular vesicles, and neural afferents may influence the central nervous system through blood-brain and blood-cerebrospinal fluid interfaces, circumventricular organs, cerebral endothelium, and brainstem-hypothalamic networks. Candidate central responses include neurotrophic and synaptic signaling, glial-state regulation, adult hippocampal neurogenesis, and neurovascular adaptation, which may correspond to group-level changes in brain structure, functional connectivity, and cognition. However, direct causal mediation across the complete human pathway remains largely untested: many cellular mechanisms derive from animal or in vitro studies, whereas human biomarker and neuroimaging findings are often indirect and process-nonspecific. Age, sex and hormonal state, genotype, disease stage, baseline function, exercise dose, recovery, and adherence further shape response heterogeneity. A stronger translational evidence base will require preregistered longitudinal interventions, source-resolved and time-resolved biomarker sampling, cross-species validation, multimodal target-engagement measures, and externally validated prediction models.
Additional Links: PMID-42952991
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@article {pmid42952991,
year = {2026},
author = {Yin, D and Luo, C and Hu, J and Bi, SZ},
title = {Exercise-related brain remodeling through bidirectional brain-body crosstalk: an integrative narrative review.},
journal = {Frontiers in integrative neuroscience},
volume = {20},
number = {},
pages = {1954740},
pmid = {42952991},
issn = {1662-5145},
abstract = {Exercise is associated with favorable brain and cognitive outcomes, yet the supporting evidence spans molecular, cellular, organ, neural-circuit, imaging, and behavioral levels that differ substantially in causal strength. This narrative review develops an integrative framework across biological levels in which exercise-related brain remodeling emerges from bidirectional brain-body crosstalk rather than from a single peripheral factor or a one-way endocrine pathway. The framework links central motor commands, sensory feedback, autonomic regulation, and cerebral hemodynamics with signal generation by skeletal muscle, liver, adipose tissue, bone, the gut microbiome, and the circulating immune-vascular milieu. Metabolites, secreted factors, extracellular vesicles, and neural afferents may influence the central nervous system through blood-brain and blood-cerebrospinal fluid interfaces, circumventricular organs, cerebral endothelium, and brainstem-hypothalamic networks. Candidate central responses include neurotrophic and synaptic signaling, glial-state regulation, adult hippocampal neurogenesis, and neurovascular adaptation, which may correspond to group-level changes in brain structure, functional connectivity, and cognition. However, direct causal mediation across the complete human pathway remains largely untested: many cellular mechanisms derive from animal or in vitro studies, whereas human biomarker and neuroimaging findings are often indirect and process-nonspecific. Age, sex and hormonal state, genotype, disease stage, baseline function, exercise dose, recovery, and adherence further shape response heterogeneity. A stronger translational evidence base will require preregistered longitudinal interventions, source-resolved and time-resolved biomarker sampling, cross-species validation, multimodal target-engagement measures, and externally validated prediction models.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Whole-body volatile organic compound profiling reveals metabolic pathway perturbations in a murine polymicrobial sepsis model: a feasibility study.
Frontiers in medicine, 13:1978491.
Sepsis rewires host metabolism, and these changes may be readable in the volatile organic compounds (VOCs) released from the body. Whether whole-body VOC profiles can be mapped onto specific disrupted biochemical pathways has not been tested. In this discovery-phase, single-time-point feasibility study, polymicrobial sepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice (14 CLP, 10 sham controls). Whole-body headspace gases were collected 12 h after surgery and analysed by thermal desorption-gas chromatography-mass spectrometry. After preprocessing, 113 features were tested univariately with Benjamini-Hochberg correction and by orthogonal partial least squares discriminant analysis (OPLS-DA). Candidate VOCs (FDR < 0.1, |log2FC| > 0.26, VIP > 1.0) were annotated against PubChem, KEGG COMPOUND, and the Human Metabolome Database. OPLS-DA separated the groups (R2X = 0.489, R2Y = 0.981, Q2 = 0.777; P = 0.001 by 1,000 permutations), and leave-one-out cross-validation classified 95.8% of animals correctly, though n = 24. Of 54 candidate VOCs, 18 had established endogenous origins; 16 fell and 2 rose in septic mice. Pathway mapping indicated four perturbed domains: lipid peroxidation (12 depleted VOCs), ketone body metabolism (3 decreased), cholesterol/isoprenoid metabolism (isoprene, decreased), and putative gut microbiota-associated metabolism (toluene and carbon disulfide, increased). All 18 endogenous VOCs kept candidate status after environment-derived VOCs were removed. Because whole-body headspace volatiles superimpose tissue metabolism, ventilation, activity, and background, these results suggest the septic volatilome may be mapped onto distinct pathway perturbations; ventilation and activity effects cannot be excluded. These findings generate testable hypotheses for non-invasive metabolic phenotyping in sepsis.
Additional Links: PMID-42953112
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@article {pmid42953112,
year = {2026},
author = {Feng, WY and Chen, Y and Zhang, XY and Fu, R and Hu, Q and Mo, FF and Wang, JF},
title = {Whole-body volatile organic compound profiling reveals metabolic pathway perturbations in a murine polymicrobial sepsis model: a feasibility study.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1978491},
pmid = {42953112},
issn = {2296-858X},
abstract = {Sepsis rewires host metabolism, and these changes may be readable in the volatile organic compounds (VOCs) released from the body. Whether whole-body VOC profiles can be mapped onto specific disrupted biochemical pathways has not been tested. In this discovery-phase, single-time-point feasibility study, polymicrobial sepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice (14 CLP, 10 sham controls). Whole-body headspace gases were collected 12 h after surgery and analysed by thermal desorption-gas chromatography-mass spectrometry. After preprocessing, 113 features were tested univariately with Benjamini-Hochberg correction and by orthogonal partial least squares discriminant analysis (OPLS-DA). Candidate VOCs (FDR < 0.1, |log2FC| > 0.26, VIP > 1.0) were annotated against PubChem, KEGG COMPOUND, and the Human Metabolome Database. OPLS-DA separated the groups (R2X = 0.489, R2Y = 0.981, Q2 = 0.777; P = 0.001 by 1,000 permutations), and leave-one-out cross-validation classified 95.8% of animals correctly, though n = 24. Of 54 candidate VOCs, 18 had established endogenous origins; 16 fell and 2 rose in septic mice. Pathway mapping indicated four perturbed domains: lipid peroxidation (12 depleted VOCs), ketone body metabolism (3 decreased), cholesterol/isoprenoid metabolism (isoprene, decreased), and putative gut microbiota-associated metabolism (toluene and carbon disulfide, increased). All 18 endogenous VOCs kept candidate status after environment-derived VOCs were removed. Because whole-body headspace volatiles superimpose tissue metabolism, ventilation, activity, and background, these results suggest the septic volatilome may be mapped onto distinct pathway perturbations; ventilation and activity effects cannot be excluded. These findings generate testable hypotheses for non-invasive metabolic phenotyping in sepsis.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Gut microbiome and gut-derived metabolites to identify the transition from metabolically healthy to unhealthy obesity: a mini review.
Frontiers in nutrition, 13:1989174.
Obesity is a metabolically heterogeneous condition with distinct metabolic phenotypes, ranging from metabolically healthy obesity (MHO) to metabolically unhealthy obesity (MUO). Although individuals with MHO initially lack cardiometabolic dysfunction, many transition to MUO over time, exponentially increasing their risk for type 2 diabetes and cardiovascular disease. In this mini-review, we synthesize recent evidence from multi-omic cohort studies evaluating gut microbiome composition and gut-derived metabolites as functional biomarkers of obesity heterogeneity and drivers of metabolic decline. While microbial diversity yields inconsistent signatures across cohorts, MHO is generally characterized by higher relative abundance of Ruminococcaceae, Oscillospira, Akkermansia, and Bifidobacterium and enrichment of other taxa predicted to be short-chain fatty acid-producers. Conversely, circulating gut-derived metabolomic signatures including altered secondary bile acid pools, elevated branched-chain amino acids, and trimethylamine N-oxide more reliably discriminate MUO from MHO than traditional measures, and correlate strongly with visceral adiposity, insulin resistance, and systemic inflammation. Furthermore, new systems biology approaches, such as integrating high-dimensional metagenomics and metabolomics via machine learning models, offer a potentially superior early indicators tool in precision medicine for identifying obesity phenotypes compared with traditional metrics (e.g., body mass index, fasting glucose). Overall, current evidence remains predominantly cross-sectional and based on secondary analyses of large cohort studies, underscoring the need for prospective longitudinal studies to validate these multi-omic biomarkers for precise phenotype identification and clinical risk assessment.
Additional Links: PMID-42953211
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@article {pmid42953211,
year = {2026},
author = {Manrique, EI and Sciglitano, L and Ortega-Santos, CP},
title = {Gut microbiome and gut-derived metabolites to identify the transition from metabolically healthy to unhealthy obesity: a mini review.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1989174},
pmid = {42953211},
issn = {2296-861X},
abstract = {Obesity is a metabolically heterogeneous condition with distinct metabolic phenotypes, ranging from metabolically healthy obesity (MHO) to metabolically unhealthy obesity (MUO). Although individuals with MHO initially lack cardiometabolic dysfunction, many transition to MUO over time, exponentially increasing their risk for type 2 diabetes and cardiovascular disease. In this mini-review, we synthesize recent evidence from multi-omic cohort studies evaluating gut microbiome composition and gut-derived metabolites as functional biomarkers of obesity heterogeneity and drivers of metabolic decline. While microbial diversity yields inconsistent signatures across cohorts, MHO is generally characterized by higher relative abundance of Ruminococcaceae, Oscillospira, Akkermansia, and Bifidobacterium and enrichment of other taxa predicted to be short-chain fatty acid-producers. Conversely, circulating gut-derived metabolomic signatures including altered secondary bile acid pools, elevated branched-chain amino acids, and trimethylamine N-oxide more reliably discriminate MUO from MHO than traditional measures, and correlate strongly with visceral adiposity, insulin resistance, and systemic inflammation. Furthermore, new systems biology approaches, such as integrating high-dimensional metagenomics and metabolomics via machine learning models, offer a potentially superior early indicators tool in precision medicine for identifying obesity phenotypes compared with traditional metrics (e.g., body mass index, fasting glucose). Overall, current evidence remains predominantly cross-sectional and based on secondary analyses of large cohort studies, underscoring the need for prospective longitudinal studies to validate these multi-omic biomarkers for precise phenotype identification and clinical risk assessment.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Faecalibacterium Mediates the Effect of Dairy Preference on Colorectal Cancer Susceptibility.
Phenomics (Cham, Switzerland), 6(4):427-438.
UNLABELLED: Current evidence supports the associations between diet, intestinal microbiome, and colorectal cancer (CRC) risk, but their causal relationships have not been extensively determined. Using large-scale genome-wide association study (GWAS) datasets of gut microbes (18,340 individuals), food preference (161,625 individuals), and CRC (24,476 cases vs. 23,073 controls), we applied a phenome-wide two-step bidirectional Mendelian randomization (MR) study to evaluate the causal effects of 45 food-liking traits on CRC susceptibility, and the mediating role of 131 microbiota. The inverse variance weighted (IVW) method was primarily employed, followed by multiple sensitivity analysis to assess the validity of the results. Among 45 categories, fatty/salty food preference was suggestively associated with a decreased risk of CRC [odds ratio (OR)IVW 0.65, 95% confidence interval (CI) 0.43-0.98, p = 0.040]. Furthermore, we identified four distinct food-microbiota association pairs, along with nine bacteria-CRC pairs. By integrating the association pairs, a putative causal pathway was found in dairy preference, increased abundance of Faecalibacterium (dairy preference-Faecalibacterium: βIVW = 0.72, 95% CI 0.30-1.13, p = 6.87 × 10[-4]), and decreased CRC risk (Faecalibacterium-CRC: ORIVW 0.91, 95% CI 0.85-0.97, p = 7.05 × 10[-3]), among which Faecalibacterium served as a potential mediator (p mediation = 0.035). Subsequent stratified analysis showed a consistent mediation in late-onset (age > 50; p = 0.029) and female (p = 0.049) populations. Our findings uncovered a novel causal pathway of dairy preference, gut Faecalibacterium levels, and CRC susceptibility, providing additional insights into CRC etiology and early prevention of CRC through dietary interventions.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at https://doi.org/10.1007/s43657-025-00241-w.
Additional Links: PMID-42953288
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@article {pmid42953288,
year = {2026},
author = {Liu, X and Wei, J and Shao, M and Chen, S and Li, H and Ji, H and Xin, J and Du, M},
title = {Faecalibacterium Mediates the Effect of Dairy Preference on Colorectal Cancer Susceptibility.},
journal = {Phenomics (Cham, Switzerland)},
volume = {6},
number = {4},
pages = {427-438},
pmid = {42953288},
issn = {2730-5848},
abstract = {UNLABELLED: Current evidence supports the associations between diet, intestinal microbiome, and colorectal cancer (CRC) risk, but their causal relationships have not been extensively determined. Using large-scale genome-wide association study (GWAS) datasets of gut microbes (18,340 individuals), food preference (161,625 individuals), and CRC (24,476 cases vs. 23,073 controls), we applied a phenome-wide two-step bidirectional Mendelian randomization (MR) study to evaluate the causal effects of 45 food-liking traits on CRC susceptibility, and the mediating role of 131 microbiota. The inverse variance weighted (IVW) method was primarily employed, followed by multiple sensitivity analysis to assess the validity of the results. Among 45 categories, fatty/salty food preference was suggestively associated with a decreased risk of CRC [odds ratio (OR)IVW 0.65, 95% confidence interval (CI) 0.43-0.98, p = 0.040]. Furthermore, we identified four distinct food-microbiota association pairs, along with nine bacteria-CRC pairs. By integrating the association pairs, a putative causal pathway was found in dairy preference, increased abundance of Faecalibacterium (dairy preference-Faecalibacterium: βIVW = 0.72, 95% CI 0.30-1.13, p = 6.87 × 10[-4]), and decreased CRC risk (Faecalibacterium-CRC: ORIVW 0.91, 95% CI 0.85-0.97, p = 7.05 × 10[-3]), among which Faecalibacterium served as a potential mediator (p mediation = 0.035). Subsequent stratified analysis showed a consistent mediation in late-onset (age > 50; p = 0.029) and female (p = 0.049) populations. Our findings uncovered a novel causal pathway of dairy preference, gut Faecalibacterium levels, and CRC susceptibility, providing additional insights into CRC etiology and early prevention of CRC through dietary interventions.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at https://doi.org/10.1007/s43657-025-00241-w.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Metabolomics-based comparison of metabolite profiles in Capparis spinosa L. from different habitats and associated soil factors.
Frontiers in plant science, 17:1914134.
INTRODUCTION: Capparis spinosa L. is a distinctive plant with edible and medicinal value, yet the factors influencing the accumulation of its effective components across diverse habitats remain unclear. This study aims to profile fruit metabolites and explore the association with rhizosphere soil environments.
METHODS: Using LC-MS/MS-based untargeted metabolomics (six biological replicates per habitat), fruit metabolites from three habitats in northern Xinjiang (Urumqi, Karamay, and Ili) were profiled. Partial least squares discriminant analysis (PLS-DA) identified differential metabolites. 16S rRNA sequencing analyzed rhizosphere soil microbial communities, and correlation analyses linked fruit metabolites with soil metabolites and microbiota.
RESULTS: A total of 1,739 metabolites were identified. PLS-DA revealed clear habitat separation, with 454, 340, and 411 differential metabolites in pairwise comparisons. Sixteen anti-inflammatory compounds (flavonoids, terpenoids, etc.) were candidate quality-associated metabolites, predominantly highest in Urumqi. Soil bacterial/fungal composition differed significantly among habitats, with Rubrobacterand Gaiella enriched in Urumqi. Correlation analysis linked 16 fruit metabolites (e.g., resveratrol, kaempferol) to 10 soil metabolites and specific soil genera.
DISCUSSION: Habitat-driven differences in soil microbial communities and metabolite levels are associated with bioactive component abundance in C. spinosa fruit, offering targets for habitat selection and microbiome-informed cultivation. Note that LC-MS/MS signal intensities are semi-quantitative; reported differences reflect relative abundance rather than absolute content.
Additional Links: PMID-42953365
PubMed:
Citation:
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@article {pmid42953365,
year = {2026},
author = {Xiayifu, X and Zhao, R and Bai, Z and Liu, X and Wang, X},
title = {Metabolomics-based comparison of metabolite profiles in Capparis spinosa L. from different habitats and associated soil factors.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1914134},
pmid = {42953365},
issn = {1664-462X},
abstract = {INTRODUCTION: Capparis spinosa L. is a distinctive plant with edible and medicinal value, yet the factors influencing the accumulation of its effective components across diverse habitats remain unclear. This study aims to profile fruit metabolites and explore the association with rhizosphere soil environments.
METHODS: Using LC-MS/MS-based untargeted metabolomics (six biological replicates per habitat), fruit metabolites from three habitats in northern Xinjiang (Urumqi, Karamay, and Ili) were profiled. Partial least squares discriminant analysis (PLS-DA) identified differential metabolites. 16S rRNA sequencing analyzed rhizosphere soil microbial communities, and correlation analyses linked fruit metabolites with soil metabolites and microbiota.
RESULTS: A total of 1,739 metabolites were identified. PLS-DA revealed clear habitat separation, with 454, 340, and 411 differential metabolites in pairwise comparisons. Sixteen anti-inflammatory compounds (flavonoids, terpenoids, etc.) were candidate quality-associated metabolites, predominantly highest in Urumqi. Soil bacterial/fungal composition differed significantly among habitats, with Rubrobacterand Gaiella enriched in Urumqi. Correlation analysis linked 16 fruit metabolites (e.g., resveratrol, kaempferol) to 10 soil metabolites and specific soil genera.
DISCUSSION: Habitat-driven differences in soil microbial communities and metabolite levels are associated with bioactive component abundance in C. spinosa fruit, offering targets for habitat selection and microbiome-informed cultivation. Note that LC-MS/MS signal intensities are semi-quantitative; reported differences reflect relative abundance rather than absolute content.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Host determinants of immune-related adverse events during immune checkpoint inhibition.
Frontiers in pharmacology, 17:1941544.
Immune checkpoint inhibitors (ICIs) have transformed the treatment of many cancers, but immune-related adverse events (irAEs) have become their principal limitation. This review argues that irAEs are not a random hazard of checkpoint blockade but a largely host-determined outcome layered on a drug-set baseline. The regimen fixes how much toxicity risk exists and, through the checkpoint it blocks, which organs are most likely affected. Within that envelope, host determinants decide which patient crosses the threshold of tolerance, and where. We synthesise the evidence for four classes of host determinant: germline genetic variation, including the IL7 locus and organ-directing human leucocyte antigen (HLA) alleles; the baseline immune landscape; the gut microbiome and metabolic state; and clinical characteristics led by pre-existing autoimmune disease. We draw two distinctions the literature often blurs. First, susceptibility should be read in two stages: determinants measurable before the first dose, which can triage patients, and on-treatment changes, which can only signal an event already emerging. Second, organ-specific toxicity is neither drug- nor host-intrinsic but the product of their intersection, with HLA restriction and shared tumour-tissue antigens offering the clearest mechanistic account of why a particular organ is struck. One theme runs throughout: many host features that raise irAE risk also predict a better antitumour response, so host stratification is a matter of optimising a benefit-to-toxicity balance rather than screening susceptible patients out. Multi-omics and systems immunology are assembling the measurements needed to act on this biology, but no host-based pre-treatment predictor is yet validated for clinical use. Realising one would shift checkpoint immunotherapy from the reactive management of toxicity toward its anticipation.
Additional Links: PMID-42953392
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Citation:
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@article {pmid42953392,
year = {2026},
author = {Alwithenani, A},
title = {Host determinants of immune-related adverse events during immune checkpoint inhibition.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1941544},
pmid = {42953392},
issn = {1663-9812},
abstract = {Immune checkpoint inhibitors (ICIs) have transformed the treatment of many cancers, but immune-related adverse events (irAEs) have become their principal limitation. This review argues that irAEs are not a random hazard of checkpoint blockade but a largely host-determined outcome layered on a drug-set baseline. The regimen fixes how much toxicity risk exists and, through the checkpoint it blocks, which organs are most likely affected. Within that envelope, host determinants decide which patient crosses the threshold of tolerance, and where. We synthesise the evidence for four classes of host determinant: germline genetic variation, including the IL7 locus and organ-directing human leucocyte antigen (HLA) alleles; the baseline immune landscape; the gut microbiome and metabolic state; and clinical characteristics led by pre-existing autoimmune disease. We draw two distinctions the literature often blurs. First, susceptibility should be read in two stages: determinants measurable before the first dose, which can triage patients, and on-treatment changes, which can only signal an event already emerging. Second, organ-specific toxicity is neither drug- nor host-intrinsic but the product of their intersection, with HLA restriction and shared tumour-tissue antigens offering the clearest mechanistic account of why a particular organ is struck. One theme runs throughout: many host features that raise irAE risk also predict a better antitumour response, so host stratification is a matter of optimising a benefit-to-toxicity balance rather than screening susceptible patients out. Multi-omics and systems immunology are assembling the measurements needed to act on this biology, but no host-based pre-treatment predictor is yet validated for clinical use. Realising one would shift checkpoint immunotherapy from the reactive management of toxicity toward its anticipation.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Research progress of polyunsaturated fatty acids in inflammatory bowel disease: from mechanisms to treatment.
Frontiers in pharmacology, 17:1971572.
Inflammatory bowel disease (IBD) imposes a growing clinical burden through recurrent intestinal inflammation, malnutrition, treatment-related toxicity, and incomplete mucosal healing. Polyunsaturated fatty acids (PUFAs) are plausible dietary regulators of this burden, yet their effects cannot be reduced to a simple anti-inflammatory role for n-3 PUFAs and a pro-inflammatory role for n-6 PUFAs. The proposed pre-clinical concept of PUFA-induced metabolic enteritis links dietary lipid exposure to epithelial stress, lipid peroxidation, and intestinal inflammation in genetically or metabolically susceptible pre-clinical models. Its human counterpart, however, remains incompletely defined. This narrative review integrates evidence across PUFA-derived lipid mediators, the gut microbiota, intestinal barrier function, mucosal immunity, and the glutathione peroxidase 4 (GPX4)-ferroptosis axis. We distinguish observational associations from interventional evidence and examine why clinical trials of eicosapentaenoic acid and docosahexaenoic acid have produced inconsistent results. We also evaluate dietary patterns, PUFA supplements, microbiome-directed approaches, specialized pro-resolving mediators, oxylipin pathways, and soluble epoxide hydrolase inhibition. Current evidence remains pre-clinical. Our review provides an approach and insights for managing IBD before PUFA-directed interventions are incorporated into precision treatment for IBD.
Additional Links: PMID-42953432
PubMed:
Citation:
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@article {pmid42953432,
year = {2026},
author = {Zhang, JL and Liu, Y and Liu, J and Yan, WN and Yu, Z},
title = {Research progress of polyunsaturated fatty acids in inflammatory bowel disease: from mechanisms to treatment.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1971572},
pmid = {42953432},
issn = {1663-9812},
abstract = {Inflammatory bowel disease (IBD) imposes a growing clinical burden through recurrent intestinal inflammation, malnutrition, treatment-related toxicity, and incomplete mucosal healing. Polyunsaturated fatty acids (PUFAs) are plausible dietary regulators of this burden, yet their effects cannot be reduced to a simple anti-inflammatory role for n-3 PUFAs and a pro-inflammatory role for n-6 PUFAs. The proposed pre-clinical concept of PUFA-induced metabolic enteritis links dietary lipid exposure to epithelial stress, lipid peroxidation, and intestinal inflammation in genetically or metabolically susceptible pre-clinical models. Its human counterpart, however, remains incompletely defined. This narrative review integrates evidence across PUFA-derived lipid mediators, the gut microbiota, intestinal barrier function, mucosal immunity, and the glutathione peroxidase 4 (GPX4)-ferroptosis axis. We distinguish observational associations from interventional evidence and examine why clinical trials of eicosapentaenoic acid and docosahexaenoic acid have produced inconsistent results. We also evaluate dietary patterns, PUFA supplements, microbiome-directed approaches, specialized pro-resolving mediators, oxylipin pathways, and soluble epoxide hydrolase inhibition. Current evidence remains pre-clinical. Our review provides an approach and insights for managing IBD before PUFA-directed interventions are incorporated into precision treatment for IBD.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
The gut-bone axis in osteoporosis: microbial mechanisms, conflicting evidence, and translational priorities.
Frontiers in immunology, 17:1966537.
Microbial effects on bone depend on the host's hormonal and inflammatory state, the microbial exposure and the tissue that receives it. This critical narrative review examines the gut-bone axis through those relationships, separating microbial associations from tested mechanisms and product-specific clinical effects. In mice, short-chain fatty acids can suppress osteoclast differentiation through metabolic reprogramming or promote bone formation through regulatory T-cell control of WNT10B production by CD8+ T cells. Intestinal T-cell trafficking also contributes to trabecular bone loss in an estrogen-deficiency model. These experiments identify causal links within defined systems; they do not establish equivalent pathways in patients. Bile acids, indole derivatives and bacterial extracellular vesicles provide further candidates, although evidence for tissue exposure and immune mediation varies. Human cohorts associate microbial features with bone density and incident fracture, but no consistent taxonomic signature has emerged across populations. Functional profiles may aid mechanistic interpretation, but their reproducibility across populations remains uncertain. Probiotic and synbiotic trials report benefit, no detectable effect or greater bone loss at particular sites. Discordance persists even between studies using the same strain accessions, making population, formulation and endpoint essential to interpretation. We distinguish microbial target engagement from bone-turnover responses, structural skeletal measures and fracture outcomes. The clinical evidence reviewed is insufficient to establish that microbiota-directed interventions reduce fragility-fracture risk. The recent, context-specific qualification of total-hip bone density as a surrogate nevertheless matters for future trial design. The most useful next studies will measure exposure and host response together, test the necessity of proposed mediators and prospectively examine host factors that may modify treatment response. This approach identifies where microbial mechanisms could complement established osteoporosis care without treating biological plausibility as clinical efficacy.
Additional Links: PMID-42953570
PubMed:
Citation:
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@article {pmid42953570,
year = {2026},
author = {Liu, Z and Yu, C},
title = {The gut-bone axis in osteoporosis: microbial mechanisms, conflicting evidence, and translational priorities.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1966537},
pmid = {42953570},
issn = {1664-3224},
mesh = {Humans ; *Osteoporosis/microbiology/metabolism/immunology ; Animals ; *Bone and Bones/metabolism/immunology ; *Gastrointestinal Microbiome/immunology ; Translational Research, Biomedical ; Probiotics ; Bone Remodeling ; Bone Density ; },
abstract = {Microbial effects on bone depend on the host's hormonal and inflammatory state, the microbial exposure and the tissue that receives it. This critical narrative review examines the gut-bone axis through those relationships, separating microbial associations from tested mechanisms and product-specific clinical effects. In mice, short-chain fatty acids can suppress osteoclast differentiation through metabolic reprogramming or promote bone formation through regulatory T-cell control of WNT10B production by CD8+ T cells. Intestinal T-cell trafficking also contributes to trabecular bone loss in an estrogen-deficiency model. These experiments identify causal links within defined systems; they do not establish equivalent pathways in patients. Bile acids, indole derivatives and bacterial extracellular vesicles provide further candidates, although evidence for tissue exposure and immune mediation varies. Human cohorts associate microbial features with bone density and incident fracture, but no consistent taxonomic signature has emerged across populations. Functional profiles may aid mechanistic interpretation, but their reproducibility across populations remains uncertain. Probiotic and synbiotic trials report benefit, no detectable effect or greater bone loss at particular sites. Discordance persists even between studies using the same strain accessions, making population, formulation and endpoint essential to interpretation. We distinguish microbial target engagement from bone-turnover responses, structural skeletal measures and fracture outcomes. The clinical evidence reviewed is insufficient to establish that microbiota-directed interventions reduce fragility-fracture risk. The recent, context-specific qualification of total-hip bone density as a surrogate nevertheless matters for future trial design. The most useful next studies will measure exposure and host response together, test the necessity of proposed mediators and prospectively examine host factors that may modify treatment response. This approach identifies where microbial mechanisms could complement established osteoporosis care without treating biological plausibility as clinical efficacy.},
}
MeSH Terms:
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Humans
*Osteoporosis/microbiology/metabolism/immunology
Animals
*Bone and Bones/metabolism/immunology
*Gastrointestinal Microbiome/immunology
Translational Research, Biomedical
Probiotics
Bone Remodeling
Bone Density
RevDate: 2026-10-29
CmpDate: 2026-10-29
Diet contributes to microbiome and niche differentiation among three sympatric cervids.
Frontiers in microbiology, 17:1980313.
BACKGROUND: Niche differentiation is a fundamental mechanism facilitating the coexistence of sympatric species, yet the extent to which dietary partitioning is associated with gut microbial differentiation remains poorly understood in wild cervids.
