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RJR: Recommended Bibliography 08 Aug 2026 at 01:54 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-08-06
CmpDate: 2026-08-06
Fermentation of legumes as a strategy to enhance nutritional and sensory properties and modulate gut microbiome and human health.
Food research international (Ottawa, Ont.), 241:119704.
Legumes represent a valuable and vegetable source of proteins and fiber with a very low environmental footprint production, therefore, both dietary guidelines and international agencies suggest increasing their production and consumption. Despite their favorable nutritional composition, they also naturally contain antinutritional factors such as phytic acid, that limit the absorption of micronutrients. This, coupled with the lower bioavailability of proteins as compared with meat, diminishes the biological and economic value of legumes. However, recent studies have shed a light on the power of fermentation to improve the protein profile of pulse and neutralize antinutritional compounds. In this review, we explore the benefits of legumes fermentation in depth, focusing on the role of microorganisms in enhancing the nutritional and sensory enhancement of legumes. Furthermore, we describe the properties and the microorganisms involved in the production of several craft-based fermented legumes typically consumed by non-Westernized populations, particularly delving into their effects on the gut microbiome and on the human health.
Additional Links: PMID-42562480
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PubMed:
Citation:
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@article {pmid42562480,
year = {2026},
author = {Marotta, R and De Filippis, F and Valentino, V and Ercolini, D},
title = {Fermentation of legumes as a strategy to enhance nutritional and sensory properties and modulate gut microbiome and human health.},
journal = {Food research international (Ottawa, Ont.)},
volume = {241},
number = {},
pages = {119704},
doi = {10.1016/j.foodres.2026.119704},
pmid = {42562480},
issn = {1873-7145},
mesh = {*Fabaceae/chemistry/metabolism ; Humans ; *Fermentation ; *Nutritive Value ; *Gastrointestinal Microbiome/physiology ; *Fermented Foods/microbiology ; },
abstract = {Legumes represent a valuable and vegetable source of proteins and fiber with a very low environmental footprint production, therefore, both dietary guidelines and international agencies suggest increasing their production and consumption. Despite their favorable nutritional composition, they also naturally contain antinutritional factors such as phytic acid, that limit the absorption of micronutrients. This, coupled with the lower bioavailability of proteins as compared with meat, diminishes the biological and economic value of legumes. However, recent studies have shed a light on the power of fermentation to improve the protein profile of pulse and neutralize antinutritional compounds. In this review, we explore the benefits of legumes fermentation in depth, focusing on the role of microorganisms in enhancing the nutritional and sensory enhancement of legumes. Furthermore, we describe the properties and the microorganisms involved in the production of several craft-based fermented legumes typically consumed by non-Westernized populations, particularly delving into their effects on the gut microbiome and on the human health.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Fabaceae/chemistry/metabolism
Humans
*Fermentation
*Nutritive Value
*Gastrointestinal Microbiome/physiology
*Fermented Foods/microbiology
RevDate: 2026-08-06
CmpDate: 2026-08-06
Benchmarking a 16S rRNA sequencing protocol for microbiome analysis in low-moisture grain environments.
Food research international (Ottawa, Ont.), 241:119710.
Microbial amplicon sequencing studies are an important tool in food and biomedical research. However, accurate interpretation of the 16S rRNA gene survey requires specialized software and an algorithm to convert raw sequencing data into reliable taxonomic profiles. Given the existence of multiple bioinformatics pipelines varying in sequence aggregation strategies, reference databases, and filtering parameters, there is little to no consensus on best practices for LMF processing systems. In this study, we systematically assessed discrepancies in taxonomic composition, alpha diversity, and beta diversity across 32 combinations of bioinformatics workflows, based on eight widely used 16S rRNA pipelines and four taxonomic databases, applied to 16S rRNA gene sequences extracted from wheat milling environments (n = 160). Weighted composite scores were used to select the top 10-performing workflow combinations for downstream analysis. Taxonomic assignments were broadly similar across workflows at the family and genus levels; however, genus-level diversity metrics were more sensitive to workflow choice. At the family level, diversity metrics were conserved across pipeline-database combinations (Chao1: 22.97 ± 2.20-24.92 ± 2.04; Shannon: 2.59 ± 0.19-2.74 ± 0.18; InvSimpson: 10.63 ± 1.25-11.27 ± 1.06; Bray-Curtis: 0.528-0.556; Jaccard: 0.557-0.582), whereas at the genus level both alpha and beta diversity exhibited wider ranges and larger dispersion (Chao1: 45.27 ± 5.68-50.20 ± 5.64; Shannon: 2.54 ± 0.24-2.73 ± 0.22; InvSimpson: 10.37 ± 1.4-11.03 ± 1.05; Bray-Curtis: 0.79-0.82; Jaccard: 0.79-0.80). Furthermore, ASV vs. OTU workflows were comparable across the evaluated metrics; however, ASVs showed numerically higher values for some genus-level measures than OTUs because they can resolve variation down to the single-nucleotide level, thereby retaining low-abundance features important for LMF safety. This work paves the way toward using bioinformatics and 16S pipelines to characterize sparse, low-density, and uneven samples in low-moisture environments.
Additional Links: PMID-42562482
Publisher:
PubMed:
Citation:
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@article {pmid42562482,
year = {2026},
author = {Doddabematti Prakash, S and Balyatanda, SB and Sytsma, J and Tenzin, K and Siliveru, K},
title = {Benchmarking a 16S rRNA sequencing protocol for microbiome analysis in low-moisture grain environments.},
journal = {Food research international (Ottawa, Ont.)},
volume = {241},
number = {},
pages = {119710},
doi = {10.1016/j.foodres.2026.119710},
pmid = {42562482},
issn = {1873-7145},
mesh = {*RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; *Benchmarking ; *Edible Grain/microbiology ; Computational Biology ; Triticum/microbiology ; *Bacteria/genetics/classification ; *Food Microbiology ; Workflow ; },
abstract = {Microbial amplicon sequencing studies are an important tool in food and biomedical research. However, accurate interpretation of the 16S rRNA gene survey requires specialized software and an algorithm to convert raw sequencing data into reliable taxonomic profiles. Given the existence of multiple bioinformatics pipelines varying in sequence aggregation strategies, reference databases, and filtering parameters, there is little to no consensus on best practices for LMF processing systems. In this study, we systematically assessed discrepancies in taxonomic composition, alpha diversity, and beta diversity across 32 combinations of bioinformatics workflows, based on eight widely used 16S rRNA pipelines and four taxonomic databases, applied to 16S rRNA gene sequences extracted from wheat milling environments (n = 160). Weighted composite scores were used to select the top 10-performing workflow combinations for downstream analysis. Taxonomic assignments were broadly similar across workflows at the family and genus levels; however, genus-level diversity metrics were more sensitive to workflow choice. At the family level, diversity metrics were conserved across pipeline-database combinations (Chao1: 22.97 ± 2.20-24.92 ± 2.04; Shannon: 2.59 ± 0.19-2.74 ± 0.18; InvSimpson: 10.63 ± 1.25-11.27 ± 1.06; Bray-Curtis: 0.528-0.556; Jaccard: 0.557-0.582), whereas at the genus level both alpha and beta diversity exhibited wider ranges and larger dispersion (Chao1: 45.27 ± 5.68-50.20 ± 5.64; Shannon: 2.54 ± 0.24-2.73 ± 0.22; InvSimpson: 10.37 ± 1.4-11.03 ± 1.05; Bray-Curtis: 0.79-0.82; Jaccard: 0.79-0.80). Furthermore, ASV vs. OTU workflows were comparable across the evaluated metrics; however, ASVs showed numerically higher values for some genus-level measures than OTUs because they can resolve variation down to the single-nucleotide level, thereby retaining low-abundance features important for LMF safety. This work paves the way toward using bioinformatics and 16S pipelines to characterize sparse, low-density, and uneven samples in low-moisture environments.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
*Benchmarking
*Edible Grain/microbiology
Computational Biology
Triticum/microbiology
*Bacteria/genetics/classification
*Food Microbiology
Workflow
RevDate: 2026-08-06
CmpDate: 2026-08-06
Wastewater irrigation reshapes the microbiome and resistome of radish sprouts: Insights from 16S rRNA and shotgun metagenomic sequencing.
Food research international (Ottawa, Ont.), 241:119739.
Water scarcity is increasing the reliance on treated wastewater in fresh produce production, yet its effects on the microbial and hygienic quality of fresh produce remain unclear. This study evaluated the influence of wastewater irrigation on the microbiome and antibiotic resistance gene (ARG) profiles of radish sprouts grown under commercially relevant conditions. Using culture-dependent methods and integrated sequencing (16S rRNA and shotgun metagenomics), we tracked microbial and resistome dynamics across the sprout production process under three irrigation regimes: swine wastewater, treated wastewater, and sterile distilled water. Wastewater irrigation markedly increased microbial loads, with aerobic plate counts exceeding 8.0 log CFU/g in final radish sprouts. Both wastewater treatments were dominated by Pseudomonas and Acinetobacter. Resistome profiling showed persistent multidrug, bacitracin, and polymyxin resistance genes in wastewater-irrigated sprouts, while sulfonamide resistance genes occurred exclusively under wastewater irrigation, suggesting wastewater-associated environmental transmission. Higher ARG subtype richness in wastewater treatments suggested that conventional wastewater treatment processes do not completely eliminate diverse ARGs. ARG-host linkage analysis suggested an elevated potential for horizontal gene transfer within edible plant tissues. Overall, wastewater irrigation altered the microbiological quality of radish sprouts and facilitated ARG persistence, underscoring the need for improved post-treatment and preventive water management to safeguard fresh produce safety.
Additional Links: PMID-42562511
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PubMed:
Citation:
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@article {pmid42562511,
year = {2026},
author = {Lee, JW and Kim, YM and Kim, YJ and Jeong, KC and Kim, SA},
title = {Wastewater irrigation reshapes the microbiome and resistome of radish sprouts: Insights from 16S rRNA and shotgun metagenomic sequencing.},
journal = {Food research international (Ottawa, Ont.)},
volume = {241},
number = {},
pages = {119739},
doi = {10.1016/j.foodres.2026.119739},
pmid = {42562511},
issn = {1873-7145},
mesh = {*Raphanus/microbiology/growth & development ; *Wastewater/microbiology ; *RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; *Agricultural Irrigation/methods ; Animals ; Metagenomics/methods ; Shotgun Sequencing ; Bacteria/genetics ; Drug Resistance, Microbial/genetics ; Swine ; },
abstract = {Water scarcity is increasing the reliance on treated wastewater in fresh produce production, yet its effects on the microbial and hygienic quality of fresh produce remain unclear. This study evaluated the influence of wastewater irrigation on the microbiome and antibiotic resistance gene (ARG) profiles of radish sprouts grown under commercially relevant conditions. Using culture-dependent methods and integrated sequencing (16S rRNA and shotgun metagenomics), we tracked microbial and resistome dynamics across the sprout production process under three irrigation regimes: swine wastewater, treated wastewater, and sterile distilled water. Wastewater irrigation markedly increased microbial loads, with aerobic plate counts exceeding 8.0 log CFU/g in final radish sprouts. Both wastewater treatments were dominated by Pseudomonas and Acinetobacter. Resistome profiling showed persistent multidrug, bacitracin, and polymyxin resistance genes in wastewater-irrigated sprouts, while sulfonamide resistance genes occurred exclusively under wastewater irrigation, suggesting wastewater-associated environmental transmission. Higher ARG subtype richness in wastewater treatments suggested that conventional wastewater treatment processes do not completely eliminate diverse ARGs. ARG-host linkage analysis suggested an elevated potential for horizontal gene transfer within edible plant tissues. Overall, wastewater irrigation altered the microbiological quality of radish sprouts and facilitated ARG persistence, underscoring the need for improved post-treatment and preventive water management to safeguard fresh produce safety.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Raphanus/microbiology/growth & development
*Wastewater/microbiology
*RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
*Agricultural Irrigation/methods
Animals
Metagenomics/methods
Shotgun Sequencing
Bacteria/genetics
Drug Resistance, Microbial/genetics
Swine
RevDate: 2026-08-06
CmpDate: 2026-08-06
Dual-stage assessment of Salmonella-specific bacteriophage formulation: Antibiofilm activity on food matrices and in vivo efficacy against the murine salmonellosis model.
Food research international (Ottawa, Ont.), 241:119738.
Foodborne infections caused by Salmonella infection remain a major global concern due to increasing multidrug resistance and biofilm formation, resulting in significant morbidity and mortality. Thus, the development of potential alternatives, including bacteriophage cocktail formulations, is emerging as a promising strategy. In this direction, we developed a Salmonella-specific phage formulation (BPF-Sal) and evaluated its stability, biocontrol efficacy, in vitro safety, antibiofilm activity and protective potential in an in vivo model. Interestingly, BPF-Sal remained stable across a wide range of pH values and temperatures while maintaining significant lytic activity. Further, it effectively reduced Salmonella contamination on chicken breast and mixed fruit matrices to below detection limits (<1 CFU/100 μL) within 6 h and 10 h, respectively, compared to conventional preservatives. In HT-29 cells, BPF-Sal (10[2]-10[1][0] PFU/mL) exhibited no cytotoxicity, preserved cellular morphology, and showed efficient phage internalization. It also displayed antibiofilm activity, reducing preformed Salmonella biofilms by 90-92% at MOI 100 and up to 98% at MOI 1000, as confirmed by crystal violet assay, scanning electron and fluorescence microscopy. In a murine salmonellosis model, oral administration of BPF-Sal conferred significant protection, preventing weight loss and reducing bacterial loads along with improved health status and histopathological outcomes. Metagenomic analysis revealed infection-induced gut dysbiosis, characterized by enrichment of Proteobacteria and depletion of beneficial taxa. BPF-Sal partially restored microbial balance, while combination therapy further improved microbiota normalization. Thus, our findings establish BPF-Sal as a safe, effective, multifunctional phage-based strategy for Salmonella biocontrol and other phage-based applications.
Additional Links: PMID-42562512
Publisher:
PubMed:
Citation:
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@article {pmid42562512,
year = {2026},
author = {Murthy, N and Nayak, KN and Tanu, and Priya, S and Priyadarshini, P},
title = {Dual-stage assessment of Salmonella-specific bacteriophage formulation: Antibiofilm activity on food matrices and in vivo efficacy against the murine salmonellosis model.},
journal = {Food research international (Ottawa, Ont.)},
volume = {241},
number = {},
pages = {119738},
doi = {10.1016/j.foodres.2026.119738},
pmid = {42562512},
issn = {1873-7145},
mesh = {Animals ; *Biofilms/growth & development ; *Salmonella Phages/physiology ; Mice ; Disease Models, Animal ; Humans ; *Salmonella Infections/microbiology/therapy/prevention & control ; *Food Microbiology ; Chickens/microbiology ; *Salmonella/virology ; *Salmonella Food Poisoning/prevention & control/microbiology ; HT29 Cells ; Meat/microbiology ; Female ; Fruit/microbiology ; },
abstract = {Foodborne infections caused by Salmonella infection remain a major global concern due to increasing multidrug resistance and biofilm formation, resulting in significant morbidity and mortality. Thus, the development of potential alternatives, including bacteriophage cocktail formulations, is emerging as a promising strategy. In this direction, we developed a Salmonella-specific phage formulation (BPF-Sal) and evaluated its stability, biocontrol efficacy, in vitro safety, antibiofilm activity and protective potential in an in vivo model. Interestingly, BPF-Sal remained stable across a wide range of pH values and temperatures while maintaining significant lytic activity. Further, it effectively reduced Salmonella contamination on chicken breast and mixed fruit matrices to below detection limits (<1 CFU/100 μL) within 6 h and 10 h, respectively, compared to conventional preservatives. In HT-29 cells, BPF-Sal (10[2]-10[1][0] PFU/mL) exhibited no cytotoxicity, preserved cellular morphology, and showed efficient phage internalization. It also displayed antibiofilm activity, reducing preformed Salmonella biofilms by 90-92% at MOI 100 and up to 98% at MOI 1000, as confirmed by crystal violet assay, scanning electron and fluorescence microscopy. In a murine salmonellosis model, oral administration of BPF-Sal conferred significant protection, preventing weight loss and reducing bacterial loads along with improved health status and histopathological outcomes. Metagenomic analysis revealed infection-induced gut dysbiosis, characterized by enrichment of Proteobacteria and depletion of beneficial taxa. BPF-Sal partially restored microbial balance, while combination therapy further improved microbiota normalization. Thus, our findings establish BPF-Sal as a safe, effective, multifunctional phage-based strategy for Salmonella biocontrol and other phage-based applications.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Biofilms/growth & development
*Salmonella Phages/physiology
Mice
Disease Models, Animal
Humans
*Salmonella Infections/microbiology/therapy/prevention & control
*Food Microbiology
Chickens/microbiology
*Salmonella/virology
*Salmonella Food Poisoning/prevention & control/microbiology
HT29 Cells
Meat/microbiology
Female
Fruit/microbiology
RevDate: 2026-08-06
CmpDate: 2026-08-06
Ecological mechanisms and functional stability of lactic acid Bacteria in synthetic microbial communities: Competition, cross-feeding, and homeostasis maintenance.
Food research international (Ottawa, Ont.), 241:119779.
Synthetic microbial communities (SynComs) play a pivotal role in advancing precision fermentation and microbiome engineering. Within these multispecies systems, lactic acid bacteria (LAB) function as ecological and metabolic cornerstones. However, the mechanisms underlying LAB-mediated community stability remain insufficiently understood. This review synthesizes current knowledge on microbial competition, cross-feeding, and community homeostasis to evaluate the ecological contributions of LAB. We compare the metabolic roles of LAB in SynComs and natural ecosystems, highlighting competitive strategies, including acidification and antimicrobial production, as well as lactate-centered syntrophic interactions. As central metabolic hubs, LAB facilitate the division of labor by transforming excess metabolic outputs into shared resources, thereby reducing metabolic inefficiencies. We further examine how functional redundancy and metabolic coupling contribute to community resilience and stability. The review also discusses emerging applications of SynComs in gut health, particularly inflammatory bowel disease (IBD), and industrial fermentation processes. We conclude that the integration of multi-omics approaches with predictive modeling will be critical for the rational design and programmable regulation of stable microbial consortia. Furthermore, this review proposes a unified hierarchical framework for understanding the stability of LAB-mediated SynComs. By integrating competition-driven colonization, cooperation mediated through cross-feeding interactions, and multidimensional homeostatic mechanisms, the framework bridges fundamental ecological theory with applied microbiome engineering. The proposed framework is primarily applicable to LAB-centered SynComs associated with food fermentation systems, acidic environments, and lactate-driven metabolic networks.
Additional Links: PMID-42562540
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PubMed:
Citation:
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@article {pmid42562540,
year = {2026},
author = {Kong, F and Xu, J and Liu, Z and Ju, N and Guo, S},
title = {Ecological mechanisms and functional stability of lactic acid Bacteria in synthetic microbial communities: Competition, cross-feeding, and homeostasis maintenance.},
journal = {Food research international (Ottawa, Ont.)},
volume = {241},
number = {},
pages = {119779},
doi = {10.1016/j.foodres.2026.119779},
pmid = {42562540},
issn = {1873-7145},
mesh = {*Lactobacillales/metabolism/physiology ; *Homeostasis ; Fermentation ; *Microbial Consortia/physiology ; *Microbiota/physiology ; Humans ; Microbial Interactions ; },
abstract = {Synthetic microbial communities (SynComs) play a pivotal role in advancing precision fermentation and microbiome engineering. Within these multispecies systems, lactic acid bacteria (LAB) function as ecological and metabolic cornerstones. However, the mechanisms underlying LAB-mediated community stability remain insufficiently understood. This review synthesizes current knowledge on microbial competition, cross-feeding, and community homeostasis to evaluate the ecological contributions of LAB. We compare the metabolic roles of LAB in SynComs and natural ecosystems, highlighting competitive strategies, including acidification and antimicrobial production, as well as lactate-centered syntrophic interactions. As central metabolic hubs, LAB facilitate the division of labor by transforming excess metabolic outputs into shared resources, thereby reducing metabolic inefficiencies. We further examine how functional redundancy and metabolic coupling contribute to community resilience and stability. The review also discusses emerging applications of SynComs in gut health, particularly inflammatory bowel disease (IBD), and industrial fermentation processes. We conclude that the integration of multi-omics approaches with predictive modeling will be critical for the rational design and programmable regulation of stable microbial consortia. Furthermore, this review proposes a unified hierarchical framework for understanding the stability of LAB-mediated SynComs. By integrating competition-driven colonization, cooperation mediated through cross-feeding interactions, and multidimensional homeostatic mechanisms, the framework bridges fundamental ecological theory with applied microbiome engineering. The proposed framework is primarily applicable to LAB-centered SynComs associated with food fermentation systems, acidic environments, and lactate-driven metabolic networks.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Lactobacillales/metabolism/physiology
*Homeostasis
Fermentation
*Microbial Consortia/physiology
*Microbiota/physiology
Humans
Microbial Interactions
RevDate: 2026-08-06
RNAi-mediated knockdown of vitellogenin genes disrupts ovary development and alters ovarian bacterial composition in Zeugodacus tau (Diptera: Tephritidae).
Journal of economic entomology pii:8753718 [Epub ahead of print].
Zeugodacus tau Walker (Diptera: Tephritidae) is an invasive pest of global significance that inflicts substantial losses to the fruit and vegetable production sectors annually. Despite the availability of the Z. tau genome in public database, functional characterization of key genes remained limited. Vitellogenin (Vg) functions as a key precursor of yolk protein and exerts a pivotal part in the insect reproductive process. Here, we identified 3 Vg genes (Vg1, Vg2, and Vg3) based on genetic data from Z. tau. Analysis of amino acid sequences demonstrated that all ZtVgs contain conserved serine residues, a putative cleavage site, and putative N-linked glycosylation sites. Molecular phylogenetic reconstruction revealed that ZtVgs exhibited the closest evolutionary affinity to their homologs found in Zeugodacus cucurbitae and Bactrocera dorsalis. Spatiotemporal expression profiling indicated that all 3 ZtVgs exhibit pronounced expression in the female fat body. Treatments with the Methoprene and 20-hydroxyecdysone (20E) significantly upregulated ZtVgs expression 24 h post application at a dose of 1 μg. RNA interference (RNAi) bioassay revealed that the suppression of 3 ZtVgs delayed ovary development and impaired female fertility. Further microbiome analysis revealed that knockdown of the 3 Vg genes led to reduced abundance of bacterial taxa affiliated with the phylum Pseudomonadota and the genus Burkholderia in the ovary. These findings elucidate the important function of Vgs in ovary development and provide insights into the association between insect Vg genes and the ovarian bacteria, thereby establishing a groundwork for subsequent investigations on the molecular mechanisms underlying their interaction.
Additional Links: PMID-42562772
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PubMed:
Citation:
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@article {pmid42562772,
year = {2026},
author = {Xu, C and Xie, Q and Li, X and Li, W},
title = {RNAi-mediated knockdown of vitellogenin genes disrupts ovary development and alters ovarian bacterial composition in Zeugodacus tau (Diptera: Tephritidae).},
journal = {Journal of economic entomology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jee/toag239},
pmid = {42562772},
issn = {1938-291X},
support = {20252BAC200396//Jiangxi Provincial Natural Science Foundation/ ; GJJ210443//Foundation Project of Jiangxi Provincial Educational Committee/ ; },
abstract = {Zeugodacus tau Walker (Diptera: Tephritidae) is an invasive pest of global significance that inflicts substantial losses to the fruit and vegetable production sectors annually. Despite the availability of the Z. tau genome in public database, functional characterization of key genes remained limited. Vitellogenin (Vg) functions as a key precursor of yolk protein and exerts a pivotal part in the insect reproductive process. Here, we identified 3 Vg genes (Vg1, Vg2, and Vg3) based on genetic data from Z. tau. Analysis of amino acid sequences demonstrated that all ZtVgs contain conserved serine residues, a putative cleavage site, and putative N-linked glycosylation sites. Molecular phylogenetic reconstruction revealed that ZtVgs exhibited the closest evolutionary affinity to their homologs found in Zeugodacus cucurbitae and Bactrocera dorsalis. Spatiotemporal expression profiling indicated that all 3 ZtVgs exhibit pronounced expression in the female fat body. Treatments with the Methoprene and 20-hydroxyecdysone (20E) significantly upregulated ZtVgs expression 24 h post application at a dose of 1 μg. RNA interference (RNAi) bioassay revealed that the suppression of 3 ZtVgs delayed ovary development and impaired female fertility. Further microbiome analysis revealed that knockdown of the 3 Vg genes led to reduced abundance of bacterial taxa affiliated with the phylum Pseudomonadota and the genus Burkholderia in the ovary. These findings elucidate the important function of Vgs in ovary development and provide insights into the association between insect Vg genes and the ovarian bacteria, thereby establishing a groundwork for subsequent investigations on the molecular mechanisms underlying their interaction.},
}
RevDate: 2026-08-07
The Benefits and Biological Risks in Breastfeeding and Sharing Human Milk: Have We Got it Right?.