METHODS: Here, we investigated winter dietary composition and fecal microbiome communities of three sympatric cervid species-moose (Alces alces), red deer (Cervus elaphus), and roe deer (Capreolus pygargus)-in Youhao National Nature Reserve, northeastern China. A total of 55 fresh fecal samples were collected in January 2024, including 19 moose, 7 red deer, and 29 roe deer samples. Dietary composition was characterized using rbcL DNA metabarcoding, while microbiome communities were assessed using full-length 16S rRNA gene sequencing.
RESULTS: Our results showed the three cervid species exhibited distinct dietary patterns, moose showed a relatively narrow woody-plant-dominated diet, whereas red deer and roe deer exhibited higher dietary diversity, and roe deer exhibited broader use of shared plant resources; microbiome communities also differed significantly among host species, with moose showing the clearest separation from red deer and roe deer in community composition and predicted microbial metabolic potentials; Procrustes analysis revealed significant concordance between dietary composition and microbiome community, and redundancy analysis also indicated that dietary plant composition explained a significant proportion of variation in microbiome community.
CONCLUSION: These findings demonstrate that trophic differentiation among sympatric cervids is accompanied by coordinated variation in gut microbial community structure and predicted functional potential. The results support a close ecological association between dietary niche differentiation and host-associated microbiome variation, while causal and directional mechanisms require confirmation through longitudinal, experimental, and direct functional studies.
Additional Links: PMID-42953620
PubMed:
Citation:
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@article {pmid42953620,
year = {2026},
author = {Liang, Y and Zhang, W and Yang, F and Zhang, Y and Wei, R and Chu, C and Sun, J and Bao, H and Li, W},
title = {Diet contributes to microbiome and niche differentiation among three sympatric cervids.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1980313},
pmid = {42953620},
issn = {1664-302X},
abstract = {BACKGROUND: Niche differentiation is a fundamental mechanism facilitating the coexistence of sympatric species, yet the extent to which dietary partitioning is associated with gut microbial differentiation remains poorly understood in wild cervids.
METHODS: Here, we investigated winter dietary composition and fecal microbiome communities of three sympatric cervid species-moose (Alces alces), red deer (Cervus elaphus), and roe deer (Capreolus pygargus)-in Youhao National Nature Reserve, northeastern China. A total of 55 fresh fecal samples were collected in January 2024, including 19 moose, 7 red deer, and 29 roe deer samples. Dietary composition was characterized using rbcL DNA metabarcoding, while microbiome communities were assessed using full-length 16S rRNA gene sequencing.
RESULTS: Our results showed the three cervid species exhibited distinct dietary patterns, moose showed a relatively narrow woody-plant-dominated diet, whereas red deer and roe deer exhibited higher dietary diversity, and roe deer exhibited broader use of shared plant resources; microbiome communities also differed significantly among host species, with moose showing the clearest separation from red deer and roe deer in community composition and predicted microbial metabolic potentials; Procrustes analysis revealed significant concordance between dietary composition and microbiome community, and redundancy analysis also indicated that dietary plant composition explained a significant proportion of variation in microbiome community.
CONCLUSION: These findings demonstrate that trophic differentiation among sympatric cervids is accompanied by coordinated variation in gut microbial community structure and predicted functional potential. The results support a close ecological association between dietary niche differentiation and host-associated microbiome variation, while causal and directional mechanisms require confirmation through longitudinal, experimental, and direct functional studies.},
}
RevDate: 2026-10-29
Integrated soil-microbe-plant regulation for maize disease control in the black soil of Northeast China.
mLife [Epub ahead of print].
The black soil region of Northeast China is a critical area for maize production in China. However, the long-term continuous cropping, coupled with residue-driven pathogen carryover, soil organic matter depletion, nutrient imbalance, and climate variability, has increased maize vulnerability to diseases. This review synthesizes current knowledge on the integrated regulation of soil, microbiomes, and plant immunity for maize disease management in this region. It assesses the physicochemical properties of the soil, the microbiota, and plant immune responses. Particular attention is paid to current biological control approaches. These plant immunity- and microbiome-based strategies include beneficial microbe-mediated immune priming, activation of induced systemic resistance, modulation of plant hormone signaling networks, RNA interference (RNAi)-based immune regulation, and microbiome-assisted enhancement of disease resistance. The underlying mechanisms include recruitment of beneficial microorganisms, suppression of pathogen growth and virulence, stabilization of protective microbial networks, activation of plant immune signaling, and enhancement of stress resilience. This review also compares these strategies in terms of disease-control efficacy, yield benefits, stability, cost, biosafety, and commercialization potential, and proposes a region-specific pathway for their integrated deployment. Establishment of a coordinated regulatory framework that combines soil-health improvement, microbiome intervention, pathogen monitoring, and plant immune enhancement will support the transition from chemical-dependent disease control to proactive and sustainable maize production systems in the black soil region of Northeast China.
Additional Links: PMID-42953682
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@article {pmid42953682,
year = {2026},
author = {Zhao, P and Hu, J and Zhou, J and Chen, RB and Zhao, JH and Deng, C and Jia, Y},
title = {Integrated soil-microbe-plant regulation for maize disease control in the black soil of Northeast China.},
journal = {mLife},
volume = {},
number = {},
pages = {},
pmid = {42953682},
issn = {2770-100X},
abstract = {The black soil region of Northeast China is a critical area for maize production in China. However, the long-term continuous cropping, coupled with residue-driven pathogen carryover, soil organic matter depletion, nutrient imbalance, and climate variability, has increased maize vulnerability to diseases. This review synthesizes current knowledge on the integrated regulation of soil, microbiomes, and plant immunity for maize disease management in this region. It assesses the physicochemical properties of the soil, the microbiota, and plant immune responses. Particular attention is paid to current biological control approaches. These plant immunity- and microbiome-based strategies include beneficial microbe-mediated immune priming, activation of induced systemic resistance, modulation of plant hormone signaling networks, RNA interference (RNAi)-based immune regulation, and microbiome-assisted enhancement of disease resistance. The underlying mechanisms include recruitment of beneficial microorganisms, suppression of pathogen growth and virulence, stabilization of protective microbial networks, activation of plant immune signaling, and enhancement of stress resilience. This review also compares these strategies in terms of disease-control efficacy, yield benefits, stability, cost, biosafety, and commercialization potential, and proposes a region-specific pathway for their integrated deployment. Establishment of a coordinated regulatory framework that combines soil-health improvement, microbiome intervention, pathogen monitoring, and plant immune enhancement will support the transition from chemical-dependent disease control to proactive and sustainable maize production systems in the black soil region of Northeast China.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Organ-specific microbiomes reveal strong bacterial compartmentalization in two tropical squid species.
microLife, 7:uqag037.
Beyond the well-established symbiosis between the bobtail squid light organ and the bioluminescent bacterium Aliivibrio fischeri, the microbiomes associated with other cephalopod tissues remain poorly characterized. Here, we examined bacterial communities associated with major organs (e.g. skin, gut, gills and nidamental gland) in two Southeast Asian squid species, Uroteuthis chinensis and Sepioteuthis lessoniana. Because host species and environmental/temporal factors were fully confounded in our sampling design, we focused on characterizing microbiome compartmentalization across organs rather than on disentangling their relative contributions. Bacterial communities were strongly structured by anatomical compartment, with each organ harboring a distinct microbiome. In U. chinensis, gill communities were dominated by Endozoicomonas, whereas the gut microbiome of S. lessoniana was dominated by Mycoplasma. Nidamental glands from both species were enriched in Ruegeria and Pikeienuella, while skin communities displayed marked interspecific differences: U. chinensis skin was enriched in Sphingomonadales and Vibrionales, whereas S. lessoniana exhibited a more diverse mix including Micrococcales, Hyphomicrobiales, and Flavobacteriales. Together, these results provide a first descriptive characterization of microbiome organization across major squid organs and establish a baseline for future studies investigating the ecological and functional roles of host-associated bacteria in cephalopods.
Additional Links: PMID-42953723
PubMed:
Citation:
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@article {pmid42953723,
year = {2026},
author = {Bettarel, Y and Gadoin, E and Bouvier, T and Auguet, JC and Crochemore, S and Mehrotra, R and Nguyen, VX and Du, HT},
title = {Organ-specific microbiomes reveal strong bacterial compartmentalization in two tropical squid species.},
journal = {microLife},
volume = {7},
number = {},
pages = {uqag037},
pmid = {42953723},
issn = {2633-6693},
abstract = {Beyond the well-established symbiosis between the bobtail squid light organ and the bioluminescent bacterium Aliivibrio fischeri, the microbiomes associated with other cephalopod tissues remain poorly characterized. Here, we examined bacterial communities associated with major organs (e.g. skin, gut, gills and nidamental gland) in two Southeast Asian squid species, Uroteuthis chinensis and Sepioteuthis lessoniana. Because host species and environmental/temporal factors were fully confounded in our sampling design, we focused on characterizing microbiome compartmentalization across organs rather than on disentangling their relative contributions. Bacterial communities were strongly structured by anatomical compartment, with each organ harboring a distinct microbiome. In U. chinensis, gill communities were dominated by Endozoicomonas, whereas the gut microbiome of S. lessoniana was dominated by Mycoplasma. Nidamental glands from both species were enriched in Ruegeria and Pikeienuella, while skin communities displayed marked interspecific differences: U. chinensis skin was enriched in Sphingomonadales and Vibrionales, whereas S. lessoniana exhibited a more diverse mix including Micrococcales, Hyphomicrobiales, and Flavobacteriales. Together, these results provide a first descriptive characterization of microbiome organization across major squid organs and establish a baseline for future studies investigating the ecological and functional roles of host-associated bacteria in cephalopods.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
The role of the microbiome in diabetic foot ulcers: Biofilm community dynamics differ with healing outcomes.
Biofilm, 12:100405.
Diabetic foot ulcers often develop into non-healing chronic wounds due to their high risk of infection resulting from exposure to various microbes, combined with a lowered immune response due to the patient's diabetic status. Recently, an increased understanding of the polymicrobial nature of chronic wound infections has given rise to questions on the role of the microbiome on healing outcomes. In our study, we aimed to investigate the microbiome composition and its pathological influence in 128 patients using the Oxford NanoPore Sequencing platform and the 16S rRNA region for sample amplification. Overall, the most abundant genera and species present in the microbiomes of these patients resembled other published studies, namely Cutibacteria, Staphylococcus and Pseudomonas. A key factor in healing outcomes was the presence of fungi, which was strongly correlated with pathogenic anaerobes such as Prevotella bivia and associated with negative outcomes. While we could not determine a direct causal link between fungi and outcomes, the data strongly suggests that fungal presence plays a role in the composition of bacterial communities in the wound environment and is potentially enabling infection persistence. Furthermore, we observed that certain bacterial species were present in all outcomes, but part of different microbial networks, hinting that healing success could be determined by these associations established in the community rather than presence of a specific pathobiont. In conclusion, while an initial look at the composition can provide an insight into the most abundant genus/species present in certain outcomes, when investigating deeper we see that associations among different taxa may play a more significant role in determining healing. We postulate that interfering with these interactions could potentially be the key to tipping the balance towards positive healing outcomes.
Additional Links: PMID-42953731
PubMed:
Citation:
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@article {pmid42953731,
year = {2026},
author = {Allkja, J and Bairoliya, S and Bakri, A and Short, B and Brown, JL and Delaney, C and Smith, P and Short, RD and Jenkins, T and Cao, B and Williams, C and Ramage, G},
title = {The role of the microbiome in diabetic foot ulcers: Biofilm community dynamics differ with healing outcomes.},
journal = {Biofilm},
volume = {12},
number = {},
pages = {100405},
pmid = {42953731},
issn = {2590-2075},
abstract = {Diabetic foot ulcers often develop into non-healing chronic wounds due to their high risk of infection resulting from exposure to various microbes, combined with a lowered immune response due to the patient's diabetic status. Recently, an increased understanding of the polymicrobial nature of chronic wound infections has given rise to questions on the role of the microbiome on healing outcomes. In our study, we aimed to investigate the microbiome composition and its pathological influence in 128 patients using the Oxford NanoPore Sequencing platform and the 16S rRNA region for sample amplification. Overall, the most abundant genera and species present in the microbiomes of these patients resembled other published studies, namely Cutibacteria, Staphylococcus and Pseudomonas. A key factor in healing outcomes was the presence of fungi, which was strongly correlated with pathogenic anaerobes such as Prevotella bivia and associated with negative outcomes. While we could not determine a direct causal link between fungi and outcomes, the data strongly suggests that fungal presence plays a role in the composition of bacterial communities in the wound environment and is potentially enabling infection persistence. Furthermore, we observed that certain bacterial species were present in all outcomes, but part of different microbial networks, hinting that healing success could be determined by these associations established in the community rather than presence of a specific pathobiont. In conclusion, while an initial look at the composition can provide an insight into the most abundant genus/species present in certain outcomes, when investigating deeper we see that associations among different taxa may play a more significant role in determining healing. We postulate that interfering with these interactions could potentially be the key to tipping the balance towards positive healing outcomes.},
}
RevDate: 2026-10-29
Correction: Oral liposomal co-delivery of ultrasmall ceria and 5-aminosalicylic acid alleviates DSS colitis via ROS scavenging and microbiome remodeling.
Correction for 'Oral liposomal co-delivery of ultrasmall ceria and 5-aminosalicylic acid alleviates DSS colitis via ROS scavenging and microbiome remodeling' by Jiahao Du et al., J. Mater. Chem. B, 2026, 14, 4956-4970, https://doi.org/10.1039/d6tb00173d.
Additional Links: PMID-42953972
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PubMed:
Citation:
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@article {pmid42953972,
year = {2026},
author = {Du, J and Sun, Y and Yu, D and Lu, S and Yu, S and Wang, M and Zhou, G and Xu, S and Zhang, L and Zhu, Y and Zhou, L},
title = {Correction: Oral liposomal co-delivery of ultrasmall ceria and 5-aminosalicylic acid alleviates DSS colitis via ROS scavenging and microbiome remodeling.},
journal = {Journal of materials chemistry. B},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6tb90156e},
pmid = {42953972},
issn = {2050-7518},
abstract = {Correction for 'Oral liposomal co-delivery of ultrasmall ceria and 5-aminosalicylic acid alleviates DSS colitis via ROS scavenging and microbiome remodeling' by Jiahao Du et al., J. Mater. Chem. B, 2026, 14, 4956-4970, https://doi.org/10.1039/d6tb00173d.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Artificial Intelligence-Driven Graph Methods for Microbiome Research: A Systematic Review.
WIREs mechanisms of disease, 18(6):.
The complexity of high-throughput sequencing data in microbiome research necessitates advanced analytical methods to decipher microbial community structures and interactions. Graph-based methods, which model taxa as nodes and their relationships as edges, have emerged as a powerful framework for this purpose. However, the rapid evolution of these techniques, from classical network analysis to modern graph representation learning, has created a fragmented and complex methodological landscape. This systematic review provides a comprehensive synthesis and structured overview of the field. We systematically review the literature and propose a three-part classification to categorize the primary contribution of each study: (1) novel methods for microbial network representation, (2) applications of classical graph analysis, and (3) the emerging use of graph representation learning for predictive modeling. We summarize the most frequent applications within each class, including keystone species identification, community clustering, and graph-based disease classification. Furthermore, we identify critical cross-cutting challenges, such as the lack of standardized tools and the need for improved model interpretability. By structuring the current landscape of graph-based methods, this review serves as a crucial guide for researchers to select appropriate models and highlights key gaps to direct future research.
Additional Links: PMID-42953986
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@article {pmid42953986,
year = {2026},
author = {Shum-Tim, C and Islam, P and Boyajian, JL and Abosalha, A and Kassab, A and Santos, M and Khan, KA and Stern, K and Emad, A and Prakash, S},
title = {Artificial Intelligence-Driven Graph Methods for Microbiome Research: A Systematic Review.},
journal = {WIREs mechanisms of disease},
volume = {18},
number = {6},
pages = {},
doi = {10.1002/wsbm.70016},
pmid = {42953986},
issn = {2692-9368},
support = {252743//Canadian Institute of Health Research/ ; 335999//Fonds de Recherche du Québec-Santé/ ; 351337//Fonds de Recherche du Québec-Santé/ ; 2020-245622//Islamic Development Bank Scholarship/ ; //Ministry of Higher Education of the Arab Republic of Egypt/ ; 504933//Natural Sciences and Engineering Research Council of Canada (NSERC)/ ; },
mesh = {*Microbiota/genetics ; *Artificial Intelligence ; Humans ; Animals ; },
abstract = {The complexity of high-throughput sequencing data in microbiome research necessitates advanced analytical methods to decipher microbial community structures and interactions. Graph-based methods, which model taxa as nodes and their relationships as edges, have emerged as a powerful framework for this purpose. However, the rapid evolution of these techniques, from classical network analysis to modern graph representation learning, has created a fragmented and complex methodological landscape. This systematic review provides a comprehensive synthesis and structured overview of the field. We systematically review the literature and propose a three-part classification to categorize the primary contribution of each study: (1) novel methods for microbial network representation, (2) applications of classical graph analysis, and (3) the emerging use of graph representation learning for predictive modeling. We summarize the most frequent applications within each class, including keystone species identification, community clustering, and graph-based disease classification. Furthermore, we identify critical cross-cutting challenges, such as the lack of standardized tools and the need for improved model interpretability. By structuring the current landscape of graph-based methods, this review serves as a crucial guide for researchers to select appropriate models and highlights key gaps to direct future research.},
}
MeSH Terms:
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hide MeSH Terms
*Microbiota/genetics
*Artificial Intelligence
Humans
Animals
RevDate: 2026-10-29
CmpDate: 2026-10-29
Small-Intestinal Motility Interrelates With Fecal Microbiota, Metabolites and Metabolic Tissue Gene Expression in Metabolic Dysfunction-Associated Steatotic Liver Disease.
Journal of neurogastroenterology and motility, 32(4):684-696.
BACKGROUND/AIMS: : Recent studies show that the gut microbiota may affect both small-intestinal motility and metabolic dysfunction-associated steatotic liver disease (MASLD). However, human studies of this triangle are lacking. Our aim was to leverage the unique potential of cine-MRI to quantify small-intestinal motility in patients with MASLD and investigate its association with gut microbiota, metabolic tissues and metabolites.
METHODS: : Fifteen patients with histology proven MASLD participated in a 12-week exercise intervention. At baseline and endpoint, small-intestinal motility and liver status were assessed using MRI. Stool consistency and composition of fecal microbiome as well as mRNA expression of liver, skeletal muscle, and subcutaneous adipose tissue biopsies were studied. Non-targeted metabolomics was performed on stool, fasted plasma, and urine samples.
RESULTS: : At baseline, small-intestinal motility did not correlate to liver histology scores or MRI-determined markers of liver fat, stiffness, or inflammation. However, small-intestinal motility did correlate with fecal microbiota, including Verrucomicrobia and Bacteroidetes phyla as well as 41 species such as Prevotella species incertae sedis (false discovery rate [FDR]-P < 0.2). Moreover, liver RNA sequencing revealed correlations of small-intestinal motility with liver mRNA expression of CBS (FDR-P < 0.001), linked to hydrogen sulfide production, and adipose tissue mRNA expression of SCARB1 and SCD1 (FDR-P < 0.05), involved in lipid metabolism. Several stool, plasma, and urine metabolites correlated with small-intestinal motility. Exercise had no effect.
CONCLUSIONS: : In MASLD patients, small-intestinal motility associates with gut microbiota, metabolites and mRNA expression in metabolic tissues. These findings warrant further investigation to determine causality and effect directionality. Additionally, this exploratory study demonstrates the potential of cine-MRI for fundamental small-intestinal motility research.
Additional Links: PMID-42954017
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PubMed:
Citation:
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@article {pmid42954017,
year = {2026},
author = {Houttu, V and Boulund, U and Holleboom, AG and Grefhorst, A and Babu, AF and Hanhineva, K and Nieuwdorp, M and Jonge, CS},
title = {Small-Intestinal Motility Interrelates With Fecal Microbiota, Metabolites and Metabolic Tissue Gene Expression in Metabolic Dysfunction-Associated Steatotic Liver Disease.},
journal = {Journal of neurogastroenterology and motility},
volume = {32},
number = {4},
pages = {684-696},
doi = {10.5056/jnm25139},
pmid = {42954017},
issn = {2093-0879},
abstract = {BACKGROUND/AIMS: : Recent studies show that the gut microbiota may affect both small-intestinal motility and metabolic dysfunction-associated steatotic liver disease (MASLD). However, human studies of this triangle are lacking. Our aim was to leverage the unique potential of cine-MRI to quantify small-intestinal motility in patients with MASLD and investigate its association with gut microbiota, metabolic tissues and metabolites.
METHODS: : Fifteen patients with histology proven MASLD participated in a 12-week exercise intervention. At baseline and endpoint, small-intestinal motility and liver status were assessed using MRI. Stool consistency and composition of fecal microbiome as well as mRNA expression of liver, skeletal muscle, and subcutaneous adipose tissue biopsies were studied. Non-targeted metabolomics was performed on stool, fasted plasma, and urine samples.
RESULTS: : At baseline, small-intestinal motility did not correlate to liver histology scores or MRI-determined markers of liver fat, stiffness, or inflammation. However, small-intestinal motility did correlate with fecal microbiota, including Verrucomicrobia and Bacteroidetes phyla as well as 41 species such as Prevotella species incertae sedis (false discovery rate [FDR]-P < 0.2). Moreover, liver RNA sequencing revealed correlations of small-intestinal motility with liver mRNA expression of CBS (FDR-P < 0.001), linked to hydrogen sulfide production, and adipose tissue mRNA expression of SCARB1 and SCD1 (FDR-P < 0.05), involved in lipid metabolism. Several stool, plasma, and urine metabolites correlated with small-intestinal motility. Exercise had no effect.
CONCLUSIONS: : In MASLD patients, small-intestinal motility associates with gut microbiota, metabolites and mRNA expression in metabolic tissues. These findings warrant further investigation to determine causality and effect directionality. Additionally, this exploratory study demonstrates the potential of cine-MRI for fundamental small-intestinal motility research.},
}
RevDate: 2026-10-29
The Microbiome-Arginine-Immune Axis in Oral Squamous Cell Carcinoma: Metabolic Competition and Therapeutic Opportunities.
Cancer investigation [Epub ahead of print].
Oral squamous cell carcinoma (OSCC) is strongly influenced by metabolic and immune dysregulation. Recent evidence highlights the role of L-arginine metabolism and arginase isoforms (ARG1/ARG2) in tumour progression, immune suppression, and metabolic reprogramming. This narrative review integrates published evidence with an independent bioinformatic reanalysis of publicly available transcriptomic and immune infiltration datasets to examine arginase signalling in oral squamous cell carcinoma and to explore how oral dysbiosis may contribute to extracellular arginine depletion and tumour-promoting immune dysfunction. These findings support the microbiome-arginine-immune axis as a promising framework for future biomarker development and metabolism-based therapeutic strategies in OSCC.
Additional Links: PMID-42954168
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PubMed:
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@article {pmid42954168,
year = {2026},
author = {Ramachandran, P and Gopalakrishnan, R and Gunasekaran, R and Kannan, K and Ganapathy, D and Pitchiah, S},
title = {The Microbiome-Arginine-Immune Axis in Oral Squamous Cell Carcinoma: Metabolic Competition and Therapeutic Opportunities.},
journal = {Cancer investigation},
volume = {},
number = {},
pages = {1-14},
doi = {10.1080/07357907.2026.2756385},
pmid = {42954168},
issn = {1532-4192},
abstract = {Oral squamous cell carcinoma (OSCC) is strongly influenced by metabolic and immune dysregulation. Recent evidence highlights the role of L-arginine metabolism and arginase isoforms (ARG1/ARG2) in tumour progression, immune suppression, and metabolic reprogramming. This narrative review integrates published evidence with an independent bioinformatic reanalysis of publicly available transcriptomic and immune infiltration datasets to examine arginase signalling in oral squamous cell carcinoma and to explore how oral dysbiosis may contribute to extracellular arginine depletion and tumour-promoting immune dysfunction. These findings support the microbiome-arginine-immune axis as a promising framework for future biomarker development and metabolism-based therapeutic strategies in OSCC.},
}
RevDate: 2026-10-29
Longitudinal changes in gut microbial evenness and dominance during anti-CD20-containing chemoimmunotherapy with concurrent trimethoprim-sulfamethoxazole prophylaxis in patients with B-cell lymphoma.
Immunological medicine [Epub ahead of print].
Reduced gut microbial diversity is associated with adverse outcomes in hematological malignancies. However, longitudinal studies during lymphoma chemoimmunotherapy rarely distinguish richness from evenness. We investigated whether microbial diversity shifts during anti-CD20-containing chemoimmunotherapy reflect loss of detected taxa or redistribution of relative abundances. In this prospective, single-center exploratory study, 40 patients with B-cell lymphoma provided pretreatment stool samples and 18 paired post-treatment samples. All 18 participants received trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis from treatment initiation through post-treatment sampling, without additional systemic antibacterial exposure between collections or during the 3 months preceding baseline. Following 16S rRNA gene V3-V4 sequencing, Pielou's evenness (q = 0.0077) and Shannon diversity (q = 0.0208) decreased post-treatment, whereas observed features and Faith's phylogenetic diversity did not change significantly (q = 0.4923 and 0.7660, respectively). Dominance significantly increased (Simpson, q = 0.0154; Berger-Parker, q = 0.0237). Beta diversity showed no detectable compositional shift, no genus-level taxon met differential-abundance criteria, and newly dominant taxa varied across individuals. These changes accompanied the combined treatment exposure in a cohort that may overrepresent clinically stable patients; the chemoimmunotherapy and TMP-SMX contributions were inseparable. These alterations appear modest and predominantly structural, with the clearest changes in evenness and dominance, and substantial uncertainty about richness.
Additional Links: PMID-42954192
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PubMed:
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@article {pmid42954192,
year = {2026},
author = {Ito, S and Otake, S and Nakagawa, M and Takahashi, H and Miura, K and Nakamura, H and Komine-Aizawa, S},
title = {Longitudinal changes in gut microbial evenness and dominance during anti-CD20-containing chemoimmunotherapy with concurrent trimethoprim-sulfamethoxazole prophylaxis in patients with B-cell lymphoma.},
journal = {Immunological medicine},
volume = {},
number = {},
pages = {1-16},
doi = {10.1080/25785826.2026.2753278},
pmid = {42954192},
issn = {2578-5826},
abstract = {Reduced gut microbial diversity is associated with adverse outcomes in hematological malignancies. However, longitudinal studies during lymphoma chemoimmunotherapy rarely distinguish richness from evenness. We investigated whether microbial diversity shifts during anti-CD20-containing chemoimmunotherapy reflect loss of detected taxa or redistribution of relative abundances. In this prospective, single-center exploratory study, 40 patients with B-cell lymphoma provided pretreatment stool samples and 18 paired post-treatment samples. All 18 participants received trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis from treatment initiation through post-treatment sampling, without additional systemic antibacterial exposure between collections or during the 3 months preceding baseline. Following 16S rRNA gene V3-V4 sequencing, Pielou's evenness (q = 0.0077) and Shannon diversity (q = 0.0208) decreased post-treatment, whereas observed features and Faith's phylogenetic diversity did not change significantly (q = 0.4923 and 0.7660, respectively). Dominance significantly increased (Simpson, q = 0.0154; Berger-Parker, q = 0.0237). Beta diversity showed no detectable compositional shift, no genus-level taxon met differential-abundance criteria, and newly dominant taxa varied across individuals. These changes accompanied the combined treatment exposure in a cohort that may overrepresent clinically stable patients; the chemoimmunotherapy and TMP-SMX contributions were inseparable. These alterations appear modest and predominantly structural, with the clearest changes in evenness and dominance, and substantial uncertainty about richness.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
A host-directed virulence factor of Clostridium perfringens is modulated by gut commensal strains.
Gut microbes, 18(1):2748768.
In a healthy host, the residential microbes help regulate the growth of pathobionts, which are common members of the human gut microbiome, preventing them from causing diseases, including infections, under certain conditions. In cases of dysbiosis, this protection may be compromised. Targeted microbiome modulation offers a promising approach to restore healthy conditions in a disrupted community and consequently prevent infections using the natural colonization resistance of the microbiome. Elucidating the interaction mechanisms between microbial species within a microbiome is crucial for understanding how a microbiome can be modulated precisely and effectively to benefit the host's well-being. Here, we investigated the interactions between the pathobiont C. perfringens and human gut commensals by combining relative abundance measurements in co-culture versus monoculture with proteome and metabolome profiling of all mono- and co-cultures. We found that commensal strains affect C. perfringens growth by competing for substrates such as amino acids or a carbon source other than glucose. We further observed that Bacteroidaceae strains altered the levels of C. perfringens proteins, among others, the host-directed θ-toxin. Our findings reinforce the notion that modulating the composition of the gut microbiome is an effective strategy to prevent infections.
Additional Links: PMID-42954253
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PubMed:
Citation:
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@article {pmid42954253,
year = {2026},
author = {Schumacher, J and Stincone, P and Rapp, J and Lucas, TN and Llaca-Bautista, C and Barletta, F and Franz, M and Maček, B and Huson, DH and Maier, L and Link, H and Petras, D and Molitor, B},
title = {A host-directed virulence factor of Clostridium perfringens is modulated by gut commensal strains.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2748768},
doi = {10.1080/19490976.2026.2748768},
pmid = {42954253},
issn = {1949-0984},
mesh = {*Clostridium perfringens/growth & development/metabolism/genetics/pathogenicity ; *Virulence Factors/metabolism/genetics ; Humans ; *Gastrointestinal Microbiome ; Symbiosis ; Bacterial Proteins/metabolism/genetics ; Coculture Techniques ; Host Microbial Interactions ; },
abstract = {In a healthy host, the residential microbes help regulate the growth of pathobionts, which are common members of the human gut microbiome, preventing them from causing diseases, including infections, under certain conditions. In cases of dysbiosis, this protection may be compromised. Targeted microbiome modulation offers a promising approach to restore healthy conditions in a disrupted community and consequently prevent infections using the natural colonization resistance of the microbiome. Elucidating the interaction mechanisms between microbial species within a microbiome is crucial for understanding how a microbiome can be modulated precisely and effectively to benefit the host's well-being. Here, we investigated the interactions between the pathobiont C. perfringens and human gut commensals by combining relative abundance measurements in co-culture versus monoculture with proteome and metabolome profiling of all mono- and co-cultures. We found that commensal strains affect C. perfringens growth by competing for substrates such as amino acids or a carbon source other than glucose. We further observed that Bacteroidaceae strains altered the levels of C. perfringens proteins, among others, the host-directed θ-toxin. Our findings reinforce the notion that modulating the composition of the gut microbiome is an effective strategy to prevent infections.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Clostridium perfringens/growth & development/metabolism/genetics/pathogenicity
*Virulence Factors/metabolism/genetics
Humans
*Gastrointestinal Microbiome
Symbiosis
Bacterial Proteins/metabolism/genetics
Coculture Techniques
Host Microbial Interactions
RevDate: 2026-10-29
Microbial profiling of Drosophila in French Guiana reveals candidate microbial taxa associated with native and invasive host.
FEMS microbiology ecology pii:9004468 [Epub ahead of print].
Invasive alien species (IAS) threaten biodiversity, human health, and economies, yet host-associated microbiome differences between invasive and native species remain poorly understood in natural systems. We investigated bacterial and fungal microbiomes of IAS and native Drosophila species collected along an anthropisation gradient in French Guiana. IAS occurrence declined strongly from coastal anthropised habitats toward rainforest localities. Using bacterial 16S rRNA and fungal ITS metabarcoding of pooled flies, we assessed microbial diversity and community structure across host species, host category (invasive vs. native), and locality. IAS-associated bacterial communities showed reduced alpha diversity and differed in structure from those of native Drosophila. Bacteriome variation was also associated with host phylogeny and locality; because host category was partially confounded with these factors, differences cannot be attributed solely to invasion status. Fungal communities were primarily associated with locality and host species. We further identified core and exclusive taxa and compared bacteriome composition with global reference datasets and microbiome literature, identifying bacterial and fungal taxa preferentially or exclusively associated with invasive or native hosts. Overall, our study characterises microbiome variation between invasive and native Drosophila in French Guiana and identifies candidate taxa for future functional investigation.
Additional Links: PMID-42954383
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PubMed:
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@article {pmid42954383,
year = {2026},
author = {Laffargue, TT and Pollet, N and Brousseau, L and Miller, WJ and Hua-Van, A and Chouteau, M},
title = {Microbial profiling of Drosophila in French Guiana reveals candidate microbial taxa associated with native and invasive host.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag121},
pmid = {42954383},
issn = {1574-6941},
abstract = {Invasive alien species (IAS) threaten biodiversity, human health, and economies, yet host-associated microbiome differences between invasive and native species remain poorly understood in natural systems. We investigated bacterial and fungal microbiomes of IAS and native Drosophila species collected along an anthropisation gradient in French Guiana. IAS occurrence declined strongly from coastal anthropised habitats toward rainforest localities. Using bacterial 16S rRNA and fungal ITS metabarcoding of pooled flies, we assessed microbial diversity and community structure across host species, host category (invasive vs. native), and locality. IAS-associated bacterial communities showed reduced alpha diversity and differed in structure from those of native Drosophila. Bacteriome variation was also associated with host phylogeny and locality; because host category was partially confounded with these factors, differences cannot be attributed solely to invasion status. Fungal communities were primarily associated with locality and host species. We further identified core and exclusive taxa and compared bacteriome composition with global reference datasets and microbiome literature, identifying bacterial and fungal taxa preferentially or exclusively associated with invasive or native hosts. Overall, our study characterises microbiome variation between invasive and native Drosophila in French Guiana and identifies candidate taxa for future functional investigation.},
}
RevDate: 2026-10-29
Microbiome science needs AI competence, not just AI literacy.
FEMS microbiology letters pii:9004453 [Epub ahead of print].
Artificial intelligence is rapidly becoming embedded in microbiome research, yet the way microbiome scientists are trained has not kept pace. Existing discussions frequently emphasize AI literacy and responsible tool use. We argue that literacy alone is insufficient in a field where data leakage, incomplete metadata, ecological confounding, inappropriate model selection and unverified generative-AI outputs can produce convincing but biologically misleading conclusions. We propose an AI-competence framework comprising five connected capabilities: data and platform fluency, machine-learning competence, advanced model competence, large-language-model and agent competence, and biological closure. The final capability-the ability to connect computational predictions to independent data, mechanistic reasoning or experimental evidence-is essential for ensuring that predictive performance becomes meaningful biology. We further propose that competence should be demonstrated through reproducible scientific artifacts rather than course completion alone. Shared datasets, computational platforms and benchmark challenges could make such training broadly accessible while establishing common standards for evaluating AI competence in microbiome science.
Additional Links: PMID-42954392
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PubMed:
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@article {pmid42954392,
year = {2026},
author = {Anand, A},
title = {Microbiome science needs AI competence, not just AI literacy.},
journal = {FEMS microbiology letters},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsle/fnag133},
pmid = {42954392},
issn = {1574-6968},
abstract = {Artificial intelligence is rapidly becoming embedded in microbiome research, yet the way microbiome scientists are trained has not kept pace. Existing discussions frequently emphasize AI literacy and responsible tool use. We argue that literacy alone is insufficient in a field where data leakage, incomplete metadata, ecological confounding, inappropriate model selection and unverified generative-AI outputs can produce convincing but biologically misleading conclusions. We propose an AI-competence framework comprising five connected capabilities: data and platform fluency, machine-learning competence, advanced model competence, large-language-model and agent competence, and biological closure. The final capability-the ability to connect computational predictions to independent data, mechanistic reasoning or experimental evidence-is essential for ensuring that predictive performance becomes meaningful biology. We further propose that competence should be demonstrated through reproducible scientific artifacts rather than course completion alone. Shared datasets, computational platforms and benchmark challenges could make such training broadly accessible while establishing common standards for evaluating AI competence in microbiome science.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Disease-specific gut microbiota-metabolite-immune networks in hematologic disorders: mechanisms, causal support, and translational strategies.
Gut microbes, 18(1):2752469.
The gut microbiota is increasingly recognized as a systemic regulator of host immunity, host metabolism, epithelial barrier integrity, and distal tissue homeostasis. Hematologic disorders provide an important setting in which these host-microbe interactions converge on immune remodeling, marrow-niche function, hematopoietic recovery, treatment response, and transplant-related complications. This narrative review synthesizes mechanistic, clinical, and translational evidence linking gut microbial dysbiosis to benign and malignant hematologic diseases, clonal and premalignant states, and hematopoietic stem cell transplantation (HSCT)-related outcomes. Rather than treating microbiome associations as a single evidence category, we distinguish five complementary evidence strata: Mendelian randomization, experimental models, prospective human cohorts, randomized human interventions, and cross-sectional studies. These study designs address different causal questions and are interpreted as complementary rather than as a single linear hierarchy. We also separate microbial composition from microbial function: taxon-level enrichment or depletion is treated primarily as context-dependent and hypothesis-generating, whereas conserved functional pathways-including short-chain fatty acids, bile-acid transformation, tryptophan metabolism, microbial translocation and barrier dysfunction, and innate immune activation-provide the principal cross-disease mechanistic framework. We integrate disease-specific microbial features, functional mediators, immune and marrow consequences, and clinical outcomes into an author-constructed evidence map, while explicitly addressing bidirectionality, reverse causality, and translational readiness. Emerging applications include microbiota-based biomarkers, treatment-response prediction, fecal microbiota transplantation, probiotics and postbiotics, antibiotic stewardship, and microbiota-dependent modulation of drug metabolism.
Additional Links: PMID-42954409
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PubMed:
Citation:
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@article {pmid42954409,
year = {2026},
author = {Yi, L and Yuan, Y and Ma, X and Li, C and Hao, Y and Ma, Q and Liu, X and Du, X and Shao, L and Wang, S and Xu, J},
title = {Disease-specific gut microbiota-metabolite-immune networks in hematologic disorders: mechanisms, causal support, and translational strategies.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2752469},
doi = {10.1080/19490976.2026.2752469},
pmid = {42954409},
issn = {1949-0984},
mesh = {Humans ; *Hematologic Diseases/microbiology/immunology/therapy ; *Gastrointestinal Microbiome/immunology ; *Dysbiosis/microbiology/immunology ; Animals ; Host Microbial Interactions/immunology ; Hematopoietic Stem Cell Transplantation ; },
abstract = {The gut microbiota is increasingly recognized as a systemic regulator of host immunity, host metabolism, epithelial barrier integrity, and distal tissue homeostasis. Hematologic disorders provide an important setting in which these host-microbe interactions converge on immune remodeling, marrow-niche function, hematopoietic recovery, treatment response, and transplant-related complications. This narrative review synthesizes mechanistic, clinical, and translational evidence linking gut microbial dysbiosis to benign and malignant hematologic diseases, clonal and premalignant states, and hematopoietic stem cell transplantation (HSCT)-related outcomes. Rather than treating microbiome associations as a single evidence category, we distinguish five complementary evidence strata: Mendelian randomization, experimental models, prospective human cohorts, randomized human interventions, and cross-sectional studies. These study designs address different causal questions and are interpreted as complementary rather than as a single linear hierarchy. We also separate microbial composition from microbial function: taxon-level enrichment or depletion is treated primarily as context-dependent and hypothesis-generating, whereas conserved functional pathways-including short-chain fatty acids, bile-acid transformation, tryptophan metabolism, microbial translocation and barrier dysfunction, and innate immune activation-provide the principal cross-disease mechanistic framework. We integrate disease-specific microbial features, functional mediators, immune and marrow consequences, and clinical outcomes into an author-constructed evidence map, while explicitly addressing bidirectionality, reverse causality, and translational readiness. Emerging applications include microbiota-based biomarkers, treatment-response prediction, fecal microbiota transplantation, probiotics and postbiotics, antibiotic stewardship, and microbiota-dependent modulation of drug metabolism.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Hematologic Diseases/microbiology/immunology/therapy
*Gastrointestinal Microbiome/immunology
*Dysbiosis/microbiology/immunology
Animals
Host Microbial Interactions/immunology
Hematopoietic Stem Cell Transplantation
RevDate: 2026-10-29
From saccharides to methane: substrate-driven microbial diversity and methanogenesis in anaerobic digestion revealed by 390 MAGs.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: Anaerobic digestion (AD) is a key technology for organic waste treatment and renewable energy production, yet its microbial processes remain poorly understood. This study employed genome-centric metagenomics to investigate synthetic AD systems fed with five substrates: starch, glucose, butyrate, propionate-valerate, and acetate. A total of 390 high-quality metagenome-assembled genomes (MAGs) were reconstructed, 64.36% of which represent potentially novel species. Substrate-driven selection shaped distinct functional consortia, with Bifidobacterium enriched in starch hydrolysis and Syntrophomonas enriched in butyrate oxidation. A complete set of acetoclastic methanogenesis-associated genes was identified in a bacterial MAG (Armatimonadota UBA5829). A complete CO2 reduction pathway was also identified in Methanothrix soehngenii. Glycine cleavage systems were prevalent in high-abundance MAGs, while key Wood-Ljungdahl pathway enzymes were absent. These findings provide genomic insights into substrate-driven assembly and methanogenic pathway distribution in synthetic AD systems.
IMPORTANCE: Anaerobic digestion is a key technology for converting organic waste into renewable energy, yet the microbial processes underlying its efficiency remain largely hidden. By reconstructing 390 microbial genomes from digestion systems fed with different sugar-derived substrates, this study unveils how specific substrates shape microbial communities and reveals unexpected metabolic pathways for methane production. These findings challenge long-standing assumptions about which organisms perform key steps in the process, provide a valuable genomic resource for the field, and offer concrete targets for improving waste-to-energy systems through microbiome engineering.
Additional Links: PMID-42954465
Publisher:
PubMed:
Citation:
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@article {pmid42954465,
year = {2026},
author = {Pan, X and Chen, X and Xie, H and Zhang, Y and Dai, Y and Yuan, C and Kong, F and Luo, F},
title = {From saccharides to methane: substrate-driven microbial diversity and methanogenesis in anaerobic digestion revealed by 390 MAGs.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0285426},
doi = {10.1128/spectrum.02854-26},
pmid = {42954465},
issn = {2165-0497},
abstract = {UNLABELLED: Anaerobic digestion (AD) is a key technology for organic waste treatment and renewable energy production, yet its microbial processes remain poorly understood. This study employed genome-centric metagenomics to investigate synthetic AD systems fed with five substrates: starch, glucose, butyrate, propionate-valerate, and acetate. A total of 390 high-quality metagenome-assembled genomes (MAGs) were reconstructed, 64.36% of which represent potentially novel species. Substrate-driven selection shaped distinct functional consortia, with Bifidobacterium enriched in starch hydrolysis and Syntrophomonas enriched in butyrate oxidation. A complete set of acetoclastic methanogenesis-associated genes was identified in a bacterial MAG (Armatimonadota UBA5829). A complete CO2 reduction pathway was also identified in Methanothrix soehngenii. Glycine cleavage systems were prevalent in high-abundance MAGs, while key Wood-Ljungdahl pathway enzymes were absent. These findings provide genomic insights into substrate-driven assembly and methanogenic pathway distribution in synthetic AD systems.
IMPORTANCE: Anaerobic digestion is a key technology for converting organic waste into renewable energy, yet the microbial processes underlying its efficiency remain largely hidden. By reconstructing 390 microbial genomes from digestion systems fed with different sugar-derived substrates, this study unveils how specific substrates shape microbial communities and reveals unexpected metabolic pathways for methane production. These findings challenge long-standing assumptions about which organisms perform key steps in the process, provide a valuable genomic resource for the field, and offer concrete targets for improving waste-to-energy systems through microbiome engineering.},
}
RevDate: 2026-10-29
Gut microbiome and metabolomics reveal the role of thioproline in attenuating colorectal cancer-associated inflammation.
mSystems [Epub ahead of print].
Colorectal cancer (CRC) is one of the top three cancers globally in terms of both incidence and mortality, and its development may be influenced by an inflammatory environment in the intestines, often associated with gut microbiota dysbiosis. Food bioactives could modulate gut microbiota through anti-inflammatory and epigenetic mechanisms. Given the significant role of thioproline as a food bioactive with antioxidant properties, its potential to modulate gut microbiota and mitigate CRC remains largely unexplored. This study aims to understand the effects of thioproline on gut microbiota community and investigate the mechanisms through which thioproline regulates gut microbiota and exerts its anticancer effects. Fecal and intestinal tissue samples were collected from health, CRC, and thioproline-treated CRC mice. The metagenome and metabolome data revealed that thioproline treatment significantly altered the gut microbiota community composition and metabolism in CRC mice. These CRC-associated gut microbiota and bacterial metabolites returned to normal levels. Moreover, under thioproline treatment, the microbial-metabolite interactions in CRC mice shifted toward patterns more closely resembling those observed in healthy mice. Thioproline treatment increased linoleic acid levels in mice, indicating its role in promoting linoleic acid metabolism to therapeutically restore homeostasis and alleviate inflammation in CRC. This was further supported by hematoxylin and eosin staining, which demonstrated that thioproline alleviated inflammation in CRC mice. Our study highlights thioproline's dual role in regulating the gut microbiota community and bacterial metabolism, modulating bacteria-host interactions, and ultimately reducing inflammation in CRC. These findings offer valuable insights for future research and therapeutic applications.IMPORTANCEColorectal cancer (CRC) is associated with gut microbiota dysbiosis and intestinal inflammation. While food bioactives can modulate the microbiome, whether thioproline exerts inhibitory effects against CRC through microbial regulation remains unknown. Using integrated metagenomics and metabolomics, we show that thioproline treatment restores the gut microbiota composition and bacterial metabolites disrupted by CRC to near-normal levels. Importantly, thioproline remodels microbial metabolite interaction networks, elevates linoleic acid levels, and alleviates intestinal inflammation. This study provides a systems-level perspective on how a single dietary bioactive compound reshapes the gut microbial ecosystem and its metabolic landscape to reduce inflammation in CRC. Our findings suggest a potential role for microbiome-targeted nutritional strategies in protecting against CRC progression through modulation of the gut microbiota and intestinal microenvironment.
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@article {pmid42954466,
year = {2026},
author = {Liu, J and Li, W and Qi, M and Zhao, J and Wu, J and Wang, Y and Yang, Y and Song, X},
title = {Gut microbiome and metabolomics reveal the role of thioproline in attenuating colorectal cancer-associated inflammation.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0054826},
doi = {10.1128/msystems.00548-26},
pmid = {42954466},
issn = {2379-5077},
abstract = {Colorectal cancer (CRC) is one of the top three cancers globally in terms of both incidence and mortality, and its development may be influenced by an inflammatory environment in the intestines, often associated with gut microbiota dysbiosis. Food bioactives could modulate gut microbiota through anti-inflammatory and epigenetic mechanisms. Given the significant role of thioproline as a food bioactive with antioxidant properties, its potential to modulate gut microbiota and mitigate CRC remains largely unexplored. This study aims to understand the effects of thioproline on gut microbiota community and investigate the mechanisms through which thioproline regulates gut microbiota and exerts its anticancer effects. Fecal and intestinal tissue samples were collected from health, CRC, and thioproline-treated CRC mice. The metagenome and metabolome data revealed that thioproline treatment significantly altered the gut microbiota community composition and metabolism in CRC mice. These CRC-associated gut microbiota and bacterial metabolites returned to normal levels. Moreover, under thioproline treatment, the microbial-metabolite interactions in CRC mice shifted toward patterns more closely resembling those observed in healthy mice. Thioproline treatment increased linoleic acid levels in mice, indicating its role in promoting linoleic acid metabolism to therapeutically restore homeostasis and alleviate inflammation in CRC. This was further supported by hematoxylin and eosin staining, which demonstrated that thioproline alleviated inflammation in CRC mice. Our study highlights thioproline's dual role in regulating the gut microbiota community and bacterial metabolism, modulating bacteria-host interactions, and ultimately reducing inflammation in CRC. These findings offer valuable insights for future research and therapeutic applications.IMPORTANCEColorectal cancer (CRC) is associated with gut microbiota dysbiosis and intestinal inflammation. While food bioactives can modulate the microbiome, whether thioproline exerts inhibitory effects against CRC through microbial regulation remains unknown. Using integrated metagenomics and metabolomics, we show that thioproline treatment restores the gut microbiota composition and bacterial metabolites disrupted by CRC to near-normal levels. Importantly, thioproline remodels microbial metabolite interaction networks, elevates linoleic acid levels, and alleviates intestinal inflammation. This study provides a systems-level perspective on how a single dietary bioactive compound reshapes the gut microbial ecosystem and its metabolic landscape to reduce inflammation in CRC. Our findings suggest a potential role for microbiome-targeted nutritional strategies in protecting against CRC progression through modulation of the gut microbiota and intestinal microenvironment.},
}
RevDate: 2026-10-29
CmpDate: 2026-10-29
Understanding the interplay between the gut microbiome, nutrition and health.
The Proceedings of the Nutrition Society, 80(4):383-385.
The Spring Conference 2021 focused on the theme of the gut microbiome and health that was divided across three separate but inter-related areas from the impact of nutrition on the gut microbiome, the cause and effect of nutrition and health on the gut microbiome to the interaction between pathogens and gut microbiota. The programme was supported by two plenary lectures, the first discussed the computational methods commonly employed to examine gut microbiota and the concluding lecture presented the interaction between the gut microbiome, nutrition and health in older populations. This short report provides a summary and highlights of the conference.
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@article {pmid42954494,
year = {2021},
author = {Ball, D and Athanasiadou, S},
title = {Understanding the interplay between the gut microbiome, nutrition and health.},
journal = {The Proceedings of the Nutrition Society},
volume = {80},
number = {4},
pages = {383-385},
doi = {10.1017/S0029665121003682},
pmid = {42954494},
issn = {1475-2719},
abstract = {The Spring Conference 2021 focused on the theme of the gut microbiome and health that was divided across three separate but inter-related areas from the impact of nutrition on the gut microbiome, the cause and effect of nutrition and health on the gut microbiome to the interaction between pathogens and gut microbiota. The programme was supported by two plenary lectures, the first discussed the computational methods commonly employed to examine gut microbiota and the concluding lecture presented the interaction between the gut microbiome, nutrition and health in older populations. This short report provides a summary and highlights of the conference.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
AI-Facilitated Discovery of Microbiome-Originated Antimicrobial Peptides: A Perspective on Combating Antibiotic Resistance Within Public Health and Food Safety Frameworks.
Microorganisms, 14(10):.
The escalating crisis of antimicrobial resistance (AMR) demands innovative therapeutic strategies beyond conventional antibiotics. Antimicrobial peptides (AMPs), particularly those originating from the human, animal, and environmental microbiome, represent a promising frontier within public health microbiology and microbial food safety. Recent advances in artificial intelligence (AI) and machine learning (ML) have revolutionized the discovery pipeline, enabling high-throughput mining of metagenomic data and de novo generation of novel peptide sequences. This perspective review synthesizes recent breakthroughs in AI-driven discovery of microbiome-originated AMPs, examines their preclinical efficacy against multidrug-resistant (MDR) pathogens under One Health and climate-sensitive frameworks and application in infectious disease treatment and discusses translational challenges including pharmacokinetics, toxicity, manufacturing scalability, and applications in food preservation and water safety. We argue that the convergence of microbiome science, deep learning, and synthetic biology positions AI-discovered AMPs as viable next-generation interventions against antibiotic resistance across human, animal, and environmental domains.
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@article {pmid42943597,
year = {2026},
author = {Atuahene, PY and Stevenson, B and Sang, Y},
title = {AI-Facilitated Discovery of Microbiome-Originated Antimicrobial Peptides: A Perspective on Combating Antibiotic Resistance Within Public Health and Food Safety Frameworks.},
journal = {Microorganisms},
volume = {14},
number = {10},
pages = {},
pmid = {42943597},
issn = {2076-2607},
support = {Evans-Allen-1013186//USDA NIFA/ ; 2020-67016-31347//NIFA AFRI/ ; 2025-38821-45500//NIFA AFRI/ ; },
abstract = {The escalating crisis of antimicrobial resistance (AMR) demands innovative therapeutic strategies beyond conventional antibiotics. Antimicrobial peptides (AMPs), particularly those originating from the human, animal, and environmental microbiome, represent a promising frontier within public health microbiology and microbial food safety. Recent advances in artificial intelligence (AI) and machine learning (ML) have revolutionized the discovery pipeline, enabling high-throughput mining of metagenomic data and de novo generation of novel peptide sequences. This perspective review synthesizes recent breakthroughs in AI-driven discovery of microbiome-originated AMPs, examines their preclinical efficacy against multidrug-resistant (MDR) pathogens under One Health and climate-sensitive frameworks and application in infectious disease treatment and discusses translational challenges including pharmacokinetics, toxicity, manufacturing scalability, and applications in food preservation and water safety. We argue that the convergence of microbiome science, deep learning, and synthetic biology positions AI-discovered AMPs as viable next-generation interventions against antibiotic resistance across human, animal, and environmental domains.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Exploratory Shotgun Metagenomic Analysis of the Fecal Microbiome and Antimicrobial-Resistance Potential in Simmental Calves with Different Diarrheal Statuses.
Microorganisms, 14(10):.
Calf diarrhea is frequently accompanied by disruption of the gastrointestinal microbiota, but the relationships between clinical status and microbial community composition, gene-content functional potential, and antimicrobial-resistance-associated features remain incompletely characterized. This exploratory study aimed to characterize these features in calves with different diarrheal statuses using shotgun metagenomics. Six approximately 2-month-old Simmental calves from Chahar Right Middle Banner, Inner Mongolia, were included, comprising two healthy calves, two calves with mild diarrhea, and two calves with severe diarrhea. Read-based taxonomic profiling was complemented by gene-abundance-weighted taxonomic annotation, and microbial functional potential was characterized using eggNOG/COG, KEGG, and CAZy annotations, together with conservatively screened CARD-associated sequence-homology candidates. The two severe-diarrhea samples exhibited lower bacterial richness and Shannon diversity, although PCoA did not show clear separation according to clinical severity. These two samples showed high representation of Proteobacteria and Enterobacteriaceae-related taxa, particularly Escherichia-related assignments, together with lower representation of Ruminococcaceae, Faecalibacterium, and Prevotella. Gene-content profiles showed higher representation of selected functions related to transport, environmental sensing, motility, secretion, and bacterial cell-envelope processes, whereas several glycan- and complex-carbohydrate-associated functions showed lower representation. Selected CARD-associated candidates were also more abundant in the severe-diarrhea samples. Within this small exploratory cohort, the two severe-diarrhea samples therefore showed concordant taxonomic and gene-content differences; however, these observations should not be interpreted as a general severity-specific microbiome signature and require validation in larger longitudinal cohorts.
Additional Links: PMID-42943608
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@article {pmid42943608,
year = {2026},
author = {Xie, M and Shang, H and Wang, F and Yang, J and Geer, N and Zhang, Q and Xu, X and Baolige, D},
title = {Exploratory Shotgun Metagenomic Analysis of the Fecal Microbiome and Antimicrobial-Resistance Potential in Simmental Calves with Different Diarrheal Statuses.},
journal = {Microorganisms},
volume = {14},
number = {10},
pages = {},
pmid = {42943608},
issn = {2076-2607},
support = {2025ZY0147//Central Government Guiding Local Science and Technology Development Fund Project/ ; 2025YFDZ0091//Inner Mongolia Autonomous Region Science and Technology Plan/ ; 2020ZD0006//Inner Mongolia Autonomous Region Major Science and Technology Project/ ; },
abstract = {Calf diarrhea is frequently accompanied by disruption of the gastrointestinal microbiota, but the relationships between clinical status and microbial community composition, gene-content functional potential, and antimicrobial-resistance-associated features remain incompletely characterized. This exploratory study aimed to characterize these features in calves with different diarrheal statuses using shotgun metagenomics. Six approximately 2-month-old Simmental calves from Chahar Right Middle Banner, Inner Mongolia, were included, comprising two healthy calves, two calves with mild diarrhea, and two calves with severe diarrhea. Read-based taxonomic profiling was complemented by gene-abundance-weighted taxonomic annotation, and microbial functional potential was characterized using eggNOG/COG, KEGG, and CAZy annotations, together with conservatively screened CARD-associated sequence-homology candidates. The two severe-diarrhea samples exhibited lower bacterial richness and Shannon diversity, although PCoA did not show clear separation according to clinical severity. These two samples showed high representation of Proteobacteria and Enterobacteriaceae-related taxa, particularly Escherichia-related assignments, together with lower representation of Ruminococcaceae, Faecalibacterium, and Prevotella. Gene-content profiles showed higher representation of selected functions related to transport, environmental sensing, motility, secretion, and bacterial cell-envelope processes, whereas several glycan- and complex-carbohydrate-associated functions showed lower representation. Selected CARD-associated candidates were also more abundant in the severe-diarrhea samples. Within this small exploratory cohort, the two severe-diarrhea samples therefore showed concordant taxonomic and gene-content differences; however, these observations should not be interpreted as a general severity-specific microbiome signature and require validation in larger longitudinal cohorts.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Comparison of Fecal Microbiome of Wild Red Deer in Different Regions Reveals Geographic Differentiation.
Microorganisms, 14(10):.