Journal of human lactation : official journal of International Lactation Consultant Association [Epub ahead of print].
BACKGROUND: Implementation of the strong recommendation by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF), and others, to increase use of donor human milk in cases where breastfeeding cannot be provided, requires a flexible, knowledge-based and risk-informed approach.
METHODS: Based on an extensive literature review, we present the evidence for potential biological risks of breastmilk in three scenarios: fresh, unmodified milk from breast to baby (breastfeeding and wet-nursing); expressed and unmodified milk stored at < 4 ºC until just before consumption; and milk modified by some form of pasteurization.
RESULTS: With the exception of contamination by some viruses and syphilis, breastfeeding is the safest way to feed a baby, despite its highly variable microbiome and virome-including organisms that, in other circumstances, can cause disease. Wet-nursing, where the donor has been appropriately screened, carries a similar risk profile to mother's own feeding. Whilst expression and storage of raw milk at < 4 °C adds a bacterial load, the additional risk, with knowledge and screening of the donor and careful attention to all steps in delivery, seems small and is smaller than using bovine-based formulae-especially in low resource circumstances. Donated milk from unknown donors carries additional risks. A decision to reduce these risks through thermal pasteurization must be weighed against the loss of breastmilk's natural protective components.
CONCLUSIONS: Not only have the biological risks of both informal and formal milk sharing for healthy infants been greatly exaggerated, but that they are often quoted without consideration of the overall risks of alternatives.
Additional Links: PMID-42562802
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PubMed:
Citation:
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@article {pmid42562802,
year = {2026},
author = {Cassey, J and Banati, R},
title = {The Benefits and Biological Risks in Breastfeeding and Sharing Human Milk: Have We Got it Right?.},
journal = {Journal of human lactation : official journal of International Lactation Consultant Association},
volume = {},
number = {},
pages = {8903344261451926},
doi = {10.1177/08903344261451926},
pmid = {42562802},
issn = {1552-5732},
abstract = {BACKGROUND: Implementation of the strong recommendation by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF), and others, to increase use of donor human milk in cases where breastfeeding cannot be provided, requires a flexible, knowledge-based and risk-informed approach.
METHODS: Based on an extensive literature review, we present the evidence for potential biological risks of breastmilk in three scenarios: fresh, unmodified milk from breast to baby (breastfeeding and wet-nursing); expressed and unmodified milk stored at < 4 ºC until just before consumption; and milk modified by some form of pasteurization.
RESULTS: With the exception of contamination by some viruses and syphilis, breastfeeding is the safest way to feed a baby, despite its highly variable microbiome and virome-including organisms that, in other circumstances, can cause disease. Wet-nursing, where the donor has been appropriately screened, carries a similar risk profile to mother's own feeding. Whilst expression and storage of raw milk at < 4 °C adds a bacterial load, the additional risk, with knowledge and screening of the donor and careful attention to all steps in delivery, seems small and is smaller than using bovine-based formulae-especially in low resource circumstances. Donated milk from unknown donors carries additional risks. A decision to reduce these risks through thermal pasteurization must be weighed against the loss of breastmilk's natural protective components.
CONCLUSIONS: Not only have the biological risks of both informal and formal milk sharing for healthy infants been greatly exaggerated, but that they are often quoted without consideration of the overall risks of alternatives.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Microbiome and resistome of the European bison (Bison bonasus).
Scientific reports, 16(1):.
After facing extinction in the early 20th century, populations of the two remnant genetic lines of European bison are now under continuous health monitoring. Faecal samples were taken from five Polish and one German herd of European bison over the course of several years. Through metagenomic sequencing, the bacterial and archaeal microbiome as well as the resistome of these samples could be characterized. Significant differences were mainly found between the bacterial microbiome of samples taken from droppings as opposed to rectal samples. Apart from this, the microbiome and resistome had low differentiation, showing no significant influence of individual factors or location. Oscillospiraceae, Lachnospiraceae and Bacteroidaceae were the dominant bacterial families, the archaeome was mostly made up by Methanobacteriaceae. Genes from resistance classes like Aminoglycosides and Macrolide, Lincosamide and Streptogramine were present. This study characterises the microbiome and resistome of the European bison with the help of metagenomics, providing novel insights into its biology.
Additional Links: PMID-42562842
PubMed:
Citation:
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@article {pmid42562842,
year = {2026},
author = {Lechleiter, N and Wedemeyer, J and Junker, J and Wilczek, M and Klich, D and Olech, W and Anusz, K and Homeier-Bachmann, T and Didkowska, A},
title = {Microbiome and resistome of the European bison (Bison bonasus).},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42562842},
issn = {2045-2322},
mesh = {Animals ; *Bison/microbiology ; *Microbiota/genetics ; Feces/microbiology ; *Bacteria/genetics/classification/drug effects/isolation & purification ; Metagenomics ; Anti-Bacterial Agents/pharmacology ; Archaea/genetics/classification/isolation & purification ; Phylogeny ; },
abstract = {After facing extinction in the early 20th century, populations of the two remnant genetic lines of European bison are now under continuous health monitoring. Faecal samples were taken from five Polish and one German herd of European bison over the course of several years. Through metagenomic sequencing, the bacterial and archaeal microbiome as well as the resistome of these samples could be characterized. Significant differences were mainly found between the bacterial microbiome of samples taken from droppings as opposed to rectal samples. Apart from this, the microbiome and resistome had low differentiation, showing no significant influence of individual factors or location. Oscillospiraceae, Lachnospiraceae and Bacteroidaceae were the dominant bacterial families, the archaeome was mostly made up by Methanobacteriaceae. Genes from resistance classes like Aminoglycosides and Macrolide, Lincosamide and Streptogramine were present. This study characterises the microbiome and resistome of the European bison with the help of metagenomics, providing novel insights into its biology.},
}
MeSH Terms:
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Animals
*Bison/microbiology
*Microbiota/genetics
Feces/microbiology
*Bacteria/genetics/classification/drug effects/isolation & purification
Metagenomics
Anti-Bacterial Agents/pharmacology
Archaea/genetics/classification/isolation & purification
Phylogeny
RevDate: 2026-08-07
Inflammatory gut-liver crosstalk: mechanisms and therapeutic targets.
Experimental & molecular medicine [Epub ahead of print].
The gut has a profound influence on the liver through their anatomical connection via the portal vein. During acute inflammation, gut tissue injury leads to increased barrier permeability, allowing the translocation of external contents that can affect hepatic function. Gut-liver crosstalk contributes to the pathophysiology of acute inflammatory disorders, such as sepsis, intestinal ischaemia-reperfusion, hepatitis and drug-induced liver injury. This organ-to-organ crosstalk is mediated by the microbiome, pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs) and various proinflammatory mediators. Different types of gut and liver resident cells as well as circulating cells also facilitate inflammatory gut-liver crosstalk. These cell types include intestinal epithelial and myeloid cells, Kupffer cells, sinusoidal endothelial cells, hepatic stellate cells, hepatocytes, lymphocytes and neutrophils. PAMPs and DAMPs activate pattern recognition receptors, such as Toll-like receptors, on various cells, leading to proinflammatory signal transduction, including NFκB activation, cytokine and chemokine production, and NETosis. Collectively, these soluble and cellular factors exacerbate acute inflammation and tissue injury via the gut-liver axis, leading to poor outcomes in critically ill patients. Potential therapeutic interventions for this deadly clinical condition include modulation of the microbiome and pharmacological inhibition of proinflammatory mediators and cellular interactions. In this article we review the pathophysiology of inflammatory gut-liver crosstalk and potential therapeutic interventions.
Additional Links: PMID-42562890
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@article {pmid42562890,
year = {2026},
author = {Murao, A and Aziz, M and Wang, P},
title = {Inflammatory gut-liver crosstalk: mechanisms and therapeutic targets.},
journal = {Experimental & molecular medicine},
volume = {},
number = {},
pages = {},
pmid = {42562890},
issn = {2092-6413},
support = {R35GM118337//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01HL076179//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; },
abstract = {The gut has a profound influence on the liver through their anatomical connection via the portal vein. During acute inflammation, gut tissue injury leads to increased barrier permeability, allowing the translocation of external contents that can affect hepatic function. Gut-liver crosstalk contributes to the pathophysiology of acute inflammatory disorders, such as sepsis, intestinal ischaemia-reperfusion, hepatitis and drug-induced liver injury. This organ-to-organ crosstalk is mediated by the microbiome, pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs) and various proinflammatory mediators. Different types of gut and liver resident cells as well as circulating cells also facilitate inflammatory gut-liver crosstalk. These cell types include intestinal epithelial and myeloid cells, Kupffer cells, sinusoidal endothelial cells, hepatic stellate cells, hepatocytes, lymphocytes and neutrophils. PAMPs and DAMPs activate pattern recognition receptors, such as Toll-like receptors, on various cells, leading to proinflammatory signal transduction, including NFκB activation, cytokine and chemokine production, and NETosis. Collectively, these soluble and cellular factors exacerbate acute inflammation and tissue injury via the gut-liver axis, leading to poor outcomes in critically ill patients. Potential therapeutic interventions for this deadly clinical condition include modulation of the microbiome and pharmacological inhibition of proinflammatory mediators and cellular interactions. In this article we review the pathophysiology of inflammatory gut-liver crosstalk and potential therapeutic interventions.},
}
RevDate: 2026-08-07
Gut microbiota modulation of gastrointestinal cancers: from dysbiosis signatures to therapeutic interventions.
Acta pharmacologica Sinica [Epub ahead of print].
The human gut microbiota constitutes the largest and most metabolically active microbial ecosystem in the body, and accumulating evidence links dynamic alterations in microbial composition and function to the initiation, progression, and treatment responses of multiple gastrointestinal (GI) cancers, including esophageal, gastric, hepatocellular, pancreatic, and colorectal malignancies. This review synthesizes current evidence on dysbiosis signatures, mechanistic pathways, and translational opportunities across major GI cancer types, with a focus on microbe-derived metabolites and microbe-associated molecular patterns that shape inflammation, epithelial barrier integrity, and antitumor immunity. Across GI cancers, recurrent patterns include enrichment of pro-inflammatory/pathobiont taxa, depletion of homeostasis-maintaining and butyrate-producing commensals, and perturbations in metabolic axes centered on bile acids and short-chain fatty acids. Mechanistically, these changes can remodel the tumor microenvironment via epithelial and immune signaling, epigenetic regulation, and metabolic reprogramming. Importantly, the gut microbiota is increasingly recognized as a modifiable determinant of the efficacy and toxicity of immune checkpoint blockade, adoptive cell therapies, chemotherapy, and radiotherapy. Despite rapid advances, key challenges persist in translating microbiome research into cancer care, including validation, standardization, variability, and safety. Future success likely depends on function-oriented, targeted modulation, supported by multi-omics, strong causal evidence, and clinical trials.
Additional Links: PMID-42562892
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@article {pmid42562892,
year = {2026},
author = {Li, XY and Xie, ZQ and Geng, MY},
title = {Gut microbiota modulation of gastrointestinal cancers: from dysbiosis signatures to therapeutic interventions.},
journal = {Acta pharmacologica Sinica},
volume = {},
number = {},
pages = {},
pmid = {42562892},
issn = {1745-7254},
abstract = {The human gut microbiota constitutes the largest and most metabolically active microbial ecosystem in the body, and accumulating evidence links dynamic alterations in microbial composition and function to the initiation, progression, and treatment responses of multiple gastrointestinal (GI) cancers, including esophageal, gastric, hepatocellular, pancreatic, and colorectal malignancies. This review synthesizes current evidence on dysbiosis signatures, mechanistic pathways, and translational opportunities across major GI cancer types, with a focus on microbe-derived metabolites and microbe-associated molecular patterns that shape inflammation, epithelial barrier integrity, and antitumor immunity. Across GI cancers, recurrent patterns include enrichment of pro-inflammatory/pathobiont taxa, depletion of homeostasis-maintaining and butyrate-producing commensals, and perturbations in metabolic axes centered on bile acids and short-chain fatty acids. Mechanistically, these changes can remodel the tumor microenvironment via epithelial and immune signaling, epigenetic regulation, and metabolic reprogramming. Importantly, the gut microbiota is increasingly recognized as a modifiable determinant of the efficacy and toxicity of immune checkpoint blockade, adoptive cell therapies, chemotherapy, and radiotherapy. Despite rapid advances, key challenges persist in translating microbiome research into cancer care, including validation, standardization, variability, and safety. Future success likely depends on function-oriented, targeted modulation, supported by multi-omics, strong causal evidence, and clinical trials.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Microbially derived glutathione from Eubacterium rectale alleviates oxidative stress and promotes intestinal epithelial recovery.
Microbiome, 14(1):.
BACKGROUND: Certain microbes inhabiting the gut have been implicated in maintaining gut homeostasis and promoting gut damage repair. Lachnospiraceae members were highly detected in dysbiotic IL-10 KO mice that displayed similar physiological outcomes as control mice. Lachnospiraceae is a highly diverse family of microbes that have been shown to display both commensal and pathogenic characteristics in the colon environment.
RESULTS: We investigated the impact of genetic variation in five Lachnospiraceae strains on lowering cellular inflammation and reactive oxygen species (ROS) levels. Cell-free spent media (CFSM) from Eubacterium rectale resulted in lowered ROS, and nitric oxide levels in stressed colon cells and colon organoids. CFSM-treated organoids showed reduced ROS accumulation, improved epithelial integrity, and partial recovery of barrier function compared to oxidatively stressed controls. We demonstrated through shotgun metagenomics, metabolomics, host RNA sequencing, and molecular techniques that glutathione (GSH) biosynthesized by E. rectale alleviated host ROS damage. We showed downregulation of cell stress and immune response genes, indicating recovery from ROS stress. Chemical depletion of GSH in CFSM confirmed the role of microbial derived GSH in alleviation of ROS in colon cells.
CONCLUSIONS: In this study, we identify E. rectale as a potential probiotic by lowering colon inflammation and ROS damage through production of reduced glutathione. Microbially derived GSH has not been well established in the Lachnospiraceae family which are a large member of the overall gut microbiota. Understanding more about the impacts of microbial functions including GSH on lowering inflammation is needed to develop potential probiotics or therapies for chronic inflammatory conditions. Video Abstract.
Additional Links: PMID-42563165
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Citation:
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@article {pmid42563165,
year = {2026},
author = {Richie, TG and Wiechman, H and Vogt, B and Ingold, C and Heeren, L and Kamke, A and Pogranichniy, S and Monk, K and Summers, T and Ran, Q and Sarkar, S and Plattner, BL and Sidebottom, AM and Chang, EB and Lee, STM},
title = {Microbially derived glutathione from Eubacterium rectale alleviates oxidative stress and promotes intestinal epithelial recovery.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {},
pmid = {42563165},
issn = {2049-2618},
mesh = {*Oxidative Stress/drug effects ; Animals ; *Glutathione/metabolism/pharmacology ; Reactive Oxygen Species/metabolism ; Mice ; Colon/microbiology/metabolism ; *Intestinal Mucosa/metabolism/microbiology/drug effects ; Nitric Oxide/metabolism ; Intestinal Barrier Function ; Gastrointestinal Microbiome ; Metagenomics ; Mice, Knockout ; Interleukin-10/genetics ; },
abstract = {BACKGROUND: Certain microbes inhabiting the gut have been implicated in maintaining gut homeostasis and promoting gut damage repair. Lachnospiraceae members were highly detected in dysbiotic IL-10 KO mice that displayed similar physiological outcomes as control mice. Lachnospiraceae is a highly diverse family of microbes that have been shown to display both commensal and pathogenic characteristics in the colon environment.
RESULTS: We investigated the impact of genetic variation in five Lachnospiraceae strains on lowering cellular inflammation and reactive oxygen species (ROS) levels. Cell-free spent media (CFSM) from Eubacterium rectale resulted in lowered ROS, and nitric oxide levels in stressed colon cells and colon organoids. CFSM-treated organoids showed reduced ROS accumulation, improved epithelial integrity, and partial recovery of barrier function compared to oxidatively stressed controls. We demonstrated through shotgun metagenomics, metabolomics, host RNA sequencing, and molecular techniques that glutathione (GSH) biosynthesized by E. rectale alleviated host ROS damage. We showed downregulation of cell stress and immune response genes, indicating recovery from ROS stress. Chemical depletion of GSH in CFSM confirmed the role of microbial derived GSH in alleviation of ROS in colon cells.
CONCLUSIONS: In this study, we identify E. rectale as a potential probiotic by lowering colon inflammation and ROS damage through production of reduced glutathione. Microbially derived GSH has not been well established in the Lachnospiraceae family which are a large member of the overall gut microbiota. Understanding more about the impacts of microbial functions including GSH on lowering inflammation is needed to develop potential probiotics or therapies for chronic inflammatory conditions. Video Abstract.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Oxidative Stress/drug effects
Animals
*Glutathione/metabolism/pharmacology
Reactive Oxygen Species/metabolism
Mice
Colon/microbiology/metabolism
*Intestinal Mucosa/metabolism/microbiology/drug effects
Nitric Oxide/metabolism
Intestinal Barrier Function
Gastrointestinal Microbiome
Metagenomics
Mice, Knockout
Interleukin-10/genetics
RevDate: 2026-08-07
CmpDate: 2026-08-07
Gut-protective metabolic phenotype for diarrhoeal remission caused by an environmental probiotic thermophile.
Microbiome, 14(1):.
BACKGROUND: Controlling diarrhoea in humans and livestock is a global challenge with diverse aetiologies. However, the dynamics of the microbiome for diarrhoeal remission are not sufficiently understood, and effective intervention strategies based on environmental microorganisms have not been fully explored.
METHODS: We investigated the metabolic structure associated with diarrhoeal remission using a combination of statistical, genomic, and proteomic approaches in a cattle model. Oral administration of the compost-derived thermophile Caldifermentibacillus hisashii significantly ameliorated persistent diarrhoea. Faecal bacterial populations and metabolites were characterised by a multi-step statistical pipeline comprising difference-in-differences (DID) analysis, Cliff's delta effect size estimation with permutation-based validation. The functional importance of the selected feature components was validated through genomic and proteomic analysis of C. hisashii N11 (AP028807.1).
RESULTS: Oral administration of C. hisashii significantly ameliorated persistent diarrhoea in calves. Although no significant differences in faecal bacterial community composition were observed, integrated analysis of faecal metabolites identified butyrate and 2-aminoisobutyrate (AIB) as the most discriminative features associated with diarrhoeal remission. Genomic and proteomic analyses of C. hisashii confirmed biosynthetic gene clusters for butyrate and AIB-containing lantibiotics, supporting the structural importance of these metabolites in diarrhoeal remission.
CONCLUSION: These findings suggest that diarrhoeal remission observed in this study involves characteristic shifts in faecal metabolite profiles rather than marked changes in overall gut microbial community composition, highlighting a protective role of C. hisashii as an environmental probiotic against diarrhoeal dysbiosis through modulation of gut microbial metabolic output. This offers a perspective that bridges environmental microbiology and gut health within a One Health framework. Video Abstract.
Additional Links: PMID-42563179
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Citation:
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@article {pmid42563179,
year = {2026},
author = {Miyamoto, H and Takahashi, H and Suda, W and Yamano, H and Inabu, Y and Kodama, H and Nakanishi, Y and Moriya, S and Satoh, T and Kato, T and Shindo, C and Tsuji, N and Matsuura, M and Ishii, C and Nakaguma, T and Etoh, T and Shiotsuka, Y and Udagawa, M and Kurotani, A and Suzuki, K and Masuya, H and Wada, S and Fukuda, S and Tashiro, Y and Miyamoto, H and Kikuchi, J and Hattori, M and Nishiuchi, T and Yamamoto, N and Ohno, H},
title = {Gut-protective metabolic phenotype for diarrhoeal remission caused by an environmental probiotic thermophile.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {},
pmid = {42563179},
issn = {2049-2618},
mesh = {Animals ; *Probiotics/administration & dosage ; *Diarrhea/veterinary/microbiology/therapy ; Feces/microbiology ; Cattle ; *Gastrointestinal Microbiome ; Proteomics ; Butyrates/metabolism ; Bacteriocins/genetics/biosynthesis ; Administration, Oral ; Genomics ; Bacteria/classification/genetics/metabolism/isolation & purification ; },
abstract = {BACKGROUND: Controlling diarrhoea in humans and livestock is a global challenge with diverse aetiologies. However, the dynamics of the microbiome for diarrhoeal remission are not sufficiently understood, and effective intervention strategies based on environmental microorganisms have not been fully explored.
METHODS: We investigated the metabolic structure associated with diarrhoeal remission using a combination of statistical, genomic, and proteomic approaches in a cattle model. Oral administration of the compost-derived thermophile Caldifermentibacillus hisashii significantly ameliorated persistent diarrhoea. Faecal bacterial populations and metabolites were characterised by a multi-step statistical pipeline comprising difference-in-differences (DID) analysis, Cliff's delta effect size estimation with permutation-based validation. The functional importance of the selected feature components was validated through genomic and proteomic analysis of C. hisashii N11 (AP028807.1).
RESULTS: Oral administration of C. hisashii significantly ameliorated persistent diarrhoea in calves. Although no significant differences in faecal bacterial community composition were observed, integrated analysis of faecal metabolites identified butyrate and 2-aminoisobutyrate (AIB) as the most discriminative features associated with diarrhoeal remission. Genomic and proteomic analyses of C. hisashii confirmed biosynthetic gene clusters for butyrate and AIB-containing lantibiotics, supporting the structural importance of these metabolites in diarrhoeal remission.
CONCLUSION: These findings suggest that diarrhoeal remission observed in this study involves characteristic shifts in faecal metabolite profiles rather than marked changes in overall gut microbial community composition, highlighting a protective role of C. hisashii as an environmental probiotic against diarrhoeal dysbiosis through modulation of gut microbial metabolic output. This offers a perspective that bridges environmental microbiology and gut health within a One Health framework. Video Abstract.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Probiotics/administration & dosage
*Diarrhea/veterinary/microbiology/therapy
Feces/microbiology
Cattle
*Gastrointestinal Microbiome
Proteomics
Butyrates/metabolism
Bacteriocins/genetics/biosynthesis
Administration, Oral
Genomics
Bacteria/classification/genetics/metabolism/isolation & purification
RevDate: 2026-08-07
Early-Life Antibiotic Exposure Disrupts Bifidobacterium in Infants: A qPCR-Based Cohort Study.
The Pediatric infectious disease journal pii:00006454-990000000-01811 [Epub ahead of print].
BACKGROUND: Early infancy represents a critical window for establishing the gut microbiome, during which Bifidobacterium species dominate and play essential roles in metabolic, immune and intestinal maturation. Antibiotic exposure during this sensitive period may disrupt microbial development, yet quantitative data on its longitudinal impact remain limited. To evaluate the effect of systemic antibiotic exposure during the first 6 months of life on the abundance of Bifidobacterium using quantitative real-time polymerase chain reaction in a prospective infant cohort.