The gut microbiome plays critical roles in nutrient metabolism and host adaptation in ruminants, yet genome-level functional differences in the fecal microbiomes across geographic populations of wild red deer remain underexplored. Here, we integrated 16S rRNA gene sequencing and shotgun metagenomics to characterize the fecal microbiome of wild red deer populations in Inner Mongolia (NMG, n = 16) and Gansu Province (GS, n = 16), China. The NMG population exhibited significantly higher α-diversity and a distinct microbial community compared to GS (adjusted p < 0.05). NMG was enriched in Clostridium, Eubacterium, and Bacillus, while GS harbored higher abundances of Ruminococcus, Oscillospira, and Faecalibacterium (adjusted p < 0.05). Functional profiling revealed that the fecal microbiome in NMG showed greater functional potential associated with amino acid, pyruvate, and butanoate metabolism pathways, whereas the fecal microbiome in GS was enriched in the genetic potential of starch/sucrose metabolism, glycan degradation, and bile acid biotransformation (adjusted p < 0.05). CAZyme analysis demonstrated that GS was enriched in glycoside hydrolases, polysaccharide lyases, and carbohydrate esterases, while NMG showed higher auxiliary activity family abundance (adjusted p < 0.05). Genome-resolved metagenomics recovered 456 species-level genome bins (SGBs), revealing that GS-enriched SGBs (Rikenellaceae, Oscillospirales CAG-272) contained CAZyme genes associated with pectin degradation, whereas NMG-enriched SGBs contained genes associated with lignin modification and chitin degradation. These findings demonstrate the significant differences in the fecal microbiomes between the two geographically distinct wild red deer populations.
Additional Links: PMID-42943642
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@article {pmid42943642,
year = {2026},
author = {Chen, S and Li, S and Li, Y and Zhang, Y and Duan, X and Xu, C and Qian, W and Si, H and Liu, H and Li, Z},
title = {Comparison of Fecal Microbiome of Wild Red Deer in Different Regions Reveals Geographic Differentiation.},
journal = {Microorganisms},
volume = {14},
number = {10},
pages = {},
pmid = {42943642},
issn = {2076-2607},
support = {20240101012JJ//Natural Science Foundation of Jilin provinces/ ; 2023YFD1302000//National Key Research and Development Program of China/ ; CARS-43//earmarked fund/ ; JLARS-2026-080204//Jilin Agricultural Research System/ ; },
abstract = {The gut microbiome plays critical roles in nutrient metabolism and host adaptation in ruminants, yet genome-level functional differences in the fecal microbiomes across geographic populations of wild red deer remain underexplored. Here, we integrated 16S rRNA gene sequencing and shotgun metagenomics to characterize the fecal microbiome of wild red deer populations in Inner Mongolia (NMG, n = 16) and Gansu Province (GS, n = 16), China. The NMG population exhibited significantly higher α-diversity and a distinct microbial community compared to GS (adjusted p < 0.05). NMG was enriched in Clostridium, Eubacterium, and Bacillus, while GS harbored higher abundances of Ruminococcus, Oscillospira, and Faecalibacterium (adjusted p < 0.05). Functional profiling revealed that the fecal microbiome in NMG showed greater functional potential associated with amino acid, pyruvate, and butanoate metabolism pathways, whereas the fecal microbiome in GS was enriched in the genetic potential of starch/sucrose metabolism, glycan degradation, and bile acid biotransformation (adjusted p < 0.05). CAZyme analysis demonstrated that GS was enriched in glycoside hydrolases, polysaccharide lyases, and carbohydrate esterases, while NMG showed higher auxiliary activity family abundance (adjusted p < 0.05). Genome-resolved metagenomics recovered 456 species-level genome bins (SGBs), revealing that GS-enriched SGBs (Rikenellaceae, Oscillospirales CAG-272) contained CAZyme genes associated with pectin degradation, whereas NMG-enriched SGBs contained genes associated with lignin modification and chitin degradation. These findings demonstrate the significant differences in the fecal microbiomes between the two geographically distinct wild red deer populations.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Light Penetration, Dissolved Oxygen, and Riparian Zone Extent Are Associated with the Structure, Gene Expression, and Lipid Production of Riverbed Microbial Communities.
Microorganisms, 14(10):.
We analyzed riverbed microbiota structure, gene expression, and fatty acid production across several sites along Little Miami River in Ohio, United States. The sites varied in stream width, shading, surrounding land use, and the size of the riparian zone. Within each site, we observed strong concordance among microbial community composition, functional gene expression, and fatty acid signature. All microbial communities were dominated by the members of phylum Proteobacteria, class Planctomycetacia, and by algal and cyanobacterial cells. The measured concentrations of chlorophyll a, dissolved oxygen, and soluble phosphorus were the main environmental determinants of microbial community structure. These were in turn dependent on the level of penetrating sunlight and, to a lesser degree, on the width of the riparian zone. The level of sunlight affected the expression of light-harvesting complexes, methanogenesis genes, anaerobic respiratory reductases and fermentation pathways, as well as functions of denitrification, ammonification, and sulfate reduction. The expression of phosphorus scavenging and antibiotic resistance genes was highest at the site lacking a riparian zone and surrounded by farmland. Overall, our findings demonstrate that riverbed microbiota exhibit consistent structural and functional responses to interacting geochemical and anthropogenic gradients. Our data also provide support for the hypothesis that phototrophic microorganisms act as central organizers of benthic community metabolism.
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@article {pmid42943644,
year = {2026},
author = {Shankar, V and Paliy, O},
title = {Light Penetration, Dissolved Oxygen, and Riparian Zone Extent Are Associated with the Structure, Gene Expression, and Lipid Production of Riverbed Microbial Communities.},
journal = {Microorganisms},
volume = {14},
number = {10},
pages = {},
pmid = {42943644},
issn = {2076-2607},
support = {DBI-1335772//U.S. National Science Foundation/ ; },
abstract = {We analyzed riverbed microbiota structure, gene expression, and fatty acid production across several sites along Little Miami River in Ohio, United States. The sites varied in stream width, shading, surrounding land use, and the size of the riparian zone. Within each site, we observed strong concordance among microbial community composition, functional gene expression, and fatty acid signature. All microbial communities were dominated by the members of phylum Proteobacteria, class Planctomycetacia, and by algal and cyanobacterial cells. The measured concentrations of chlorophyll a, dissolved oxygen, and soluble phosphorus were the main environmental determinants of microbial community structure. These were in turn dependent on the level of penetrating sunlight and, to a lesser degree, on the width of the riparian zone. The level of sunlight affected the expression of light-harvesting complexes, methanogenesis genes, anaerobic respiratory reductases and fermentation pathways, as well as functions of denitrification, ammonification, and sulfate reduction. The expression of phosphorus scavenging and antibiotic resistance genes was highest at the site lacking a riparian zone and surrounded by farmland. Overall, our findings demonstrate that riverbed microbiota exhibit consistent structural and functional responses to interacting geochemical and anthropogenic gradients. Our data also provide support for the hypothesis that phototrophic microorganisms act as central organizers of benthic community metabolism.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Ecological Editing: Decoupling Microbial Signals from Metabolic Noise to Reprogram the Gut Ecosystem.
Microorganisms, 14(10):.
The translation of microbiome therapeutics is hampered by the stochasticity of faecal microbiota transplantation (FMT), an empirical transfer of undefined biomass confounded by donor heterogeneity, procedural variability, and immunogenic debris. As the field moves towards precision medicine, microbiome engineering is diverging into two philosophies: the subtractive paradigm, which purifies the native ecosystem by removing deleterious metabolites, and the additive paradigm, which assembles functional guilds de novo. In this review, we propose that density-based ecological purification, termed quantitative fractionated microbiota (QFM), may act as an immunological sieve, using washed microbiota transplantation (WMT) as its best-characterised clinical exemplar, to separate therapeutic signals (viable microbiota and bacteriophages) from metabolic noise (for example, pro-inflammatory lipid mediators and glucocorticoid metabolites). We explicitly frame this separation as a conceptual working model rather than an established mechanism: the quantitative assays, cut-off values, and units required to operationalise a signal-to-noise distinction do not yet exist, and we set out what would be needed to develop them. Conversely, live biotherapeutic products (LBPs) offer compositional precision but face a critical bottleneck, namely engraftment failure in colonisation-resistant hosts. We propose that the future lies less in competition between these modalities than in their convergence, which we term the soil-and-seed framework. In this framework, subtractive ecological priming (QFM/WMT) may transiently lower colonisation resistance by liberating niche space and by reducing soluble inflammatory exposure, thereby preparing the mucosa for subsequent engraftment of additive consortia. We describe this hybrid strategy as a hypothesis with an explicit validation roadmap. If it holds, this shift would move microbiome therapy from stochastic biomass transfer towards predictable ecosystem engineering.
Additional Links: PMID-42943648
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@article {pmid42943648,
year = {2026},
author = {He, Y and Zhu, X and Huang, Z and Yang, X and Yi, B},
title = {Ecological Editing: Decoupling Microbial Signals from Metabolic Noise to Reprogram the Gut Ecosystem.},
journal = {Microorganisms},
volume = {14},
number = {10},
pages = {},
pmid = {42943648},
issn = {2076-2607},
support = {82404050//National Natural Science Foundation of China/ ; 82560565//National Natural Science Foundation of China/ ; 20252BAC250152//Key Project of the Natural Science Foundation of Jiangxi Province/ ; 20252BAC250125//Key Project of the Natural Science Foundation of Jiangxi Province/ ; 20252BAC200530//Youth Project of the Natural Science Foundation of Jiangxi Province/ ; GJJ2403619//Scientific and Technological Research Project of the Jiangxi Provincial Department of Education/ ; GJJ2503436//Scientific and Technological Research Project of the Jiangxi Provincial Department of Education/ ; SKJP1320242247//Jiangxi Provincial Health Commission Science and Technology Program/ ; },
abstract = {The translation of microbiome therapeutics is hampered by the stochasticity of faecal microbiota transplantation (FMT), an empirical transfer of undefined biomass confounded by donor heterogeneity, procedural variability, and immunogenic debris. As the field moves towards precision medicine, microbiome engineering is diverging into two philosophies: the subtractive paradigm, which purifies the native ecosystem by removing deleterious metabolites, and the additive paradigm, which assembles functional guilds de novo. In this review, we propose that density-based ecological purification, termed quantitative fractionated microbiota (QFM), may act as an immunological sieve, using washed microbiota transplantation (WMT) as its best-characterised clinical exemplar, to separate therapeutic signals (viable microbiota and bacteriophages) from metabolic noise (for example, pro-inflammatory lipid mediators and glucocorticoid metabolites). We explicitly frame this separation as a conceptual working model rather than an established mechanism: the quantitative assays, cut-off values, and units required to operationalise a signal-to-noise distinction do not yet exist, and we set out what would be needed to develop them. Conversely, live biotherapeutic products (LBPs) offer compositional precision but face a critical bottleneck, namely engraftment failure in colonisation-resistant hosts. We propose that the future lies less in competition between these modalities than in their convergence, which we term the soil-and-seed framework. In this framework, subtractive ecological priming (QFM/WMT) may transiently lower colonisation resistance by liberating niche space and by reducing soluble inflammatory exposure, thereby preparing the mucosa for subsequent engraftment of additive consortia. We describe this hybrid strategy as a hypothesis with an explicit validation roadmap. If it holds, this shift would move microbiome therapy from stochastic biomass transfer towards predictable ecosystem engineering.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Oleanolic Acid-Loaded Cyclodextrin Metal-Organic Framework Ameliorates NAFLD via Modulation of Gut Microbiota and Liver Metabolism.
Molecules (Basel, Switzerland), 31(20):.
Oleanolic acid (OA) possesses hepatoprotective properties, but its clinical application is hampered by poor aqueous solubility. This study aimed to enhance OA solubility and investigate its therapeutic mechanism for NAFLD by encapsulating it in a γ-cyclodextrin metal-organic framework (OA@CDMOF). The OA@CDMOF complex was synthesized and characterized. Its effects on a high-fat diet (HFD)-induced NAFLD mouse model (MOD) were evaluated by combined liver metabolomics and 16S rRNA amplicon sequencing analyses. When encapsulated into CDMOF to yield an OA@CDMOF complex, the solubility of OA significantly improved. OA@CDMOF administration ameliorated HFD-induced metabolic alterations and liver injury. It modulated the gut microbiota composition, notably enriching the phylum Firmicutes while decreasing the abundance of Bacteroidota. Liver metabolomic analysis revealed that OA@CDMOF was associated with changes in metabolites related to glycerophospholipid, purine, glutathione, and vitamin B6 metabolism. Furthermore, it was associated with changes in metabolites related to lipolysis in adipocytes, pentose and glucuronate interconversions, and key signaling pathways, including AMPK, FoxO, and cGMP-PKG. Importantly, OA@CDMOF showed protective effects comparable to those of free OA, with no statistically significant difference between the two groups. This study elucidates the mechanism by which OA@CDMOF alleviates NAFLD through modulation of the gut microbiome and host metabolism. Our findings provide novel insights into the hepatoprotective role of OA@CDMOF and suggest a promising nanostrategy for NAFLD intervention.
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@article {pmid42943735,
year = {2026},
author = {Zhu, H and Tang, M and Li, M and Zhang, Z and Kang, L and Wang, Q and Wang, R and Hua, C and Zhou, H and Zhou, W and Wu, Y and Wang, Z},
title = {Oleanolic Acid-Loaded Cyclodextrin Metal-Organic Framework Ameliorates NAFLD via Modulation of Gut Microbiota and Liver Metabolism.},
journal = {Molecules (Basel, Switzerland)},
volume = {31},
number = {20},
pages = {},
pmid = {42943735},
issn = {1420-3049},
support = {32372452//National Natural Science Foundation of China/ ; WJ202510R02//State Administration for Market Regulation/ ; PAPD//Jiangsu Higher Education Institutions/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Non-alcoholic Fatty Liver Disease/drug therapy/metabolism/etiology/microbiology ; *Liver/metabolism/drug effects ; *Oleanolic Acid/pharmacology/chemistry ; Mice ; *Metal-Organic Frameworks/chemistry/pharmacology ; Male ; Diet, High-Fat/adverse effects ; *Cyclodextrins/chemistry ; Disease Models, Animal ; Metabolomics/methods ; Mice, Inbred C57BL ; },
abstract = {Oleanolic acid (OA) possesses hepatoprotective properties, but its clinical application is hampered by poor aqueous solubility. This study aimed to enhance OA solubility and investigate its therapeutic mechanism for NAFLD by encapsulating it in a γ-cyclodextrin metal-organic framework (OA@CDMOF). The OA@CDMOF complex was synthesized and characterized. Its effects on a high-fat diet (HFD)-induced NAFLD mouse model (MOD) were evaluated by combined liver metabolomics and 16S rRNA amplicon sequencing analyses. When encapsulated into CDMOF to yield an OA@CDMOF complex, the solubility of OA significantly improved. OA@CDMOF administration ameliorated HFD-induced metabolic alterations and liver injury. It modulated the gut microbiota composition, notably enriching the phylum Firmicutes while decreasing the abundance of Bacteroidota. Liver metabolomic analysis revealed that OA@CDMOF was associated with changes in metabolites related to glycerophospholipid, purine, glutathione, and vitamin B6 metabolism. Furthermore, it was associated with changes in metabolites related to lipolysis in adipocytes, pentose and glucuronate interconversions, and key signaling pathways, including AMPK, FoxO, and cGMP-PKG. Importantly, OA@CDMOF showed protective effects comparable to those of free OA, with no statistically significant difference between the two groups. This study elucidates the mechanism by which OA@CDMOF alleviates NAFLD through modulation of the gut microbiome and host metabolism. Our findings provide novel insights into the hepatoprotective role of OA@CDMOF and suggest a promising nanostrategy for NAFLD intervention.},
}
MeSH Terms:
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Animals
*Gastrointestinal Microbiome/drug effects
*Non-alcoholic Fatty Liver Disease/drug therapy/metabolism/etiology/microbiology
*Liver/metabolism/drug effects
*Oleanolic Acid/pharmacology/chemistry
Mice
*Metal-Organic Frameworks/chemistry/pharmacology
Male
Diet, High-Fat/adverse effects
*Cyclodextrins/chemistry
Disease Models, Animal
Metabolomics/methods
Mice, Inbred C57BL
RevDate: 2026-10-28
CmpDate: 2026-10-27
Next-Generation Functional Nanoplatforms: Engineering Plant-Derived Extracellular Vesicles for Targeted Bioactive Delivery and Health Applications.
Molecules (Basel, Switzerland), 31(20):.
Plant-derived extracellular vesicles (PDEVs) are being recognized as a capable novel class of natural nanocarriers that have important uses in delivering bioactives and facilitating innovations in functional foods and precision health technologies. PDEVs are lipid-bilayer-enclosed vesicular structures that commonly occur at the nanoscale, although their reported sizes vary depending on the plant source, isolation procedure, and measurement method. They contain diverse biomolecules, including lipids, proteins, microRNAs, and phytochemicals, and have been investigated for their potential roles in interspecies communication and the delivery of bioactive compounds. Compared with some conventional nanocarriers, PDEVs have shown favorable biocompatibility and stability under certain experimental conditions; however, these properties are dependent on the plant source, isolation method, cargo, formulation, and experimental model; therefore, they are uniquely positioned for oral delivery systems. This review presents a complete picture of the process of PDEV biogenesis, the molecular architecture of PDEVs, and their cargo. We evaluate and compare the source materials of PDEVs to determine whether they will influence how effectively the bioactive agent is delivered to its intended target and produce the therapeutic effect. Additionally, we present a review of the advances in technology for the analysis of PDEVs: methods of extraction, purification, and characterization of PDEV; current and future techniques for loading cargo into PDEVs; methods of modifying the surfaces of PDEVs; and methods of developing, producing, and delivering hybrid systems of PDEVs. Finally, a comprehensive review of the use of PDEVs in delivering nutraceuticals, modulating the gut microbiome, delivering probiotic systems, and exhibiting anti-inflammatory, antioxidant, and anti-cancer effects. Even as these positive advancements occur, challenges related to scalability, standardization, and purity remain significant barriers to industrial translation. PDEVs are well-positioned to serve as a sustainable, next-generation nanoplatform at the intersection of nanotechnology, food science, and biomedicine. PDEVs also provide unprecedented opportunities to advance functional foods and precision nutrition.
Additional Links: PMID-42943823
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@article {pmid42943823,
year = {2026},
author = {Awlqadr, FH and Saeed, MN and Ramddan, AB and Sdiq, AFH and Hama, HK and Hossain, MS and Noreen, S and Raza, H and Kiss, AP},
title = {Next-Generation Functional Nanoplatforms: Engineering Plant-Derived Extracellular Vesicles for Targeted Bioactive Delivery and Health Applications.},
journal = {Molecules (Basel, Switzerland)},
volume = {31},
number = {20},
pages = {},
pmid = {42943823},
issn = {1420-3049},
mesh = {*Extracellular Vesicles/chemistry/metabolism ; Humans ; *Plants/chemistry/metabolism ; *Drug Delivery Systems ; Phytochemicals/chemistry ; Animals ; },
abstract = {Plant-derived extracellular vesicles (PDEVs) are being recognized as a capable novel class of natural nanocarriers that have important uses in delivering bioactives and facilitating innovations in functional foods and precision health technologies. PDEVs are lipid-bilayer-enclosed vesicular structures that commonly occur at the nanoscale, although their reported sizes vary depending on the plant source, isolation procedure, and measurement method. They contain diverse biomolecules, including lipids, proteins, microRNAs, and phytochemicals, and have been investigated for their potential roles in interspecies communication and the delivery of bioactive compounds. Compared with some conventional nanocarriers, PDEVs have shown favorable biocompatibility and stability under certain experimental conditions; however, these properties are dependent on the plant source, isolation method, cargo, formulation, and experimental model; therefore, they are uniquely positioned for oral delivery systems. This review presents a complete picture of the process of PDEV biogenesis, the molecular architecture of PDEVs, and their cargo. We evaluate and compare the source materials of PDEVs to determine whether they will influence how effectively the bioactive agent is delivered to its intended target and produce the therapeutic effect. Additionally, we present a review of the advances in technology for the analysis of PDEVs: methods of extraction, purification, and characterization of PDEV; current and future techniques for loading cargo into PDEVs; methods of modifying the surfaces of PDEVs; and methods of developing, producing, and delivering hybrid systems of PDEVs. Finally, a comprehensive review of the use of PDEVs in delivering nutraceuticals, modulating the gut microbiome, delivering probiotic systems, and exhibiting anti-inflammatory, antioxidant, and anti-cancer effects. Even as these positive advancements occur, challenges related to scalability, standardization, and purity remain significant barriers to industrial translation. PDEVs are well-positioned to serve as a sustainable, next-generation nanoplatform at the intersection of nanotechnology, food science, and biomedicine. PDEVs also provide unprecedented opportunities to advance functional foods and precision nutrition.},
}
MeSH Terms:
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*Extracellular Vesicles/chemistry/metabolism
Humans
*Plants/chemistry/metabolism
*Drug Delivery Systems
Phytochemicals/chemistry
Animals
RevDate: 2026-10-28
CmpDate: 2026-10-27
The Gut Virome in Gastrointestinal Cancers: Mechanisms, Biomarkers, and Translational Opportunities.
Viruses, 18(10):.
The gastrointestinal tract contains a dense multi-kingdom ecosystem in which bacteria, fungi, archaea, viruses, the mucosa, and the immune system interact. Although cancer microbiome research has focused mainly on bacteria, the gut virome dominated by bacteriophages may influence gastrointestinal carcinogenesis by reshaping bacterial communities, transferring functional genes, modulating inflammation, and altering treatment response. The strongest evidence comes from colorectal cancer, where multiple cohorts show altered phage diversity, temperate-phage enrichment, disrupted phage-bacteria networks, and reproducible stool-based diagnostic signals. Emerging studies in pancreatic cancer, esophageal adenocarcinoma, hepatocellular carcinoma, and precursor lesions suggest that virome disruption extends beyond colorectal cancer, although evidence remains uneven. Classic oncogenic viruses, including Epstein-Barr virus and hepatitis viruses, provide complementary examples of direct viral carcinogenesis in digestive organs. Anelloviruses are widespread in healthy individuals and are not established causes of cancer, but their abundance and composition may reflect immune status, inflammation, tissue injury, and altered host viral ecology. Virome-related interventions remain clinically immature: fecal microbiota transplantation has reached small phase I/II studies in gastrointestinal cancers, whereas phage, fecal-filtrate, and fecal virome approaches remain preclinical or non-oncology; direct oncolytic viruses have reached late-phase testing. Major barriers include viral dark matter, specimen and assay heterogeneity, disease-related confounding, limited external validation, and weak causal evidence. Standardized, mechanistically anchored, multi-kingdom studies are needed to establish clinical utility.
Additional Links: PMID-42944051
PubMed:
Citation:
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@article {pmid42944051,
year = {2026},
author = {Ghidini, M and Sberna, G and Guerrera, LP and Maggi, F and Novazzi, F},
title = {The Gut Virome in Gastrointestinal Cancers: Mechanisms, Biomarkers, and Translational Opportunities.},
journal = {Viruses},
volume = {18},
number = {10},
pages = {},
pmid = {42944051},
issn = {1999-4915},
mesh = {Humans ; *Gastrointestinal Neoplasms/virology/therapy ; *Virome ; *Gastrointestinal Microbiome ; Animals ; Bacteriophages ; Gastrointestinal Tract/virology ; Translational Research, Biomedical ; Biomarkers, Tumor ; Oncogenic Viruses ; Bacteria/virology ; },
abstract = {The gastrointestinal tract contains a dense multi-kingdom ecosystem in which bacteria, fungi, archaea, viruses, the mucosa, and the immune system interact. Although cancer microbiome research has focused mainly on bacteria, the gut virome dominated by bacteriophages may influence gastrointestinal carcinogenesis by reshaping bacterial communities, transferring functional genes, modulating inflammation, and altering treatment response. The strongest evidence comes from colorectal cancer, where multiple cohorts show altered phage diversity, temperate-phage enrichment, disrupted phage-bacteria networks, and reproducible stool-based diagnostic signals. Emerging studies in pancreatic cancer, esophageal adenocarcinoma, hepatocellular carcinoma, and precursor lesions suggest that virome disruption extends beyond colorectal cancer, although evidence remains uneven. Classic oncogenic viruses, including Epstein-Barr virus and hepatitis viruses, provide complementary examples of direct viral carcinogenesis in digestive organs. Anelloviruses are widespread in healthy individuals and are not established causes of cancer, but their abundance and composition may reflect immune status, inflammation, tissue injury, and altered host viral ecology. Virome-related interventions remain clinically immature: fecal microbiota transplantation has reached small phase I/II studies in gastrointestinal cancers, whereas phage, fecal-filtrate, and fecal virome approaches remain preclinical or non-oncology; direct oncolytic viruses have reached late-phase testing. Major barriers include viral dark matter, specimen and assay heterogeneity, disease-related confounding, limited external validation, and weak causal evidence. Standardized, mechanistically anchored, multi-kingdom studies are needed to establish clinical utility.},
}
MeSH Terms:
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Humans
*Gastrointestinal Neoplasms/virology/therapy
*Virome
*Gastrointestinal Microbiome
Animals
Bacteriophages
Gastrointestinal Tract/virology
Translational Research, Biomedical
Biomarkers, Tumor
Oncogenic Viruses
Bacteria/virology
RevDate: 2026-10-28
CmpDate: 2026-10-27
Red Tide Algal Toxin-Induced Intestinal Injury in Marine Fish: Mechanisms, Gut Microecology, and Aquaculture Health Risk Assessment.
Veterinary sciences, 13(10):.
Harmful algal blooms (HABs) can cause rapid, extensive mortality in exposed marine fish, often before fish-level diagnostic sampling can guide an emergency response. This review compares the toxin-specific evidence for intestinal injury caused by paralytic shellfish toxins, okadaic acid and Dinophysistoxins, brevetoxins, and fish-killing blooms, while distinguishing direct evidence in marine fish from evidence in other models. Intestinal barrier disruption, inflammation, and microbiome changes are valuable for explaining sublethal exposure, survivor recovery, and post-event attribution. They are not proposed as operational triggers during an acute fish kill. Practical management instead depends chiefly on site-specific environmental surveillance before exposure, predefined emergency actions when a bloom approaches, and longer-term reduction in avoidable nutrient and waste inputs where these contribute to local bloom risk. A four-stage framework links environmental hazard, fish exposure, biological effects, and production or food-safety outcomes with quantitative indicators and explicit uncertainty at each transition. This revised scope places mechanistic intestinal toxicology within the ecological time scale and operational limits of marine aquaculture.
Additional Links: PMID-42944108
PubMed:
Citation:
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@article {pmid42944108,
year = {2026},
author = {Hang, L and Xu, H and Ding, Y and Chen, P and Song, X and Shi, D and Chen, Z},
title = {Red Tide Algal Toxin-Induced Intestinal Injury in Marine Fish: Mechanisms, Gut Microecology, and Aquaculture Health Risk Assessment.},
journal = {Veterinary sciences},
volume = {13},
number = {10},
pages = {},
pmid = {42944108},
issn = {2306-7381},
abstract = {Harmful algal blooms (HABs) can cause rapid, extensive mortality in exposed marine fish, often before fish-level diagnostic sampling can guide an emergency response. This review compares the toxin-specific evidence for intestinal injury caused by paralytic shellfish toxins, okadaic acid and Dinophysistoxins, brevetoxins, and fish-killing blooms, while distinguishing direct evidence in marine fish from evidence in other models. Intestinal barrier disruption, inflammation, and microbiome changes are valuable for explaining sublethal exposure, survivor recovery, and post-event attribution. They are not proposed as operational triggers during an acute fish kill. Practical management instead depends chiefly on site-specific environmental surveillance before exposure, predefined emergency actions when a bloom approaches, and longer-term reduction in avoidable nutrient and waste inputs where these contribute to local bloom risk. A four-stage framework links environmental hazard, fish exposure, biological effects, and production or food-safety outcomes with quantitative indicators and explicit uncertainty at each transition. This revised scope places mechanistic intestinal toxicology within the ecological time scale and operational limits of marine aquaculture.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Descriptive, Exploratory Analysis of Microbial Community Composition Across Stages of Canine Periodontal Disease Revealed by 16S rRNA Sequencing in Dogs.
Veterinary sciences, 13(10):.
Periodontal disease (PD) is one of the most prevalent oral conditions in dogs, yet the microbial dynamics underlying its progression remain incompletely understood. This exploratory study aimed to describe the canine oral microbiome across four clinical stages using 16S rRNA gene sequencing. Dogs were categorized as Healthy (Stage 0), Gingivitis (Stage 1), Early Periodontitis (Stage 2), and Moderate-Advanced Periodontitis (Stages 3-4) according to American Veterinary Dental College (AVDC) criteria. Pooled subgingival plaque samples from the groups were analyzed for microbial diversity, taxonomic composition, and ecological patterns. Alpha diversity differed among the four pooled profiles, with the highest observed richness in the Early Periodontitis (Stage 2) pool and the lowest in the Moderate-Advanced Periodontitis (Stages 3-4) pool. Beta diversity analyses showed separation among the pooled profiles, particularly between the healthy and severe groups. Taxonomic profiling identified higher relative abundances of sequences assigned to Porphyromonas gingivalis and Treponema denticola in the more advanced disease stage pools, while Fusobacterium nucleatum reached its highest relative abundance in the Early Periodontitis (Stage 2) pool. Visualization of abundance profiles across the four pooled libraries revealed concordant trends among selected treponeme taxa and Fusobacterium nucleatum, as well as inverse trends for other taxa. These findings provide a descriptive, group-level characterization of microbial community differences across AVDC-defined stages of canine periodontal disease based on pooled samples and generate hypotheses for future individual-level studies.
Additional Links: PMID-42944112
PubMed:
Citation:
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@article {pmid42944112,
year = {2026},
author = {Pizauro, LJL and Gualberto, NGS and Santos, KC and Pirovani, CP and Santana, JO and Castro, LMC and Dias, RPM and Nunes, MSC and Carlos, RSA},
title = {Descriptive, Exploratory Analysis of Microbial Community Composition Across Stages of Canine Periodontal Disease Revealed by 16S rRNA Sequencing in Dogs.},
journal = {Veterinary sciences},
volume = {13},
number = {10},
pages = {},
pmid = {42944112},
issn = {2306-7381},
abstract = {Periodontal disease (PD) is one of the most prevalent oral conditions in dogs, yet the microbial dynamics underlying its progression remain incompletely understood. This exploratory study aimed to describe the canine oral microbiome across four clinical stages using 16S rRNA gene sequencing. Dogs were categorized as Healthy (Stage 0), Gingivitis (Stage 1), Early Periodontitis (Stage 2), and Moderate-Advanced Periodontitis (Stages 3-4) according to American Veterinary Dental College (AVDC) criteria. Pooled subgingival plaque samples from the groups were analyzed for microbial diversity, taxonomic composition, and ecological patterns. Alpha diversity differed among the four pooled profiles, with the highest observed richness in the Early Periodontitis (Stage 2) pool and the lowest in the Moderate-Advanced Periodontitis (Stages 3-4) pool. Beta diversity analyses showed separation among the pooled profiles, particularly between the healthy and severe groups. Taxonomic profiling identified higher relative abundances of sequences assigned to Porphyromonas gingivalis and Treponema denticola in the more advanced disease stage pools, while Fusobacterium nucleatum reached its highest relative abundance in the Early Periodontitis (Stage 2) pool. Visualization of abundance profiles across the four pooled libraries revealed concordant trends among selected treponeme taxa and Fusobacterium nucleatum, as well as inverse trends for other taxa. These findings provide a descriptive, group-level characterization of microbial community differences across AVDC-defined stages of canine periodontal disease based on pooled samples and generate hypotheses for future individual-level studies.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Integrating Host Transcriptomics and Metagenomics in the Periparturient Dairy Cow: From Molecular Signatures to Host-Microbiome Interfaces.
Veterinary sciences, 13(10):.
The periparturient or transition period-roughly three weeks before to three weeks after calving-compresses the most severe metabolic, endocrine and immunological demands of the production cycle into a few weeks and accounts for most clinical disease and involuntary culling in dairy herds. Conventional surveillance relies on downstream indicators-non-esterified fatty acids, β-hydroxybutyrate, calcium and acute-phase proteins-that document failed adaptation without resolving its regulatory origins. Two omics platforms now close that gap. Transcriptomics shows that the liver, adipose tissue, mammary gland, endometrium, rumen epithelium and circulating leukocytes each execute a distinct, temporally ordered program organized around lipid mobilization, gluconeogenesis, endoplasmic reticulum stress, redox defense and inflammatory resolution, layered over a regulatory tier of non-coding RNAs. Metagenomics shows in parallel that rumen, hindgut, uterine, vaginal, teat-apex and colostrum communities are restructured by parturition and by the dietary shift into lactation, with reproducible dysbiotic signatures accompanying ketosis, fatty liver, metritis, endometritis and intramammary infection. Critically, the two layers are mechanistically coupled: microbial short-chain fatty acids, secondary bile acids, purine derivatives and amino acids reprogram hepatic and immune cell transcription, while host lipolysis, inflammation and mineral demand reshape community structure. This review synthesizes both groups of literature within a single framework, formalizes five host-microbiome interfaces supported by paired measurements and identifies the biomarker, nutritional and genetic-selection opportunities that emerge only when host and microbial evidence are read together.
Additional Links: PMID-42944114
PubMed:
Citation:
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@article {pmid42944114,
year = {2026},
author = {Ma, Q and Tharwat, M and Ullah, A and Liu, J and Alkheraif, AA and Khan, MZ},
title = {Integrating Host Transcriptomics and Metagenomics in the Periparturient Dairy Cow: From Molecular Signatures to Host-Microbiome Interfaces.},
journal = {Veterinary sciences},
volume = {13},
number = {10},
pages = {},
pmid = {42944114},
issn = {2306-7381},
support = {QU-APC-2026//Qassim University/ ; },
abstract = {The periparturient or transition period-roughly three weeks before to three weeks after calving-compresses the most severe metabolic, endocrine and immunological demands of the production cycle into a few weeks and accounts for most clinical disease and involuntary culling in dairy herds. Conventional surveillance relies on downstream indicators-non-esterified fatty acids, β-hydroxybutyrate, calcium and acute-phase proteins-that document failed adaptation without resolving its regulatory origins. Two omics platforms now close that gap. Transcriptomics shows that the liver, adipose tissue, mammary gland, endometrium, rumen epithelium and circulating leukocytes each execute a distinct, temporally ordered program organized around lipid mobilization, gluconeogenesis, endoplasmic reticulum stress, redox defense and inflammatory resolution, layered over a regulatory tier of non-coding RNAs. Metagenomics shows in parallel that rumen, hindgut, uterine, vaginal, teat-apex and colostrum communities are restructured by parturition and by the dietary shift into lactation, with reproducible dysbiotic signatures accompanying ketosis, fatty liver, metritis, endometritis and intramammary infection. Critically, the two layers are mechanistically coupled: microbial short-chain fatty acids, secondary bile acids, purine derivatives and amino acids reprogram hepatic and immune cell transcription, while host lipolysis, inflammation and mineral demand reshape community structure. This review synthesizes both groups of literature within a single framework, formalizes five host-microbiome interfaces supported by paired measurements and identifies the biomarker, nutritional and genetic-selection opportunities that emerge only when host and microbial evidence are read together.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Effects of Eucommia ulmoides Leaf-Astragalus membranaceus Complex on Antioxidant Capacity, Immune Function, Gut Microbiota and Serum Metabolome of Yellow-Feather Broilers.
Veterinary sciences, 13(10):.
Background: Phytogenic feed additives may provide sustainable alternatives for improving poultry productivity and health. This study evaluated the chemical composition, antioxidant activity, and in vivo effects of a 1:1 Eucommia ulmoides leaf-Astragalus membranaceus complex (EG) in yellow-feathered broilers. Methods: The nutritional composition, bioactive compounds, and antioxidant activity of EG were characterized. A total of 200 one-day-old yellow-feathered broilers were randomly allocated into four dietary treatments with five replicates per group and 10 birds per replicate: the control group (CG) receiving a basal diet and three EG supplementation groups receiving diets supplemented with 0.5% (EG (0.5%)), 1.0% (EG (1.0%)), 2.0% (EG (2.0%)) Eucommia ulmoides leaf-Astragalus membranaceus complex for 42 days. Growth performance, serum antioxidant and immune indicators, intestinal microbiota composition, and serum metabolomic profiles were analyzed. Results: EG contained 46.53% polysaccharides and exhibited concentration-dependent radical-scavenging activity. Supplementation with EG (0.5%) consistently increased body weight and average daily gain and reduced the feed conversion ratio without affecting feed intake. EG increased serum antioxidant enzyme activities and immunoglobulin concentrations but did not affect routine biochemical parameters. The EG (0.5%) group was therefore selected for microbiome and metabolome analyses. EG altered jejunal and cecal microbial composition without significantly affecting α-diversity and increased cecal Faecalibacterium and Blautia at day 21 and Faecalibacterium and Parabacteroides at day 42. Metabolomics identified 103 differential metabolites associated mainly with amino acid, glycerophospholipid, and energy metabolism. Spearman's analysis further associated Bacteroidota, Bacillota, Enterococcus, and Blautia with amino acid, carbohydrate, and lipid-related metabolites. Conclusions: These findings indicate that EG (0.5%) may improve growth and feed efficiency while modulating antioxidant status, humoral immune indices, intestinal microbial composition, and systemic metabolism in yellow-feathered broilers.
Additional Links: PMID-42944140
PubMed:
Citation:
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@article {pmid42944140,
year = {2026},
author = {Ma, H and Yao, Y and Wei, Y},
title = {Effects of Eucommia ulmoides Leaf-Astragalus membranaceus Complex on Antioxidant Capacity, Immune Function, Gut Microbiota and Serum Metabolome of Yellow-Feather Broilers.},
journal = {Veterinary sciences},
volume = {13},
number = {10},
pages = {},
pmid = {42944140},
issn = {2306-7381},
support = {YCKJ-2022057//Yuncheng Science and Technology Program/ ; },
abstract = {Background: Phytogenic feed additives may provide sustainable alternatives for improving poultry productivity and health. This study evaluated the chemical composition, antioxidant activity, and in vivo effects of a 1:1 Eucommia ulmoides leaf-Astragalus membranaceus complex (EG) in yellow-feathered broilers. Methods: The nutritional composition, bioactive compounds, and antioxidant activity of EG were characterized. A total of 200 one-day-old yellow-feathered broilers were randomly allocated into four dietary treatments with five replicates per group and 10 birds per replicate: the control group (CG) receiving a basal diet and three EG supplementation groups receiving diets supplemented with 0.5% (EG (0.5%)), 1.0% (EG (1.0%)), 2.0% (EG (2.0%)) Eucommia ulmoides leaf-Astragalus membranaceus complex for 42 days. Growth performance, serum antioxidant and immune indicators, intestinal microbiota composition, and serum metabolomic profiles were analyzed. Results: EG contained 46.53% polysaccharides and exhibited concentration-dependent radical-scavenging activity. Supplementation with EG (0.5%) consistently increased body weight and average daily gain and reduced the feed conversion ratio without affecting feed intake. EG increased serum antioxidant enzyme activities and immunoglobulin concentrations but did not affect routine biochemical parameters. The EG (0.5%) group was therefore selected for microbiome and metabolome analyses. EG altered jejunal and cecal microbial composition without significantly affecting α-diversity and increased cecal Faecalibacterium and Blautia at day 21 and Faecalibacterium and Parabacteroides at day 42. Metabolomics identified 103 differential metabolites associated mainly with amino acid, glycerophospholipid, and energy metabolism. Spearman's analysis further associated Bacteroidota, Bacillota, Enterococcus, and Blautia with amino acid, carbohydrate, and lipid-related metabolites. Conclusions: These findings indicate that EG (0.5%) may improve growth and feed efficiency while modulating antioxidant status, humoral immune indices, intestinal microbial composition, and systemic metabolism in yellow-feathered broilers.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
A Systematic Comparison of Differential Metabolites and Functional Pathways in the Gut Contents of Yaks and Plateau Yellow Cattle Across Altitudinal Gradients.
Veterinary sciences, 13(10):.
The yak (Bos grunniens) is a crucial species adapted to the extreme high-altitude environment of the Tibetan Plateau. However, a systematic understanding of how gut metabolic homeostasis contributes to this adaptation, particularly across altitudinal gradients and in comparison with sympatric species, remains limited. This study employed untargeted metabolomics to profile the intestinal contents of high-altitude yaks (HYs, 3800 m), low-altitude yaks (LYs, 2500 m), and plateau yellow cattle (PC, 3500 m) from the Gannan region. Multivariate analysis revealed distinct clustering of the three groups, with PLS-DA model validation parameters (R2Y(cum) > 0.997, Q2(cum) > 0.990), confirming significant species-specific and altitude-adaptive differentiation in the gut metabolome. A suite of differentially abundant metabolites (DAMs) was identified: HYs were enriched with stress- and inflammation-related molecules (e.g., prostaglandin E2, uric acid-indicative of oxidative stress and inflammatory responses) and steroid metabolites; LYs showed a profile oriented towards basic anabolism and antioxidant defense (e.g., L-galactono-1,4-lactone, allantoin); PC were characterized by unique lipid derivatives (e.g., 5-hexyl-2-furanhexanoic acid) and fungal-origin metabolites. Pathway enrichment analysis pinpointed Linoleic acid metabolism as one of the most significantly enriched pathways, with key hydroxyoctadecadienoic acids (HODEs) and related oxylipins significantly upregulated in HYs. Other significantly enriched pathways included Tryptophan metabolism, ABC transporters, and Protein digestion and absorption. Our findings suggest that high-altitude adaptation in yaks is associated with remodeling of the intestinal metabolic network. The identified signature metabolites and consistently enriched candidate pathways provide novel insights into potential host-microbiome-associated mechanisms and establish a metabolic foundation for the conservation of plateau livestock genetic resources and the development of precision husbandry strategies. However, these findings should be interpreted as hypothesis-generating because altitude, species, diet, and environment were not fully decoupled.
Additional Links: PMID-42944158
PubMed:
Citation:
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@article {pmid42944158,
year = {2026},
author = {Li, D and Zhang, J and Zhang, L and Liu, X and Chen, P},
title = {A Systematic Comparison of Differential Metabolites and Functional Pathways in the Gut Contents of Yaks and Plateau Yellow Cattle Across Altitudinal Gradients.},
journal = {Veterinary sciences},
volume = {13},
number = {10},
pages = {},
pmid = {42944158},
issn = {2306-7381},
support = {QY-HS-2025A-01//The 2025 County-Level Science and Technology Plan Project of the East-West Collaboration Financial Assistance Fund/ ; 26CXNA042//The 2026 Provincial Science and Technology Program of the Gansu Provincial Department of Science and Technology/ ; },
abstract = {The yak (Bos grunniens) is a crucial species adapted to the extreme high-altitude environment of the Tibetan Plateau. However, a systematic understanding of how gut metabolic homeostasis contributes to this adaptation, particularly across altitudinal gradients and in comparison with sympatric species, remains limited. This study employed untargeted metabolomics to profile the intestinal contents of high-altitude yaks (HYs, 3800 m), low-altitude yaks (LYs, 2500 m), and plateau yellow cattle (PC, 3500 m) from the Gannan region. Multivariate analysis revealed distinct clustering of the three groups, with PLS-DA model validation parameters (R2Y(cum) > 0.997, Q2(cum) > 0.990), confirming significant species-specific and altitude-adaptive differentiation in the gut metabolome. A suite of differentially abundant metabolites (DAMs) was identified: HYs were enriched with stress- and inflammation-related molecules (e.g., prostaglandin E2, uric acid-indicative of oxidative stress and inflammatory responses) and steroid metabolites; LYs showed a profile oriented towards basic anabolism and antioxidant defense (e.g., L-galactono-1,4-lactone, allantoin); PC were characterized by unique lipid derivatives (e.g., 5-hexyl-2-furanhexanoic acid) and fungal-origin metabolites. Pathway enrichment analysis pinpointed Linoleic acid metabolism as one of the most significantly enriched pathways, with key hydroxyoctadecadienoic acids (HODEs) and related oxylipins significantly upregulated in HYs. Other significantly enriched pathways included Tryptophan metabolism, ABC transporters, and Protein digestion and absorption. Our findings suggest that high-altitude adaptation in yaks is associated with remodeling of the intestinal metabolic network. The identified signature metabolites and consistently enriched candidate pathways provide novel insights into potential host-microbiome-associated mechanisms and establish a metabolic foundation for the conservation of plateau livestock genetic resources and the development of precision husbandry strategies. However, these findings should be interpreted as hypothesis-generating because altitude, species, diet, and environment were not fully decoupled.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
The Gut-Mammary Axis in Dairy Cattle: A Review of Gut Microbiota-Driven Influences on Lactation.
Veterinary sciences, 13(10):.
The gut microbiota is increasingly recognized as an important regulator of cattle health and productivity, particularly in shaping lactation performance. This review synthesizes current research on how gut microbial communities influence milk yield, composition, and lactational physiology. The diverse microbial populations in the ruminant gastrointestinal tract produce key metabolites, including short-chain fatty acids, microbial amino acids, and vitamins, that support host energy balance and nutrient utilization during lactation. We discuss the role of the gut microbiota in the gut-mammary axis and how microbial fermentation influences immune modulation, mastitis, and nutrient metabolism, all of which affect mammary gland development and milk synthesis. The review also examines how factors such as diet composition, feed additives (e.g., prebiotics, probiotics, and postbiotics), antimicrobial use, and environmental stressors alter microbiota structure and function. These changes can promote microbial resilience or dysbiosis, thereby affecting lactation either positively or negatively. Understanding these complex interactions offers promising avenues for microbiome-targeted interventions to enhance dairy performance and animal well-being. Future research should emphasize integrated multi-omics approaches to identify causal pathways and inform precision strategies for improving lactation efficiency in cattle.
Additional Links: PMID-42944202
PubMed:
Citation:
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@article {pmid42944202,
year = {2026},
author = {Ahmad, K and Islam, T and Jamal, QMS and Srivastava, S and Rabbee, MF},
title = {The Gut-Mammary Axis in Dairy Cattle: A Review of Gut Microbiota-Driven Influences on Lactation.},
journal = {Veterinary sciences},
volume = {13},
number = {10},
pages = {},
pmid = {42944202},
issn = {2306-7381},
support = {QU-APC-2026//Qassim University/ ; },
abstract = {The gut microbiota is increasingly recognized as an important regulator of cattle health and productivity, particularly in shaping lactation performance. This review synthesizes current research on how gut microbial communities influence milk yield, composition, and lactational physiology. The diverse microbial populations in the ruminant gastrointestinal tract produce key metabolites, including short-chain fatty acids, microbial amino acids, and vitamins, that support host energy balance and nutrient utilization during lactation. We discuss the role of the gut microbiota in the gut-mammary axis and how microbial fermentation influences immune modulation, mastitis, and nutrient metabolism, all of which affect mammary gland development and milk synthesis. The review also examines how factors such as diet composition, feed additives (e.g., prebiotics, probiotics, and postbiotics), antimicrobial use, and environmental stressors alter microbiota structure and function. These changes can promote microbial resilience or dysbiosis, thereby affecting lactation either positively or negatively. Understanding these complex interactions offers promising avenues for microbiome-targeted interventions to enhance dairy performance and animal well-being. Future research should emphasize integrated multi-omics approaches to identify causal pathways and inform precision strategies for improving lactation efficiency in cattle.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-27
Machine Learning in Mammals' Health: Integrating Multi-Omics Data for Precision Nutrition and Sustainable Production.
Veterinary sciences, 13(10):.
Precision nutrition in modern mammalian production aims to transition from static feeding regimens toward dynamic and customized strategies by unraveling complex interactions among genetics, environment, the gut microbiome, and host physiology. Machine learning provides a powerful analytical framework to navigate high-dimensional multi-omics datasets. However, existing applications frequently lack systematic criteria for algorithm selection and remain largely confined to observational statistical associations without progressing toward causal verification. This perspective delineates a coherent translational chain spanning three interconnected operational scenarios: key functional microbiota screening to identify whom to intervene on, multi-omics biomarker identification to define when to intervene, and host pathway characterization to reveal how the animal responds. We critically examine the operational boundaries, interpretability trade-offs, and failure modes of classical algorithms including LASSO, support vector machines, random forest, and graph neural networks across these domains. Furthermore, we address critical field bottlenecks such as high dimensionality, small-sample overfitting, batch effects, and black-box opacity, while highlighting emerging paradigms including multimodal data fusion, transfer learning, and causal machine learning to bridge the gap between data-driven screening and actionable nutritional interventions. Ultimately, transforming machine learning from an auxiliary predictive tool into an autonomous precision nutrition engine requires shifting the research focus from isolated model accuracy to reproducible and causally validated biological targets.
Additional Links: PMID-42944216
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@article {pmid42944216,
year = {2026},
author = {Huang, W and Yu, X and Xia, Y and Li, W and Zhao, X},
title = {Machine Learning in Mammals' Health: Integrating Multi-Omics Data for Precision Nutrition and Sustainable Production.},
journal = {Veterinary sciences},
volume = {13},
number = {10},
pages = {},
pmid = {42944216},
issn = {2306-7381},
support = {CSTB2023NSCQ-MSX0786//Natural Science Foundation of Chongqing/ ; KJQN202500214//Chongqing Municipality Education Commission/ ; NW-CSTB2025NYKJGGXM-DPJSLXMX0003//Agricultural Science and Technology R&D Program of Chongqing/ ; },
abstract = {Precision nutrition in modern mammalian production aims to transition from static feeding regimens toward dynamic and customized strategies by unraveling complex interactions among genetics, environment, the gut microbiome, and host physiology. Machine learning provides a powerful analytical framework to navigate high-dimensional multi-omics datasets. However, existing applications frequently lack systematic criteria for algorithm selection and remain largely confined to observational statistical associations without progressing toward causal verification. This perspective delineates a coherent translational chain spanning three interconnected operational scenarios: key functional microbiota screening to identify whom to intervene on, multi-omics biomarker identification to define when to intervene, and host pathway characterization to reveal how the animal responds. We critically examine the operational boundaries, interpretability trade-offs, and failure modes of classical algorithms including LASSO, support vector machines, random forest, and graph neural networks across these domains. Furthermore, we address critical field bottlenecks such as high dimensionality, small-sample overfitting, batch effects, and black-box opacity, while highlighting emerging paradigms including multimodal data fusion, transfer learning, and causal machine learning to bridge the gap between data-driven screening and actionable nutritional interventions. Ultimately, transforming machine learning from an auxiliary predictive tool into an autonomous precision nutrition engine requires shifting the research focus from isolated model accuracy to reproducible and causally validated biological targets.},
}
RevDate: 2026-10-27
Local Microenvironment in Adenoid Hypertrophy and Its Clinical Relevance.
Current medical science [Epub ahead of print].
Adenoid hypertrophy (AH) is among the most common otolaryngologic disorders in childhood, and its development cannot be adequately explained by a single inflammatory process. Increasing evidence suggests that the adenoid functions not only as an important component of upper airway mucosal immunity but also as a critical site for persistent microbial colonization and local immune remodeling. This review examines AH from structural, immunologic, and microecological perspectives, offering an integrated analytical framework to better understand coordinated imbalance within the adenoidal microenvironment. Furthermore, we investigate the relationships between distinct microenvironmental patterns and clinical phenotypes and discuss both current therapeutic strategies and emerging precision intervention approaches. Collectively, existing evidence indicates that AH is a multifaceted disorder closely associated with microenvironmental reprogramming, and its clinical heterogeneity appears to be attributed to diverse underlying biological processes.
Additional Links: PMID-42944802
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@article {pmid42944802,
year = {2026},
author = {Ma, JY and Chen, AN and Yao, Y and Wang, H},
title = {Local Microenvironment in Adenoid Hypertrophy and Its Clinical Relevance.},
journal = {Current medical science},
volume = {},
number = {},
pages = {},
pmid = {42944802},
issn = {2523-899X},
support = {81873694//National Natural Science Foundation of China/ ; 81873694//National Natural Science Foundation of China/ ; 81873694//National Natural Science Foundation of China/ ; 2022BCA005//the key Research and Development Program of Hubei Province/ ; },
abstract = {Adenoid hypertrophy (AH) is among the most common otolaryngologic disorders in childhood, and its development cannot be adequately explained by a single inflammatory process. Increasing evidence suggests that the adenoid functions not only as an important component of upper airway mucosal immunity but also as a critical site for persistent microbial colonization and local immune remodeling. This review examines AH from structural, immunologic, and microecological perspectives, offering an integrated analytical framework to better understand coordinated imbalance within the adenoidal microenvironment. Furthermore, we investigate the relationships between distinct microenvironmental patterns and clinical phenotypes and discuss both current therapeutic strategies and emerging precision intervention approaches. Collectively, existing evidence indicates that AH is a multifaceted disorder closely associated with microenvironmental reprogramming, and its clinical heterogeneity appears to be attributed to diverse underlying biological processes.},
}
RevDate: 2026-10-27
CmpDate: 2026-10-27
Periodontitis Beyond ASCVD: Emerging Cardiovascular Phenotypes in Perio-Medicine.
Clinical oral investigations, 30(11):.
BACKGROUND: Periodontitis is increasingly recognized as a chronic inflammatory disease with systemic implications beyond the oral cavity. Within perio-medicine, its association with cardiovascular disease has been extensively investigated, particularly in relation to atherosclerotic cardiovascular disease (ASCVD). However, the field is now expanding toward a broader and more phenotype-specific cardiovascular framework.
OBJECTIVE: This narrative review critically examines how the periodontitis-cardiovascular field has evolved from a predominantly ASCVD-centered model toward a broader spectrum of cardiovascular phenotypes, with particular emphasis on differences in evidence maturity, contemporary mechanistic concepts, and unresolved translational questions.
METHODS: A structured literature search was conducted in PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library. Evidence from mechanistic, observational, and interventional studies was qualitatively synthesized according to its contribution to established clinical associations, supportive mechanistic evidence, emerging cardiovascular phenotypes, and unresolved questions regarding causality and clinical translation.
RESULTS: The association between periodontitis and coronary atherosclerotic disease represents the most mature component of the literature, with substantial observational and meta-analytic support, while ischemic cerebrovascular disease is also supported by consistent but more heterogeneous evidence. Beyond ASCVD, atrial fibrillation and heart failure currently represent the most developed emerging cardiovascular phenotypes, whereas evidence concerning abdominal aortic aneurysm and venous thromboembolism remains more preliminary and hypothesis-generating. Contemporary mechanistic models extend beyond bacteremia and systemic inflammation to include endothelial dysfunction, thrombo-inflammatory signaling, trained immunity, immune-cell trafficking, functional dysregulation of the oral microbiome, and shared biological vulnerabilities. However, these pathways differ markedly in cardiovascular-specific evidentiary maturity and should not be interpreted as equivalent evidence of human causality. Periodontal therapy can improve inflammatory biomarkers, endothelial function, selected metabolic parameters, and blood pressure in specific populations, but a persistent translational gap remains between surrogate-marker improvement and demonstrated reduction in major adverse cardiovascular events. Periodontitis may also contribute to chronic systemic inflammatory burden in susceptible individuals, although its role within cardiovascular residual inflammatory risk remains an emerging hypothesis.
CONCLUSIONS: The periodontal-cardiovascular field is evolving from a predominantly ASCVD-centered model toward a phenotype-specific continuum of evidence maturity. Periodontitis is best interpreted as a potential modifier of cardiovascular vulnerability rather than as an established causal determinant. Future research should prioritize adequately powered cardiovascular-outcome trials, standardized periodontal phenotyping, and prospective validation of emerging phenotypes and mechanistic frameworks before periodontal information can be considered clinically actionable for cardiovascular prevention.
Additional Links: PMID-42944993
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@article {pmid42944993,
year = {2026},
author = {Sansavini, M and Pieretto, G and Samra, M and Bacci, C},
title = {Periodontitis Beyond ASCVD: Emerging Cardiovascular Phenotypes in Perio-Medicine.},
journal = {Clinical oral investigations},
volume = {30},
number = {11},
pages = {},
pmid = {42944993},
issn = {1436-3771},
mesh = {Humans ; Phenotype ; *Periodontitis/complications ; *Cardiovascular Diseases/etiology ; *Atherosclerosis/etiology ; },
abstract = {BACKGROUND: Periodontitis is increasingly recognized as a chronic inflammatory disease with systemic implications beyond the oral cavity. Within perio-medicine, its association with cardiovascular disease has been extensively investigated, particularly in relation to atherosclerotic cardiovascular disease (ASCVD). However, the field is now expanding toward a broader and more phenotype-specific cardiovascular framework.
OBJECTIVE: This narrative review critically examines how the periodontitis-cardiovascular field has evolved from a predominantly ASCVD-centered model toward a broader spectrum of cardiovascular phenotypes, with particular emphasis on differences in evidence maturity, contemporary mechanistic concepts, and unresolved translational questions.
METHODS: A structured literature search was conducted in PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library. Evidence from mechanistic, observational, and interventional studies was qualitatively synthesized according to its contribution to established clinical associations, supportive mechanistic evidence, emerging cardiovascular phenotypes, and unresolved questions regarding causality and clinical translation.
RESULTS: The association between periodontitis and coronary atherosclerotic disease represents the most mature component of the literature, with substantial observational and meta-analytic support, while ischemic cerebrovascular disease is also supported by consistent but more heterogeneous evidence. Beyond ASCVD, atrial fibrillation and heart failure currently represent the most developed emerging cardiovascular phenotypes, whereas evidence concerning abdominal aortic aneurysm and venous thromboembolism remains more preliminary and hypothesis-generating. Contemporary mechanistic models extend beyond bacteremia and systemic inflammation to include endothelial dysfunction, thrombo-inflammatory signaling, trained immunity, immune-cell trafficking, functional dysregulation of the oral microbiome, and shared biological vulnerabilities. However, these pathways differ markedly in cardiovascular-specific evidentiary maturity and should not be interpreted as equivalent evidence of human causality. Periodontal therapy can improve inflammatory biomarkers, endothelial function, selected metabolic parameters, and blood pressure in specific populations, but a persistent translational gap remains between surrogate-marker improvement and demonstrated reduction in major adverse cardiovascular events. Periodontitis may also contribute to chronic systemic inflammatory burden in susceptible individuals, although its role within cardiovascular residual inflammatory risk remains an emerging hypothesis.