METHODS: Seventy healthy term infants were enrolled at birth and followed at 1, 3 and 6 months. Stool samples were analyzed using quantitative real-time polymerase chain reaction targeting genus-level Bifidobacterium. Infants were categorized into antibiotic-exposed (n = 27) and nonexposed (n = 43). Demographic and clinical variables were compared, and longitudinal and multivariate analyses were used to assess factors associated with Bifidobacterium abundance.
RESULTS: No significant baseline differences were observed between groups. Antibiotic-exposed infants demonstrated significantly lower Bifidobacterium levels at all measured time points (P < 0.001). Nonexposed infants showed the expected rise in Bifidobacterium from 1 to 3 months, whereas exposed infants exhibited a significant decline from 1 to 6 months (P = 0.009). Multivariate regression analysis indicated that clinical factors, such as delivery mode, feeding type, gestational age and maternal intrapartum antibiotics, were not significant predictors of Bifidobacterium levels among exposed infants.
CONCLUSIONS: Antibiotic exposure in the first 6 months leads to persistent suppression of Bifidobacterium, disrupting normal microbiome maturation. These findings underscore the importance of cautious antibiotic use in early infancy and highlight the need for strategies to restore microbial balance following antibiotic therapy.
Additional Links: PMID-42563207
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PubMed:
Citation:
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@article {pmid42563207,
year = {2026},
author = {Abdel-Hady, DM and Sabry Zeid, M and Hamdy Mohamed, E and El Sayed Zaki, M and Mohamed Reda El-Lakany, R and Mohamed Reda Mahmoud El-Lakany, N and Ahmed Noureldin, M},
title = {Early-Life Antibiotic Exposure Disrupts Bifidobacterium in Infants: A qPCR-Based Cohort Study.},
journal = {The Pediatric infectious disease journal},
volume = {},
number = {},
pages = {},
doi = {10.1097/INF.0000000000005360},
pmid = {42563207},
issn = {1532-0987},
abstract = {BACKGROUND: Early infancy represents a critical window for establishing the gut microbiome, during which Bifidobacterium species dominate and play essential roles in metabolic, immune and intestinal maturation. Antibiotic exposure during this sensitive period may disrupt microbial development, yet quantitative data on its longitudinal impact remain limited. To evaluate the effect of systemic antibiotic exposure during the first 6 months of life on the abundance of Bifidobacterium using quantitative real-time polymerase chain reaction in a prospective infant cohort.
METHODS: Seventy healthy term infants were enrolled at birth and followed at 1, 3 and 6 months. Stool samples were analyzed using quantitative real-time polymerase chain reaction targeting genus-level Bifidobacterium. Infants were categorized into antibiotic-exposed (n = 27) and nonexposed (n = 43). Demographic and clinical variables were compared, and longitudinal and multivariate analyses were used to assess factors associated with Bifidobacterium abundance.
RESULTS: No significant baseline differences were observed between groups. Antibiotic-exposed infants demonstrated significantly lower Bifidobacterium levels at all measured time points (P < 0.001). Nonexposed infants showed the expected rise in Bifidobacterium from 1 to 3 months, whereas exposed infants exhibited a significant decline from 1 to 6 months (P = 0.009). Multivariate regression analysis indicated that clinical factors, such as delivery mode, feeding type, gestational age and maternal intrapartum antibiotics, were not significant predictors of Bifidobacterium levels among exposed infants.
CONCLUSIONS: Antibiotic exposure in the first 6 months leads to persistent suppression of Bifidobacterium, disrupting normal microbiome maturation. These findings underscore the importance of cautious antibiotic use in early infancy and highlight the need for strategies to restore microbial balance following antibiotic therapy.},
}
RevDate: 2026-08-07
Crop Resilience to Combined Drought and Salinity Stress in Drylands: From Soil Processes to Genomic Solutions.
Plant, cell & environment [Epub ahead of print].
Drought and soil salinization increasingly co‑occur, threatening global food security, particularly in dryland farming systems where these stresses can interact additively, synergistically or antagonistically to reduce crop yields. This review critically distinguishes these interaction types and moves beyond single‑stress frameworks to provide a multiscale synthesis of plant responses, soil water-salt dynamics, root‑system plasticity, rhizosphere microbiome modulation, emerging breeding modelling and agronomic tools. This review provides a detailed overview of the multilevel damage from these co-occurring stresses, including osmotic shock, ionic toxicity and systemic oxidative damage, and examines plant strategies such as ion homoeostasis, osmotic adjustment and antioxidant responses. Beyond plant-centric views, the review explores epigenetic reprogramming for stress memory and the potential of rhizosphere microbiome engineering with plant growth-promoting rhizobacteria as a biological stress-alleviation strategy. It critically examines how high-throughput multiomics techniques, combined with innovative breeding methods, provide a transformative approach to decode complex tolerance traits and accelerate cultivar development. These techniques cover genomics, epigenomics, transcriptomics, proteomics and metabolomics, while the breeding methods include genomic selection and CRISPR-Cas gene editing. Despite progress, key challenges remain: validating combined stress resilience under field conditions, harnessing epigenetic inheritance and integrating microbial solutions into breeding pipelines. We propose a unified framework that merges mechanistic discovery, microbiome-assisted breeding, soil and water management and systems-level predictive modelling. This integrative approach is essential for developing climate-resilient crops to sustain dryland agriculture.
Additional Links: PMID-42563405
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PubMed:
Citation:
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@article {pmid42563405,
year = {2026},
author = {Adil, M and Gul, I and Lu, S and Bashir, S and Razzaq, S and Lu, H and Daud, M and Iqbal, Y and Tao, Y},
title = {Crop Resilience to Combined Drought and Salinity Stress in Drylands: From Soil Processes to Genomic Solutions.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70804},
pmid = {42563405},
issn = {1365-3040},
support = {41871079//National Natural Science Foundation of China/ ; SKLECRA2023//Chinese Research Academy of Environmental Sciences/ ; //Open Foundation of State Key Laboratory of Environmental Criteria and Risk Assessment/ ; },
abstract = {Drought and soil salinization increasingly co‑occur, threatening global food security, particularly in dryland farming systems where these stresses can interact additively, synergistically or antagonistically to reduce crop yields. This review critically distinguishes these interaction types and moves beyond single‑stress frameworks to provide a multiscale synthesis of plant responses, soil water-salt dynamics, root‑system plasticity, rhizosphere microbiome modulation, emerging breeding modelling and agronomic tools. This review provides a detailed overview of the multilevel damage from these co-occurring stresses, including osmotic shock, ionic toxicity and systemic oxidative damage, and examines plant strategies such as ion homoeostasis, osmotic adjustment and antioxidant responses. Beyond plant-centric views, the review explores epigenetic reprogramming for stress memory and the potential of rhizosphere microbiome engineering with plant growth-promoting rhizobacteria as a biological stress-alleviation strategy. It critically examines how high-throughput multiomics techniques, combined with innovative breeding methods, provide a transformative approach to decode complex tolerance traits and accelerate cultivar development. These techniques cover genomics, epigenomics, transcriptomics, proteomics and metabolomics, while the breeding methods include genomic selection and CRISPR-Cas gene editing. Despite progress, key challenges remain: validating combined stress resilience under field conditions, harnessing epigenetic inheritance and integrating microbial solutions into breeding pipelines. We propose a unified framework that merges mechanistic discovery, microbiome-assisted breeding, soil and water management and systems-level predictive modelling. This integrative approach is essential for developing climate-resilient crops to sustain dryland agriculture.},
}
RevDate: 2026-08-07
Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.
American journal of physiology. Gastrointestinal and liver physiology [Epub ahead of print].
Metabolic syndrome (MetS), characterized by abdominal obesity, insulin resistance, dyslipidemia, and hypertension, affects a substantial proportion of the global population and increases the risk for cardiovascular disease, diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD). Despite its prevalence, there are currently no effective pharmacological therapies targeting MetS, highlighting the need to identify novel etiological mechanisms, particularly within the gastrointestinal (GI) tract. Using a mouse model of MetS and healthy lean controls, we assessed the colonic microenvironment through metabolomic, transcriptomic, and microbiome analyses. Colonic organoids were cultured to further explore epithelial alterations. Additionally, human MetS fecal metabolomics data were cross-compared with the mouse model to validate translational relevance. MetS mice exhibited upregulation of colonic anabolic pathways, including glycolysis, the pentose phosphate pathway, and the tryptophan/kynurenine pathway, without evidence of intestinal inflammation. Microbiome analysis revealed an increased abundance of the genus Lactobacillus in MS NASH mice. Colonic organoids from MetS mice showed altered goblet cell differentiation. Comparative analysis with human MetS fecal metabolomics demonstrated similar dysregulated pathways, underscoring the translational relevance of these findings. Our study reveals significant metabolic and microbial alterations in the colon of MS NASH mice, implicating a dysfunctional GI tract as a potential etiological factor in MetS. These findings highlight specific metabolic pathways and microbial signatures that could serve as future therapeutic targets for MetS.
Additional Links: PMID-42563426
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PubMed:
Citation:
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@article {pmid42563426,
year = {2026},
author = {Rivas, JA and Scieszka, DP and Peralta-Herrera, E and Madera Enriquez, C and Merkley, SD and Nava, AL and Gullapalli, RR and Guo, Y and Castillo, EF},
title = {Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00121.2026},
pmid = {42563426},
issn = {1522-1547},
support = {IRG-21-146-25//American Cancer Society (ACS)/ ; P30CA118100//Center for Strategic Scientific Initiatives, National Cancer Institute (CSSI)/ ; UL1TR001449//HHS | NIH | National Center for Advancing Translational Sciences (NCATS)/ ; P20GM121176//HHS | NIH | National Institute of General Medical Sciences (NIGMS)/ ; T32 GM144834//HHS | NIH | National Institute of General Medical Sciences (NIGMS)/ ; },
abstract = {Metabolic syndrome (MetS), characterized by abdominal obesity, insulin resistance, dyslipidemia, and hypertension, affects a substantial proportion of the global population and increases the risk for cardiovascular disease, diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD). Despite its prevalence, there are currently no effective pharmacological therapies targeting MetS, highlighting the need to identify novel etiological mechanisms, particularly within the gastrointestinal (GI) tract. Using a mouse model of MetS and healthy lean controls, we assessed the colonic microenvironment through metabolomic, transcriptomic, and microbiome analyses. Colonic organoids were cultured to further explore epithelial alterations. Additionally, human MetS fecal metabolomics data were cross-compared with the mouse model to validate translational relevance. MetS mice exhibited upregulation of colonic anabolic pathways, including glycolysis, the pentose phosphate pathway, and the tryptophan/kynurenine pathway, without evidence of intestinal inflammation. Microbiome analysis revealed an increased abundance of the genus Lactobacillus in MS NASH mice. Colonic organoids from MetS mice showed altered goblet cell differentiation. Comparative analysis with human MetS fecal metabolomics demonstrated similar dysregulated pathways, underscoring the translational relevance of these findings. Our study reveals significant metabolic and microbial alterations in the colon of MS NASH mice, implicating a dysfunctional GI tract as a potential etiological factor in MetS. These findings highlight specific metabolic pathways and microbial signatures that could serve as future therapeutic targets for MetS.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Mechanistic pathways linking gut microbial metabolites, microbial structural products, and host-microbe co-metabolites to mitochondrial function.
Gut microbes, 18(1):2694140.
Gut-derived microbial metabolites modulate host mitochondrial function. To our knowledge, no prior systematic review has synthesized evidence linking these metabolites to direct mitochondrial endpoints across all major metabolite classes. PubMed, Scopus, and Web of Science were systematically searched through March 2026 for studies examining direct mitochondrial endpoints in relation to ten classes of gut-derived metabolites. Gut-derived microbial metabolites exert diverse effects on mitochondrial function, ranging from bioenergetic enhancement to direct toxicity. After contextual evidence was excluded from the certainty assessment, four metabolite-mitochondrial outcome groupings had moderate certainty: butyrate, propionate, indoxyl sulfate, and lipopolysaccharide. Evidence for p-cresyl sulfate, H2S, and urolithin A was rated low; evidence for the remaining metabolite classes was low or very low. Butyrate generally enhances mitochondrial biogenesis, ATP generation, and electron transport chain activity across multiple experimental models. Indoxyl sulfate generally impaired mitochondrial function, whereas p-cresyl sulfate produced concentration- and model-dependent effects. PGC-1α emerges as a central regulatory node, integrating microbial metabolic signals to control mitochondrial biogenesis and oxidative metabolism. Many microbial metabolites demonstrate concentration-dependent biphasic effects. These findings support a mechanistic microbiome-mitochondrial framework in which diverse gut-derived molecules converge on a limited set of mitochondrial control nodes: electron transport chain activity, reactive oxygen species handling, biogenesis, and mitophagy. The evidence base is predominantly preclinical; these insights should be considered hypothesis-generating.
Additional Links: PMID-42563439
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@article {pmid42563439,
year = {2026},
author = {Frye, RE and Rossignol, DA},
title = {Mechanistic pathways linking gut microbial metabolites, microbial structural products, and host-microbe co-metabolites to mitochondrial function.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2694140},
doi = {10.1080/19490976.2026.2694140},
pmid = {42563439},
issn = {1949-0984},
mesh = {*Mitochondria/metabolism/physiology ; *Gastrointestinal Microbiome/physiology ; Humans ; Animals ; *Bacteria/metabolism/classification ; *Host Microbial Interactions ; Butyrates/metabolism ; Organelle Biogenesis ; Propionates/metabolism ; Cresols ; Sulfuric Acid Esters ; },
abstract = {Gut-derived microbial metabolites modulate host mitochondrial function. To our knowledge, no prior systematic review has synthesized evidence linking these metabolites to direct mitochondrial endpoints across all major metabolite classes. PubMed, Scopus, and Web of Science were systematically searched through March 2026 for studies examining direct mitochondrial endpoints in relation to ten classes of gut-derived metabolites. Gut-derived microbial metabolites exert diverse effects on mitochondrial function, ranging from bioenergetic enhancement to direct toxicity. After contextual evidence was excluded from the certainty assessment, four metabolite-mitochondrial outcome groupings had moderate certainty: butyrate, propionate, indoxyl sulfate, and lipopolysaccharide. Evidence for p-cresyl sulfate, H2S, and urolithin A was rated low; evidence for the remaining metabolite classes was low or very low. Butyrate generally enhances mitochondrial biogenesis, ATP generation, and electron transport chain activity across multiple experimental models. Indoxyl sulfate generally impaired mitochondrial function, whereas p-cresyl sulfate produced concentration- and model-dependent effects. PGC-1α emerges as a central regulatory node, integrating microbial metabolic signals to control mitochondrial biogenesis and oxidative metabolism. Many microbial metabolites demonstrate concentration-dependent biphasic effects. These findings support a mechanistic microbiome-mitochondrial framework in which diverse gut-derived molecules converge on a limited set of mitochondrial control nodes: electron transport chain activity, reactive oxygen species handling, biogenesis, and mitophagy. The evidence base is predominantly preclinical; these insights should be considered hypothesis-generating.},
}
MeSH Terms:
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*Mitochondria/metabolism/physiology
*Gastrointestinal Microbiome/physiology
Humans
Animals
*Bacteria/metabolism/classification
*Host Microbial Interactions
Butyrates/metabolism
Organelle Biogenesis
Propionates/metabolism
Cresols
Sulfuric Acid Esters
RevDate: 2026-08-07
The gut microbiome plays a modifiable role in MS progression?-Commentary.
Multiple sclerosis (Houndmills, Basingstoke, England) [Epub ahead of print].
Additional Links: PMID-42563483
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PubMed:
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@article {pmid42563483,
year = {2026},
author = {Hedström, AK},
title = {The gut microbiome plays a modifiable role in MS progression?-Commentary.},
journal = {Multiple sclerosis (Houndmills, Basingstoke, England)},
volume = {},
number = {},
pages = {13524585261471368},
doi = {10.1177/13524585261471368},
pmid = {42563483},
issn = {1477-0970},
}
RevDate: 2026-08-07
The gut microbiome plays a modifiable role in MS progression-No.
Multiple sclerosis (Houndmills, Basingstoke, England) [Epub ahead of print].
Additional Links: PMID-42563487
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PubMed:
Citation:
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@article {pmid42563487,
year = {2026},
author = {Afzal, S and Fox, RJ},
title = {The gut microbiome plays a modifiable role in MS progression-No.},
journal = {Multiple sclerosis (Houndmills, Basingstoke, England)},
volume = {},
number = {},
pages = {13524585261471355},
doi = {10.1177/13524585261471355},
pmid = {42563487},
issn = {1477-0970},
}
RevDate: 2026-08-07
From Gut to Heart: The Emerging Role of Dietary Fermentable Fiber in Heart Failure with Preserved Ejection Fraction.
American journal of physiology. Heart and circulatory physiology [Epub ahead of print].
Heart failure with preserved ejection fraction (HFpEF) is a multisystemic syndrome that accounts for more than half of all heart failure cases and causes a substantial burden of morbidity and mortality. In contrast to heart failure with reduced ejection fraction (HFrEF), few disease-modifying therapies exist for HFpEF, reflecting differences in pathophysiology. Low fermentable fiber (FF) intake, gut dysbiosis, and depletion of short-chain fatty acids (SCFAs), microbial metabolites central to immune, metabolic, and vascular homeostasis, are increasingly linked to the pathophysiology of HFpEF. Here, we synthesize preclinical and clinical evidence on FF and SCFAs and evaluate their therapeutic relevance to HFpEF. Preclinical studies demonstrate that FF supplementation or direct SCFA administration improves cardiometabolic function and attenuates cardiac remodeling through SCFA receptor signaling, enhanced nitric oxide bioavailability, reduced inflammation, and metabolic support of the energy-starved failing heart. Supporting the translational relevance of these findings, a systematic review of 27 human randomized controlled trials showed that FF interventions exert microbiome-mediated effects, enriching SCFA-producing taxa and augmenting fecal and circulating SCFA levels, while improving insulin sensitivity and reducing abdominal adiposity and LDL cholesterol. Direct SCFA supplementation increases SCFA availability and provides modest metabolic benefits, including reduced adiposity and liver fat. However, its effects are inconsistent. Collectively, these findings provide a mechanistic and translational rationale for FF-based interventions in HFpEF. To date, no clinical trials have evaluated the effects of FF on HFpEF-specific outcomes. Clinical studies are therefore needed to determine whether increasing FF intake can improve symptoms, cardiac function, and disease progression in HFpEF.
Additional Links: PMID-42563498
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Citation:
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@article {pmid42563498,
year = {2026},
author = {Darbar, F and Priyadarshini, M and Wang, Y and Safdary, Z and Mahmoud, AM and DiDomenico, RJ and Rosas, P},
title = {From Gut to Heart: The Emerging Role of Dietary Fermentable Fiber in Heart Failure with Preserved Ejection Fraction.},
journal = {American journal of physiology. Heart and circulatory physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpheart.00177.2026},
pmid = {42563498},
issn = {1522-1539},
support = {K01HL155241//HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; },
abstract = {Heart failure with preserved ejection fraction (HFpEF) is a multisystemic syndrome that accounts for more than half of all heart failure cases and causes a substantial burden of morbidity and mortality. In contrast to heart failure with reduced ejection fraction (HFrEF), few disease-modifying therapies exist for HFpEF, reflecting differences in pathophysiology. Low fermentable fiber (FF) intake, gut dysbiosis, and depletion of short-chain fatty acids (SCFAs), microbial metabolites central to immune, metabolic, and vascular homeostasis, are increasingly linked to the pathophysiology of HFpEF. Here, we synthesize preclinical and clinical evidence on FF and SCFAs and evaluate their therapeutic relevance to HFpEF. Preclinical studies demonstrate that FF supplementation or direct SCFA administration improves cardiometabolic function and attenuates cardiac remodeling through SCFA receptor signaling, enhanced nitric oxide bioavailability, reduced inflammation, and metabolic support of the energy-starved failing heart. Supporting the translational relevance of these findings, a systematic review of 27 human randomized controlled trials showed that FF interventions exert microbiome-mediated effects, enriching SCFA-producing taxa and augmenting fecal and circulating SCFA levels, while improving insulin sensitivity and reducing abdominal adiposity and LDL cholesterol. Direct SCFA supplementation increases SCFA availability and provides modest metabolic benefits, including reduced adiposity and liver fat. However, its effects are inconsistent. Collectively, these findings provide a mechanistic and translational rationale for FF-based interventions in HFpEF. To date, no clinical trials have evaluated the effects of FF on HFpEF-specific outcomes. Clinical studies are therefore needed to determine whether increasing FF intake can improve symptoms, cardiac function, and disease progression in HFpEF.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Multi‑omics insights into uveitis: From mechanisms to precision medicine (Review).
International journal of molecular medicine, 58(4):.
Uveitis encompasses a group of intraocular inflammatory disorders that notably contribute to global visual morbidity. Persistent challenges include early diagnosis, accurate subtype classification and individualized treatment. Recent advances in omics technologies, including genomics, epigenetics, transcriptomics, single‑cell omics, proteomics, metabolomics, lipidomics and microbiome profiling, have reshaped the current understanding of uveitis pathogenesis by uncovering disease‑associated genetic variants, dynamic transcriptional landscapes, inflammatory proteins, metabolic alterations, and microbe‑host interactions. Notably, single‑cell RNA sequencing offers unprecedented insights into retinal immune cell heterogeneity and functional states, while radiomics is emerging as a valuable platform for imaging biomarkers. The present review summarizes key findings from multi‑omics studies in uveitis, described the sample sources and analytical strategies employed, and highlighted the transformative potential of integrative omics in precision ophthalmology. Multi‑omics approaches hold promise for identifying novel biomarkers and therapeutic targets, refining disease classification, and enabling tailored interventions for patients with uveitis.
Additional Links: PMID-42563687
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PubMed:
Citation:
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@article {pmid42563687,
year = {2026},
author = {Liu, C and Wu, Q and Yuan, M and Liu, M and Wang, X and Shen, J and Cao, X},
title = {Multi‑omics insights into uveitis: From mechanisms to precision medicine (Review).},
journal = {International journal of molecular medicine},
volume = {58},
number = {4},
pages = {},
doi = {10.3892/ijmm.2026.5947},
pmid = {42563687},
issn = {1791-244X},
mesh = {Humans ; Multiomics ; *Uveitis/genetics/metabolism/therapy/diagnosis ; *Precision Medicine/methods ; Biomarkers/metabolism ; Genomics/methods ; Metabolomics/methods ; Proteomics/methods ; Animals ; },
abstract = {Uveitis encompasses a group of intraocular inflammatory disorders that notably contribute to global visual morbidity. Persistent challenges include early diagnosis, accurate subtype classification and individualized treatment. Recent advances in omics technologies, including genomics, epigenetics, transcriptomics, single‑cell omics, proteomics, metabolomics, lipidomics and microbiome profiling, have reshaped the current understanding of uveitis pathogenesis by uncovering disease‑associated genetic variants, dynamic transcriptional landscapes, inflammatory proteins, metabolic alterations, and microbe‑host interactions. Notably, single‑cell RNA sequencing offers unprecedented insights into retinal immune cell heterogeneity and functional states, while radiomics is emerging as a valuable platform for imaging biomarkers. The present review summarizes key findings from multi‑omics studies in uveitis, described the sample sources and analytical strategies employed, and highlighted the transformative potential of integrative omics in precision ophthalmology. Multi‑omics approaches hold promise for identifying novel biomarkers and therapeutic targets, refining disease classification, and enabling tailored interventions for patients with uveitis.},
}
MeSH Terms:
show MeSH Terms
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Humans
Multiomics
*Uveitis/genetics/metabolism/therapy/diagnosis
*Precision Medicine/methods
Biomarkers/metabolism
Genomics/methods
Metabolomics/methods
Proteomics/methods
Animals
RevDate: 2026-08-07
CmpDate: 2026-08-07
Clinical effects of a 0.5% selenium sulfide shampoo on dandruff and scalp microbiota in adolescents: a prospective single-arm clinical study.
Frontiers in medicine, 13:1866777.
INTRODUCTION: This prospective, exploratory single-arm pilot study evaluated the clinical efficacy, safety, and scalp microecological effects of a 0.5% selenium sulfide shampoo in adolescents with dandruff.
METHODS: Following a 2-week washout, 31 adolescents applied the shampoo three to four times weekly for 4 weeks. Investigator assessments, patient-reported pruritus scores, instrumental assessments (transepidermal water loss, stratum corneum hydration, sebum spot size), and scalp microbiome analysis were performed at baseline (week 0) and at week 4 (or week 2 for some measures).
RESULTS: Investigator assessments showed significant improvements: median dandruff scores declined from 16 to 6, erythema scores from 12 to 2, total scalp oiliness scores from 153 to 127, and total hair lift scores increased from 107 to 122 at week 4. Patient-reported pruritus scores decreased from 109 at baseline to 60, 48, and 37 at weeks 1, 2, and 4, respectively (P<0.001). Instrumental assessments demonstrated reduced transepidermal water loss (35.66 ± 8.18 to 31.12 ± 4.36 g/m[2]·h, P < 0.01), increased stratum corneum hydration (30.49 ± 10.28 to 35.01 ± 9.64 a.u., P < 0.001), and decreased sebum spot size at week 2 (953.65 ± 892.50 to 692.33 ± 456.19 pixels, P < 0.05). Genus-level microbiome profiling revealed significantly elevated Cutibacterium abundance (P < 0.001), alongside reduced levels of Staphylococcus and Malassezia (both P < 0.01). No adverse events were reported.
CONCLUSION: The 0.5% selenium sulfide shampoo significantly improved clinical symptoms of dandruff in adolescents, with favorable safety, barrier-protective effects, promoted beneficial compositional shifts in the scalp microbial community toward a healthier profile.
Additional Links: PMID-42564041
PubMed:
Citation:
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@article {pmid42564041,
year = {2026},
author = {Jiang, W and Zhang, R and Wang, L and Xu, Y and Tan, Y},
title = {Clinical effects of a 0.5% selenium sulfide shampoo on dandruff and scalp microbiota in adolescents: a prospective single-arm clinical study.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1866777},
pmid = {42564041},
issn = {2296-858X},
abstract = {INTRODUCTION: This prospective, exploratory single-arm pilot study evaluated the clinical efficacy, safety, and scalp microecological effects of a 0.5% selenium sulfide shampoo in adolescents with dandruff.
METHODS: Following a 2-week washout, 31 adolescents applied the shampoo three to four times weekly for 4 weeks. Investigator assessments, patient-reported pruritus scores, instrumental assessments (transepidermal water loss, stratum corneum hydration, sebum spot size), and scalp microbiome analysis were performed at baseline (week 0) and at week 4 (or week 2 for some measures).
RESULTS: Investigator assessments showed significant improvements: median dandruff scores declined from 16 to 6, erythema scores from 12 to 2, total scalp oiliness scores from 153 to 127, and total hair lift scores increased from 107 to 122 at week 4. Patient-reported pruritus scores decreased from 109 at baseline to 60, 48, and 37 at weeks 1, 2, and 4, respectively (P<0.001). Instrumental assessments demonstrated reduced transepidermal water loss (35.66 ± 8.18 to 31.12 ± 4.36 g/m[2]·h, P < 0.01), increased stratum corneum hydration (30.49 ± 10.28 to 35.01 ± 9.64 a.u., P < 0.001), and decreased sebum spot size at week 2 (953.65 ± 892.50 to 692.33 ± 456.19 pixels, P < 0.05). Genus-level microbiome profiling revealed significantly elevated Cutibacterium abundance (P < 0.001), alongside reduced levels of Staphylococcus and Malassezia (both P < 0.01). No adverse events were reported.
CONCLUSION: The 0.5% selenium sulfide shampoo significantly improved clinical symptoms of dandruff in adolescents, with favorable safety, barrier-protective effects, promoted beneficial compositional shifts in the scalp microbial community toward a healthier profile.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Bryophytes in heavy metal-polluted environments: trait-based sensitivity, tolerance mechanisms, biomonitoring applications, and restoration potential.
Frontiers in plant science, 17:1891423.
Heavy metal contamination remains a persistent environmental challenge due to its non-degradable nature, long residence time, and cumulative ecological impacts. Bryophytes have long been recognized as effective bioindicators because of their high sensitivity and strong metal accumulation capacity. However, current research on bryophyte-metal interactions remains fragmented, with limited integration between mechanistic understanding and ecological application. In this review, we develop a trait-informed, hypothesis-generating framework that links bryophyte characteristics to heavy metal exposure, physiological responses, and ecological functions. We first examine the structural, physicochemical, and ecological attributes that govern metal interception and exposure variability, and then synthesize current evidence for extracellular immobilization, intracellular detoxification, regulatory coordination, redox buffering, and metabolic reprogramming. We further evaluate bryophyte-associated microbiomes while distinguishing functional plausibility from direct causal evidence. On the applied side, we assess bryophytes as biologically interpretable biomonitoring systems and as realistic agents of ecological stabilization and engineered biosorption. Finally, we identify key limitations, including taxonomic bias, inconsistent trait parameterization, limited experimental validation, and challenges in translating laboratory findings to field conditions. This framework currently supports directional and testable expectations rather than universal quantitative prediction, and its predictive capacity will depend on standardized cross-species experiments and field validation.
Additional Links: PMID-42564062
PubMed:
Citation:
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@article {pmid42564062,
year = {2026},
author = {Huang, WZ and Huang, W and Jin, LZ and Yu, CH and Yu, MJ and Chen, WW and Wu, YH},
title = {Bryophytes in heavy metal-polluted environments: trait-based sensitivity, tolerance mechanisms, biomonitoring applications, and restoration potential.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1891423},
pmid = {42564062},
issn = {1664-462X},
abstract = {Heavy metal contamination remains a persistent environmental challenge due to its non-degradable nature, long residence time, and cumulative ecological impacts. Bryophytes have long been recognized as effective bioindicators because of their high sensitivity and strong metal accumulation capacity. However, current research on bryophyte-metal interactions remains fragmented, with limited integration between mechanistic understanding and ecological application. In this review, we develop a trait-informed, hypothesis-generating framework that links bryophyte characteristics to heavy metal exposure, physiological responses, and ecological functions. We first examine the structural, physicochemical, and ecological attributes that govern metal interception and exposure variability, and then synthesize current evidence for extracellular immobilization, intracellular detoxification, regulatory coordination, redox buffering, and metabolic reprogramming. We further evaluate bryophyte-associated microbiomes while distinguishing functional plausibility from direct causal evidence. On the applied side, we assess bryophytes as biologically interpretable biomonitoring systems and as realistic agents of ecological stabilization and engineered biosorption. Finally, we identify key limitations, including taxonomic bias, inconsistent trait parameterization, limited experimental validation, and challenges in translating laboratory findings to field conditions. This framework currently supports directional and testable expectations rather than universal quantitative prediction, and its predictive capacity will depend on standardized cross-species experiments and field validation.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Bacterial and gut microbiota-derived extracellular vesicles as emerging sources of cancer biomarkers: molecular mechanisms, diagnostic approaches, and therapeutic applications.
Frontiers in cellular and infection microbiology, 16:1806945.
Extracellular vesicles (EVs) originating from bacteria and gut microbiota have recently been recognized as pivotal agents in the communication between host and microbes, exhibiting considerable promise as innovative biomarkers and therapeutic instruments in the realm of oncology. These nanoscale vesicles encapsulate a heterogeneous array of molecular constituents, including metabolites, proteins, nucleic acids, and toxins, which possess the capacity to influence tumor proliferation, apoptosis, immune responses, and metastasis. Recent investigations underscore their bifunctional nature: specific bacterial EVs can facilitate oncogenesis by altering signaling cascades such as BRCA1/EXO1/TP53BP1 or TGF-β1/Smad, while others may suppress tumor growth through the induction of oxidative stress, mitophagy, or the activation of antitumor immunity via STING or cGAS pathways. The metabolomic and molecular characterizations of bacterial and fecal EVs afford a distinctive, non-invasive perspective into tumor biology and the interactions between host and microbiome. Sophisticated diagnostic methodologies, encompassing targeted metabolomics, high-throughput sequencing, and flow cytometry-based characterization of EVs, have enabled the discovery of EV-derived cancer biomarkers with exceptional specificity and sensitivity. Moreover, engineered EVs that transport therapeutic agents, including prodrugs, microRNAs, or photosensitizers, exhibit significant anticancer efficacy in preclinical experimental models. This review consolidates contemporary understanding regarding the molecular mechanisms, diagnostic capabilities, and therapeutic implications of bacterial and gut microbiota-derived EVs in the context of cancer.
Additional Links: PMID-42564071
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Citation:
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@article {pmid42564071,
year = {2026},
author = {Ying, H},
title = {Bacterial and gut microbiota-derived extracellular vesicles as emerging sources of cancer biomarkers: molecular mechanisms, diagnostic approaches, and therapeutic applications.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1806945},
pmid = {42564071},
issn = {2235-2988},
mesh = {Humans ; *Extracellular Vesicles/metabolism ; *Biomarkers, Tumor/metabolism ; *Neoplasms/diagnosis/therapy ; *Gastrointestinal Microbiome ; *Bacteria/metabolism ; Animals ; },
abstract = {Extracellular vesicles (EVs) originating from bacteria and gut microbiota have recently been recognized as pivotal agents in the communication between host and microbes, exhibiting considerable promise as innovative biomarkers and therapeutic instruments in the realm of oncology. These nanoscale vesicles encapsulate a heterogeneous array of molecular constituents, including metabolites, proteins, nucleic acids, and toxins, which possess the capacity to influence tumor proliferation, apoptosis, immune responses, and metastasis. Recent investigations underscore their bifunctional nature: specific bacterial EVs can facilitate oncogenesis by altering signaling cascades such as BRCA1/EXO1/TP53BP1 or TGF-β1/Smad, while others may suppress tumor growth through the induction of oxidative stress, mitophagy, or the activation of antitumor immunity via STING or cGAS pathways. The metabolomic and molecular characterizations of bacterial and fecal EVs afford a distinctive, non-invasive perspective into tumor biology and the interactions between host and microbiome. Sophisticated diagnostic methodologies, encompassing targeted metabolomics, high-throughput sequencing, and flow cytometry-based characterization of EVs, have enabled the discovery of EV-derived cancer biomarkers with exceptional specificity and sensitivity. Moreover, engineered EVs that transport therapeutic agents, including prodrugs, microRNAs, or photosensitizers, exhibit significant anticancer efficacy in preclinical experimental models. This review consolidates contemporary understanding regarding the molecular mechanisms, diagnostic capabilities, and therapeutic implications of bacterial and gut microbiota-derived EVs in the context of cancer.},
}
MeSH Terms:
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Humans
*Extracellular Vesicles/metabolism
*Biomarkers, Tumor/metabolism
*Neoplasms/diagnosis/therapy
*Gastrointestinal Microbiome
*Bacteria/metabolism
Animals
RevDate: 2026-08-07
CmpDate: 2026-08-07
Microbiome as a prediction of immunotherapy response in lung cancer.
Frontiers in immunology, 17:1849553.
Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of lung cancer (LC), offering durable responses in non-small cell lung cancer (NSCLC) and, to a lesser extent, small cell lung cancer (SCLC). Nevertheless, clinical outcomes remain highly heterogeneous, with many patients experiencing primary or acquired resistance and/or immune-related adverse events (irAEs) that impair their quality of life and treatment adherence. The human microbiome, particularly in the gut and oral compartments, has emerged as a critical modulator of systemic antitumor immunity and a promising noninvasive predictive biomarker for ICI efficacy and toxicity. This narrative review synthesizes the current evidence on microbiome composition, diversity, and function in patients with LC receiving ICIs as monotherapy, dual blockade, or in combination regimens, as well as clinically relevant biomarkers associated with treatment response and toxicity. Higher gut microbial alpha diversity and enrichment of beneficial taxa (e.g., Akkermansia muciniphila, Faecalibacterium prausnitzii, and certain Firmicutes) are consistently linked to improved progression-free survival (PFS) and overall survival (OS), mediated by microbial metabolites such as short-chain fatty acids and inosine, which enhance T-cell priming, tumor microenvironment remodeling, and gut-lung axis communication. Microbiome-disruptive exposures, particularly antibiotics and proton pump inhibitors (PPIs), induce dysbiosis and are strongly associated with poorer survival outcomes. Mechanistic insights from preclinical models and clinical cohorts, alongside clinical confounders, underscore the complementary role of the microbiome relative to established markers such as programmed death-ligand 1 (PD-L1) and tumor mutational burden. Prospective standardization of metagenomic profiling and microbiome-modulating interventions represents a key next step in translating these findings into personalized immunotherapy strategies for LC.
Additional Links: PMID-42564172
PubMed:
Citation:
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@article {pmid42564172,
year = {2026},
author = {Rojas, L and Zuluaga, J and Cardona, AF},
title = {Microbiome as a prediction of immunotherapy response in lung cancer.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1849553},
pmid = {42564172},
issn = {1664-3224},
mesh = {Humans ; *Lung Neoplasms/immunology/drug therapy/microbiology/therapy ; *Immune Checkpoint Inhibitors/therapeutic use/adverse effects ; *Immunotherapy/methods ; *Gastrointestinal Microbiome/immunology/drug effects ; Treatment Outcome ; Animals ; *Microbiota/immunology ; },
abstract = {Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of lung cancer (LC), offering durable responses in non-small cell lung cancer (NSCLC) and, to a lesser extent, small cell lung cancer (SCLC). Nevertheless, clinical outcomes remain highly heterogeneous, with many patients experiencing primary or acquired resistance and/or immune-related adverse events (irAEs) that impair their quality of life and treatment adherence. The human microbiome, particularly in the gut and oral compartments, has emerged as a critical modulator of systemic antitumor immunity and a promising noninvasive predictive biomarker for ICI efficacy and toxicity. This narrative review synthesizes the current evidence on microbiome composition, diversity, and function in patients with LC receiving ICIs as monotherapy, dual blockade, or in combination regimens, as well as clinically relevant biomarkers associated with treatment response and toxicity. Higher gut microbial alpha diversity and enrichment of beneficial taxa (e.g., Akkermansia muciniphila, Faecalibacterium prausnitzii, and certain Firmicutes) are consistently linked to improved progression-free survival (PFS) and overall survival (OS), mediated by microbial metabolites such as short-chain fatty acids and inosine, which enhance T-cell priming, tumor microenvironment remodeling, and gut-lung axis communication. Microbiome-disruptive exposures, particularly antibiotics and proton pump inhibitors (PPIs), induce dysbiosis and are strongly associated with poorer survival outcomes. Mechanistic insights from preclinical models and clinical cohorts, alongside clinical confounders, underscore the complementary role of the microbiome relative to established markers such as programmed death-ligand 1 (PD-L1) and tumor mutational burden. Prospective standardization of metagenomic profiling and microbiome-modulating interventions represents a key next step in translating these findings into personalized immunotherapy strategies for LC.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Lung Neoplasms/immunology/drug therapy/microbiology/therapy
*Immune Checkpoint Inhibitors/therapeutic use/adverse effects
*Immunotherapy/methods
*Gastrointestinal Microbiome/immunology/drug effects
Treatment Outcome
Animals
*Microbiota/immunology
RevDate: 2026-08-07
CmpDate: 2026-08-07
Rhizosphere microbiomes in drought-tolerant and drought-sensitive bermudagrass genotypes: root exudate association.
Frontiers in microbiology, 17:1868900.
INTRODUCTION: Plant-microbiome interactions in the rhizosphere are critical for plant adaptation to environmental stress; however, the coordinated roles of root exudates and microbiome dynamics remain poorly understood.
METHODS: Integrating untargeted metabolomics and shotgun metagenomics, we analyzed drought responses in drought-tolerant and drought-sensitive bermudagrass genotypes.
RESULTS: Drought stress shaped the root exudate chemistry, which likely reprogrammed microbiome functions, such as TccC toxins and the Type VI secretion system, without considerable broad taxonomic shifts. A few metabolites, including riboflavin and 1-carboxy-6-hydroxy-3,4-dihydro-beta-carboline, were associated with Massilia putida, particularly in the rhizosphere of the drought-tolerant genotype.
DISCUSSION: Our data suggest a potential explanation for a genotype-driven strategy of microbiome modulation via metabolite signaling.
Additional Links: PMID-42564309
PubMed:
Citation:
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@article {pmid42564309,
year = {2026},
author = {Akther, SM and Krakko, D and Shi, W},
title = {Rhizosphere microbiomes in drought-tolerant and drought-sensitive bermudagrass genotypes: root exudate association.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1868900},
pmid = {42564309},
issn = {1664-302X},
abstract = {INTRODUCTION: Plant-microbiome interactions in the rhizosphere are critical for plant adaptation to environmental stress; however, the coordinated roles of root exudates and microbiome dynamics remain poorly understood.
METHODS: Integrating untargeted metabolomics and shotgun metagenomics, we analyzed drought responses in drought-tolerant and drought-sensitive bermudagrass genotypes.
RESULTS: Drought stress shaped the root exudate chemistry, which likely reprogrammed microbiome functions, such as TccC toxins and the Type VI secretion system, without considerable broad taxonomic shifts. A few metabolites, including riboflavin and 1-carboxy-6-hydroxy-3,4-dihydro-beta-carboline, were associated with Massilia putida, particularly in the rhizosphere of the drought-tolerant genotype.
DISCUSSION: Our data suggest a potential explanation for a genotype-driven strategy of microbiome modulation via metabolite signaling.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Gut microbiota in asthma: mechanisms, clinical evidence, and therapeutic opportunities.
Frontiers in cellular and infection microbiology, 16:1842331.
Asthma is a heterogeneous chronic airway inflammatory disease associated with high global prevalence and substantial clinical burden. Conventional therapies remain limited in controlling refractory phenotypes and preventing disease progression. The gut-lung axis has emerged as a fundamental regulatory network connecting intestinal homeostasis with pulmonary immune function, and mounting evidence has established a close mechanistic link between gut dysbiosis and the onset, persistence, and exacerbation of asthma. This review comprehensively integrates evidence from epidemiological investigations, animal models, clinical observational studies, and randomized controlled trials published between 2011 and 2025 to elucidate the crosstalk mechanisms of the gut-lung axis in asthma, characterize compositional and functional alterations of the gut microbiome, evaluate microbiota-targeted interventions such as probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation, and discuss current translational challenges. We highlight that the gut microbiota orchestrates airway inflammatory responses through fine-tuning immune cell differentiation, mediating microbial metabolite signaling, and maintaining intestinal barrier function, with discernible microbial signatures evident across allergic versus non-allergic and pediatric versus adult asthma phenotypes. Despite promising preclinical and preliminary clinical findings, causal evidence remains insufficient, and intervention heterogeneity limits clinical application. This review underscores the potential of microbiome-based precision strategies and identifies key directions for future mechanistic research and clinical translation.
Additional Links: PMID-42564344
PubMed:
Citation:
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@article {pmid42564344,
year = {2026},
author = {Ruan, Z and Sheng, F and Lin, M and Wu, S and Hu, C and Shao, Z and Hu, H and Xu, L},
title = {Gut microbiota in asthma: mechanisms, clinical evidence, and therapeutic opportunities.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1842331},
pmid = {42564344},
issn = {2235-2988},
mesh = {Humans ; *Asthma/therapy/microbiology/immunology ; Animals ; *Gastrointestinal Microbiome ; Dysbiosis ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Disease Models, Animal ; Lung/immunology ; Prebiotics/administration & dosage ; },
abstract = {Asthma is a heterogeneous chronic airway inflammatory disease associated with high global prevalence and substantial clinical burden. Conventional therapies remain limited in controlling refractory phenotypes and preventing disease progression. The gut-lung axis has emerged as a fundamental regulatory network connecting intestinal homeostasis with pulmonary immune function, and mounting evidence has established a close mechanistic link between gut dysbiosis and the onset, persistence, and exacerbation of asthma. This review comprehensively integrates evidence from epidemiological investigations, animal models, clinical observational studies, and randomized controlled trials published between 2011 and 2025 to elucidate the crosstalk mechanisms of the gut-lung axis in asthma, characterize compositional and functional alterations of the gut microbiome, evaluate microbiota-targeted interventions such as probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation, and discuss current translational challenges. We highlight that the gut microbiota orchestrates airway inflammatory responses through fine-tuning immune cell differentiation, mediating microbial metabolite signaling, and maintaining intestinal barrier function, with discernible microbial signatures evident across allergic versus non-allergic and pediatric versus adult asthma phenotypes. Despite promising preclinical and preliminary clinical findings, causal evidence remains insufficient, and intervention heterogeneity limits clinical application. This review underscores the potential of microbiome-based precision strategies and identifies key directions for future mechanistic research and clinical translation.},
}
MeSH Terms:
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Humans
*Asthma/therapy/microbiology/immunology
Animals
*Gastrointestinal Microbiome
Dysbiosis
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Disease Models, Animal
Lung/immunology
Prebiotics/administration & dosage
RevDate: 2026-08-07
CmpDate: 2026-08-07
Pharmaceutical wastewater irrigation and metabolite-based environmental pharmacognosy: a perspective on quality and safety risks for medicinal plants.
Frontiers in pharmacology, 17:1878168.
Medicinal plants are increasingly cultivated in agroecosystems irrigated with treated or untreated wastewater, biosolids and contaminated surface water. Pharmaceutical residues are recognised contaminants of emerging concern, but their implications for botanical-drug quality, therapeutic consistency and safety remain insufficiently characterised. This Perspective argues that pharmaceutical wastewater irrigation is a plausible yet underexamined driver of metabolite reprogramming in medicinal plants. Chronic exposure to antibiotics, non-steroidal anti-inflammatory drugs, antiepileptics, antidepressants, hormones and transformation products may alter secondary metabolism through oxidative stress, xenobiotic detoxification, rhizosphere microbiome disturbance and modified nutrient signalling. These processes may change phenolic, flavonoid, alkaloid, terpenoid, glycoside and volatile metabolites that underpin pharmacognostic quality and ethnopharmacological reliability. Medicinal plants may also accumulate parent pharmaceuticals, transformation products and, under some conditions, microbial signatures associated with antibiotic resistance. Building on Carter et al.'s source-pathway-receptor framework and Helmecke et al.'s regulatory risk synthesis, we shift attention from residue burden to how exposure history alters the medicinal metabolome. Evidence from antibiotic-induced metabolite changes in Pinellia ternata supports this proposition, while indicating compound- and context-specific effects. We advance a balanced position: metabolite reprogramming is biologically credible, but food-crop studies often report de minimis residue risks and inconsistent rhizosphere-resistome effects. Future work should integrate wastewater profiling, matched controls, targeted and untargeted metabolomics, transformation-product discovery, microbiome analysis, digestion and bioaccessibility testing, bioactivity assays and probabilistic mixture-risk assessment.