CONCLUSIONS: The periodontal-cardiovascular field is evolving from a predominantly ASCVD-centered model toward a phenotype-specific continuum of evidence maturity. Periodontitis is best interpreted as a potential modifier of cardiovascular vulnerability rather than as an established causal determinant. Future research should prioritize adequately powered cardiovascular-outcome trials, standardized periodontal phenotyping, and prospective validation of emerging phenotypes and mechanistic frameworks before periodontal information can be considered clinically actionable for cardiovascular prevention.},
}
MeSH Terms:
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Humans
Phenotype
*Periodontitis/complications
*Cardiovascular Diseases/etiology
*Atherosclerosis/etiology
RevDate: 2026-10-27
CmpDate: 2026-10-27
Prepartum Heat Stress Dysregulates Immune Resilience in Postpartum Dairy Cows.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 40(20):.
Increasing environmental temperatures pose a major challenge to animal welfare by inducing heat stress and increasing the incidence of disease. Immune resilience is essential for maintaining animal health; however, the mechanisms linking heat stress to immune dysfunction and disease remain unclear. We hypothesized that prepartum heat stress would result in persistent disruption of immune resilience after calving when cows were no longer heat stressed. During summer, non-lactating, pregnant cows were subjected to either prepartum cooling (fans, water soakers, and shade; n = 31) or heat stress (shade only; n = 31) for the last 46 days of gestation. After calving, all cows received cooling. Postpartum health, peripheral blood, and endometrial samples were evaluated up to 21 days postpartum. Prepartum heat stress increased the incidence of postpartum diseases compared to cooled cows, with little change to the uterine microbiome. Prepartum heat stress increased postpartum white blood cell counts and mean platelet volume, while lipopolysaccharide-stimulated expression of CXCL8, IL1B, and TNF tended to be attenuated in whole blood. Interestingly, prepartum heat stress increased lipopolysaccharide-stimulated secretion of IL-6 and IL-8 in whole blood. In parallel, prepartum heat stress induced mild but persistent changes to the postpartum endometrial transcriptome associated with immunological pathways. Furthermore, prepartum heat stress attenuated basal expression of CXCL8, IL6, and TNF in cultured endometrial cells. Collectively, these findings demonstrate that prepartum heat stress increases disease incidence and disrupts peripheral and endometrial immune resilience independent of changes to the microbiome in postpartum cows.
Additional Links: PMID-42945143
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@article {pmid42945143,
year = {2026},
author = {Tariq, A and Sagheer, M and Kertz, NC and Seekford, ZK and de Bari, MAT and Macay, GA and Pandey, S and Zhai, Y and Jeong, KC and Dahl, GE and Bromfield, JJ},
title = {Prepartum Heat Stress Dysregulates Immune Resilience in Postpartum Dairy Cows.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {20},
pages = {},
pmid = {42945143},
issn = {1530-6860},
support = {2020-67015-31015//USDA | National Institute of Food and Agriculture (NIFA)/ ; //Higher Education Commission, Pakistan (HEC)/ ; },
mesh = {Animals ; Female ; Cattle ; *Postpartum Period/immunology ; *Heat-Shock Response/immunology ; Pregnancy ; *Heat Stress Disorders/immunology/veterinary ; Lipopolysaccharides ; Hot Temperature ; },
abstract = {Increasing environmental temperatures pose a major challenge to animal welfare by inducing heat stress and increasing the incidence of disease. Immune resilience is essential for maintaining animal health; however, the mechanisms linking heat stress to immune dysfunction and disease remain unclear. We hypothesized that prepartum heat stress would result in persistent disruption of immune resilience after calving when cows were no longer heat stressed. During summer, non-lactating, pregnant cows were subjected to either prepartum cooling (fans, water soakers, and shade; n = 31) or heat stress (shade only; n = 31) for the last 46 days of gestation. After calving, all cows received cooling. Postpartum health, peripheral blood, and endometrial samples were evaluated up to 21 days postpartum. Prepartum heat stress increased the incidence of postpartum diseases compared to cooled cows, with little change to the uterine microbiome. Prepartum heat stress increased postpartum white blood cell counts and mean platelet volume, while lipopolysaccharide-stimulated expression of CXCL8, IL1B, and TNF tended to be attenuated in whole blood. Interestingly, prepartum heat stress increased lipopolysaccharide-stimulated secretion of IL-6 and IL-8 in whole blood. In parallel, prepartum heat stress induced mild but persistent changes to the postpartum endometrial transcriptome associated with immunological pathways. Furthermore, prepartum heat stress attenuated basal expression of CXCL8, IL6, and TNF in cultured endometrial cells. Collectively, these findings demonstrate that prepartum heat stress increases disease incidence and disrupts peripheral and endometrial immune resilience independent of changes to the microbiome in postpartum cows.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Female
Cattle
*Postpartum Period/immunology
*Heat-Shock Response/immunology
Pregnancy
*Heat Stress Disorders/immunology/veterinary
Lipopolysaccharides
Hot Temperature
RevDate: 2026-10-28
CmpDate: 2026-10-27
Microbial community structure of Penaeus vannamei post-larvae naturally infected with multiple viruses in hatchery tanks.
PloS one, 21(10):e0361576.
BACKGROUND: This study offers an observational evaluation of how viral and bacterial infections co-occur with alterations in the microbiome and survival of Penaeus vannamei post-larvae, one of the most economically important species in global aquaculture.
METHODS: Eleven commercial larval production tanks were classified into three distinct infection scenarios using histology and PCR: Baculovirus penaei (BP) monoinfection, mixed infections (BP, white spot syndrome virus [WSSV], and acute hepatopancreatic necrosis disease [AHPND]-causing bacteria), and non-infected controls. High-molecular-weight DNA was subjected to shotgun metagenomic sequencing on the Illumina NovaSeq 6000 platform, followed by evaluation of microbial diversity, community structure, and infection-associated microbial signatures.
RESULTS: Although BP was the most abundant viral genus across infected groups, severe mortality was observed only under mixed-infection conditions, which were closely associated with AHPND-causing bacteria presence and microbiome disruption rather than with BP alone. Deep metagenomic sequencing revealed reduced, distinct microbiome structures in shrimp infected with BP and in those with mixed infections, compared to non-infected individuals. Non-infected post-larvae maintained complex and well-balanced bacterial communities, predominantly composed of Donghicola and Muricauda. Nudiviridae and Oscillospiraceae showed comparable relative abundances in BP-only and mixed-infection groups. In contrast, mixed infections were characterized by a relative increase in Vibrio, together with the PCR-detection of PirAB toxin genes, whereas WSSV remained detectable in the metagenomic dataset despite its comparatively low relative abundance, while the infection remained thermally suppressed and asymptomatic in the larvae. Functionally, infected larval microbiomes were enriched for transposases, retrotransposons, and virulence-factor genes. The near-complete BP-GR25 genome (119,245 bp) was assembled and annotated from larval metagenomes.
CONCLUSION: These results highlight the value of high-throughput sequencing in the early detection of pathogens in aquaculture, where subtle microbial shifts during postlarval stages can be valuable indicators of health status for production.
Additional Links: PMID-42945300
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@article {pmid42945300,
year = {2026},
author = {Andrade, B and Ramírez, M and Reyes, G},
title = {Microbial community structure of Penaeus vannamei post-larvae naturally infected with multiple viruses in hatchery tanks.},
journal = {PloS one},
volume = {21},
number = {10},
pages = {e0361576},
pmid = {42945300},
issn = {1932-6203},
mesh = {Animals ; *Penaeidae/virology/microbiology ; Larva/virology/microbiology ; Aquaculture ; *Microbiota ; Metagenomics ; Metagenome ; },
abstract = {BACKGROUND: This study offers an observational evaluation of how viral and bacterial infections co-occur with alterations in the microbiome and survival of Penaeus vannamei post-larvae, one of the most economically important species in global aquaculture.
METHODS: Eleven commercial larval production tanks were classified into three distinct infection scenarios using histology and PCR: Baculovirus penaei (BP) monoinfection, mixed infections (BP, white spot syndrome virus [WSSV], and acute hepatopancreatic necrosis disease [AHPND]-causing bacteria), and non-infected controls. High-molecular-weight DNA was subjected to shotgun metagenomic sequencing on the Illumina NovaSeq 6000 platform, followed by evaluation of microbial diversity, community structure, and infection-associated microbial signatures.
RESULTS: Although BP was the most abundant viral genus across infected groups, severe mortality was observed only under mixed-infection conditions, which were closely associated with AHPND-causing bacteria presence and microbiome disruption rather than with BP alone. Deep metagenomic sequencing revealed reduced, distinct microbiome structures in shrimp infected with BP and in those with mixed infections, compared to non-infected individuals. Non-infected post-larvae maintained complex and well-balanced bacterial communities, predominantly composed of Donghicola and Muricauda. Nudiviridae and Oscillospiraceae showed comparable relative abundances in BP-only and mixed-infection groups. In contrast, mixed infections were characterized by a relative increase in Vibrio, together with the PCR-detection of PirAB toxin genes, whereas WSSV remained detectable in the metagenomic dataset despite its comparatively low relative abundance, while the infection remained thermally suppressed and asymptomatic in the larvae. Functionally, infected larval microbiomes were enriched for transposases, retrotransposons, and virulence-factor genes. The near-complete BP-GR25 genome (119,245 bp) was assembled and annotated from larval metagenomes.
CONCLUSION: These results highlight the value of high-throughput sequencing in the early detection of pathogens in aquaculture, where subtle microbial shifts during postlarval stages can be valuable indicators of health status for production.},
}
MeSH Terms:
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Animals
*Penaeidae/virology/microbiology
Larva/virology/microbiology
Aquaculture
*Microbiota
Metagenomics
Metagenome
RevDate: 2026-10-27
CmpDate: 2026-10-27
Supervised and covariate-adjusted dimension reduction for prediction and visualization using microbiome data.
Briefings in bioinformatics, 27(5):.
Given that the gut microbiome has been shown to play a critical role in human health, discerning the relationship between microbial taxa and disease outcomes or phenotypes is of interest. Often, this involves association testing, predictive modeling, and visualizing trends in the data. Principal coordinates analysis (PCoA) is a commonly used dimension reduction technique in microbiome studies. PCoA relies on pairwise distances between samples and serves as a nonlinear alternative to the classic principal component analysis when non-Euclidean distances are used. Its low-dimensional embeddings provide intuitive visualizations but do not incorporate outcome-related information. Therefore, the low-dimensional principal coordinates may have poor performance in visualizing outcome differences, as well as in downstream disease prediction tasks. Additionally, covariates, such as demographics, lifestyle factors, and technical artifacts, can obscure true biological signals, leading to masked or spurious associations and limited generalizability. To address these limitations, we propose a supervised and covariate adjusted PCoA algorithm. By utilizing outcome information, while simultaneously minimizing the influence of nuisance variables, our method produces low-dimensional embeddings that better separate disease outcomes in visualizations and result in improved accuracy in downstream regression and classification tasks. We demonstrate the effectiveness of the proposed method and highlight its ability to extract important associations between the microbiome and disease outcomes while mitigating nuisance variation through simulations and application to real microbiome profiling studies.
Additional Links: PMID-42945345
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@article {pmid42945345,
year = {2026},
author = {Zang, C and Tang, L and Deek, RA},
title = {Supervised and covariate-adjusted dimension reduction for prediction and visualization using microbiome data.},
journal = {Briefings in bioinformatics},
volume = {27},
number = {5},
pages = {},
pmid = {42945345},
issn = {1477-4054},
support = {R56LM014522/LM/NLM NIH HHS/United States ; S10OD028483/OD/NIH HHS/United States ; //University of Pittsburgh's CTSI Trans-disciplinary Collaboration Pilot Award/ ; RRID:SCR_022735//University of Pittsburgh Center for Research Computing and Data/ ; },
mesh = {Humans ; Principal Component Analysis ; Algorithms ; *Microbiota ; Dimensionality Reduction ; *Gastrointestinal Microbiome ; *Computational Biology/methods ; Prediction Algorithms ; },
abstract = {Given that the gut microbiome has been shown to play a critical role in human health, discerning the relationship between microbial taxa and disease outcomes or phenotypes is of interest. Often, this involves association testing, predictive modeling, and visualizing trends in the data. Principal coordinates analysis (PCoA) is a commonly used dimension reduction technique in microbiome studies. PCoA relies on pairwise distances between samples and serves as a nonlinear alternative to the classic principal component analysis when non-Euclidean distances are used. Its low-dimensional embeddings provide intuitive visualizations but do not incorporate outcome-related information. Therefore, the low-dimensional principal coordinates may have poor performance in visualizing outcome differences, as well as in downstream disease prediction tasks. Additionally, covariates, such as demographics, lifestyle factors, and technical artifacts, can obscure true biological signals, leading to masked or spurious associations and limited generalizability. To address these limitations, we propose a supervised and covariate adjusted PCoA algorithm. By utilizing outcome information, while simultaneously minimizing the influence of nuisance variables, our method produces low-dimensional embeddings that better separate disease outcomes in visualizations and result in improved accuracy in downstream regression and classification tasks. We demonstrate the effectiveness of the proposed method and highlight its ability to extract important associations between the microbiome and disease outcomes while mitigating nuisance variation through simulations and application to real microbiome profiling studies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Principal Component Analysis
Algorithms
*Microbiota
Dimensionality Reduction
*Gastrointestinal Microbiome
*Computational Biology/methods
Prediction Algorithms
RevDate: 2026-10-27
Introduction to the special issue on RBD 40 years old: Perspectives on extensive clinical and research intersections.
Sleep medicine, 149:109330 pii:S1389-9457(26)00569-1 [Epub ahead of print].
This Introduction to the special issue in Sleep Medicine marking the 40th anniversary of the first publication on REM sleep behavior disorder (RBD) in 1986 provides a brief historical background with early timelines, followed by current RBD and REM-without-atonia diagnostic considerations; and updates on RBD global epidemiology, RBD in younger populations, and the spectrum of RBD comorbidities and biomarkers. Other topics covered include RBD gut microbiome dysbiosis, proteome abnormalities, and neuroinflammation; RBD international research consortia; RBD economic burden and adverse quality of life; and neurodegeneration risk disclosure for newly diagnosed idiopathic/isolated RBD patients. Thirty-four RBD clinical and research intersections are depicted in a figure. Two recent review articles are cited that identified more than 4200 peer-reviewed journal articles published to date on RBD. The six articles contained in this special RBD issue cover animal models and basic science; genetics; pathogenesis; measurement and diagnosis; neurodegeneration, neuroimaging, and phenoconversion biomarkers; and cognition. RBD epitomizes the close collaboration and cross-fertilization of clinical and basic science research.
Additional Links: PMID-42945712
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@article {pmid42945712,
year = {2026},
author = {Schenck, CH},
title = {Introduction to the special issue on RBD 40 years old: Perspectives on extensive clinical and research intersections.},
journal = {Sleep medicine},
volume = {149},
number = {},
pages = {109330},
doi = {10.1016/j.sleep.2026.109330},
pmid = {42945712},
issn = {1878-5506},
abstract = {This Introduction to the special issue in Sleep Medicine marking the 40th anniversary of the first publication on REM sleep behavior disorder (RBD) in 1986 provides a brief historical background with early timelines, followed by current RBD and REM-without-atonia diagnostic considerations; and updates on RBD global epidemiology, RBD in younger populations, and the spectrum of RBD comorbidities and biomarkers. Other topics covered include RBD gut microbiome dysbiosis, proteome abnormalities, and neuroinflammation; RBD international research consortia; RBD economic burden and adverse quality of life; and neurodegeneration risk disclosure for newly diagnosed idiopathic/isolated RBD patients. Thirty-four RBD clinical and research intersections are depicted in a figure. Two recent review articles are cited that identified more than 4200 peer-reviewed journal articles published to date on RBD. The six articles contained in this special RBD issue cover animal models and basic science; genetics; pathogenesis; measurement and diagnosis; neurodegeneration, neuroimaging, and phenoconversion biomarkers; and cognition. RBD epitomizes the close collaboration and cross-fertilization of clinical and basic science research.},
}
RevDate: 2026-10-27
Antibiotics and outcomes of cancer immunotherapy: An updated meta-analysis and clinical applications.
Cancer cell pii:S1535-6108(26)00431-9 [Epub ahead of print].
The gut microbiome is a modifiable determinant of response to immune checkpoint inhibitors (ICI), positioning antibiotic exposure as a critical yet under-recognized risk factor for worse survival outcomes in immuno-oncology. As nearly 30% of ICI-treated patients receive antibiotics and indications of cancer immunotherapy are expanding, this issue represents a global challenge in oncology. Here, we paint an updated and comprehensive landscape of antibiotic exposure in immuno-oncology, provide actionable clinical recommendations, and envision future avenues for improvement. First, we describe the biological mechanisms by which antibiotic-induced dysbiosis contributes to ICI resistance. Next, through an updated meta-analysis of 116 cohorts and 97,850 cancer patients treated with ICI, we found a significant association between antibiotic exposure and survival outcomes (overall survival, hazard ratio [HR]: 1.49, 95% confidence interval [CI]: 1.34-1.65; progression-free survival, HR: 1.44, 95% CI: 1.31-1.58). Finally, we discuss antibiotics stewardship and microbiome-centered strategies to prevent, diagnose, and/or repair dysbiosis.
Additional Links: PMID-42945960
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@article {pmid42945960,
year = {2026},
author = {Porcari, S and Bolte, LA and Björk, JR and Elkrief, A and Derosa, L and Ferrari, M and Pezzullo, AM and Severino, A and Fusco, W and Messaoudene, M and Costa Silva, CA and Fidelle, M and Routy, B and Mählmann, L and Thomas, AM and Ciccarese, C and Nero, C and Fagotti, A and Tortora, G and Gasbarrini, A and Iacovelli, R and Bria, E and Futreal, A and McQuade, J and Kroemer, G and Hospers, GAP and de Haan, JJ and Wargo, J and Segata, N and Weersma, RK and Ianiro, G and Zitvogel, L and , },
title = {Antibiotics and outcomes of cancer immunotherapy: An updated meta-analysis and clinical applications.},
journal = {Cancer cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ccell.2026.09.012},
pmid = {42945960},
issn = {1878-3686},
abstract = {The gut microbiome is a modifiable determinant of response to immune checkpoint inhibitors (ICI), positioning antibiotic exposure as a critical yet under-recognized risk factor for worse survival outcomes in immuno-oncology. As nearly 30% of ICI-treated patients receive antibiotics and indications of cancer immunotherapy are expanding, this issue represents a global challenge in oncology. Here, we paint an updated and comprehensive landscape of antibiotic exposure in immuno-oncology, provide actionable clinical recommendations, and envision future avenues for improvement. First, we describe the biological mechanisms by which antibiotic-induced dysbiosis contributes to ICI resistance. Next, through an updated meta-analysis of 116 cohorts and 97,850 cancer patients treated with ICI, we found a significant association between antibiotic exposure and survival outcomes (overall survival, hazard ratio [HR]: 1.49, 95% confidence interval [CI]: 1.34-1.65; progression-free survival, HR: 1.44, 95% CI: 1.31-1.58). Finally, we discuss antibiotics stewardship and microbiome-centered strategies to prevent, diagnose, and/or repair dysbiosis.},
}
RevDate: 2026-10-27
Lactose, Lactose Maldigestion and Lactose Intolerance: Definitions, Misunderstandings, Mechanisms, and Public Health Implications.
Advances in nutrition (Bethesda, Md.) pii:S2161-8313(26)00174-2 [Epub ahead of print].
Lactose is the principal carbohydrate in milk, serving a critical role in infant energy metabolism as well as contributing to neurodevelopment, and the establishment of a healthy gut microbiota. Later in life, lactose digestion capacity varies widely across human populations owing to the genetically determined decline of intestinal lactase expression after weaning-a condition termed 'lactase non-persistence'. Approximately two-thirds of the global adult population exhibits reduced lactase activity, yet the clinical consequences of this enzymatic reduction are far less uniform than commonly assumed. This review provides a comprehensive examination of lactose functionality, the physiology of lactose digestion, and the consequences of lactase persistence and non-persistence. We present formal definitions for the spectrum of terms used in lactose research-including lactase persistence, lactase non-persistence, lactose maldigestion, and lactose intolerance-and argue that the critical distinction between lactose maldigestion (a physiological state) and lactose intolerance (a clinical syndrome) is frequently overlooked in both research and public health. Drawing on evidence from double-blind randomised controlled trials , microbiome intervention studies, and global epidemiological data, the evidence indicates that the majority of individuals with lactose maldigestion do not develop clinically meaningful symptoms at moderate intake levels of most dairy products. We further discuss the mechanism of colonic adaptation, whereby gradual lactose exposure selectively enriches Bifidobacterium populations capable of fermenting lactose without excessive gas production resulting in greater lactose tolerance. Finally, we examine the public health implications of these findings, noting that food-based dietary guidelines worldwide-including those in populations with high prevalence of lactase non-persistence-consistently recommend dairy consumption owing to its established associations with reduced risk of type 2 diabetes, colorectal cancer, and improved bone health.
Additional Links: PMID-42946056
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PubMed:
Citation:
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@article {pmid42946056,
year = {2026},
author = {Geurts, J and Pot, B and Knipping, K and Braat, M and Peters, S},
title = {Lactose, Lactose Maldigestion and Lactose Intolerance: Definitions, Misunderstandings, Mechanisms, and Public Health Implications.},
journal = {Advances in nutrition (Bethesda, Md.)},
volume = {},
number = {},
pages = {100760},
doi = {10.1016/j.advnut.2026.100760},
pmid = {42946056},
issn = {2156-5376},
abstract = {Lactose is the principal carbohydrate in milk, serving a critical role in infant energy metabolism as well as contributing to neurodevelopment, and the establishment of a healthy gut microbiota. Later in life, lactose digestion capacity varies widely across human populations owing to the genetically determined decline of intestinal lactase expression after weaning-a condition termed 'lactase non-persistence'. Approximately two-thirds of the global adult population exhibits reduced lactase activity, yet the clinical consequences of this enzymatic reduction are far less uniform than commonly assumed. This review provides a comprehensive examination of lactose functionality, the physiology of lactose digestion, and the consequences of lactase persistence and non-persistence. We present formal definitions for the spectrum of terms used in lactose research-including lactase persistence, lactase non-persistence, lactose maldigestion, and lactose intolerance-and argue that the critical distinction between lactose maldigestion (a physiological state) and lactose intolerance (a clinical syndrome) is frequently overlooked in both research and public health. Drawing on evidence from double-blind randomised controlled trials , microbiome intervention studies, and global epidemiological data, the evidence indicates that the majority of individuals with lactose maldigestion do not develop clinically meaningful symptoms at moderate intake levels of most dairy products. We further discuss the mechanism of colonic adaptation, whereby gradual lactose exposure selectively enriches Bifidobacterium populations capable of fermenting lactose without excessive gas production resulting in greater lactose tolerance. Finally, we examine the public health implications of these findings, noting that food-based dietary guidelines worldwide-including those in populations with high prevalence of lactase non-persistence-consistently recommend dairy consumption owing to its established associations with reduced risk of type 2 diabetes, colorectal cancer, and improved bone health.},
}
RevDate: 2026-10-27
Gut microbiome profiles associated with simple liver steatosis in MASLD.
Gut pii:gutjnl-2025-337572 [Epub ahead of print].
Additional Links: PMID-42946473
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PubMed:
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@article {pmid42946473,
year = {2026},
author = {Pradhan, M and Molinaro, A and Ginanni Corradini, S and Silecchia, G and Ferri, F and Capoccia, D and Lv, B and Wu, H and Huber-Schönauer, U and Völkerer, A and Mischitelli, M and Parlati, L and Bergström, G and Datz, C and Leonetti, F and Tilg, H and Tremaroli, V and Bäckhed, F},
title = {Gut microbiome profiles associated with simple liver steatosis in MASLD.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-337572},
pmid = {42946473},
issn = {1468-3288},
}
RevDate: 2026-10-28
Longitudinal Skin Bacterial Cluster Associated With Protection Against Allergic Co-Morbidity in Pediatric Atopic Dermatitis.
Allergy [Epub ahead of print].
BACKGROUND: Atopic dermatitis (AD) is an inflammatory skin condition that often portends the development of allergic comorbidities. Despite evidence supporting the role of the skin microbiome in AD, its temporal patterns and associations with risk or protection for allergic co-morbidity remain unclear. Our objective is to characterize core species of the pediatric AD bacterial microbiome, assess microbial networks and clusters, and identify global microbial changes relevant to AD and the atopic march.
METHODS: We performed metagenomic shotgun sequencing on 353 non-lesional skin samples from children in the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohort across 5 annual visits. We assessed taxonomic composition and analyzed longitudinal skin microbial patterns with progression to allergic co-morbidities.
RESULTS: We identified 436 distinct species. Shannon diversity and richness declined with age, and socioeconomic factors explained the variance in species composition. Staphylococcus aureus (SA) was more abundant in severe AD. Cluster 5, comprised of typically gut-associated microbes, was more abundant in non-sensitized children who did not develop allergic co-morbidities over time.
CONCLUSIONS: Our analyses revealed key patterns in core taxa, diversity and abundance of the skin microbiome over time in early life and highlighted previously unexplored factors such as socioeconomic status as key contributors to the variability in species composition. Abundance of SA confers risk, while gut-associated microbes may offer protection, influencing the clinical trajectory of AD and the atopic march. Thus, these results provide a novel and comprehensive understanding of the temporal dynamics of the skin microbiota in pediatric AD.
Additional Links: PMID-42946695
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PubMed:
Citation:
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@article {pmid42946695,
year = {2026},
author = {Dahal, A and Chang, WC and Grashel, B and Morgan, D and Spagna, D and Kim, DH and Sachdeva, S and Phelan, KJ and Satish, L and Biagini, JM and Haslam, DB and Ollberding, NJ and Khurana Hershey, GK},
title = {Longitudinal Skin Bacterial Cluster Associated With Protection Against Allergic Co-Morbidity in Pediatric Atopic Dermatitis.},
journal = {Allergy},
volume = {},
number = {},
pages = {},
doi = {10.1111/all.70554},
pmid = {42946695},
issn = {1398-9995},
support = {U19AI070235//National Institute of Allergy and Infectious Diseases/ ; F30AI181481//National Institute of Allergy and Infectious Diseases/ ; T32GM149200/GM/NIGMS NIH HHS/United States ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) is an inflammatory skin condition that often portends the development of allergic comorbidities. Despite evidence supporting the role of the skin microbiome in AD, its temporal patterns and associations with risk or protection for allergic co-morbidity remain unclear. Our objective is to characterize core species of the pediatric AD bacterial microbiome, assess microbial networks and clusters, and identify global microbial changes relevant to AD and the atopic march.
METHODS: We performed metagenomic shotgun sequencing on 353 non-lesional skin samples from children in the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohort across 5 annual visits. We assessed taxonomic composition and analyzed longitudinal skin microbial patterns with progression to allergic co-morbidities.
RESULTS: We identified 436 distinct species. Shannon diversity and richness declined with age, and socioeconomic factors explained the variance in species composition. Staphylococcus aureus (SA) was more abundant in severe AD. Cluster 5, comprised of typically gut-associated microbes, was more abundant in non-sensitized children who did not develop allergic co-morbidities over time.
CONCLUSIONS: Our analyses revealed key patterns in core taxa, diversity and abundance of the skin microbiome over time in early life and highlighted previously unexplored factors such as socioeconomic status as key contributors to the variability in species composition. Abundance of SA confers risk, while gut-associated microbes may offer protection, influencing the clinical trajectory of AD and the atopic march. Thus, these results provide a novel and comprehensive understanding of the temporal dynamics of the skin microbiota in pediatric AD.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
mHolmes improves cross anatomical cadaveric microbiome forecasting for postmortem interval estimation.
Nature communications, 17(1):.
Forensic microbiology leverages postmortem microbiome succession as a promising biomarker for estimating the postmortem interval (PMI). However, current methods are constrained by sparse sampling (typically 3-5 time points) and limited cross-anatomical generalizability, leading to imprecise PMI estimates with errors often exceeding ±3 days, particularly in cases of dismembered remains. To address these limitations, we developed mHolmes, a Transformer-based transfer learning framework for forecasting cadaveric microbiome dynamics. Trained on daily longitudinal data from 34 cadavers over 21 days, mHolmes achieves daily predictions of microbial dynamics, with reduced error (MAE < 2 days) in cross-anatomical forecasting tasks (e.g., hip to face). Shapley Additive exPlanations (SHAP) analysis supports interpretability by identifying seven bacterial classes as candidate PMI-associated features. This study supports mHolmes as a robust forecasting framework that addresses key limitations in sparse and cross anatomical microbiome data, improves PMI estimation from incomplete observations, and has potential forensic applications in body part matching and higher resolution timeline reconstruction.