Additional Links: PMID-42564438
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Citation:
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@article {pmid42564438,
year = {2026},
author = {Diovu, EO and Nnadi, CO and Paul-Chima, UO},
title = {Pharmaceutical wastewater irrigation and metabolite-based environmental pharmacognosy: a perspective on quality and safety risks for medicinal plants.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1878168},
pmid = {42564438},
issn = {1663-9812},
abstract = {Medicinal plants are increasingly cultivated in agroecosystems irrigated with treated or untreated wastewater, biosolids and contaminated surface water. Pharmaceutical residues are recognised contaminants of emerging concern, but their implications for botanical-drug quality, therapeutic consistency and safety remain insufficiently characterised. This Perspective argues that pharmaceutical wastewater irrigation is a plausible yet underexamined driver of metabolite reprogramming in medicinal plants. Chronic exposure to antibiotics, non-steroidal anti-inflammatory drugs, antiepileptics, antidepressants, hormones and transformation products may alter secondary metabolism through oxidative stress, xenobiotic detoxification, rhizosphere microbiome disturbance and modified nutrient signalling. These processes may change phenolic, flavonoid, alkaloid, terpenoid, glycoside and volatile metabolites that underpin pharmacognostic quality and ethnopharmacological reliability. Medicinal plants may also accumulate parent pharmaceuticals, transformation products and, under some conditions, microbial signatures associated with antibiotic resistance. Building on Carter et al.'s source-pathway-receptor framework and Helmecke et al.'s regulatory risk synthesis, we shift attention from residue burden to how exposure history alters the medicinal metabolome. Evidence from antibiotic-induced metabolite changes in Pinellia ternata supports this proposition, while indicating compound- and context-specific effects. We advance a balanced position: metabolite reprogramming is biologically credible, but food-crop studies often report de minimis residue risks and inconsistent rhizosphere-resistome effects. Future work should integrate wastewater profiling, matched controls, targeted and untargeted metabolomics, transformation-product discovery, microbiome analysis, digestion and bioaccessibility testing, bioactivity assays and probabilistic mixture-risk assessment.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Faecal carriage of multidrug-resistant Enterobacterales in hospitalisaed and outpatient children in northern India: A cross-sectional study.
African journal of laboratory medicine, 15(1):3027.
BACKGROUND: Asymptomatic intestinal carriage of multidrug-resistant (MDR) Enterobacterales in children is increasingly recognised as an important reservoir for transmission and subsequent infection. However, data from northern India remain limited, warranting evaluation of its burden and associated risk factors.
OBJECTIVE: To determine the prevalence of MDR Enterobacterales carriage among children and to identify associated risk factors, including recent hospitalisation, antimicrobial exposure, and hygiene practices.
METHODS: This cross-sectional study was conducted at a tertiary care hospital in northern India from January to June 2025. Children aged ≤ 14 years were enrolled after obtaining informed consent from parents or legal guardians. A total of 340 stool samples were processed using standard microbiological methods. Bacterial identification was performed using conventional biochemical tests, and antimicrobial susceptibility testing was carried out according to Clinical and Laboratory Standards Institute guidelines, 2025 edition. Multidrug-resistant was defined as resistance to at least one agent in three or more antimicrobial classes. Demographic and clinical data were analysed using SPSS version 25.0; p < 0.05 was considered statistically significant.
RESULTS: Among 340 enrolled children, Enterobacterales were isolated from 309 (90.9%). Multidrug-resistant Enterobacterales were identified in 87 children, yielding a prevalence of 28.2% among Enterobacterales-positive children and 25.6% overall. Escherichia coli (66.7%) and Klebsiella spp. (33.3%) were the predominant MDR organisms. Extended-spectrum β-lactamase production was detected in 18.1% of isolates. Multidrug-resistant carriage was significantly higher among inpatients (p < 0.001).
CONCLUSION: Asymptomatic carriage of MDR Enterobacterales is common, particularly among hospitalised children, highlighting the importance of strengthened antimicrobial stewardship and infection prevention strategies in paediatric care.
WHAT THIS STUDY ADDS: This study demonstrates a high prevalence of asymptomatic multidrug-resistant Enterobacterales carriage among children in northern India, particularly among hospitalised children, highlighting the need for ongoing surveillance, infection prevention and antimicrobial stewardship.
Additional Links: PMID-42564505
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Citation:
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@article {pmid42564505,
year = {2026},
author = {Goyal, A and Kaur, J and Chauhan, S},
title = {Faecal carriage of multidrug-resistant Enterobacterales in hospitalisaed and outpatient children in northern India: A cross-sectional study.},
journal = {African journal of laboratory medicine},
volume = {15},
number = {1},
pages = {3027},
pmid = {42564505},
issn = {2225-2002},
abstract = {BACKGROUND: Asymptomatic intestinal carriage of multidrug-resistant (MDR) Enterobacterales in children is increasingly recognised as an important reservoir for transmission and subsequent infection. However, data from northern India remain limited, warranting evaluation of its burden and associated risk factors.
OBJECTIVE: To determine the prevalence of MDR Enterobacterales carriage among children and to identify associated risk factors, including recent hospitalisation, antimicrobial exposure, and hygiene practices.
METHODS: This cross-sectional study was conducted at a tertiary care hospital in northern India from January to June 2025. Children aged ≤ 14 years were enrolled after obtaining informed consent from parents or legal guardians. A total of 340 stool samples were processed using standard microbiological methods. Bacterial identification was performed using conventional biochemical tests, and antimicrobial susceptibility testing was carried out according to Clinical and Laboratory Standards Institute guidelines, 2025 edition. Multidrug-resistant was defined as resistance to at least one agent in three or more antimicrobial classes. Demographic and clinical data were analysed using SPSS version 25.0; p < 0.05 was considered statistically significant.
RESULTS: Among 340 enrolled children, Enterobacterales were isolated from 309 (90.9%). Multidrug-resistant Enterobacterales were identified in 87 children, yielding a prevalence of 28.2% among Enterobacterales-positive children and 25.6% overall. Escherichia coli (66.7%) and Klebsiella spp. (33.3%) were the predominant MDR organisms. Extended-spectrum β-lactamase production was detected in 18.1% of isolates. Multidrug-resistant carriage was significantly higher among inpatients (p < 0.001).
CONCLUSION: Asymptomatic carriage of MDR Enterobacterales is common, particularly among hospitalised children, highlighting the importance of strengthened antimicrobial stewardship and infection prevention strategies in paediatric care.
WHAT THIS STUDY ADDS: This study demonstrates a high prevalence of asymptomatic multidrug-resistant Enterobacterales carriage among children in northern India, particularly among hospitalised children, highlighting the need for ongoing surveillance, infection prevention and antimicrobial stewardship.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
The Gut Microbiome and Diet Interact to Dictate Personalized Response to Broccoli Sprout Consumption.
Food science & nutrition, 14(8):e72211.
Broccoli sprouts produce sulforaphane (SFN), a dietary isothiocyanate with anti-cancer and anti-inflammatory properties. Human intervention trials observe large variation in metabolite generation and bioactivity with broccoli sprout consumption across individuals. We hypothesize that interactions between pre-intervention diet and personalized gut microbiome composition contribute to this variation. This exploratory analysis leverages a small existing dataset to test novel mediation pathways, with the goal of identifying associations for future validation in larger, prospectively designed studies. In a trial of 38 healthy adults, we analyzed participant-recorded 7-day food diaries, profiled baseline gut microbiome compositions, and quantified urinary SFN metabolites over 72 h after broccoli sprout consumption. Using regression-based mediation analysis, we modeled two complementary predictions: (1) that specific gut bacterial genera mediate how pre-intervention diet composition influences SFN metabolism, and (2) that particular dietary components mediate how gut microbiome composition influences SFN metabolism. These analyses found that seven genera, including Collinsella, Ruminococcus, and Bifidobacterium, mediated relationships between pre-intervention diet and SFN metabolites, particularly the bioactive forms. Unsupervised clustering further revealed three distinct baseline gut microbiome community "types," each exhibiting differential production of SFN-nitrile, a biologically inert metabolite, with effects mediated by the consumption of specific carbohydrate classes. Together, these findings indicate that microbiome structure, in concert with diet, shapes individual SFN metabolic outcomes. Considering pre-intervention diet and gut microbiome may therefore enhance the design and personalization of cruciferous vegetable interventions.
Additional Links: PMID-42564592
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Citation:
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@article {pmid42564592,
year = {2026},
author = {Alexiev, A and Beaver, LM and Bouranis, JA and Wong, CP and Stevens, JF and Sharpton, TJ and Ho, E},
title = {The Gut Microbiome and Diet Interact to Dictate Personalized Response to Broccoli Sprout Consumption.},
journal = {Food science & nutrition},
volume = {14},
number = {8},
pages = {e72211},
pmid = {42564592},
issn = {2048-7177},
abstract = {Broccoli sprouts produce sulforaphane (SFN), a dietary isothiocyanate with anti-cancer and anti-inflammatory properties. Human intervention trials observe large variation in metabolite generation and bioactivity with broccoli sprout consumption across individuals. We hypothesize that interactions between pre-intervention diet and personalized gut microbiome composition contribute to this variation. This exploratory analysis leverages a small existing dataset to test novel mediation pathways, with the goal of identifying associations for future validation in larger, prospectively designed studies. In a trial of 38 healthy adults, we analyzed participant-recorded 7-day food diaries, profiled baseline gut microbiome compositions, and quantified urinary SFN metabolites over 72 h after broccoli sprout consumption. Using regression-based mediation analysis, we modeled two complementary predictions: (1) that specific gut bacterial genera mediate how pre-intervention diet composition influences SFN metabolism, and (2) that particular dietary components mediate how gut microbiome composition influences SFN metabolism. These analyses found that seven genera, including Collinsella, Ruminococcus, and Bifidobacterium, mediated relationships between pre-intervention diet and SFN metabolites, particularly the bioactive forms. Unsupervised clustering further revealed three distinct baseline gut microbiome community "types," each exhibiting differential production of SFN-nitrile, a biologically inert metabolite, with effects mediated by the consumption of specific carbohydrate classes. Together, these findings indicate that microbiome structure, in concert with diet, shapes individual SFN metabolic outcomes. Considering pre-intervention diet and gut microbiome may therefore enhance the design and personalization of cruciferous vegetable interventions.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Gut microbiota and pathobiont exposure influences disease incidence in non-obese diabetic mice.
Frontiers in microbiology, 17:1844128.
While the non-obese diabetic (NOD) mouse is the most widely used animal model of type 1 diabetes (T1D), it suffers from poor reproducibility in disease incidence often attributed to variables in the environment, including the gut microbiota (GM). Prior research suggests a protective effect of segmented filamentous bacteria (SFB) on disease incidence, but it is unclear whether other pathobiont organisms or resident GM affect disease incidence. The objectives of the current study were to determine the effect of supplier-origin GMs and three different microbial challenges (SFB, Helicobacter hepaticus, and Mouse Hepatitis Virus [MHV]) on early-stage insulitis and lifelong disease incidence in NOD mice. The fecal microbiome was assessed pre- and post-disease onset to identify shifts in composition and predicted function of the GM. Results show that all three microbes influence T1D incidence and insulitis severity. Overall, SFB, MHV, and a high-richness microbiome were associated with lower disease incidence, while H. hepaticus and a low-richness microbiome were associated with higher disease incidence. H. hepaticus, but not SFB or MHV, was associated with significant changes in beta-diversity of the GM. While immune outcomes were not included, these findings provide guidance on microbes affecting disease incidence in NOD mice and evidence that such microbes may contribute to poor reproducibility in NOD mice or other mouse models.
Additional Links: PMID-42565114
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@article {pmid42565114,
year = {2026},
author = {Russell, AL and Olthoff, B and Zhang, C and Lutz, C and Franklin, CL and Ericsson, AC},
title = {Gut microbiota and pathobiont exposure influences disease incidence in non-obese diabetic mice.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1844128},
pmid = {42565114},
issn = {1664-302X},
abstract = {While the non-obese diabetic (NOD) mouse is the most widely used animal model of type 1 diabetes (T1D), it suffers from poor reproducibility in disease incidence often attributed to variables in the environment, including the gut microbiota (GM). Prior research suggests a protective effect of segmented filamentous bacteria (SFB) on disease incidence, but it is unclear whether other pathobiont organisms or resident GM affect disease incidence. The objectives of the current study were to determine the effect of supplier-origin GMs and three different microbial challenges (SFB, Helicobacter hepaticus, and Mouse Hepatitis Virus [MHV]) on early-stage insulitis and lifelong disease incidence in NOD mice. The fecal microbiome was assessed pre- and post-disease onset to identify shifts in composition and predicted function of the GM. Results show that all three microbes influence T1D incidence and insulitis severity. Overall, SFB, MHV, and a high-richness microbiome were associated with lower disease incidence, while H. hepaticus and a low-richness microbiome were associated with higher disease incidence. H. hepaticus, but not SFB or MHV, was associated with significant changes in beta-diversity of the GM. While immune outcomes were not included, these findings provide guidance on microbes affecting disease incidence in NOD mice and evidence that such microbes may contribute to poor reproducibility in NOD mice or other mouse models.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Quantifying the Contributions of Food, Glucose, Sleep, and Microbiome Data to Personalized Glycemic Response Prediction.
Current developments in nutrition, 10(8):109429.
BACKGROUND: Individual glycemic responses to foods vary and can be predicted using microbiome, activity, and dietary data. However, these data are expensive and invasive to collect, and it is not known how much each modality contributes to accuracy.
OBJECTIVES: We aim to quantify the contributions of dietary, sleep, continuous glucose monitor (CGM), and microbiome features for glycemic response prediction; understand how much personal data are required for training; and evaluate how microbiome sample timing impacts model accuracy.
METHODS: We used data from 8334 participants in the Human Phenotype Project cohort study who provided demographic, anthropometric, dietary, and CGM data. Participants self-reported meals in a dietary tracking application for a mean of 10.78 d, during which they wore CGMs. We trained CatBoost models to predict postprandial glycemic response (PPGR) using 2-h incremental area under the curve and peak 2-h postprandial glucose rise (Glumax). We conducted ablation studies with varied feature combinations to assess the contribution of each data modality. We used 3 train/test splits (split-by-meal, 5-d personal training, and split-by-person) to assess the impact of personal training data. Lastly, we evaluated accuracy as a function of microbiome sample timing (from before meal logs to ≤60 d after).
RESULTS: The model combining all features performed best, and CGM was the most informative feature. Models trained with more personal data had the best performance (PPGR split-by-meal R = 0.731; split-by-person R = 0.590), and personal training data had a larger effect on accuracy than microbiome. Microbiome features improved predictions most when collected within 7 d of meal logs and did not improve performance without personal training data or for samples collected >14 d after meal logs.
CONCLUSIONS: Although CGM was the most important feature group, combining it with personal training data and timely microbiome samples led to the most accurate models in our analysis. These findings can help researchers understand the tradeoffs between the time and effort of data collection and how data types impact model performance.
Additional Links: PMID-42565182
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Citation:
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@article {pmid42565182,
year = {2026},
author = {Shen, Y and Choi, E and Kleinberg, S},
title = {Quantifying the Contributions of Food, Glucose, Sleep, and Microbiome Data to Personalized Glycemic Response Prediction.},
journal = {Current developments in nutrition},
volume = {10},
number = {8},
pages = {109429},
pmid = {42565182},
issn = {2475-2991},
abstract = {BACKGROUND: Individual glycemic responses to foods vary and can be predicted using microbiome, activity, and dietary data. However, these data are expensive and invasive to collect, and it is not known how much each modality contributes to accuracy.
OBJECTIVES: We aim to quantify the contributions of dietary, sleep, continuous glucose monitor (CGM), and microbiome features for glycemic response prediction; understand how much personal data are required for training; and evaluate how microbiome sample timing impacts model accuracy.
METHODS: We used data from 8334 participants in the Human Phenotype Project cohort study who provided demographic, anthropometric, dietary, and CGM data. Participants self-reported meals in a dietary tracking application for a mean of 10.78 d, during which they wore CGMs. We trained CatBoost models to predict postprandial glycemic response (PPGR) using 2-h incremental area under the curve and peak 2-h postprandial glucose rise (Glumax). We conducted ablation studies with varied feature combinations to assess the contribution of each data modality. We used 3 train/test splits (split-by-meal, 5-d personal training, and split-by-person) to assess the impact of personal training data. Lastly, we evaluated accuracy as a function of microbiome sample timing (from before meal logs to ≤60 d after).
RESULTS: The model combining all features performed best, and CGM was the most informative feature. Models trained with more personal data had the best performance (PPGR split-by-meal R = 0.731; split-by-person R = 0.590), and personal training data had a larger effect on accuracy than microbiome. Microbiome features improved predictions most when collected within 7 d of meal logs and did not improve performance without personal training data or for samples collected >14 d after meal logs.
CONCLUSIONS: Although CGM was the most important feature group, combining it with personal training data and timely microbiome samples led to the most accurate models in our analysis. These findings can help researchers understand the tradeoffs between the time and effort of data collection and how data types impact model performance.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Conjunctival Sac-Derived Lactobacillus mucosae MM-1 Metabolite Indole-3-Lactic Acid Attenuates Lens-Induced Myopia in Mice via AHR Activation and TGF-β/Smad Inhibition.
Microbial biotechnology, 19(8):e70426.
Emerging research has revealed a diverse microbiota in the high myopia (HM) conjunctival sac, highlighting the therapeutic potential of modulating this community to influence disease outcomes. However, current research on targeted modulation of this microbiota for myopia intervention lacks in-depth investigation and definitive conclusions regarding its efficacy and underlying mechanisms. In this study, high-throughput sequencing and culturomics were first used to screen the conjunctival sac microbiota of healthy people, identifying Lactobacillus mucosae MM-1 as a potential probiotic for myopia control. Then, animal studies further confirmed that L. mucosae MM-1 significantly attenuated lens-induced myopia, improved COL1A1 expression and scleral integrity and elevated Lactobacillus abundance. Furthermore, untargeted metabolomics analysis suggested that indole-3-lactic acid (ILA) may be a key substance for L. mucosae MM-1 to exert its effects for myopia control. Mechanistically, pharmacological ILA supplementation supports the involvement of AHR in TGF-β/Smad pathway inhibition, accompanied by altered COL1A1 and α-SMA expression and attenuation of lens-induced myopia in mice. Therefore, these findings suggest that L. mucosae MM-1 may attenuate lens-induced myopia in mice, at least in part, through ILA-mediated regulation of the TGF-β/Smad pathway, and offer a theoretical foundation for future therapeutic strategies based on conjunctival sac microbiome manipulation.
Additional Links: PMID-42565253
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@article {pmid42565253,
year = {2026},
author = {Li, Y and Wu, Q and Zhang, X and Liu, L and Ding, L and Xu, J and Cheng, C and Peng, Y and Yu, K and Yao, W and Pi, Y and Li, J and Wu, D and Wei, J and Yu, Y and Chen, T},
title = {Conjunctival Sac-Derived Lactobacillus mucosae MM-1 Metabolite Indole-3-Lactic Acid Attenuates Lens-Induced Myopia in Mice via AHR Activation and TGF-β/Smad Inhibition.},
journal = {Microbial biotechnology},
volume = {19},
number = {8},
pages = {e70426},
doi = {10.1111/1751-7915.70426},
pmid = {42565253},
issn = {1751-7915},
support = {YC2024-B072//Graduate Innovation Special Fund of Jiangxi Province/ ; },
mesh = {Animals ; *Lactobacillus/metabolism/isolation & purification ; *Receptors, Aryl Hydrocarbon/metabolism ; Mice ; *Transforming Growth Factor beta/metabolism/antagonists & inhibitors ; *Myopia/metabolism/drug therapy ; *Smad Proteins/metabolism/antagonists & inhibitors ; *Conjunctiva/microbiology ; Humans ; *Probiotics/administration & dosage ; Signal Transduction/drug effects ; Male ; Disease Models, Animal ; *Indoles/metabolism ; Microbiota ; Collagen Type I/metabolism ; },
abstract = {Emerging research has revealed a diverse microbiota in the high myopia (HM) conjunctival sac, highlighting the therapeutic potential of modulating this community to influence disease outcomes. However, current research on targeted modulation of this microbiota for myopia intervention lacks in-depth investigation and definitive conclusions regarding its efficacy and underlying mechanisms. In this study, high-throughput sequencing and culturomics were first used to screen the conjunctival sac microbiota of healthy people, identifying Lactobacillus mucosae MM-1 as a potential probiotic for myopia control. Then, animal studies further confirmed that L. mucosae MM-1 significantly attenuated lens-induced myopia, improved COL1A1 expression and scleral integrity and elevated Lactobacillus abundance. Furthermore, untargeted metabolomics analysis suggested that indole-3-lactic acid (ILA) may be a key substance for L. mucosae MM-1 to exert its effects for myopia control. Mechanistically, pharmacological ILA supplementation supports the involvement of AHR in TGF-β/Smad pathway inhibition, accompanied by altered COL1A1 and α-SMA expression and attenuation of lens-induced myopia in mice. Therefore, these findings suggest that L. mucosae MM-1 may attenuate lens-induced myopia in mice, at least in part, through ILA-mediated regulation of the TGF-β/Smad pathway, and offer a theoretical foundation for future therapeutic strategies based on conjunctival sac microbiome manipulation.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Lactobacillus/metabolism/isolation & purification
*Receptors, Aryl Hydrocarbon/metabolism
Mice
*Transforming Growth Factor beta/metabolism/antagonists & inhibitors
*Myopia/metabolism/drug therapy
*Smad Proteins/metabolism/antagonists & inhibitors
*Conjunctiva/microbiology
Humans
*Probiotics/administration & dosage
Signal Transduction/drug effects
Male
Disease Models, Animal
*Indoles/metabolism
Microbiota
Collagen Type I/metabolism
RevDate: 2026-08-07
The efficacy of microbiome transplantation in treating vaginosis and its impact on vaginosis recurrence: a meta-analysis of randomized controlled trials.
Ginekologia polska pii:VM/OJS/J/106234 [Epub ahead of print].
OBJECTIVES: Bacterial vaginosis (BV) is a recurrent condition with significant health implications. Microbiome transplantation has emerged as a potential treatment strategy. This meta-analysis assesses its efficacy in treating vaginosis and preventing recurrence.
METHODS: A systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating microbiome transplantation for vaginosis treatment were conducted. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were calculated for short- and long-term efficacy. Sensitivity and publication bias analyses were performed.
RESULTS: In the short-term follow-up, microbiome transplantation significantly reduced vaginosis recurrence (pooled RR = 0.628, 95% CI: 0.543-0.726, p < 0.001). However, heterogeneity was moderate (I² = 60.8%). Sensitivity analyses confirmed the robustness of findings. Long-term follow-up results showed a pooled RR of 0.746 (95% CI: 0.670-0.831, p < 0.001), though with higher heterogeneity (I² = 72.8%). After sensitivity adjustments, meta-analysis yielded a pooled RR of 0.865 (95% CI: 0.735-1.019, p = 0.083), suggesting reduced long-term efficacy. No significant publication bias was detected.
CONCLUSIONS: Microbiome transplantation effectively reduces short-term vaginosis recurrence. However, long-term efficacy diminishes upon sensitivity adjustment, necessitating further investigation.
Additional Links: PMID-42565380
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PubMed:
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@article {pmid42565380,
year = {2026},
author = {Yang, S and Guo, C and Zhang, J and Ma, M and Tian, J and Zhang, Y},
title = {The efficacy of microbiome transplantation in treating vaginosis and its impact on vaginosis recurrence: a meta-analysis of randomized controlled trials.},
journal = {Ginekologia polska},
volume = {},
number = {},
pages = {},
doi = {10.5603/gpl.106234},
pmid = {42565380},
issn = {2543-6767},
abstract = {OBJECTIVES: Bacterial vaginosis (BV) is a recurrent condition with significant health implications. Microbiome transplantation has emerged as a potential treatment strategy. This meta-analysis assesses its efficacy in treating vaginosis and preventing recurrence.
METHODS: A systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating microbiome transplantation for vaginosis treatment were conducted. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were calculated for short- and long-term efficacy. Sensitivity and publication bias analyses were performed.
RESULTS: In the short-term follow-up, microbiome transplantation significantly reduced vaginosis recurrence (pooled RR = 0.628, 95% CI: 0.543-0.726, p < 0.001). However, heterogeneity was moderate (I² = 60.8%). Sensitivity analyses confirmed the robustness of findings. Long-term follow-up results showed a pooled RR of 0.746 (95% CI: 0.670-0.831, p < 0.001), though with higher heterogeneity (I² = 72.8%). After sensitivity adjustments, meta-analysis yielded a pooled RR of 0.865 (95% CI: 0.735-1.019, p = 0.083), suggesting reduced long-term efficacy. No significant publication bias was detected.