Additional Links: PMID-42946700
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@article {pmid42946700,
year = {2026},
author = {Han, J and Zhang, Y and Zhang, H and Zhou, K and Chen, X and Ning, K},
title = {mHolmes improves cross anatomical cadaveric microbiome forecasting for postmortem interval estimation.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42946700},
issn = {2041-1723},
mesh = {Humans ; *Microbiota ; *Postmortem Changes ; Cadaver ; *Forensic Microbiology/methods ; Bacteria/classification/isolation & purification/genetics ; },
abstract = {Forensic microbiology leverages postmortem microbiome succession as a promising biomarker for estimating the postmortem interval (PMI). However, current methods are constrained by sparse sampling (typically 3-5 time points) and limited cross-anatomical generalizability, leading to imprecise PMI estimates with errors often exceeding ±3 days, particularly in cases of dismembered remains. To address these limitations, we developed mHolmes, a Transformer-based transfer learning framework for forecasting cadaveric microbiome dynamics. Trained on daily longitudinal data from 34 cadavers over 21 days, mHolmes achieves daily predictions of microbial dynamics, with reduced error (MAE < 2 days) in cross-anatomical forecasting tasks (e.g., hip to face). Shapley Additive exPlanations (SHAP) analysis supports interpretability by identifying seven bacterial classes as candidate PMI-associated features. This study supports mHolmes as a robust forecasting framework that addresses key limitations in sparse and cross anatomical microbiome data, improves PMI estimation from incomplete observations, and has potential forensic applications in body part matching and higher resolution timeline reconstruction.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
*Postmortem Changes
Cadaver
*Forensic Microbiology/methods
Bacteria/classification/isolation & purification/genetics
RevDate: 2026-10-28
CmpDate: 2026-10-28
An Antimicrobial Oosporein Pigment-producing Fungus Associated with the Lac Insect.
Microbial ecology, 89(1):.
Insects host diverse fungal communities that produce biologically active secondary metabolites. Here, we use culture-dependent and culture-independent methods to characterise fungi associated with the lac insect Kerria lacca - a species well known for its natural red lac pigment. We isolated several fungi from the external surface of the insects. Of these, only Acremonium sp. 'ALR' was found to produce a red pigment under laboratory conditions. We therefore investigated this pigment in relation to the insect's lac pigment. The pigment from Acremonium sp. ALR was identified as oosporein. In vitro bioassays demonstrated that the fungus exhibits broad-spectrum antimicrobial activity, inhibiting the growth of bacteria and fungi, including sooty moulds associated with the lac insect's honeydew. The fungus belongs to the order Hypocreales, which includes the lac insect's yeast-like symbiont and many entomopathogenic fungi that produce toxins and chemically reactive pigments. We detected the fungus on the cuticle of K. lacca nymphs and adult females, as well as in the wax deposits near the site of emergence of crawler nymphs. We hypothesise that the fungus may adhere to the nymphs' cuticles during their emergence and can get passively transmitted during the host's life stages. However, oosporein was detected in neither the lac insects nor their resin, based on liquid chromatography mass spectrometry analysis. Conversely, lac pigments were not detected in the pigment extracts of Acremonium sp. ALR, demonstrating that the two pigments are chemically distinct and that the Acremonium sp. ALR did not impact the lac insect's own pigment synthesis.
Additional Links: PMID-42946867
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@article {pmid42946867,
year = {2026},
author = {Vaishally, and Shukla, SP},
title = {An Antimicrobial Oosporein Pigment-producing Fungus Associated with the Lac Insect.},
journal = {Microbial ecology},
volume = {89},
number = {1},
pages = {},
pmid = {42946867},
issn = {1432-184X},
support = {Ramalingaswami Fellowship//Department of Biotechnology, Ministry of Science and Technology, India/ ; SRG/2021/000600//Department of Science and Technology, Ministry of Science and Technology, India/ ; },
mesh = {Animals ; *Pigments, Biological/metabolism/pharmacology/biosynthesis ; *Hemiptera/microbiology ; Female ; *Acremonium/metabolism/isolation & purification/genetics ; *Anti-Infective Agents/metabolism/pharmacology ; *Hypocreales/isolation & purification/metabolism/genetics ; Bacteria/drug effects ; Nymph/microbiology ; },
abstract = {Insects host diverse fungal communities that produce biologically active secondary metabolites. Here, we use culture-dependent and culture-independent methods to characterise fungi associated with the lac insect Kerria lacca - a species well known for its natural red lac pigment. We isolated several fungi from the external surface of the insects. Of these, only Acremonium sp. 'ALR' was found to produce a red pigment under laboratory conditions. We therefore investigated this pigment in relation to the insect's lac pigment. The pigment from Acremonium sp. ALR was identified as oosporein. In vitro bioassays demonstrated that the fungus exhibits broad-spectrum antimicrobial activity, inhibiting the growth of bacteria and fungi, including sooty moulds associated with the lac insect's honeydew. The fungus belongs to the order Hypocreales, which includes the lac insect's yeast-like symbiont and many entomopathogenic fungi that produce toxins and chemically reactive pigments. We detected the fungus on the cuticle of K. lacca nymphs and adult females, as well as in the wax deposits near the site of emergence of crawler nymphs. We hypothesise that the fungus may adhere to the nymphs' cuticles during their emergence and can get passively transmitted during the host's life stages. However, oosporein was detected in neither the lac insects nor their resin, based on liquid chromatography mass spectrometry analysis. Conversely, lac pigments were not detected in the pigment extracts of Acremonium sp. ALR, demonstrating that the two pigments are chemically distinct and that the Acremonium sp. ALR did not impact the lac insect's own pigment synthesis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Pigments, Biological/metabolism/pharmacology/biosynthesis
*Hemiptera/microbiology
Female
*Acremonium/metabolism/isolation & purification/genetics
*Anti-Infective Agents/metabolism/pharmacology
*Hypocreales/isolation & purification/metabolism/genetics
Bacteria/drug effects
Nymph/microbiology
RevDate: 2026-10-28
CmpDate: 2026-10-28
Cervicovaginal zinc and copper profiles across vaginitis phenotypes and hydrogel assignment: an exploratory pilot study.
BMC women's health, 26(1):.
Zinc (Zn) and copper (Cu) support epithelial integrity, nutritional immunity, and host-microbiome interactions, yet cervicovaginal trace-metal dynamics across vaginitis phenotypes remain poorly defined. We prospectively quantified cervicovaginal lavage (CVL) Zn and Cu by ICP-OES in an exploratory secondary analysis nested within a single-center randomized trial involving 56 symptomatic women and asymptomatic controls (mean age, 36.0 ± 11.8 years; mean BMI, 23.1 ± 4.9 kg/m[2]). We examined whether CVL trace-element concentrations varied according to culture-defined phenotype and randomized hydrogel exposure. CVL Zn concentrations were higher in the Candida albicans-positive (120.2 ± 95.6 µg/L) and symptomatic culture-positive bacterial phenotypes (83.8 ± 55.2 µg/L) than in controls (58.6 ± 27.2 µg/L), whereas Cu showed less consistent variation. Among participants assigned to hydrogel, phenotype-specific differences from controls were not statistically significant. In the fluconazole-only group, higher Zn concentrations were observed in the C. albicans-positive phenotype (154.3 ± 113.5 vs. 54.2 ± 23.8 µg/L), accompanied by higher Cu concentrations (12.13 ± 4.76 vs. 5.76 ± 2.86 µg/L). These exploratory findings indicate that cervicovaginal trace-element profiles may vary across symptomatic culture-defined phenotypes and treatment groups. Our findings should be interpreted as hypothesis-generating. Biological and clinical relevance remains uncertain and warrants confirmation in adequately powered, longitudinal studies using dilution-normalized CVL measurements. Trial registration: The study protocol was approved by the Hungarian National Institutional Review Medical Research Council (approval No. 3282-7/2023/EUIG). The parent trial is registered at ClinicalTrials.gov (NCT05895162; 2023-05-15). Each participant signed a written informed consent form. All procedures performed in studies involving human participants were under the ethical standards of the Hungarian National Institutional Review Medical Research Council and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. This article does not contain any studies with animals performed by any of the authors.
Additional Links: PMID-42947086
PubMed:
Citation:
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@article {pmid42947086,
year = {2026},
author = {Kunkli, A and Rátonyi, D and Kozma, B and Farkas, B and Majoros, L and Póka, R and Sipos, AG and Takacs, P and Krasznai, ZT and Kozma, B},
title = {Cervicovaginal zinc and copper profiles across vaginitis phenotypes and hydrogel assignment: an exploratory pilot study.},
journal = {BMC women's health},
volume = {26},
number = {1},
pages = {},
pmid = {42947086},
issn = {1472-6874},
mesh = {Female ; Humans ; Pilot Projects ; *Zinc/analysis/metabolism ; *Copper/analysis ; Adult ; Phenotype ; *Cervix Uteri/chemistry/metabolism/microbiology ; Candida albicans/isolation & purification ; *Vagina/microbiology/chemistry/metabolism ; Fluconazole/therapeutic use ; Hydrogels ; Middle Aged ; *Vaginitis/microbiology/metabolism/drug therapy ; Antifungal Agents/therapeutic use ; Prospective Studies ; Candidiasis, Vulvovaginal/drug therapy ; Hydrogel, Polyethylene Glycol Dimethacrylate ; },
abstract = {Zinc (Zn) and copper (Cu) support epithelial integrity, nutritional immunity, and host-microbiome interactions, yet cervicovaginal trace-metal dynamics across vaginitis phenotypes remain poorly defined. We prospectively quantified cervicovaginal lavage (CVL) Zn and Cu by ICP-OES in an exploratory secondary analysis nested within a single-center randomized trial involving 56 symptomatic women and asymptomatic controls (mean age, 36.0 ± 11.8 years; mean BMI, 23.1 ± 4.9 kg/m[2]). We examined whether CVL trace-element concentrations varied according to culture-defined phenotype and randomized hydrogel exposure. CVL Zn concentrations were higher in the Candida albicans-positive (120.2 ± 95.6 µg/L) and symptomatic culture-positive bacterial phenotypes (83.8 ± 55.2 µg/L) than in controls (58.6 ± 27.2 µg/L), whereas Cu showed less consistent variation. Among participants assigned to hydrogel, phenotype-specific differences from controls were not statistically significant. In the fluconazole-only group, higher Zn concentrations were observed in the C. albicans-positive phenotype (154.3 ± 113.5 vs. 54.2 ± 23.8 µg/L), accompanied by higher Cu concentrations (12.13 ± 4.76 vs. 5.76 ± 2.86 µg/L). These exploratory findings indicate that cervicovaginal trace-element profiles may vary across symptomatic culture-defined phenotypes and treatment groups. Our findings should be interpreted as hypothesis-generating. Biological and clinical relevance remains uncertain and warrants confirmation in adequately powered, longitudinal studies using dilution-normalized CVL measurements. Trial registration: The study protocol was approved by the Hungarian National Institutional Review Medical Research Council (approval No. 3282-7/2023/EUIG). The parent trial is registered at ClinicalTrials.gov (NCT05895162; 2023-05-15). Each participant signed a written informed consent form. All procedures performed in studies involving human participants were under the ethical standards of the Hungarian National Institutional Review Medical Research Council and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. This article does not contain any studies with animals performed by any of the authors.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
Humans
Pilot Projects
*Zinc/analysis/metabolism
*Copper/analysis
Adult
Phenotype
*Cervix Uteri/chemistry/metabolism/microbiology
Candida albicans/isolation & purification
*Vagina/microbiology/chemistry/metabolism
Fluconazole/therapeutic use
Hydrogels
Middle Aged
*Vaginitis/microbiology/metabolism/drug therapy
Antifungal Agents/therapeutic use
Prospective Studies
Candidiasis, Vulvovaginal/drug therapy
Hydrogel, Polyethylene Glycol Dimethacrylate
RevDate: 2026-10-28
CmpDate: 2026-10-28
Dietary index for gut microbiota and risk of metabolic syndrome: the mediating role of hepatic steatosis in a prospective cohort study.
Diabetology & metabolic syndrome, 18(1):.
BACKGROUND: Metabolic syndrome (MetS) is a growing public health concern, with emerging evidence implicating that gut microbiota plays a role in MetS pathogenesis. The Dietary Index for Gut Microbiota (DI-GM) quantifies diet quality in relation to microbial diversity. This study examined the association between DI-GM and MetS risk, evaluating hepatic steatosis as a potential mediator.
METHODS: This prospective cohort included 4,503 adults (20-70 years) from the Monitoring of Metabolic Diseases Risk Factors in Tehran (MMRT) study, followed over five years. Dietary intake was assessed using a validated 125-item food frequency questionnaire to calculate DI-GM scores. Hepatic steatosis was quantified via controlled attenuation parameter (CAP) using transient elastography. MetS was defined according to Adult Treatment Panel III criteria. Multivariable logistic regression and mediation analyses evaluated associations.
RESULTS: Higher DI‑GM scores were associated with lower MetS incidence. In the fully adjusted model (Model 2), participants in the highest DI‑GM quartile had a 66% lower odds of MetS compared with the lowest quartile (OR = 0.34; 95% CI: 0.27-0.43; P‑trend < 0.001). Each one‑unit increase in the DI‑GM score was associated with an 18% decrease in the odds of MetS (OR = 0.82; 95% CI: 0.78-0.85; P < 0.001). All five MetS components showed significant inverse associations, with the strongest effects observed for elevated waist circumference, hypertriglyceridemia, and low high‑density lipoprotein cholesterol. In mediation analysis, hepatic steatosis accounted for approximately 65% of the DI‑GM-MetS association (indirect effect: -0.0263; P < 0.01), although causal interpretation is limited by the observational design.
CONCLUSION: Greater adherence to a gut microbiota-supportive diet, as measured by DI-GM, is associated with a reduced risk of MetS, largely mediated by reductions in hepatic fat. These findings highlight the potential of microbiome-oriented dietary interventions for MetS prevention.
Additional Links: PMID-42947171
PubMed:
Citation:
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@article {pmid42947171,
year = {2026},
author = {Etesami, E and Kamrani, F and Nikparast, A and Sepehrinia, M and Homayounfar, R and Razzaz, JM},
title = {Dietary index for gut microbiota and risk of metabolic syndrome: the mediating role of hepatic steatosis in a prospective cohort study.},
journal = {Diabetology & metabolic syndrome},
volume = {18},
number = {1},
pages = {},
pmid = {42947171},
issn = {1758-5996},
abstract = {BACKGROUND: Metabolic syndrome (MetS) is a growing public health concern, with emerging evidence implicating that gut microbiota plays a role in MetS pathogenesis. The Dietary Index for Gut Microbiota (DI-GM) quantifies diet quality in relation to microbial diversity. This study examined the association between DI-GM and MetS risk, evaluating hepatic steatosis as a potential mediator.
METHODS: This prospective cohort included 4,503 adults (20-70 years) from the Monitoring of Metabolic Diseases Risk Factors in Tehran (MMRT) study, followed over five years. Dietary intake was assessed using a validated 125-item food frequency questionnaire to calculate DI-GM scores. Hepatic steatosis was quantified via controlled attenuation parameter (CAP) using transient elastography. MetS was defined according to Adult Treatment Panel III criteria. Multivariable logistic regression and mediation analyses evaluated associations.
RESULTS: Higher DI‑GM scores were associated with lower MetS incidence. In the fully adjusted model (Model 2), participants in the highest DI‑GM quartile had a 66% lower odds of MetS compared with the lowest quartile (OR = 0.34; 95% CI: 0.27-0.43; P‑trend < 0.001). Each one‑unit increase in the DI‑GM score was associated with an 18% decrease in the odds of MetS (OR = 0.82; 95% CI: 0.78-0.85; P < 0.001). All five MetS components showed significant inverse associations, with the strongest effects observed for elevated waist circumference, hypertriglyceridemia, and low high‑density lipoprotein cholesterol. In mediation analysis, hepatic steatosis accounted for approximately 65% of the DI‑GM-MetS association (indirect effect: -0.0263; P < 0.01), although causal interpretation is limited by the observational design.
CONCLUSION: Greater adherence to a gut microbiota-supportive diet, as measured by DI-GM, is associated with a reduced risk of MetS, largely mediated by reductions in hepatic fat. These findings highlight the potential of microbiome-oriented dietary interventions for MetS prevention.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
Comparative pilot study using mucosal brushing and mucosal biopsy for detecting duodenal microbiome in functional dyspepsia.
Gut pathogens, 18(1):.
BACKGROUND: Functional dyspepsia (FD) is a prevalent gastrointestinal disorder affecting quality of life, with recent studies suggesting a role of the duodenal microbiome in its pathogenesis via the gut-brain axis. The optimal specimen sampling collection method and the specific microbial features associated with FD remain unclear.
OBJECTIVES: This pilot study compared mucosal brushing and biopsy for duodenal microbiome sampling, with an exploratory secondary aim of assessing microbial differences between FD and non-FD controls.
METHODS: Patients undergoing esophago-gastro-duodenoscopy (EGD) were recruited from February 2024 to May 2025. FD patients were identified using the Rome IV criteria, and non-FD controls without upper GI symptoms were included. Duodenal samples were collected via mucosal brushing and biopsy, followed by DNA extraction and 16 S rRNA sequencing of the V1-V2 region. α-diversity (richness, Shannon, Simpson) and β-diversity (Bray-Curtis dissimilarity) were assessed between FD and non-FD controls and between sampling methods. Paired Wilcoxon signed-rank tests compared sampling methods, while linear regression models adjusted for age, sex, and BMI compared FD and non-FD controls within each method. Microbial associations with FD were examined using generalized linear models, adjusting for age, sex, and BMI, with Benjamini-Hochberg FDR correction.
RESULTS: Forty participants (FD n = 20; non-FD controls n = 20) were included, yielding 80 paired samples. Brushing showed higher retention of non-chimeric reads and lower filtering losses than biopsy (all p < 0.0001). Brushing also yielded greater alpha diversity-genus richness (81[33] vs. 19[17]), Shannon (3.68[0.46] vs. 2.60[0.89]), and Simpson (0.96[0.03] vs. 0.89[0.08]); all p < 0.0001-and a distinct community structure (PERMANOVA R²=0.16, p = 0.001). Within each sampling method, FD and non-FD controls did not differ in alpha or beta diversity after adjustment. Exploratory differential abundance modeling identified Streptococcus as numerically higher in FD across both methods, although no genus survived FDR correction (all q > 0.05).
CONCLUSION: Mucosal brushing collects luminal/mucus-associated microbiota and therefore yielded higher bacterial biomass and greater microbial diversity than mucosal biopsy. No significant differences in alpha or beta diversity were detected between FD and non-FD controls within either method, although the study was not powered to exclude such differences. Exploratory analyses suggested numerically higher Streptococcus abundance in FD that did not survive FDR correction. This hypothesis-generating finding requires validation in larger studies.
GOV IDENTIFIER: NCT06326918.
Additional Links: PMID-42947191
PubMed:
Citation:
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@article {pmid42947191,
year = {2026},
author = {Samuthpongtorn, C and Vimonsuntirungsri, T and Tangkijvanich, P and Pittayanon, R},
title = {Comparative pilot study using mucosal brushing and mucosal biopsy for detecting duodenal microbiome in functional dyspepsia.},
journal = {Gut pathogens},
volume = {18},
number = {1},
pages = {},
pmid = {42947191},
issn = {1757-4749},
support = {GA68/053//the Ratchadapiseksompotch Fund, Faculty of Medicine/ ; },
abstract = {BACKGROUND: Functional dyspepsia (FD) is a prevalent gastrointestinal disorder affecting quality of life, with recent studies suggesting a role of the duodenal microbiome in its pathogenesis via the gut-brain axis. The optimal specimen sampling collection method and the specific microbial features associated with FD remain unclear.
OBJECTIVES: This pilot study compared mucosal brushing and biopsy for duodenal microbiome sampling, with an exploratory secondary aim of assessing microbial differences between FD and non-FD controls.
METHODS: Patients undergoing esophago-gastro-duodenoscopy (EGD) were recruited from February 2024 to May 2025. FD patients were identified using the Rome IV criteria, and non-FD controls without upper GI symptoms were included. Duodenal samples were collected via mucosal brushing and biopsy, followed by DNA extraction and 16 S rRNA sequencing of the V1-V2 region. α-diversity (richness, Shannon, Simpson) and β-diversity (Bray-Curtis dissimilarity) were assessed between FD and non-FD controls and between sampling methods. Paired Wilcoxon signed-rank tests compared sampling methods, while linear regression models adjusted for age, sex, and BMI compared FD and non-FD controls within each method. Microbial associations with FD were examined using generalized linear models, adjusting for age, sex, and BMI, with Benjamini-Hochberg FDR correction.
RESULTS: Forty participants (FD n = 20; non-FD controls n = 20) were included, yielding 80 paired samples. Brushing showed higher retention of non-chimeric reads and lower filtering losses than biopsy (all p < 0.0001). Brushing also yielded greater alpha diversity-genus richness (81[33] vs. 19[17]), Shannon (3.68[0.46] vs. 2.60[0.89]), and Simpson (0.96[0.03] vs. 0.89[0.08]); all p < 0.0001-and a distinct community structure (PERMANOVA R²=0.16, p = 0.001). Within each sampling method, FD and non-FD controls did not differ in alpha or beta diversity after adjustment. Exploratory differential abundance modeling identified Streptococcus as numerically higher in FD across both methods, although no genus survived FDR correction (all q > 0.05).
CONCLUSION: Mucosal brushing collects luminal/mucus-associated microbiota and therefore yielded higher bacterial biomass and greater microbial diversity than mucosal biopsy. No significant differences in alpha or beta diversity were detected between FD and non-FD controls within either method, although the study was not powered to exclude such differences. Exploratory analyses suggested numerically higher Streptococcus abundance in FD that did not survive FDR correction. This hypothesis-generating finding requires validation in larger studies.
GOV IDENTIFIER: NCT06326918.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
Colobine gut microbiome vulnerability to captivity: a meta-analysis of herbivorous primates.
Animal microbiome, 8(1):.
BACKGROUND: Colobine monkey species have a multi-cavity forestomach adapted to a folivorous diet and foregut fermentation, making their gut microbiome essential for efficient digestion of plant fibre. In captivity, these species frequently experience gastrointestinal disorders associated with dietary changes and microbial dysbiosis. Understanding how their microbiome differs from that of other primates is therefore critical for improving health and husbandry. This study used a meta-analysis of global primate microbiome data to compare the faecal microbiome of colobines with those of other herbivorous primates, focusing on the effects of captivity.
RESULTS: Data from 16 studies involving 35 primate species and 7 primate families/subfamilies, comprising 1,690 faecal samples generated using 16 S rRNA amplicon sequencing, were re-analysed using standardised bioinformatic and compositional-statistical pipelines. Significant differences in microbial diversity and composition were observed among wild primates across families/subfamilies, diets, and fermentation strategies. Colobinae had a distinctive microbiome characterised by low Shannon diversity and high relative abundance of Firmicutes, particularly Ruminococcaceae and Lachnospiraceae, which were also prominent members of the wild colobinae core microbiome. Across all families/subfamilies and within colobinae, observed Shannon diversity was lower in captivity; however, multivariable mixed-effects models showed that alpha-diversity estimates were highly sensitive to study identity, species representation and methodological covariates. In contrast, beta-diversity and ALDEx2 analyses provided consistent evidence of captivity-associated compositional restructuring. Captive colobinae were enriched in Bacteroidetes and Spirochaetes, and families such as Prevotellaceae, Rikenellaceae, Methanobacteriaceae, Spirochaetaceae and Bacteroidaceae, whereas wild colobines were enriched in fibre-associated taxa, including Ruminococcaceae and Lachnospiraceae.
CONCLUSIONS: Captivity alters the gut microbiota of colobine primates, affecting microbial diversity and core fibre-fermenting taxa important for gastrointestinal health. However, adjusted alpha-diversity models revealed substantial confounding by study, species, and methodological variables, indicating that diversity effects should be interpreted cautiously. Their specialised folivorous diet and foregut-fermenting physiology appear to produce a highly efficient yet fragile microbial ecosystem poorly adapted to ex-situ conditions. The strongest evidence for captivity-associated disruption was consistent alterations in faecal microbial composition, highlighting the need for diet formulations and microbiome-based health monitoring tailored to the unique digestive ecology of colobines to mitigate the high prevalence of gastrointestinal disorders in captivity.
Additional Links: PMID-42947200
PubMed:
Citation:
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@article {pmid42947200,
year = {2026},
author = {Todó-Llorens, M and Rooney, N and Peachey, L},
title = {Colobine gut microbiome vulnerability to captivity: a meta-analysis of herbivorous primates.},
journal = {Animal microbiome},
volume = {8},
number = {1},
pages = {},
pmid = {42947200},
issn = {2524-4671},
abstract = {BACKGROUND: Colobine monkey species have a multi-cavity forestomach adapted to a folivorous diet and foregut fermentation, making their gut microbiome essential for efficient digestion of plant fibre. In captivity, these species frequently experience gastrointestinal disorders associated with dietary changes and microbial dysbiosis. Understanding how their microbiome differs from that of other primates is therefore critical for improving health and husbandry. This study used a meta-analysis of global primate microbiome data to compare the faecal microbiome of colobines with those of other herbivorous primates, focusing on the effects of captivity.
RESULTS: Data from 16 studies involving 35 primate species and 7 primate families/subfamilies, comprising 1,690 faecal samples generated using 16 S rRNA amplicon sequencing, were re-analysed using standardised bioinformatic and compositional-statistical pipelines. Significant differences in microbial diversity and composition were observed among wild primates across families/subfamilies, diets, and fermentation strategies. Colobinae had a distinctive microbiome characterised by low Shannon diversity and high relative abundance of Firmicutes, particularly Ruminococcaceae and Lachnospiraceae, which were also prominent members of the wild colobinae core microbiome. Across all families/subfamilies and within colobinae, observed Shannon diversity was lower in captivity; however, multivariable mixed-effects models showed that alpha-diversity estimates were highly sensitive to study identity, species representation and methodological covariates. In contrast, beta-diversity and ALDEx2 analyses provided consistent evidence of captivity-associated compositional restructuring. Captive colobinae were enriched in Bacteroidetes and Spirochaetes, and families such as Prevotellaceae, Rikenellaceae, Methanobacteriaceae, Spirochaetaceae and Bacteroidaceae, whereas wild colobines were enriched in fibre-associated taxa, including Ruminococcaceae and Lachnospiraceae.
CONCLUSIONS: Captivity alters the gut microbiota of colobine primates, affecting microbial diversity and core fibre-fermenting taxa important for gastrointestinal health. However, adjusted alpha-diversity models revealed substantial confounding by study, species, and methodological variables, indicating that diversity effects should be interpreted cautiously. Their specialised folivorous diet and foregut-fermenting physiology appear to produce a highly efficient yet fragile microbial ecosystem poorly adapted to ex-situ conditions. The strongest evidence for captivity-associated disruption was consistent alterations in faecal microbial composition, highlighting the need for diet formulations and microbiome-based health monitoring tailored to the unique digestive ecology of colobines to mitigate the high prevalence of gastrointestinal disorders in captivity.},
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
Role of Intestinal Stem Cells in the Pathogenesis and Repair of Necrotizing Enterocolitis.
Expert reviews in molecular medicine, 28:e51 pii:S1462399426100842.
BACKGROUND: Necrotizing enterocolitis (NEC) is a leading gastrointestinal emergency in preterm infants, characterized by severe epithelial injury, dysregulated inflammation, and defective mucosal repair. Intestinal stem cells (ISCs) at the crypt base are essential for epithelial renewal and barrier restoration after injury.
METHODS: We summarized recent advances in the molecular and cellular mechanisms governing ISC injury and regeneration in NEC, emphasizing canonical repair pathways, niche-derived regulatory circuits, and emerging ISC-targeted therapies.
RESULTS: NEC disrupts ISC survival, proliferation, and differentiation through aberrant innate immune activation, microbial dysbiosis, and impairment of Wnt, Notch, and epidermal growth factor (EGF) signalling. ISC function is also shaped by interactions with Paneth cells, mesenchymal niche components, immune cells, and microbial metabolites. Disruption of this niche compromises crypt regeneration, perpetuates barrier dysfunction, and amplifies intestinal inflammation. Restoring ISC activity and niche integrity has therefore prompted interest in growth factor supplementation, microbiota modulation, immune-based interventions, and stem cell-oriented approaches.
CONCLUSIONS: ISC-centred regenerative failure provides an integrated framework linking epithelial biology, immunology, and microbiome research in NEC. Restoring ISC function and niche integrity represents a promising therapeutic direction with experimental and translational relevance.
Additional Links: PMID-42947211
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PubMed:
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@article {pmid42947211,
year = {2026},
author = {Zhang, F and Zhang, X and Zhang, Z},
title = {Role of Intestinal Stem Cells in the Pathogenesis and Repair of Necrotizing Enterocolitis.},
journal = {Expert reviews in molecular medicine},
volume = {28},
number = {},
pages = {e51},
doi = {10.1017/erm.2026.10084},
pmid = {42947211},
issn = {1462-3994},
mesh = {Humans ; *Enterocolitis, Necrotizing/pathology/etiology/metabolism/therapy ; *Stem Cells/metabolism/cytology ; Animals ; *Intestinal Mucosa/metabolism/pathology ; *Intestines/pathology/cytology ; Regeneration ; Signal Transduction ; },
abstract = {BACKGROUND: Necrotizing enterocolitis (NEC) is a leading gastrointestinal emergency in preterm infants, characterized by severe epithelial injury, dysregulated inflammation, and defective mucosal repair. Intestinal stem cells (ISCs) at the crypt base are essential for epithelial renewal and barrier restoration after injury.