CONCLUSIONS: Microbiome transplantation effectively reduces short-term vaginosis recurrence. However, long-term efficacy diminishes upon sensitivity adjustment, necessitating further investigation.},
}
RevDate: 2026-08-07
Monounsaturated fatty acid biosynthesis is critical for streptococcal envelope homeostasis and stress tolerance.
Journal of bacteriology [Epub ahead of print].
The genus Streptococcus contains some of the most important commensals and pathogens of the human microbiome. To obtain the fatty acids required for cell membranes, Streptococcus either produce fatty acids de novo through the fatty acid biosynthesis (fab) pathway or uptake host fatty acids through the fatty acid kinase (fak) pathway. Although both the fab and fak pathways represent potential therapeutic targets to prevent or treat infection, progress is limited because of an incomplete understanding of taxon-to-taxon variability in streptococcal lipid metabolism. Here, we examined the role of de novo monounsaturated fatty acid (MUFA) synthesis in physiology and virulence-associated traits in Streptococcus mutans, Streptococcus pyogenes, and Streptococcus pneumoniae, three major pathogens that cause disease at distinct body sites. In all three species, deletion of fabM abolished MUFA production and caused severe growth defects, decreased stress tolerance, increased antibiotic susceptibility, and defects in cell viability, morphology, and division. In S. mutans, loss of fabM also markedly reduced competence signaling and production of the mutacin IV bacteriocin. Deletion of fabM increased susceptibility to killing by human neutrophils in S. mutans and S. pneumoniae, but not S. pyogenes. Together, these findings illustrate that MUFA synthesis is broadly important for streptococcal physiology and cell membrane homeostasis, while its contribution to pathogenesis is strongly species- and context-dependent, providing leads to guide the development of novel therapeutic and/or preventative strategies.IMPORTANCEStreptococcus spp. exert profound effects on human health, with several species causing significant morbidity and mortality. Although streptococcal fatty acid biosynthesis and utilization are attractive metabolic targets for development of therapeutics, this opportunity is vexed by an incomplete understanding of taxon-to-taxon variability in lipid metabolism. In this study, the role of de novo monounsaturated fatty acid (MUFA) synthesis in physiology and virulence-associated traits was examined in Streptococcus mutans, Streptococcus pyogenes, and Streptococcus pneumoniae, three major pathogens that cause disease at distinct body sites. MUFA synthesis was important for stress and antibiotic tolerance across all three species, while its impact on virulence was species- and context-dependent. Overall, these discoveries provide leads to guide the development of novel therapeutic and/or preventative strategies.
Additional Links: PMID-42565831
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@article {pmid42565831,
year = {2026},
author = {Baker, JL and Tang, J and Guo, M and Farias-da-Silva, FF and Barbisan, M and Burnside, M and Crofton, K and Williams, S and Rao, S and Lee, M and Drucker, SG and Kim, D and Higashi, D and Merritt, J and Hirose, Y and Veening, J-W and Nizet, V},
title = {Monounsaturated fatty acid biosynthesis is critical for streptococcal envelope homeostasis and stress tolerance.},
journal = {Journal of bacteriology},
volume = {},
number = {},
pages = {e0002626},
doi = {10.1128/jb.00026-26},
pmid = {42565831},
issn = {1098-5530},
abstract = {The genus Streptococcus contains some of the most important commensals and pathogens of the human microbiome. To obtain the fatty acids required for cell membranes, Streptococcus either produce fatty acids de novo through the fatty acid biosynthesis (fab) pathway or uptake host fatty acids through the fatty acid kinase (fak) pathway. Although both the fab and fak pathways represent potential therapeutic targets to prevent or treat infection, progress is limited because of an incomplete understanding of taxon-to-taxon variability in streptococcal lipid metabolism. Here, we examined the role of de novo monounsaturated fatty acid (MUFA) synthesis in physiology and virulence-associated traits in Streptococcus mutans, Streptococcus pyogenes, and Streptococcus pneumoniae, three major pathogens that cause disease at distinct body sites. In all three species, deletion of fabM abolished MUFA production and caused severe growth defects, decreased stress tolerance, increased antibiotic susceptibility, and defects in cell viability, morphology, and division. In S. mutans, loss of fabM also markedly reduced competence signaling and production of the mutacin IV bacteriocin. Deletion of fabM increased susceptibility to killing by human neutrophils in S. mutans and S. pneumoniae, but not S. pyogenes. Together, these findings illustrate that MUFA synthesis is broadly important for streptococcal physiology and cell membrane homeostasis, while its contribution to pathogenesis is strongly species- and context-dependent, providing leads to guide the development of novel therapeutic and/or preventative strategies.IMPORTANCEStreptococcus spp. exert profound effects on human health, with several species causing significant morbidity and mortality. Although streptococcal fatty acid biosynthesis and utilization are attractive metabolic targets for development of therapeutics, this opportunity is vexed by an incomplete understanding of taxon-to-taxon variability in lipid metabolism. In this study, the role of de novo monounsaturated fatty acid (MUFA) synthesis in physiology and virulence-associated traits was examined in Streptococcus mutans, Streptococcus pyogenes, and Streptococcus pneumoniae, three major pathogens that cause disease at distinct body sites. MUFA synthesis was important for stress and antibiotic tolerance across all three species, while its impact on virulence was species- and context-dependent. Overall, these discoveries provide leads to guide the development of novel therapeutic and/or preventative strategies.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Bacteria-nanoplastic interactions: mechanisms, ecological consequences, and advances in biodegradation technologies.
Archives of microbiology, 208(11):.
Nanoplastics (< 1 μm) represent a pervasive class of environmental contaminants with unique physicochemical properties that profoundly influence microbial ecosystems. Their high surface-area-to-volume ratio, weathering-induced functionalization, and ability to adsorb chemical pollutants and biomolecules facilitate intricate interactions with bacterial communities. This review systematically examines nanoplastic-bacteria interactions, highlighting mechanisms such as oxidative stress induction, membrane perturbation, DNA damage, metabolic reprogramming, biofilm modulation, and enhanced horizontal gene transfer, which collectively reshape microbial structure and function. Emphasis is placed on the plastisphere microbiome as a dynamic hotspot for pollutant accumulation, pathogen enrichment, and resistance gene exchange. Bacterial biodegradation pathways, including enzymatic hydrolysis, oxidative processes, biosurfactant-mediated interactions, and multispecies consortia activity, are analyzed in detail. Advanced analytical tools, such as nanoscale imaging, spectroscopy, flow cytometry, meta-omics, and AI-assisted computational modeling, are discussed for their role in elucidating nanoplastic-microbe dynamics. Environmental and human health implications, including microbiome disruption, immunotoxicity, and ecological perturbations, are evaluated. Finally, emerging biotechnological strategies for enhancing biodegradation are explored, and critical research gaps are identified. This review provides a comprehensive framework for understanding nanoplastic-bacteria interactions, offering strategic insights for environmental monitoring, risk assessment, and bioremediation development.
Additional Links: PMID-42565868
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Citation:
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@article {pmid42565868,
year = {2026},
author = {Abuelhaded, K and Mohamed, HH and Alam-ElDein, KM},
title = {Bacteria-nanoplastic interactions: mechanisms, ecological consequences, and advances in biodegradation technologies.},
journal = {Archives of microbiology},
volume = {208},
number = {11},
pages = {},
pmid = {42565868},
issn = {1432-072X},
mesh = {Biodegradation, Environmental ; *Bacteria/metabolism/genetics ; *Environmental Pollutants/metabolism ; *Microplastics/metabolism/chemistry ; Microbiota ; Gene Transfer, Horizontal ; Humans ; },
abstract = {Nanoplastics (< 1 μm) represent a pervasive class of environmental contaminants with unique physicochemical properties that profoundly influence microbial ecosystems. Their high surface-area-to-volume ratio, weathering-induced functionalization, and ability to adsorb chemical pollutants and biomolecules facilitate intricate interactions with bacterial communities. This review systematically examines nanoplastic-bacteria interactions, highlighting mechanisms such as oxidative stress induction, membrane perturbation, DNA damage, metabolic reprogramming, biofilm modulation, and enhanced horizontal gene transfer, which collectively reshape microbial structure and function. Emphasis is placed on the plastisphere microbiome as a dynamic hotspot for pollutant accumulation, pathogen enrichment, and resistance gene exchange. Bacterial biodegradation pathways, including enzymatic hydrolysis, oxidative processes, biosurfactant-mediated interactions, and multispecies consortia activity, are analyzed in detail. Advanced analytical tools, such as nanoscale imaging, spectroscopy, flow cytometry, meta-omics, and AI-assisted computational modeling, are discussed for their role in elucidating nanoplastic-microbe dynamics. Environmental and human health implications, including microbiome disruption, immunotoxicity, and ecological perturbations, are evaluated. Finally, emerging biotechnological strategies for enhancing biodegradation are explored, and critical research gaps are identified. This review provides a comprehensive framework for understanding nanoplastic-bacteria interactions, offering strategic insights for environmental monitoring, risk assessment, and bioremediation development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Biodegradation, Environmental
*Bacteria/metabolism/genetics
*Environmental Pollutants/metabolism
*Microplastics/metabolism/chemistry
Microbiota
Gene Transfer, Horizontal
Humans
RevDate: 2026-08-07
CmpDate: 2026-08-07
Optimization and application of probiotics complex for grouper based on dynamic model.
World journal of microbiology & biotechnology, 42(8):.
This study applied systematic microecological method to develop multi-strain probiotics for grouper aquaculture, focusing on rational strain selection and interaction optimization. Five strains from marine source were initially screened through functional and safety assessments. Based on single-strain growth kinetics and pairwise interaction data, the generalized Lotka-Volterra model and multiple linear regression were employed to identify an optimal consortium consisting of Bacillus subtilis, Bacillus megaterium, and Bacillus velezensis (1: 1: 1), which exhibited significantly antagonism against Vibrio harveyi (p < 0.05) and higher digestive enzyme activities among thirty predefined combinations. In vitro tests using intestinal communities from the purebred grouper Epinephelus coioides (Ec) and the hybrid grouper E. fuscoguttatus ♀ × E. lanceolatus ♂ (Elf) revealed host-specific microbiome characteristics. The consortium exerted stronger effects in Elf than single-strain treatments. Supplementation of probiotic complex enhanced network stability, enriched beneficial genera (e.g., Bacillus), and suppressed opportunistic pathogens (e.g., Vibrio). Finally, in a 42-day feeding trial in juvenile Elf grouper, both single bacteria (B. velezensis at 10[7] CFU/g feed) and the multi-strain consortium (total 10[7] CFU/g feed) improved growth performance and disease resistance compared to the control. The consortium further increased weight-specific growth rate by 23.41% (p < 0.05), feed intake by 25.92% (p < 0.05), and survival rate after pathogenic challenge by 40.0% (p < 0.05). Both treatments reshaped gut microbiome correlation networks, reducing the dominance of Vibrio and Photobacterium while increasing the centrality of beneficial Cetobacterium in the consortium group. This work validated the effectiveness of the gLV model for screening and designing probiotic consortia, providing a promising solution for precision aquaculture of grouper.
Additional Links: PMID-42565884
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Citation:
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@article {pmid42565884,
year = {2026},
author = {Chen, C and Song, W and Ai, C and Zhao, J},
title = {Optimization and application of probiotics complex for grouper based on dynamic model.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {8},
pages = {},
pmid = {42565884},
issn = {1573-0972},
support = {3502Z20226031//Xiamen Science and Technology Program of China/ ; XMUPTI2024004//Xiamen University Pingtan Institute/ ; },
mesh = {Animals ; *Probiotics/administration & dosage/pharmacology ; Bacillus/growth & development ; Vibrio ; *Bass/microbiology/growth & development ; Aquaculture/methods ; Bacillus subtilis/growth & development ; Bacillus megaterium/growth & development ; Animal Feed/microbiology/analysis ; Gastrointestinal Microbiome ; Fish Diseases/prevention & control/microbiology ; },
abstract = {This study applied systematic microecological method to develop multi-strain probiotics for grouper aquaculture, focusing on rational strain selection and interaction optimization. Five strains from marine source were initially screened through functional and safety assessments. Based on single-strain growth kinetics and pairwise interaction data, the generalized Lotka-Volterra model and multiple linear regression were employed to identify an optimal consortium consisting of Bacillus subtilis, Bacillus megaterium, and Bacillus velezensis (1: 1: 1), which exhibited significantly antagonism against Vibrio harveyi (p < 0.05) and higher digestive enzyme activities among thirty predefined combinations. In vitro tests using intestinal communities from the purebred grouper Epinephelus coioides (Ec) and the hybrid grouper E. fuscoguttatus ♀ × E. lanceolatus ♂ (Elf) revealed host-specific microbiome characteristics. The consortium exerted stronger effects in Elf than single-strain treatments. Supplementation of probiotic complex enhanced network stability, enriched beneficial genera (e.g., Bacillus), and suppressed opportunistic pathogens (e.g., Vibrio). Finally, in a 42-day feeding trial in juvenile Elf grouper, both single bacteria (B. velezensis at 10[7] CFU/g feed) and the multi-strain consortium (total 10[7] CFU/g feed) improved growth performance and disease resistance compared to the control. The consortium further increased weight-specific growth rate by 23.41% (p < 0.05), feed intake by 25.92% (p < 0.05), and survival rate after pathogenic challenge by 40.0% (p < 0.05). Both treatments reshaped gut microbiome correlation networks, reducing the dominance of Vibrio and Photobacterium while increasing the centrality of beneficial Cetobacterium in the consortium group. This work validated the effectiveness of the gLV model for screening and designing probiotic consortia, providing a promising solution for precision aquaculture of grouper.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Probiotics/administration & dosage/pharmacology
Bacillus/growth & development
Vibrio
*Bass/microbiology/growth & development
Aquaculture/methods
Bacillus subtilis/growth & development
Bacillus megaterium/growth & development
Animal Feed/microbiology/analysis
Gastrointestinal Microbiome
Fish Diseases/prevention & control/microbiology
RevDate: 2026-08-07
Lichen biomonitoring revisited: a multi-level framework incorporating symbiotic response and microbiome dynamics as early-warning indicators.
Environmental science and pollution research international [Epub ahead of print].
Lichens are among the most widely used biological indicators of environmental quality because they integrate atmospheric pollutants and respond sensitively to environmental change. However, recent advances in lichen biology have expanded biomonitoring beyond traditional measures of pollutant accumulation, physiological injury, and community composition, creating the need for an updated synthesis. This review integrates current evidence on the biological basis, response mechanisms, environmental applications, and emerging frontiers of lichen biomonitoring. Classical approaches have been successfully applied to monitor air pollution, heavy metals, nitrogen deposition, and other environmental stressors, while recent studies demonstrate that symbiotic interactions and lichen-associated microbiomes provide additional, potentially earlier indicators of ecosystem disturbance. Building on this evidence, we propose a multi-level framework integrating six complementary biological domains: pollutant accumulation, physiological responses, community dynamics, functional traits, symbiotic interactions, and microbiome dynamics. This framework links established and emerging response pathways into a unified biomonitoring concept while acknowledging remaining challenges, including environmental variability, species-specific responses, methodological standardization, and geographic bias. Integrating conventional and emerging biological endpoints provides a more comprehensive and mechanistic foundation for lichen biomonitoring in a rapidly changing environment.
Additional Links: PMID-42565949
PubMed:
Citation:
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@article {pmid42565949,
year = {2026},
author = {Temu, SG and Myovela, HH and Hussein, JM},
title = {Lichen biomonitoring revisited: a multi-level framework incorporating symbiotic response and microbiome dynamics as early-warning indicators.},
journal = {Environmental science and pollution research international},
volume = {},
number = {},
pages = {},
pmid = {42565949},
issn = {1614-7499},
abstract = {Lichens are among the most widely used biological indicators of environmental quality because they integrate atmospheric pollutants and respond sensitively to environmental change. However, recent advances in lichen biology have expanded biomonitoring beyond traditional measures of pollutant accumulation, physiological injury, and community composition, creating the need for an updated synthesis. This review integrates current evidence on the biological basis, response mechanisms, environmental applications, and emerging frontiers of lichen biomonitoring. Classical approaches have been successfully applied to monitor air pollution, heavy metals, nitrogen deposition, and other environmental stressors, while recent studies demonstrate that symbiotic interactions and lichen-associated microbiomes provide additional, potentially earlier indicators of ecosystem disturbance. Building on this evidence, we propose a multi-level framework integrating six complementary biological domains: pollutant accumulation, physiological responses, community dynamics, functional traits, symbiotic interactions, and microbiome dynamics. This framework links established and emerging response pathways into a unified biomonitoring concept while acknowledging remaining challenges, including environmental variability, species-specific responses, methodological standardization, and geographic bias. Integrating conventional and emerging biological endpoints provides a more comprehensive and mechanistic foundation for lichen biomonitoring in a rapidly changing environment.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Co-supplementation of fructooligosaccharide with soy isoflavone restores the gut-brain axis dysfunction via modulation of gut microbiome in estrogen-deprived rat model.
Molecular biology reports, 53(1):.
BACKGROUND: The gut-brain axis (GBA) plays a critical role in regulating neurocognitive and gastrointestinal functions through integrated neuronal, immune, endocrine, and microbial pathways. Estrogen deficiency causes gut dysbiosis and associated GBA dysfunction. Strategies that may modulate GBA dysfunction in the postmenopausal phase need to be explored. Our present research aimed to examine the synergistic effect of soy isoflavone (SIF) and fructooligosaccharide (FOS) in combination on GBA dysfunction in an estrogen-deprived rat model.
METHODS: To induce similar postmenopausal complications, female SD rats were bilaterally ovariectomized (OVX) and were orally administered a combination of FOS (50 mg/kg) & SIF (40 mg/kg) and 17β-estradiol (10 μg/kg) for 28 days. At the end, the uterus, hippocampus, & proximal colon health was measured.
RESULTS: Co-supplementation of FOS with SIF in estrogen-deprived rats synergistically improves body weight, neurobehavior, brain-derived neurotrophic factor levels, and monoamine neurotransmission. We also observed marked restoration of oxidative stress, inflammation, and apoptosis in the hippocampus and colon. With this, we also observed restoration of gut health as indicated by increased mucosal layer integrity, promoting tight junction (TJ) genes, and rebalancing the gut microbiome (GM). The combination approach also selectively activates ER-β expression in the hippocampus without affecting serum estradiol levels & uterine weight. Collectively, the combination approach acts as a selective estrogen receptor modulator and improves GBA functioning.
CONCLUSION: Thus, the combination approach may attenuate GBA dysfunction in estrogen-deprived rats by selectively activating the ER-β receptor and modulating oxidative stress, inflammation, and apoptosis while preserving the mucosal layer, TJ genes, and GM.
Additional Links: PMID-42566093
PubMed:
Citation:
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@article {pmid42566093,
year = {2026},
author = {Chaudhary, R and Bansal, N and Kaur, A and Gupta, S and Chopra, K and Bansal, S},
title = {Co-supplementation of fructooligosaccharide with soy isoflavone restores the gut-brain axis dysfunction via modulation of gut microbiome in estrogen-deprived rat model.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42566093},
issn = {1573-4978},
support = {ANRF/ECRG/2024/001702/LS//Anusandhan National Research Foundation (ANRF), Prime Minister Early Career Research Grant (PMECRG) Program/ ; },
mesh = {Animals ; *Oligosaccharides/pharmacology/metabolism ; Female ; *Isoflavones/pharmacology ; Rats ; *Gastrointestinal Microbiome/drug effects ; Rats, Sprague-Dawley ; *Estrogens/deficiency/metabolism ; *Brain-Gut Axis/drug effects ; Glycine max/chemistry ; Disease Models, Animal ; Oxidative Stress/drug effects ; Ovariectomy ; Brain/drug effects/metabolism ; Hippocampus/drug effects/metabolism ; Apoptosis/drug effects ; Dietary Supplements ; },
abstract = {BACKGROUND: The gut-brain axis (GBA) plays a critical role in regulating neurocognitive and gastrointestinal functions through integrated neuronal, immune, endocrine, and microbial pathways. Estrogen deficiency causes gut dysbiosis and associated GBA dysfunction. Strategies that may modulate GBA dysfunction in the postmenopausal phase need to be explored. Our present research aimed to examine the synergistic effect of soy isoflavone (SIF) and fructooligosaccharide (FOS) in combination on GBA dysfunction in an estrogen-deprived rat model.
METHODS: To induce similar postmenopausal complications, female SD rats were bilaterally ovariectomized (OVX) and were orally administered a combination of FOS (50 mg/kg) & SIF (40 mg/kg) and 17β-estradiol (10 μg/kg) for 28 days. At the end, the uterus, hippocampus, & proximal colon health was measured.
RESULTS: Co-supplementation of FOS with SIF in estrogen-deprived rats synergistically improves body weight, neurobehavior, brain-derived neurotrophic factor levels, and monoamine neurotransmission. We also observed marked restoration of oxidative stress, inflammation, and apoptosis in the hippocampus and colon. With this, we also observed restoration of gut health as indicated by increased mucosal layer integrity, promoting tight junction (TJ) genes, and rebalancing the gut microbiome (GM). The combination approach also selectively activates ER-β expression in the hippocampus without affecting serum estradiol levels & uterine weight. Collectively, the combination approach acts as a selective estrogen receptor modulator and improves GBA functioning.
CONCLUSION: Thus, the combination approach may attenuate GBA dysfunction in estrogen-deprived rats by selectively activating the ER-β receptor and modulating oxidative stress, inflammation, and apoptosis while preserving the mucosal layer, TJ genes, and GM.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Oligosaccharides/pharmacology/metabolism
Female
*Isoflavones/pharmacology
Rats
*Gastrointestinal Microbiome/drug effects
Rats, Sprague-Dawley
*Estrogens/deficiency/metabolism
*Brain-Gut Axis/drug effects
Glycine max/chemistry
Disease Models, Animal
Oxidative Stress/drug effects
Ovariectomy
Brain/drug effects/metabolism
Hippocampus/drug effects/metabolism
Apoptosis/drug effects
Dietary Supplements
RevDate: 2026-08-07
Context Dependent Effects of Probiotics: A Systems Perspective on the Interpretation of Experimental Findings.
Probiotics and antimicrobial proteins [Epub ahead of print].
Current definitions of probiotics emphasize their beneficial effects on the host but do not fully capture the complexity of their interactions within the host. Most experimental models remain reductionist, focusing on individual probiotic strains rather than the biological systems in which they operate. However, the effects of probiotics emerge within a dynamic context shaped by the resident microbiota, host metabolism, and immune responses. From this perspective, the present article discusses selected examples illustrating how commonly used experimental models may influence the interpretation of the mechanisms underlying observed probiotic effects. These examples include DSS induced colitis models, specific pathogen free (SPF) animal models, experimental design based on single endpoint measurements, assessment of microbial colonization, and probiotic dosing defined by colony forming units (CFU). The examples presented suggest that probiotic effects should be interpreted as properties emerging from the entire biological system, resulting from interactions among the host, the resident microbiota, and experimental conditions, rather than as direct effects of individual probiotic strains. This systems-oriented perspective may support more accurate interpretation of experimental findings and contribute to the further refinement of experimental models used in probiotic research.
Additional Links: PMID-42566148
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Citation:
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@article {pmid42566148,
year = {2026},
author = {Walczuk, U},
title = {Context Dependent Effects of Probiotics: A Systems Perspective on the Interpretation of Experimental Findings.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42566148},
issn = {1867-1314},
abstract = {Current definitions of probiotics emphasize their beneficial effects on the host but do not fully capture the complexity of their interactions within the host. Most experimental models remain reductionist, focusing on individual probiotic strains rather than the biological systems in which they operate. However, the effects of probiotics emerge within a dynamic context shaped by the resident microbiota, host metabolism, and immune responses. From this perspective, the present article discusses selected examples illustrating how commonly used experimental models may influence the interpretation of the mechanisms underlying observed probiotic effects. These examples include DSS induced colitis models, specific pathogen free (SPF) animal models, experimental design based on single endpoint measurements, assessment of microbial colonization, and probiotic dosing defined by colony forming units (CFU). The examples presented suggest that probiotic effects should be interpreted as properties emerging from the entire biological system, resulting from interactions among the host, the resident microbiota, and experimental conditions, rather than as direct effects of individual probiotic strains. This systems-oriented perspective may support more accurate interpretation of experimental findings and contribute to the further refinement of experimental models used in probiotic research.},
}
RevDate: 2026-08-07
Live Biotherapeutic Products (LBPs) as Promising Microbiome-Based Medicines for Colorectal Cancer (CRC): Mechanistic Basis, Therapeutic Applications, and Translational Challenges.