METHODS: We summarized recent advances in the molecular and cellular mechanisms governing ISC injury and regeneration in NEC, emphasizing canonical repair pathways, niche-derived regulatory circuits, and emerging ISC-targeted therapies.
RESULTS: NEC disrupts ISC survival, proliferation, and differentiation through aberrant innate immune activation, microbial dysbiosis, and impairment of Wnt, Notch, and epidermal growth factor (EGF) signalling. ISC function is also shaped by interactions with Paneth cells, mesenchymal niche components, immune cells, and microbial metabolites. Disruption of this niche compromises crypt regeneration, perpetuates barrier dysfunction, and amplifies intestinal inflammation. Restoring ISC activity and niche integrity has therefore prompted interest in growth factor supplementation, microbiota modulation, immune-based interventions, and stem cell-oriented approaches.
CONCLUSIONS: ISC-centred regenerative failure provides an integrated framework linking epithelial biology, immunology, and microbiome research in NEC. Restoring ISC function and niche integrity represents a promising therapeutic direction with experimental and translational relevance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Enterocolitis, Necrotizing/pathology/etiology/metabolism/therapy
*Stem Cells/metabolism/cytology
Animals
*Intestinal Mucosa/metabolism/pathology
*Intestines/pathology/cytology
Regeneration
Signal Transduction
RevDate: 2026-10-28
CmpDate: 2026-10-28
PROMISE: a PROspective randomised double-blind parallel group placebo-controlled multicentre trial of faecal MIcrobiota tranSplantation to improve outcomEs in patients with cirrhosis over 24 months-study protocol for a clinical trial.
Trials, 27(1):.
BACKGROUND: Patients with cirrhosis have reduced gut bacterial diversity and a gut microbiota dominated by pathobionts. These changes, coupled with increased gut permeability and bacterial translocation, increase susceptibility to infection and death. There is also considerable concern that high antimicrobial exposure in the cirrhotic population drives the development of antimicrobial resistance (AMR). We previously performed a randomised feasibility trial of endoscopically administered jejunal faecal microbiota transplant (FMT) slurry derived from stringently screened donors, and showed it to be safe and well-tolerated in patients with cirrhosis (PROFIT Trial: NCT02862249). FMT was associated with reduced enteropathogenic bacteria in the gut, augmented ammonia excretion, ameliorated systemic inflammation, and enhanced innate immune responses to pathogen challenge. The trial was not powered to detect differences in clinical outcomes. The PROMISE study will evaluate the efficacy of lyophilised encapsulated FMT to reduce infection, decompensating events and mortality in patients with cirrhosis secondary to alcohol-related liver disease (ALD), metabolic dysfunction-associated steatotic liver disease (MASLD) cirrhosis and metabolic dysfunction and alcohol-related liver disease (MetALD).
METHODS: The PROMISE study is a phase 3 multicentre, randomised, double-blinded, placebo-controlled trial that will evaluate encapsulated lyophilised FMT in 300 participants with ALD, MetALD or MASLD cirrhosis (Model for End-Stage Liver Disease Sodium (MELD-Na) score 8-16). Participants will be randomly allocated (1:1) to receive FMT or matched placebo capsules every 91 days for 21 months, with 24-month follow-up. The primary endpoint is time-to-infection or decompensating event resulting in presentation to the emergency department or hospitalisation. Secondary endpoints include all hepatic decompensation, all-cause infection, antibiotic usage, incidence of AMR, hospitalisation rates, liver disease severity scores, quality of life scores, Hospital Anxiety and Depression Scale score (HADS), alcohol use, and mortality. Mechanistic endpoints include quantification of plasma bacterial DNA, plasma and faecal cytokines/biomarkers, plasma and faecal metabolome, faecal proteome, faecal microbiome composition and diversity (including resistome) and monocyte and mucosal-associated invariant T (MAIT) cell frequency, phenotype and function. Recruitment commenced in June 2023. Results will be disseminated via peer-reviewed journals, international conferences and patient support groups.
DISCUSSION: The PROMISE study will assess the efficacy and evaluate the mechanisms of action of FMT in patients with ALD, MASLD and MetALD cirrhosis. FMT may provide an alternative non-antibiotic treatment for these patients through ecological reconstitution of microbial balance.
TRIAL REGISTRATION: ISRCTN, ISRCTN17863382. Registered on 25th March 2022, https://www.isrctn.com/ISRCTNISRCTN17863382 .
CLINICALTRIALS: gov NCT06461208. Registered on 4th June 2024, https://clinicaltrials.gov/study/NCT06461208#study-overview .
Additional Links: PMID-42947250
PubMed:
Citation:
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@article {pmid42947250,
year = {2026},
author = {Kronsten, VT and Ntuli, Y and Paintsil, EK and Woodhouse, CA and Tranah, TH and Cheung, S and Hagan, D and Merrick, B and Cape, A and Maher, F and Sultana, K and Prossomariti, D and Rodrigues, S and Masterson, C and Hebditch, V and Zamalloa, A and Mullish, BH and Singanayagam, A and Patel, VC and Thursz, MR and , and Goldenberg, SD and Carter, B and Edwards, LA and Shawcross, DL},
title = {PROMISE: a PROspective randomised double-blind parallel group placebo-controlled multicentre trial of faecal MIcrobiota tranSplantation to improve outcomEs in patients with cirrhosis over 24 months-study protocol for a clinical trial.},
journal = {Trials},
volume = {27},
number = {1},
pages = {},
pmid = {42947250},
issn = {1745-6215},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; Double-Blind Method ; Multicenter Studies as Topic ; Randomized Controlled Trials as Topic ; Treatment Outcome ; *Liver Cirrhosis/therapy/microbiology ; Prospective Studies ; *Gastrointestinal Microbiome ; Time Factors ; Clinical Trials, Phase III as Topic ; },
abstract = {BACKGROUND: Patients with cirrhosis have reduced gut bacterial diversity and a gut microbiota dominated by pathobionts. These changes, coupled with increased gut permeability and bacterial translocation, increase susceptibility to infection and death. There is also considerable concern that high antimicrobial exposure in the cirrhotic population drives the development of antimicrobial resistance (AMR). We previously performed a randomised feasibility trial of endoscopically administered jejunal faecal microbiota transplant (FMT) slurry derived from stringently screened donors, and showed it to be safe and well-tolerated in patients with cirrhosis (PROFIT Trial: NCT02862249). FMT was associated with reduced enteropathogenic bacteria in the gut, augmented ammonia excretion, ameliorated systemic inflammation, and enhanced innate immune responses to pathogen challenge. The trial was not powered to detect differences in clinical outcomes. The PROMISE study will evaluate the efficacy of lyophilised encapsulated FMT to reduce infection, decompensating events and mortality in patients with cirrhosis secondary to alcohol-related liver disease (ALD), metabolic dysfunction-associated steatotic liver disease (MASLD) cirrhosis and metabolic dysfunction and alcohol-related liver disease (MetALD).
METHODS: The PROMISE study is a phase 3 multicentre, randomised, double-blinded, placebo-controlled trial that will evaluate encapsulated lyophilised FMT in 300 participants with ALD, MetALD or MASLD cirrhosis (Model for End-Stage Liver Disease Sodium (MELD-Na) score 8-16). Participants will be randomly allocated (1:1) to receive FMT or matched placebo capsules every 91 days for 21 months, with 24-month follow-up. The primary endpoint is time-to-infection or decompensating event resulting in presentation to the emergency department or hospitalisation. Secondary endpoints include all hepatic decompensation, all-cause infection, antibiotic usage, incidence of AMR, hospitalisation rates, liver disease severity scores, quality of life scores, Hospital Anxiety and Depression Scale score (HADS), alcohol use, and mortality. Mechanistic endpoints include quantification of plasma bacterial DNA, plasma and faecal cytokines/biomarkers, plasma and faecal metabolome, faecal proteome, faecal microbiome composition and diversity (including resistome) and monocyte and mucosal-associated invariant T (MAIT) cell frequency, phenotype and function. Recruitment commenced in June 2023. Results will be disseminated via peer-reviewed journals, international conferences and patient support groups.
DISCUSSION: The PROMISE study will assess the efficacy and evaluate the mechanisms of action of FMT in patients with ALD, MASLD and MetALD cirrhosis. FMT may provide an alternative non-antibiotic treatment for these patients through ecological reconstitution of microbial balance.
TRIAL REGISTRATION: ISRCTN, ISRCTN17863382. Registered on 25th March 2022, https://www.isrctn.com/ISRCTNISRCTN17863382 .
CLINICALTRIALS: gov NCT06461208. Registered on 4th June 2024, https://clinicaltrials.gov/study/NCT06461208#study-overview .},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fecal Microbiota Transplantation/methods/adverse effects
Double-Blind Method
Multicenter Studies as Topic
Randomized Controlled Trials as Topic
Treatment Outcome
*Liver Cirrhosis/therapy/microbiology
Prospective Studies
*Gastrointestinal Microbiome
Time Factors
Clinical Trials, Phase III as Topic
RevDate: 2026-10-28
CmpDate: 2026-10-28
Bacillus probiotic blend modulates ileal microbiome to improve growth performance and prevent necrotic enteritis in broiler chickens.
Animal microbiome, 8(1):.
The intensification of poultry production has led to an increased prevalence of necrotic enteritis (NE), a costly disease caused by Clostridium perfringens, traditionally managed through antibiotic use. However, concerns over antibiotic resistance have driven the search for alternative solutions. This study evaluates the efficacy of a three-strain Bacillus probiotic blend as an alternative for preventing NE in broiler chickens. The three Bacillus strains, Bacillus subtilis ATCC PTA126786, B. velezensis ATCC PTA127064, and B. velezensis ATCC PTA 127065, were selected based on their probiotic attributes, especially their ability to inhibit the growth of C. perfringens and other poultry pathogens. Our results from in vivo experiments showed that dietary supplementation with the probiotic blend significantly reduced NE-associated mortality and improved growth performance metrics such as average daily gain and feed conversion ratio. Metagenomic analyses of ileal contents of chickens supplemented with the Bacillus blend revealed a significant reduction in the abundances of C. perfringens, Enterococcus cecorum, and Eimeria acervulina following NE challenge, despite modest changes in overall microbiome composition. Importantly, the observed probiotic efficacy was strongly associated with the Bacillus strains colonization in the gut, as measured by the Bacillus genome recovery in ileal content samples. These findings highlight the potential of Bacillus-based probiotics as an effective alternative to antibiotics in poultry production, contributing to improved animal health and sustainability.
Additional Links: PMID-42947262
PubMed:
Citation:
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@article {pmid42947262,
year = {2026},
author = {Baxter, N and Plata, G and Bown, L and Shields, J and Augspurger, N and Kumar, A and Susanti, D},
title = {Bacillus probiotic blend modulates ileal microbiome to improve growth performance and prevent necrotic enteritis in broiler chickens.},
journal = {Animal microbiome},
volume = {8},
number = {1},
pages = {},
pmid = {42947262},
issn = {2524-4671},
abstract = {The intensification of poultry production has led to an increased prevalence of necrotic enteritis (NE), a costly disease caused by Clostridium perfringens, traditionally managed through antibiotic use. However, concerns over antibiotic resistance have driven the search for alternative solutions. This study evaluates the efficacy of a three-strain Bacillus probiotic blend as an alternative for preventing NE in broiler chickens. The three Bacillus strains, Bacillus subtilis ATCC PTA126786, B. velezensis ATCC PTA127064, and B. velezensis ATCC PTA 127065, were selected based on their probiotic attributes, especially their ability to inhibit the growth of C. perfringens and other poultry pathogens. Our results from in vivo experiments showed that dietary supplementation with the probiotic blend significantly reduced NE-associated mortality and improved growth performance metrics such as average daily gain and feed conversion ratio. Metagenomic analyses of ileal contents of chickens supplemented with the Bacillus blend revealed a significant reduction in the abundances of C. perfringens, Enterococcus cecorum, and Eimeria acervulina following NE challenge, despite modest changes in overall microbiome composition. Importantly, the observed probiotic efficacy was strongly associated with the Bacillus strains colonization in the gut, as measured by the Bacillus genome recovery in ileal content samples. These findings highlight the potential of Bacillus-based probiotics as an effective alternative to antibiotics in poultry production, contributing to improved animal health and sustainability.},
}
RevDate: 2026-10-28
Towards precision microbiome medicine through ecological network balance.
Clinical and translational medicine, 16(11):.
Additional Links: PMID-42947314
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PubMed:
Citation:
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@article {pmid42947314,
year = {2026},
author = {López, RC and Bonachela, JA and Dominguez-Bello, MG and Manhart, M and Levin, SA and Blaser, MJ and Muñoz, MA},
title = {Towards precision microbiome medicine through ecological network balance.},
journal = {Clinical and translational medicine},
volume = {16},
number = {11},
pages = {},
doi = {10.1002/ctm2.70875},
pmid = {42947314},
issn = {2001-1326},
support = {PID2023-149174NB-I00//Spanish Ministry and Agencia Estatal de Investigación MICIU/AEI/10.13039/501100011033/ ; DMS-2052616//National Science Foundation/ ; },
}
RevDate: 2026-10-28
CmpDate: 2026-10-28
Comprehensive Microbiome Profiling of Cheese Production Environments Using Long-Read Sequencing.
Environmental microbiology, 28(10):.
Environmental microbiota in cheese-production facilities can influence both product quality and hygienic conditions. This study characterised airborne and surface-associated microbial communities in production and ripening rooms of eight Slovak bryndza cheese facilities using culture-dependent methods and long-amplicon Nanopore sequencing. Air samples were collected with PBS-filled impingers and surface-swab suspensions were processed for DNA extraction. Bacterial 16S rRNA and fungal 28S rRNA gene amplicons were sequenced and taxonomically classified using Kraken2 and EMU. Community analyses included alpha-diversity estimates, Bray-Curtis ordination, PERMANOVA and supplementary ALDEx2 comparisons. Microbial loads varied among facilities and rooms, with elevated bacterial or fungal counts detected in several ripening environments. Sequencing revealed diverse bacterial and fungal communities comprising ripening-associated microorganisms, environmental contaminants, potential spoilage organisms and low-abundance taxa of hygienic relevance. Surface material had limited effects on overall bacterial and fungal community composition, although selected differences in fungal richness were observed among materials and individual facilities showed distinct microbial profiles. To our knowledge, this is among the first studies applying long-amplicon Nanopore sequencing to jointly characterise airborne and surface-associated bacterial and fungal communities in dairy-production environments. These findings support integrated environmental monitoring that considers microbial load, community diversity and facility-specific production conditions.
Additional Links: PMID-42947318
Publisher:
PubMed:
Citation:
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@article {pmid42947318,
year = {2026},
author = {Klištincová, N and Farkas, Z and Bučková, M and Puškárová, A and Kválová, K and Planý, M and Pavlović, J and Koreňová, J and Kuchta, T and Pangallo, D},
title = {Comprehensive Microbiome Profiling of Cheese Production Environments Using Long-Read Sequencing.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {},
doi = {10.1111/1462-2920.70461},
pmid = {42947318},
issn = {1462-2920},
support = {APVV-20-0001//Slovak Research and Development Agency/ ; },
mesh = {*Cheese/microbiology ; *Microbiota/genetics ; *Bacteria/classification/genetics/isolation & purification ; *Fungi/classification/genetics/isolation & purification ; RNA, Ribosomal, 16S/genetics ; *Air Microbiology ; RNA, Ribosomal, 28S/genetics ; },
abstract = {Environmental microbiota in cheese-production facilities can influence both product quality and hygienic conditions. This study characterised airborne and surface-associated microbial communities in production and ripening rooms of eight Slovak bryndza cheese facilities using culture-dependent methods and long-amplicon Nanopore sequencing. Air samples were collected with PBS-filled impingers and surface-swab suspensions were processed for DNA extraction. Bacterial 16S rRNA and fungal 28S rRNA gene amplicons were sequenced and taxonomically classified using Kraken2 and EMU. Community analyses included alpha-diversity estimates, Bray-Curtis ordination, PERMANOVA and supplementary ALDEx2 comparisons. Microbial loads varied among facilities and rooms, with elevated bacterial or fungal counts detected in several ripening environments. Sequencing revealed diverse bacterial and fungal communities comprising ripening-associated microorganisms, environmental contaminants, potential spoilage organisms and low-abundance taxa of hygienic relevance. Surface material had limited effects on overall bacterial and fungal community composition, although selected differences in fungal richness were observed among materials and individual facilities showed distinct microbial profiles. To our knowledge, this is among the first studies applying long-amplicon Nanopore sequencing to jointly characterise airborne and surface-associated bacterial and fungal communities in dairy-production environments. These findings support integrated environmental monitoring that considers microbial load, community diversity and facility-specific production conditions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Cheese/microbiology
*Microbiota/genetics
*Bacteria/classification/genetics/isolation & purification
*Fungi/classification/genetics/isolation & purification
RNA, Ribosomal, 16S/genetics
*Air Microbiology
RNA, Ribosomal, 28S/genetics
RevDate: 2026-10-28
CmpDate: 2026-10-28
Morphogenomic description of Cranifera cranifera (Chitwood, 1932) Kloss, 1960 from captive Blaptica dubia Serville, 1838 cockroach.
Journal of helminthology, 100:e151 pii:S0022149X26102569.
Nematodes of the superfamily Thelastomatoidea are found in the digestive system of various arthropods, feeding on their host microbiome. They are sometimes considered to be ecologically intermediate forms between free-living rhabditids and parasitic Spirurina, while phylogenetically they are nested within the latter. In addition to new morphological data on the male morphology, this manuscript presents the first nuclear genome assembly of a thelastomatid species, Cranifera cranifera, using a long-read sequencing approach, making a total of three nuclear genomes available for superfamily Thelastomatoidea. The C. cranifera nuclear genome assembly presented here is 243 Mb long, consists of 7563 contigs, has an N50 of 43 kb, and includes 94% of the BUSCO nematoda_odb12 genes. The mitochondrial genome is 24644 bases long, includes a complete set of protein-coding, rRNA, and tRNA genes, and a repetitive region 9731 bases long, which includes multiple copies of tRNA-Asn(gtt) and tRNA-Lys(ttt). The nuclear assembly also contained two sequence variants of the 28S rRNA and two of the 18S rRNA genes, highlighting the presence of intragenomic variation within the rRNA operon. The newly generated assemblies (nuclear and organelle) will add to a growing body of genomic resources for underrepresented and understudied animal parasitic nematodes from Clade 3, enabling comprehensive studies in their phylogeny and trait evolution in the future.
Additional Links: PMID-42947561
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PubMed:
Citation:
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@article {pmid42947561,
year = {2026},
author = {Morffe, J and Guiglielmoni, N and Wassey, N and Gueddach, K and Schuster, A and Becker, K and Bast, J and Schiffer, P and Holovachov, O},
title = {Morphogenomic description of Cranifera cranifera (Chitwood, 1932) Kloss, 1960 from captive Blaptica dubia Serville, 1838 cockroach.},
journal = {Journal of helminthology},
volume = {100},
number = {},
pages = {e151},
doi = {10.1017/S0022149X26102569},
pmid = {42947561},
issn = {1475-2697},
support = {dha.2024.4.3-192//Artdatabanken, Sveriges Lantbruksuniversitet/ ; BA 58004-1//Deutsche Forschungsgemeinschaft/ ; BA 58004-1//Deutsche Forschungsgemeinschaft/ ; },
mesh = {Animals ; Male ; Phylogeny ; *Cockroaches/parasitology ; Genome, Mitochondrial ; *Genome, Helminth ; *Rhabditida/genetics/anatomy & histology/classification ; Sequence Analysis, DNA ; },
abstract = {Nematodes of the superfamily Thelastomatoidea are found in the digestive system of various arthropods, feeding on their host microbiome. They are sometimes considered to be ecologically intermediate forms between free-living rhabditids and parasitic Spirurina, while phylogenetically they are nested within the latter. In addition to new morphological data on the male morphology, this manuscript presents the first nuclear genome assembly of a thelastomatid species, Cranifera cranifera, using a long-read sequencing approach, making a total of three nuclear genomes available for superfamily Thelastomatoidea. The C. cranifera nuclear genome assembly presented here is 243 Mb long, consists of 7563 contigs, has an N50 of 43 kb, and includes 94% of the BUSCO nematoda_odb12 genes. The mitochondrial genome is 24644 bases long, includes a complete set of protein-coding, rRNA, and tRNA genes, and a repetitive region 9731 bases long, which includes multiple copies of tRNA-Asn(gtt) and tRNA-Lys(ttt). The nuclear assembly also contained two sequence variants of the 28S rRNA and two of the 18S rRNA genes, highlighting the presence of intragenomic variation within the rRNA operon. The newly generated assemblies (nuclear and organelle) will add to a growing body of genomic resources for underrepresented and understudied animal parasitic nematodes from Clade 3, enabling comprehensive studies in their phylogeny and trait evolution in the future.},
}
MeSH Terms:
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Animals
Male
Phylogeny
*Cockroaches/parasitology
Genome, Mitochondrial
*Genome, Helminth
*Rhabditida/genetics/anatomy & histology/classification
Sequence Analysis, DNA
RevDate: 2026-10-28
Supraoptimal Mycorrhizal Colonisation Elicits Defence and Depletes Rhizosphere Inhabiting Massilia in Mild Salt‑Stressed Maize: A Split‑Root Comparison of Locally Colonised Roots.
Plant, cell & environment [Epub ahead of print].
Environmental conditions, such as light availability, affect the growth‑promoting effects of arbuscular mycorrhizal (AM) symbiosis. However, how the root‑rhizosphere continuum responds when mycorrhizal structures become unsuitable due to environmental deterioration remains unresolved. Using a split‑root system under mild salinity and low light, we generated two AM colonisation states (moderate and supraoptimal) and focused on roots with similar colonisation rates to compare local responses under different whole‑plant symbiotic backgrounds. Supraoptimal colonisation reduced the mycorrhizal growth response compared with moderate colonisation, and this reduction was uncoupled from ion homoeostasis. Root transcriptomics and rhizosphere exudates revealed that supraoptimal colonisation induced jasmonate/ethylene‑mediated defence responses, downregulated carbon transporter genes, and shifted exudation from symbiosis‑supporting lipids/terpenoids toward defence‑related amino acid derivatives. Consequently, supraoptimal colonisation reduced beneficial bacteria, notably Massilia, and simplified co‑occurrence networks. We propose a model in which salt stress and low light drive a host‑mediated "defence‑symbiosis" trade‑off, reducing the mycorrhizal growth response under supraoptimal AM colonisation. These findings provide a mechanistic framework for optimising AM applications in saline systems.
Additional Links: PMID-42947608
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PubMed:
Citation:
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@article {pmid42947608,
year = {2026},
author = {Wang, C and Zheng, G and Chen, Y and Zhang, L and Li, X and Ning, P and Quan, M and Wang, D and Xie, Z},
title = {Supraoptimal Mycorrhizal Colonisation Elicits Defence and Depletes Rhizosphere Inhabiting Massilia in Mild Salt‑Stressed Maize: A Split‑Root Comparison of Locally Colonised Roots.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.71000},
pmid = {42947608},
issn = {1365-3040},
support = {KF2024-6//the Open Research Fund Program of State Key Laboratory of Nutrient Use and Management/ ; ZR2024QD021//Shandong Provincial Natural Science Foundation/ ; 32270065//the National Natural Science Foundation of China/ ; tscy20251061//Taishan Industrial Experts Programme/ ; },
abstract = {Environmental conditions, such as light availability, affect the growth‑promoting effects of arbuscular mycorrhizal (AM) symbiosis. However, how the root‑rhizosphere continuum responds when mycorrhizal structures become unsuitable due to environmental deterioration remains unresolved. Using a split‑root system under mild salinity and low light, we generated two AM colonisation states (moderate and supraoptimal) and focused on roots with similar colonisation rates to compare local responses under different whole‑plant symbiotic backgrounds. Supraoptimal colonisation reduced the mycorrhizal growth response compared with moderate colonisation, and this reduction was uncoupled from ion homoeostasis. Root transcriptomics and rhizosphere exudates revealed that supraoptimal colonisation induced jasmonate/ethylene‑mediated defence responses, downregulated carbon transporter genes, and shifted exudation from symbiosis‑supporting lipids/terpenoids toward defence‑related amino acid derivatives. Consequently, supraoptimal colonisation reduced beneficial bacteria, notably Massilia, and simplified co‑occurrence networks. We propose a model in which salt stress and low light drive a host‑mediated "defence‑symbiosis" trade‑off, reducing the mycorrhizal growth response under supraoptimal AM colonisation. These findings provide a mechanistic framework for optimising AM applications in saline systems.},
}
RevDate: 2026-10-28
The Modern Exposome in Early-Onset Carcinogenesis.
Carcinogenesis pii:9003447 [Epub ahead of print].
Additional Links: PMID-42947638
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42947638,
year = {2026},
author = {Hofseth, LJ and Bailey, AM and Pine, SR and Giovannucci, EL},
title = {The Modern Exposome in Early-Onset Carcinogenesis.},
journal = {Carcinogenesis},
volume = {},
number = {},
pages = {},
doi = {10.1093/carcin/bgag078},
pmid = {42947638},
issn = {1460-2180},
}
RevDate: 2026-10-28
Multiple Exposures to Antibiotics Affect Tumor Development in a Mouse Model of Early-Onset Colorectal Cancer.
Carcinogenesis pii:9003448 [Epub ahead of print].
Early-onset colorectal cancer (EOCRC), defined as colorectal cancer in individuals under 50 years old, is a growing global epidemic, with incidence and mortality rates steadily increasing over the past several decades. Although EOCRC has been linked to established colorectal cancer risk factors, its underlying causes remain poorly understood. We propose that EOCRC may result from exposure to environmental factors, collectively known as the exposome, that have increased globally across EOCRC birth cohorts. Based on our current knowledge of EOCRC, the use of antibiotics is a potential exposome that may increase the risk for EOCRC. We hypothesized that exposure to antibiotics alters the gut microbiota resulting in dysbiosis that promotes inflammation in the distal colon and rectum, leading to increased risk of developing EOCRC. To test this, we examined the effects of repeated exposure to two commonly prescribed classes of pediatric antibiotics on gut microbiome composition, colonic inflammation, and tumor development following exposure to a carcinogen in a mouse model of EOCRC. A/J mice were subjected to multiple rounds of antibiotics followed by treatment with azoxymethane (AOM) to initiate tumor development, and assessment of colon tumor development. Antibiotic treatment induced dysbiosis and both local and systemic inflammation. Subsequent exposure to AOM showed that the two classes of antibiotics had different effects on tumor development in the distal colon and influenced the risk for EOCRC development in different ways.
Additional Links: PMID-42947647
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42947647,
year = {2026},
author = {Jani, N and Hinsch, V and Joseph, M and Ball, R and Johnson, K and Sikirzzhytski, V and Gowda, V and Ebel, L and Ganesh Babu, S and Hasnie, I and Villanueva, H and Baird, M and Hogan, K and Hofseth, L and Kubinak, J and Peña, MMO},
title = {Multiple Exposures to Antibiotics Affect Tumor Development in a Mouse Model of Early-Onset Colorectal Cancer.},
journal = {Carcinogenesis},
volume = {},
number = {},
pages = {},
doi = {10.1093/carcin/bgag077},
pmid = {42947647},
issn = {1460-2180},
abstract = {Early-onset colorectal cancer (EOCRC), defined as colorectal cancer in individuals under 50 years old, is a growing global epidemic, with incidence and mortality rates steadily increasing over the past several decades. Although EOCRC has been linked to established colorectal cancer risk factors, its underlying causes remain poorly understood. We propose that EOCRC may result from exposure to environmental factors, collectively known as the exposome, that have increased globally across EOCRC birth cohorts. Based on our current knowledge of EOCRC, the use of antibiotics is a potential exposome that may increase the risk for EOCRC. We hypothesized that exposure to antibiotics alters the gut microbiota resulting in dysbiosis that promotes inflammation in the distal colon and rectum, leading to increased risk of developing EOCRC. To test this, we examined the effects of repeated exposure to two commonly prescribed classes of pediatric antibiotics on gut microbiome composition, colonic inflammation, and tumor development following exposure to a carcinogen in a mouse model of EOCRC. A/J mice were subjected to multiple rounds of antibiotics followed by treatment with azoxymethane (AOM) to initiate tumor development, and assessment of colon tumor development. Antibiotic treatment induced dysbiosis and both local and systemic inflammation. Subsequent exposure to AOM showed that the two classes of antibiotics had different effects on tumor development in the distal colon and influenced the risk for EOCRC development in different ways.},
}
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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.