Probiotics and antimicrobial proteins [Epub ahead of print].
Colorectal cancer (CRC) is the third most prevalent and second deadliest cancer worldwide. The gut microbiota profoundly influences this cancer by modulating immune responses and therapeutic efficacy. Recently, live biotherapeutic products (LBPs), comprising live resident microorganisms in the gut, have emerged as promising agents to reprogram host immunity and enhance treatment efficacy in preclinical CRC models. However, translation of these findings to clinical practice remains limited due to heterogeneous study designs, poorly defined mechanisms in human hosts, unresolved manufacturing and safety concerns, and lack of personalized treatment strategies. This review briefly introduces LBPs as a new class of medicines, categorize them as single strains, composite strains, and engineered strains, and details their multifaceted mechanisms against CRC, including direct immunomodulation to enhance anti-tumor activity, production of protective metabolites like short-chain fatty acids (SCFAs), and restoring gut microbiota. Additionally, the synergistic potential of LBPs with conventional chemo- and immunotherapies and current LBPs in clinical trials for CRC are summarized, highlighting their translational progress. We further address the manufacturing, regulatory, and safety barriers constraining clinical adoption and propose strategies for integrating preclinical and clinical evidence to meet patient needs. By consolidating current knowledge of LBPs as an emerging oncology drug class, this review offers a practical framework for advancing LBPs from preclinical promise to clinical practice, supporting the development of personalized medicine.
Additional Links: PMID-42566149
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Citation:
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@article {pmid42566149,
year = {2026},
author = {Nomiri, S and Yazdani, F and Heidary, H and Sadeghi, A and Tarzemani, S and Sadeghloo, Z and Saeedi Niasar, M and Tillotson, G and Safarpour, H and Raeisi, H},
title = {Live Biotherapeutic Products (LBPs) as Promising Microbiome-Based Medicines for Colorectal Cancer (CRC): Mechanistic Basis, Therapeutic Applications, and Translational Challenges.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42566149},
issn = {1867-1314},
abstract = {Colorectal cancer (CRC) is the third most prevalent and second deadliest cancer worldwide. The gut microbiota profoundly influences this cancer by modulating immune responses and therapeutic efficacy. Recently, live biotherapeutic products (LBPs), comprising live resident microorganisms in the gut, have emerged as promising agents to reprogram host immunity and enhance treatment efficacy in preclinical CRC models. However, translation of these findings to clinical practice remains limited due to heterogeneous study designs, poorly defined mechanisms in human hosts, unresolved manufacturing and safety concerns, and lack of personalized treatment strategies. This review briefly introduces LBPs as a new class of medicines, categorize them as single strains, composite strains, and engineered strains, and details their multifaceted mechanisms against CRC, including direct immunomodulation to enhance anti-tumor activity, production of protective metabolites like short-chain fatty acids (SCFAs), and restoring gut microbiota. Additionally, the synergistic potential of LBPs with conventional chemo- and immunotherapies and current LBPs in clinical trials for CRC are summarized, highlighting their translational progress. We further address the manufacturing, regulatory, and safety barriers constraining clinical adoption and propose strategies for integrating preclinical and clinical evidence to meet patient needs. By consolidating current knowledge of LBPs as an emerging oncology drug class, this review offers a practical framework for advancing LBPs from preclinical promise to clinical practice, supporting the development of personalized medicine.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
Engineering rhizobacterial communities for soil and plant health.
Microbiology (Reading, England), 172(8):.
Rhizobacteria play a central role in supporting plant growth, contributing to nutrient acquisition, stress tolerance and disease suppression. Harnessing and improving rhizosphere microbial communities therefore represents a promising avenue towards more sustainable agriculture. Recent advances in microbiome ecology and synthetic biology have enabled the rational design of microbial consortia. Synthetic communities are widely used as tractable models to study ecological interactions and are increasingly explored as biofertilizers and biocontrol agents. Here, we define engineered microbial communities (EngComs) as microbial consortia augmented with strains carrying synthetic genetic circuits. These systems extend SynCom approaches by enabling programmable functions, such as intercellular communication, division of labour, biosensing and controlled nutrient mobilization, ultimately improving functional stability in complex environments. Beyond bacteria-bacteria interactions, we highlight emerging strategies to engineer plant-microbe interfaces through synthetic signalling pathways and multi-input genetic circuits that enable context-dependent responses. Despite this progress, the engineering of rhizobacteria for real soil environments remains at an early stage. Most systems are still characterized in simplified or artificial conditions, and key challenges persist, including environmental complexity, genetic stability, biocontainment and regulatory constraints. Addressing these limitations will be essential to translate engineered functions from laboratory settings to the field. Overall, continued integration of synthetic biology with ecological and biophysical understanding of the rhizosphere will pave the way for programmable plant-microbe systems, offering new opportunities to enhance crop productivity while reducing environmental impact.
Additional Links: PMID-42566244
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PubMed:
Citation:
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@article {pmid42566244,
year = {2026},
author = {Garcia-Perez, E and Perrin, L and Malone, JG and Thompson, CMA and Guiziou, S},
title = {Engineering rhizobacterial communities for soil and plant health.},
journal = {Microbiology (Reading, England)},
volume = {172},
number = {8},
pages = {},
doi = {10.1099/mic.0.001748},
pmid = {42566244},
issn = {1465-2080},
mesh = {*Soil Microbiology ; Rhizosphere ; *Plants/microbiology ; Synthetic Biology ; *Microbial Consortia ; Bacteria/genetics/metabolism ; Genetic Engineering ; *Microbiota ; },
abstract = {Rhizobacteria play a central role in supporting plant growth, contributing to nutrient acquisition, stress tolerance and disease suppression. Harnessing and improving rhizosphere microbial communities therefore represents a promising avenue towards more sustainable agriculture. Recent advances in microbiome ecology and synthetic biology have enabled the rational design of microbial consortia. Synthetic communities are widely used as tractable models to study ecological interactions and are increasingly explored as biofertilizers and biocontrol agents. Here, we define engineered microbial communities (EngComs) as microbial consortia augmented with strains carrying synthetic genetic circuits. These systems extend SynCom approaches by enabling programmable functions, such as intercellular communication, division of labour, biosensing and controlled nutrient mobilization, ultimately improving functional stability in complex environments. Beyond bacteria-bacteria interactions, we highlight emerging strategies to engineer plant-microbe interfaces through synthetic signalling pathways and multi-input genetic circuits that enable context-dependent responses. Despite this progress, the engineering of rhizobacteria for real soil environments remains at an early stage. Most systems are still characterized in simplified or artificial conditions, and key challenges persist, including environmental complexity, genetic stability, biocontainment and regulatory constraints. Addressing these limitations will be essential to translate engineered functions from laboratory settings to the field. Overall, continued integration of synthetic biology with ecological and biophysical understanding of the rhizosphere will pave the way for programmable plant-microbe systems, offering new opportunities to enhance crop productivity while reducing environmental impact.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Soil Microbiology
Rhizosphere
*Plants/microbiology
Synthetic Biology
*Microbial Consortia
Bacteria/genetics/metabolism
Genetic Engineering
*Microbiota
RevDate: 2026-08-07
Alterations in the feline oral microbiome in common oral diseases - A comprehensive review.
European journal of microbiology & immunology pii:1886.2026.00040 [Epub ahead of print].
The most prevalent diagnostic conditions in domestic cats (Felis catus) are oral diseases, affecting up to 90% of older cats. Periodontal disease (PD), feline chronic gingivostomatitis (FCGS), and tooth resorption (TR) are the principal clinically relevant entities, each with distinct histopathological and microbiological features. Certain molecular techniques, including 16S rRNA sequencing, shotgun metagenomics, and metatranscriptomics, have substantially advanced our understanding of the feline oral microbiome alterations. This review summarizes the findings of the healthy oral microbiome and its disease-associated shifts in PD, FCGS, TR, and feline immunodeficiency virus (FIV)-associated pathology. The healthy oral cavity is dominated by Proteobacteria, Bacteroidota, Bacillota, Fusobacteria, and Actinobacteria, notably Porphyromonas, Moraxella, Capnocytophaga, and Fusobacterium. Dental disease is characterised by expansion of Bacteroidota and Spirochaetota, enrichment of Treponema, Peptostreptococcus, Filifactor, and Fusobacterium nucleatum, and depletion of commensals. The contributions of fungi, viruses, and host immunity are critically evaluated, alongside the development of microbiome-based diagnostics and therapeutics. We argue that dysbiosis is a unifying (albeit not monocausal) feature of feline oral pathology and identify gaps in current knowledge that require further investigation.
Additional Links: PMID-42566284
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@article {pmid42566284,
year = {2026},
author = {Oláh, ÁA and Dudás-Györki, Z and Dunay, IR and Dunay, MP},
title = {Alterations in the feline oral microbiome in common oral diseases - A comprehensive review.},
journal = {European journal of microbiology & immunology},
volume = {},
number = {},
pages = {},
doi = {10.1556/1886.2026.00040},
pmid = {42566284},
issn = {2062-509X},
abstract = {The most prevalent diagnostic conditions in domestic cats (Felis catus) are oral diseases, affecting up to 90% of older cats. Periodontal disease (PD), feline chronic gingivostomatitis (FCGS), and tooth resorption (TR) are the principal clinically relevant entities, each with distinct histopathological and microbiological features. Certain molecular techniques, including 16S rRNA sequencing, shotgun metagenomics, and metatranscriptomics, have substantially advanced our understanding of the feline oral microbiome alterations. This review summarizes the findings of the healthy oral microbiome and its disease-associated shifts in PD, FCGS, TR, and feline immunodeficiency virus (FIV)-associated pathology. The healthy oral cavity is dominated by Proteobacteria, Bacteroidota, Bacillota, Fusobacteria, and Actinobacteria, notably Porphyromonas, Moraxella, Capnocytophaga, and Fusobacterium. Dental disease is characterised by expansion of Bacteroidota and Spirochaetota, enrichment of Treponema, Peptostreptococcus, Filifactor, and Fusobacterium nucleatum, and depletion of commensals. The contributions of fungi, viruses, and host immunity are critically evaluated, alongside the development of microbiome-based diagnostics and therapeutics. We argue that dysbiosis is a unifying (albeit not monocausal) feature of feline oral pathology and identify gaps in current knowledge that require further investigation.},
}
RevDate: 2026-08-07
From Dysbiosis to systemic health: Microbiome modulation as a unified therapeutic framework.
Acta microbiologica et immunologica Hungarica pii:030.2026.03015 [Epub ahead of print].
The gut microbiome is a dynamic microbial ecosystem regulating gastrointestinal, metabolic, immune, and neurobehavioral physiology. Dysbiosis has been linked to irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and systemic disorders including metabolic syndrome, autoimmune conditions, and neurodegenerative diseases. This narrative review synthesizes mechanistic, clinical, and translational evidence to delineate molecular pathways of microbiome-targeted interventions, evaluates clinical outcomes in IBS and IBD, and proposes a unified framework linking gastrointestinal modulation to systemic health. A structured literature search across PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar (2012-2024) identified approximately 68 eligible sources, appraised using Cochrane Risk of Bias 2.0 and AMSTAR-2. Five principal molecular pathways were identified: competitive pathogen exclusion, epithelial barrier reinforcement, immune modulation, short-chain fatty acid (SCFA) production, and neurotransmitter signaling. Clinically, dietary strategies, biological agents (probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation [FMT]), advanced modalities (rifaximin, psychobiotics, bacteriophage therapy), and lifestyle interventions collectively engage these pathways. The same mechanisms underpin emerging applications in metabolic, autoimmune, neurological, and cardiovascular disease. We propose a three-tier model progressing from molecular mechanisms through gastrointestinal outcomes to systemic benefits, with precision medicine and standardized trial designs as prerequisites for therapeutic translation.
Additional Links: PMID-42566286
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PubMed:
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@article {pmid42566286,
year = {2026},
author = {Dhiman, NK and Ahmad, SR},
title = {From Dysbiosis to systemic health: Microbiome modulation as a unified therapeutic framework.},
journal = {Acta microbiologica et immunologica Hungarica},
volume = {},
number = {},
pages = {},
doi = {10.1556/030.2026.03015},
pmid = {42566286},
issn = {1588-2640},
abstract = {The gut microbiome is a dynamic microbial ecosystem regulating gastrointestinal, metabolic, immune, and neurobehavioral physiology. Dysbiosis has been linked to irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and systemic disorders including metabolic syndrome, autoimmune conditions, and neurodegenerative diseases. This narrative review synthesizes mechanistic, clinical, and translational evidence to delineate molecular pathways of microbiome-targeted interventions, evaluates clinical outcomes in IBS and IBD, and proposes a unified framework linking gastrointestinal modulation to systemic health. A structured literature search across PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar (2012-2024) identified approximately 68 eligible sources, appraised using Cochrane Risk of Bias 2.0 and AMSTAR-2. Five principal molecular pathways were identified: competitive pathogen exclusion, epithelial barrier reinforcement, immune modulation, short-chain fatty acid (SCFA) production, and neurotransmitter signaling. Clinically, dietary strategies, biological agents (probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation [FMT]), advanced modalities (rifaximin, psychobiotics, bacteriophage therapy), and lifestyle interventions collectively engage these pathways. The same mechanisms underpin emerging applications in metabolic, autoimmune, neurological, and cardiovascular disease. We propose a three-tier model progressing from molecular mechanisms through gastrointestinal outcomes to systemic benefits, with precision medicine and standardized trial designs as prerequisites for therapeutic translation.},
}
RevDate: 2026-08-07
Nanoscale Strategies for Improving Plant Salinity Tolerance.
Journal of agricultural and food chemistry pii:5247101 [Epub ahead of print].
Soil salinity poses a major threat to global food security, impairing plant physiology through ionic toxicity, osmotic stress, and oxidative damage. However, conventional breeding and genetic engineering approaches face limitations due to the complexity of stress responses and regulatory hurdles. Nanotechnology, through the unique properties of nanomaterials (NMs), offers a promising alternative. This review synthesizes recent advances in nanoscale strategies for early salt stress sensing, the regulation of ion homeostasis, and reactive oxygen species scavenging. It further examines how NMs enhance nutrient use efficiency under saline conditions and discusses emerging applications in microbiome engineering and nontransgenic genetic improvements. The integration of machine learning to optimize NM design and application is also discussed. By synthesizing insights across these disciplines, this review provides a holistic framework for developing next-generation, nanotechnology-driven solutions to mitigate salinity stress, bridging the fundamental research with field-scale application for sustainable agriculture.
Additional Links: PMID-42566294
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PubMed:
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@article {pmid42566294,
year = {2026},
author = {Tanveer, M and Ud Din Khan, W and Fotopoulos, V and Shabala, S and Wang, L and White, JC},
title = {Nanoscale Strategies for Improving Plant Salinity Tolerance.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.6c01761},
pmid = {42566294},
issn = {1520-5118},
support = {NA//Xinjiang Institute of Ecology and Geography, Chinese Academy of Sciences/ ; },
abstract = {Soil salinity poses a major threat to global food security, impairing plant physiology through ionic toxicity, osmotic stress, and oxidative damage. However, conventional breeding and genetic engineering approaches face limitations due to the complexity of stress responses and regulatory hurdles. Nanotechnology, through the unique properties of nanomaterials (NMs), offers a promising alternative. This review synthesizes recent advances in nanoscale strategies for early salt stress sensing, the regulation of ion homeostasis, and reactive oxygen species scavenging. It further examines how NMs enhance nutrient use efficiency under saline conditions and discusses emerging applications in microbiome engineering and nontransgenic genetic improvements. The integration of machine learning to optimize NM design and application is also discussed. By synthesizing insights across these disciplines, this review provides a holistic framework for developing next-generation, nanotechnology-driven solutions to mitigate salinity stress, bridging the fundamental research with field-scale application for sustainable agriculture.},
}
RevDate: 2026-08-07
CmpDate: 2026-08-07
The gut-immune-brain axis in CNS tumors: Causal roles of microbiota and inflammatory proteins unveiled by Mendelian randomization and single-cell transcriptomics.
Medicine, 105(32):e50109.
There is a growing number of research suggesting that there is an association between gut microbiota and central nervous system (CNS) tumor. However, the causal relationships and the mediation effects of inflammatory proteins in the associations are unclear. We extracted genetic variants associated with gut microbiota, inflammatory proteins, and 4 subtypes of CNS tumors from published genome-wide association studies and performed a Mendelian randomization analysis to identify potential causal effects. The inverse variance weighted method was used as the main method. Mediation analysis and single-cell RNA-seq analysis were performed to explore the mediation effects and the expression in cells. This study identified 73 gut microbial taxa and 11 inflammatory proteins that were significantly associated with CNS tumors. The inflammatory proteins may act as intermediate mediators in the potential causal association between gut microbiota and 4 CNS tumor subtypes. Mediation analysis suggested that CX3CL1 may partially mediate the relationship between gut microbiota and Glioblastoma, while Eotaxin, CSF-1, IL-15RA and the other 5 cytokines may serve as subtype-specific potential mediators for the remaining 3 tumor types. Our research supports a hypothesized "gut-immune-brain" axis that may mediate the effects of gut microbiota on different CNS tumor subtypes, with distinct immune proteins implicated for each. These findings strongly suggest potential targets for microbiome therapy and immune therapy, though the underlying mechanistic links require experimental validation.
Additional Links: PMID-42566596
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@article {pmid42566596,
year = {2026},
author = {Cao, X and Guo, H and Wang, K and Wu, Q and Wang, X and Shao, J},
title = {The gut-immune-brain axis in CNS tumors: Causal roles of microbiota and inflammatory proteins unveiled by Mendelian randomization and single-cell transcriptomics.},
journal = {Medicine},
volume = {105},
number = {32},
pages = {e50109},
doi = {10.1097/MD.0000000000050109},
pmid = {42566596},
issn = {1536-5964},
support = {2020THRC-DJ-SNW//Wuxi Taihu Lake Talent Plan - Supports for Leading Talents in Medical and Health Profession/ ; ZD2022038//Key Project of the Jiangsu Provincial Health Commission/ ; },
mesh = {Humans ; Mendelian Randomization Analysis ; *Gastrointestinal Microbiome/immunology/genetics ; *Central Nervous System Neoplasms/genetics/immunology/microbiology ; Genome-Wide Association Study ; Single-Cell Analysis ; Transcriptome ; *Brain ; Single-Cell Gene Expression Analysis ; Cytokines/genetics ; Inflammation ; },
abstract = {There is a growing number of research suggesting that there is an association between gut microbiota and central nervous system (CNS) tumor. However, the causal relationships and the mediation effects of inflammatory proteins in the associations are unclear. We extracted genetic variants associated with gut microbiota, inflammatory proteins, and 4 subtypes of CNS tumors from published genome-wide association studies and performed a Mendelian randomization analysis to identify potential causal effects. The inverse variance weighted method was used as the main method. Mediation analysis and single-cell RNA-seq analysis were performed to explore the mediation effects and the expression in cells. This study identified 73 gut microbial taxa and 11 inflammatory proteins that were significantly associated with CNS tumors. The inflammatory proteins may act as intermediate mediators in the potential causal association between gut microbiota and 4 CNS tumor subtypes. Mediation analysis suggested that CX3CL1 may partially mediate the relationship between gut microbiota and Glioblastoma, while Eotaxin, CSF-1, IL-15RA and the other 5 cytokines may serve as subtype-specific potential mediators for the remaining 3 tumor types. Our research supports a hypothesized "gut-immune-brain" axis that may mediate the effects of gut microbiota on different CNS tumor subtypes, with distinct immune proteins implicated for each. These findings strongly suggest potential targets for microbiome therapy and immune therapy, though the underlying mechanistic links require experimental validation.},
}
MeSH Terms:
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Humans
Mendelian Randomization Analysis
*Gastrointestinal Microbiome/immunology/genetics
*Central Nervous System Neoplasms/genetics/immunology/microbiology
Genome-Wide Association Study
Single-Cell Analysis
Transcriptome
*Brain
Single-Cell Gene Expression Analysis
Cytokines/genetics
Inflammation
RevDate: 2026-08-07
Four Decades of Stress, Depression, and Close Relationships: Lessons from Psychoneuroimmunology.
Annual review of psychology [Epub ahead of print].
Human psychoneuroimmunology research has demonstrated that stress, depression, and close relationships reliably shape immune and endocrine function in ways that matter for health. Across studies of examination stress, laboratory stressors, marital discord, cancer survivorship, and dementia caregiving, psychosocial adversity predicts more infections, weaker vaccine responses and faster erosion of vaccine protection, slower wound healing, heightened inflammation, and accelerated cellular aging. Depression also sensitizes immune function, producing larger inflammatory responses when individuals encounter stressors. Loneliness, low support, and distressed relationships can amplify stress reactivity and are linked to greater inflammatory and metabolic vulnerability, including postprandial inflammatory and endothelial responses. More recent work has extended these pathways to the gut microbiome and intestinal permeability (leaky gut), integrating microbial, neuroendocrine, and immune mechanisms. Collectively, the evidence supports a biobehavioral model in which social stress accelerates immune aging and increases risk for inflammation-related disease, while behavioral and nutritional interventions can modify these trajectories.
Additional Links: PMID-42566682
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@article {pmid42566682,
year = {2026},
author = {Kiecolt-Glaser, JK},
title = {Four Decades of Stress, Depression, and Close Relationships: Lessons from Psychoneuroimmunology.},
journal = {Annual review of psychology},
volume = {},
number = {},
pages = {},
doi = {10.1146/annurev-psych-020226-033326},
pmid = {42566682},
issn = {1545-2085},
abstract = {Human psychoneuroimmunology research has demonstrated that stress, depression, and close relationships reliably shape immune and endocrine function in ways that matter for health. Across studies of examination stress, laboratory stressors, marital discord, cancer survivorship, and dementia caregiving, psychosocial adversity predicts more infections, weaker vaccine responses and faster erosion of vaccine protection, slower wound healing, heightened inflammation, and accelerated cellular aging. Depression also sensitizes immune function, producing larger inflammatory responses when individuals encounter stressors. Loneliness, low support, and distressed relationships can amplify stress reactivity and are linked to greater inflammatory and metabolic vulnerability, including postprandial inflammatory and endothelial responses. More recent work has extended these pathways to the gut microbiome and intestinal permeability (leaky gut), integrating microbial, neuroendocrine, and immune mechanisms. Collectively, the evidence supports a biobehavioral model in which social stress accelerates immune aging and increases risk for inflammation-related disease, while behavioral and nutritional interventions can modify these trajectories.},
}
RevDate: 2026-08-07
Biomimetic delivery systems for overcoming drug resistance in gastrointestinal cancers.
Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy, 89:101465 pii:S1368-7646(26)00116-0 [Epub ahead of print].
Gastrointestinal (GI) cancers remain a major cause of cancer-related mortality worldwide, and multidrug resistance (MDR) is a critical barrier to durable therapeutic response. In GI malignancies, MDR arises from multilayered and interdependent factors, including insufficient intracellular drug accumulation, altered drug activation and metabolic detoxification, target rewiring and phenotypic plasticity, apoptosis-autophagy-mediated stress adaptation, and extrinsic protection from the tumor microenvironment, cancer stem cells, metastatic niches, and microbiome-associated mechanisms. Biomimetic delivery systems (BDSs), including cell membrane-coated nanocarriers, extracellular vesicles, and living or virus-mediated platforms, provide biological interface functions that may improve drug circulation, tumor recognition, tissue penetration, membrane interaction, and active trafficking. However, their therapeutic value in MDR GI cancers should not be judged merely by improved delivery efficiency, but by whether they address defined resistance bottlenecks and generate evidence of genuine re-sensitization in resistant disease contexts. Current evidence indicates that many BDSs remain at the level of exposure enhancement or mechanism-aligned sensitization, whereas only a limited subset has demonstrated functional restoration of treatment response in established resistant models. This review organizes current BDS strategies according to their dominant mechanistic functions: enhancing drug accumulation and intratumoral delivery, reversing cellular drug resistance, remodeling resistance-supportive tumor microenvironment, targeting cancer stem cells (CSCs) and metastatic niches, and enabling site-directed intervention using living carriers and living therapeutics. By linking GI cancer-focused MDR biology to function-oriented biomimetic design, this review establishes an evidence-based framework for distinguishing delivery enhancement from true MDR reversal and outlines platform-specific requirements for clinical translation.
Additional Links: PMID-42567032
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PubMed:
Citation:
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@article {pmid42567032,
year = {2026},
author = {Wu, G and Li, AX and Gu, YW and Cheng, XL and Mao, RC and Wang, XJ and He, MY and Chai, QQ and Li, FN and Liu, HY and Zhang, WX and Zheng, XY and Wu, Z and Wu, X and Liu, JY},
title = {Biomimetic delivery systems for overcoming drug resistance in gastrointestinal cancers.},
journal = {Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy},
volume = {89},
number = {},
pages = {101465},
doi = {10.1016/j.drup.2026.101465},
pmid = {42567032},
issn = {1532-2084},
abstract = {Gastrointestinal (GI) cancers remain a major cause of cancer-related mortality worldwide, and multidrug resistance (MDR) is a critical barrier to durable therapeutic response. In GI malignancies, MDR arises from multilayered and interdependent factors, including insufficient intracellular drug accumulation, altered drug activation and metabolic detoxification, target rewiring and phenotypic plasticity, apoptosis-autophagy-mediated stress adaptation, and extrinsic protection from the tumor microenvironment, cancer stem cells, metastatic niches, and microbiome-associated mechanisms. Biomimetic delivery systems (BDSs), including cell membrane-coated nanocarriers, extracellular vesicles, and living or virus-mediated platforms, provide biological interface functions that may improve drug circulation, tumor recognition, tissue penetration, membrane interaction, and active trafficking. However, their therapeutic value in MDR GI cancers should not be judged merely by improved delivery efficiency, but by whether they address defined resistance bottlenecks and generate evidence of genuine re-sensitization in resistant disease contexts. Current evidence indicates that many BDSs remain at the level of exposure enhancement or mechanism-aligned sensitization, whereas only a limited subset has demonstrated functional restoration of treatment response in established resistant models. This review organizes current BDS strategies according to their dominant mechanistic functions: enhancing drug accumulation and intratumoral delivery, reversing cellular drug resistance, remodeling resistance-supportive tumor microenvironment, targeting cancer stem cells (CSCs) and metastatic niches, and enabling site-directed intervention using living carriers and living therapeutics. By linking GI cancer-focused MDR biology to function-oriented biomimetic design, this review establishes an evidence-based framework for distinguishing delivery enhancement from true MDR reversal and outlines platform-specific requirements for clinical translation.},
}
RevDate: 2026-08-05
Zoo gut plastispheres enable pathogen escape and adaptation.
The ISME journal pii:8752697 [Epub ahead of print].
In zoos, intensive human contact and artificial feeding may create pathways for microplastic (MP) ingestion and gut colonization. We hypothesized that ingested MPs form intestinal plastispheres with elevated pathogenic potential and enhanced environmental persistence. To test this, we surveyed feces from 15 zoo-dwelling species and coupled particle characterization, feces-derived intestinal simulations, metagenomic sequencing, and a subsequent water-exposure experiment. Zoo feces contained more abundant MPs than reported for wild counterparts, with fragments predominating and polyethylene terephthalate (PET)/polystyrene (PS) dominating polymer profiles. MP burdens tracked human-animal interaction patterns, with human-fed species (e.g., Tiger, Elephant) carrying the highest loads (88-212 items/g). MPs supported dense biofilms whose composition diverged from bulk gut communities, exhibiting greater compositional variability and substrate-specific assembly. Metagenomic analyses revealed coordinated enrichment of potentially pathogenic taxa, virulence factor genes (VFGs), and antibiotic resistance genes (ARGs), with ARG profiles dominated by efflux- and inactivation-related mechanisms and tightly associated with mobile genetic elements. Elevated Type II/III/IV/VI secretion systems and effector delivery-related VFGs occurred within extracellular polymeric substance-rich biofilms, suggesting enhanced potential for ARG retention and horizontal gene transfer. During the 35-day aquatic exposure, MP-associated communities persisted longer than non-plastic particle-associated communities and free gut microbiota, suggesting that plastic-specific properties promote microbial persistence. PET/PS plastispheres showed the slowest declines in bacterial activity and favored the persistence of Enterococcus, Enterobacter, and Clostridium. Overall, intestinal MPs in zoo animals may select, enrich, and export high-risk microbiomes, highlighting the need for MP mitigation and evidence-based management of zoos and adjacent ecosystems.
Additional Links: PMID-42555106
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PubMed:
Citation:
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@article {pmid42555106,
year = {2026},
author = {Luo, Z and Liu, Y and Wu, H and Xiao, Y and Li, Y and Liu, M and Li, C and Zhu, D and Jin, LN and Dong, T and Yan, W},
title = {Zoo gut plastispheres enable pathogen escape and adaptation.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag207},
pmid = {42555106},
issn = {1751-7370},
abstract = {In zoos, intensive human contact and artificial feeding may create pathways for microplastic (MP) ingestion and gut colonization. We hypothesized that ingested MPs form intestinal plastispheres with elevated pathogenic potential and enhanced environmental persistence. To test this, we surveyed feces from 15 zoo-dwelling species and coupled particle characterization, feces-derived intestinal simulations, metagenomic sequencing, and a subsequent water-exposure experiment. Zoo feces contained more abundant MPs than reported for wild counterparts, with fragments predominating and polyethylene terephthalate (PET)/polystyrene (PS) dominating polymer profiles. MP burdens tracked human-animal interaction patterns, with human-fed species (e.g., Tiger, Elephant) carrying the highest loads (88-212 items/g). MPs supported dense biofilms whose composition diverged from bulk gut communities, exhibiting greater compositional variability and substrate-specific assembly. Metagenomic analyses revealed coordinated enrichment of potentially pathogenic taxa, virulence factor genes (VFGs), and antibiotic resistance genes (ARGs), with ARG profiles dominated by efflux- and inactivation-related mechanisms and tightly associated with mobile genetic elements. Elevated Type II/III/IV/VI secretion systems and effector delivery-related VFGs occurred within extracellular polymeric substance-rich biofilms, suggesting enhanced potential for ARG retention and horizontal gene transfer. During the 35-day aquatic exposure, MP-associated communities persisted longer than non-plastic particle-associated communities and free gut microbiota, suggesting that plastic-specific properties promote microbial persistence. PET/PS plastispheres showed the slowest declines in bacterial activity and favored the persistence of Enterococcus, Enterobacter, and Clostridium. Overall, intestinal MPs in zoo animals may select, enrich, and export high-risk microbiomes, highlighting the need for MP mitigation and evidence-based management of zoos and adjacent ecosystems.},
}
RevDate: 2026-08-05
Viral lysis accelerates microbial succession patterns resembling diatom senescence.
The ISME journal pii:8752695 [Epub ahead of print].
Diatom blooms influence carbon cycling through organic matter production and its deposition or remineralization - processes mediated by the microbial community. Viruses can influence diatom bloom dynamics and even terminate blooms, yet interactions between diatoms, their viruses, and associated bacteria remain poorly resolved. Here, we examined how infection of the toxigenic diatom Pseudo-nitzschia galaxiae by its ssRNA virus PnGalRNAV reshapes host physiology, microbiome structure, and organic-matter processing in non-axenic batch cultures. Using epi-fluorescence microscopy, 16S rRNA amplicon sequencing, and metatranscriptomics, we linked microbial composition, localisation, and functional activity during viral lysis. Infection rapidly collapsed diatom growth and induced a senescence-like host state, with broad repression of photosynthesis, silicon metabolism, and core biosynthetic pathways, alongside induction of heat-shock and other stress-related genes. Concurrently, phycosphere-associated bacteria declined, detritosphere-associated bacteria increased, and community composition shifted from Marinobacter (Gammaproteobacteria) dominated, towards Flavobacteriaceae (Bacteroidetes) dominated, especially by Polaribacter. In non-infected controls Alphaproteobacteria proved to benefit from the stable healthy phycospheres with a distinct DOM pool. Bacterial metatranscriptomes showed significant upregulation of polysaccharide-degradation-associated genes in infected cultures, indicating active utilisation of lysis-derived diatom glycans. Similar compositional and metabolic profiles in infected cultures and later-stage senescent controls suggest infection accelerated senescence-associated microbial processes. Overall, viral lysis converted a productive diatom culture into a detrital, DOM-rich environment that selects for specialised polysaccharide degraders, redirects carbon through the viral shunt and may accelerate nutrient recycling in coastal systems. Extending this approach to natural microbial communities and diverse diatom-virus systems will help determine whether these mechanisms are broadly conserved.
Additional Links: PMID-42555112
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PubMed:
Citation:
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@article {pmid42555112,
year = {2026},
author = {Timotej, TD and Ion, GA and Tinkara, R and Tinkara, T},
title = {Viral lysis accelerates microbial succession patterns resembling diatom senescence.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag206},
pmid = {42555112},
issn = {1751-7370},
abstract = {Diatom blooms influence carbon cycling through organic matter production and its deposition or remineralization - processes mediated by the microbial community. Viruses can influence diatom bloom dynamics and even terminate blooms, yet interactions between diatoms, their viruses, and associated bacteria remain poorly resolved. Here, we examined how infection of the toxigenic diatom Pseudo-nitzschia galaxiae by its ssRNA virus PnGalRNAV reshapes host physiology, microbiome structure, and organic-matter processing in non-axenic batch cultures. Using epi-fluorescence microscopy, 16S rRNA amplicon sequencing, and metatranscriptomics, we linked microbial composition, localisation, and functional activity during viral lysis. Infection rapidly collapsed diatom growth and induced a senescence-like host state, with broad repression of photosynthesis, silicon metabolism, and core biosynthetic pathways, alongside induction of heat-shock and other stress-related genes. Concurrently, phycosphere-associated bacteria declined, detritosphere-associated bacteria increased, and community composition shifted from Marinobacter (Gammaproteobacteria) dominated, towards Flavobacteriaceae (Bacteroidetes) dominated, especially by Polaribacter. In non-infected controls Alphaproteobacteria proved to benefit from the stable healthy phycospheres with a distinct DOM pool. Bacterial metatranscriptomes showed significant upregulation of polysaccharide-degradation-associated genes in infected cultures, indicating active utilisation of lysis-derived diatom glycans. Similar compositional and metabolic profiles in infected cultures and later-stage senescent controls suggest infection accelerated senescence-associated microbial processes. Overall, viral lysis converted a productive diatom culture into a detrital, DOM-rich environment that selects for specialised polysaccharide degraders, redirects carbon through the viral shunt and may accelerate nutrient recycling in coastal systems. Extending this approach to natural microbial communities and diverse diatom-virus systems will help determine whether these mechanisms are broadly conserved.},
}
RevDate: 2026-08-05
Pharmacotherapeutic strategies for the treatment of severe juvenile acne.
Expert opinion on pharmacotherapy [Epub ahead of print].
INTRODUCTION: Severe juvenile acne vulgaris represents a highly prevalent chronic inflammatory disorder that may significantly impair quality of life and lead to permanent scarring during adolescence. Increasing understanding of acne pathophysiology has progressively modified therapeutic approaches, with growing emphasis on early intervention, antimicrobial stewardship, and individualized systemic treatment strategies.
AREAS COVERED: This narrative review summarizes current evidence regarding pharmacotherapeutic strategies for severe juvenile acne, with particular focus on systemic therapies. A literature search was conducted in PubMed, Embase, Google Scholar, Cochrane Library, and ClinicalTrials.gov from database inception to March 2026. The pathogenic mechanisms underlying juvenile acne, including sebaceous hyperactivity, follicular hyperkeratinization, Cutibacterium acnes, dysbiosis, immune-inflammatory activation, and hormonal influences, are discussed.
EXPERT OPINION: Severe juvenile acne should not be underestimated as a physiologic condition of adolescence, as delayed or inadequate treatment may result in substantial physical and psychological sequelae. Oral isotretinoin remains the gold-standard therapy for severe nodulocystic, scarring, or treatment-resistant acne. Timely specialist assessment is essential in high-risk adolescents to avoid unnecessary delay when the licensed criteria for isotretinoin treatment are fulfilled; however, its use must remain consistent with applicable product information, regulatory requirements, and risk-minimization measures. Simultaneously, prolonged systemic antibiotic exposure should be minimized through stewardship-oriented approaches integrating benzoyl peroxide combinations and shorter treatment durations. Future therapeutic strategies will likely move toward increasingly individualized, microbiome-conscious, and inflammation-targeted approaches aimed not only at lesion clearance but also at prevention of long-term scarring and psychosocial burden.
Additional Links: PMID-42555374
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PubMed:
Citation:
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@article {pmid42555374,
year = {2026},
author = {Palagiano, C and Potestio, L and Brescia, C and Napolitano, M},
title = {Pharmacotherapeutic strategies for the treatment of severe juvenile acne.},
journal = {Expert opinion on pharmacotherapy},
volume = {},
number = {},
pages = {},
doi = {10.1080/14656566.2026.2715706},
pmid = {42555374},
issn = {1744-7666},
abstract = {INTRODUCTION: Severe juvenile acne vulgaris represents a highly prevalent chronic inflammatory disorder that may significantly impair quality of life and lead to permanent scarring during adolescence. Increasing understanding of acne pathophysiology has progressively modified therapeutic approaches, with growing emphasis on early intervention, antimicrobial stewardship, and individualized systemic treatment strategies.
AREAS COVERED: This narrative review summarizes current evidence regarding pharmacotherapeutic strategies for severe juvenile acne, with particular focus on systemic therapies. A literature search was conducted in PubMed, Embase, Google Scholar, Cochrane Library, and ClinicalTrials.gov from database inception to March 2026. The pathogenic mechanisms underlying juvenile acne, including sebaceous hyperactivity, follicular hyperkeratinization, Cutibacterium acnes, dysbiosis, immune-inflammatory activation, and hormonal influences, are discussed.
EXPERT OPINION: Severe juvenile acne should not be underestimated as a physiologic condition of adolescence, as delayed or inadequate treatment may result in substantial physical and psychological sequelae. Oral isotretinoin remains the gold-standard therapy for severe nodulocystic, scarring, or treatment-resistant acne. Timely specialist assessment is essential in high-risk adolescents to avoid unnecessary delay when the licensed criteria for isotretinoin treatment are fulfilled; however, its use must remain consistent with applicable product information, regulatory requirements, and risk-minimization measures. Simultaneously, prolonged systemic antibiotic exposure should be minimized through stewardship-oriented approaches integrating benzoyl peroxide combinations and shorter treatment durations. Future therapeutic strategies will likely move toward increasingly individualized, microbiome-conscious, and inflammation-targeted approaches aimed not only at lesion clearance but also at prevention of long-term scarring and psychosocial burden.},
}
RevDate: 2026-08-05
CmpDate: 2026-08-05
Harnessing the gut microbiome to combat tuberculosis: a technological and clinical review.
Frontiers in cellular and infection microbiology, 16:1847443.
Tuberculosis (TB), especially multidrug-resistant and extensively drug-resistant strains, remains a severe global health threat. Advances in high-throughput sequencing, omics technologies and artificial intelligence have revealed the critical involvement of the gut microbiome (GM) in TB pathogenesis, diagnosis and treatment via the gut-lung axis. The GM modulates host immunity and metabolism; TB patients typically show reduced microbial diversity and enriched pro-inflammatory taxa closely linked to disease severity and treatment responses. Omics research has identified promising biomarkers and pathways for early diagnosis and personalized management, while artificial intelligence improves diagnostic accuracy and treatment outcome prediction. GM-targeted interventions, including probiotics, dietary adjustment and fecal microbiota transplantation, can enhance therapeutic efficacy and relieve adverse drug reactions. Current limitations include insufficient validation of the gut-lung axis' causal mechanisms, lagged clinical translation of biomarkers, biases and errors in diagnosis and prediction, data privacy and security concerns, gaps in intervention research, and poor accessibility of related technologies in resource-scarce medical regions. Future studies need rigorous causal analyses, real-time monitoring tools and large-scale multicenter trials to validate microbiome-based strategies. This review highlights the translational potential of GM interventions to optimize personalized TB prevention, diagnosis and treatment and improve clinical outcomes.
Additional Links: PMID-42555388
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Citation:
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@article {pmid42555388,
year = {2026},
author = {Sun, W and Xiao, M and Ali, SL and Jin, C and Khan, A and Shakirullah, and Ni, R and An, Y and Zhang, M and Tian, Y and Kaushik, S and Zhang, Y and Gong, W},
title = {Harnessing the gut microbiome to combat tuberculosis: a technological and clinical review.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1847443},
pmid = {42555388},
issn = {2235-2988},
mesh = {Humans ; *Tuberculosis/therapy/diagnosis/microbiology/prevention & control ; *Gastrointestinal Microbiome ; Artificial Intelligence ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Biomarkers ; Multiomics ; },
abstract = {Tuberculosis (TB), especially multidrug-resistant and extensively drug-resistant strains, remains a severe global health threat. Advances in high-throughput sequencing, omics technologies and artificial intelligence have revealed the critical involvement of the gut microbiome (GM) in TB pathogenesis, diagnosis and treatment via the gut-lung axis. The GM modulates host immunity and metabolism; TB patients typically show reduced microbial diversity and enriched pro-inflammatory taxa closely linked to disease severity and treatment responses. Omics research has identified promising biomarkers and pathways for early diagnosis and personalized management, while artificial intelligence improves diagnostic accuracy and treatment outcome prediction. GM-targeted interventions, including probiotics, dietary adjustment and fecal microbiota transplantation, can enhance therapeutic efficacy and relieve adverse drug reactions. Current limitations include insufficient validation of the gut-lung axis' causal mechanisms, lagged clinical translation of biomarkers, biases and errors in diagnosis and prediction, data privacy and security concerns, gaps in intervention research, and poor accessibility of related technologies in resource-scarce medical regions. Future studies need rigorous causal analyses, real-time monitoring tools and large-scale multicenter trials to validate microbiome-based strategies. This review highlights the translational potential of GM interventions to optimize personalized TB prevention, diagnosis and treatment and improve clinical outcomes.},
}
MeSH Terms:
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Humans
*Tuberculosis/therapy/diagnosis/microbiology/prevention & control
*Gastrointestinal Microbiome
Artificial Intelligence
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Biomarkers
Multiomics
RevDate: 2026-08-05
CmpDate: 2026-08-05
Uncovering the Hidden Diversity and Antimicrobial Resistance of Uropathogens in a Tertiary-Care Hospital in Bangladesh.
International journal of microbiology, 2026:8327078.
Urinary tract infections (UTIs) are among the most common bacterial infections worldwide; however, their diagnosis in low- and middle-income countries often relies on conventional culture and biochemical methods with limited sensitivity. This study evaluated the limitations of routine diagnostic approaches and explored the microbial diversity and antimicrobial resistance (AMR) profiles of uropathogens in a tertiary-care hospital in Bangladesh using integrated culture-based and molecular methods. Among 30 patient urine samples collected in 2025, 10 were selected for detailed analysis due to funding and resource limitations; therefore, the findings should be interpreted as exploratory and may be subject to selection bias. Of these 10 samples, routine hospital diagnostics identified only eight isolates, whereas extended biochemical analysis detected 29 isolates, indicating substantial underestimation of microbial diversity in standard practice. Antibiotic susceptibility testing revealed a high prevalence of multidrug resistance, with 83% and 80% of isolates resistant to ampicillin and clindamycin, respectively. In contrast, nitrofurantoin and fosfomycin retained effectiveness against most isolates, supporting their continued clinical utility. 16S rRNA gene sequencing further revealed complex and heterogeneous microbial communities, with several samples dominated by Escherichia-Shigella, whereas others exhibited polymicrobial profiles including commensal and opportunistic genera. Despite taxonomic variability, microbial diversity did not differ significantly between inpatient and outpatient groups. Functional pathway prediction demonstrated a largely conserved metabolic profile across samples, including pathways associated with virulence, iron acquisition, and AMR. Overall, this study demonstrates that conventional diagnostic methods substantially underestimate uropathogen diversity and may contribute to misdiagnosis and inappropriate antibiotic use. Integrating molecular approaches into routine clinical workflows could improve pathogen detection, enhance AMR surveillance, and support more effective management of UTIs in Bangladesh and similar resource-limited settings.
Additional Links: PMID-42555404
PubMed:
Citation:
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@article {pmid42555404,
year = {2026},
author = {Hosen, MA and Rahman, T and Rahatuzzaman, and Kabir, RB and Ahsan, CR and Rahman, M and Yasmin, M and Jubair, M},
title = {Uncovering the Hidden Diversity and Antimicrobial Resistance of Uropathogens in a Tertiary-Care Hospital in Bangladesh.},
journal = {International journal of microbiology},
volume = {2026},
number = {},
pages = {8327078},
pmid = {42555404},
issn = {1687-918X},
abstract = {Urinary tract infections (UTIs) are among the most common bacterial infections worldwide; however, their diagnosis in low- and middle-income countries often relies on conventional culture and biochemical methods with limited sensitivity. This study evaluated the limitations of routine diagnostic approaches and explored the microbial diversity and antimicrobial resistance (AMR) profiles of uropathogens in a tertiary-care hospital in Bangladesh using integrated culture-based and molecular methods. Among 30 patient urine samples collected in 2025, 10 were selected for detailed analysis due to funding and resource limitations; therefore, the findings should be interpreted as exploratory and may be subject to selection bias. Of these 10 samples, routine hospital diagnostics identified only eight isolates, whereas extended biochemical analysis detected 29 isolates, indicating substantial underestimation of microbial diversity in standard practice. Antibiotic susceptibility testing revealed a high prevalence of multidrug resistance, with 83% and 80% of isolates resistant to ampicillin and clindamycin, respectively. In contrast, nitrofurantoin and fosfomycin retained effectiveness against most isolates, supporting their continued clinical utility. 16S rRNA gene sequencing further revealed complex and heterogeneous microbial communities, with several samples dominated by Escherichia-Shigella, whereas others exhibited polymicrobial profiles including commensal and opportunistic genera. Despite taxonomic variability, microbial diversity did not differ significantly between inpatient and outpatient groups. Functional pathway prediction demonstrated a largely conserved metabolic profile across samples, including pathways associated with virulence, iron acquisition, and AMR. Overall, this study demonstrates that conventional diagnostic methods substantially underestimate uropathogen diversity and may contribute to misdiagnosis and inappropriate antibiotic use. Integrating molecular approaches into routine clinical workflows could improve pathogen detection, enhance AMR surveillance, and support more effective management of UTIs in Bangladesh and similar resource-limited settings.},
}
RevDate: 2026-08-05
CmpDate: 2026-08-05
AUTO-brewery syndrome and the human microbiome: Insights into endogenous ethanol production and human diseases.
Food science and biotechnology, 35(9):2415-2436.
Auto-Brewery Syndrome (ABS) is a metabolic condition where microbiota dysbiosis undergoes ethanolic fermentation within the gastrointestinal tract. Because the microbial ethanolic fermentation of dietary carbohydrates occurs entirely within the host's gastrointestinal tract, resulting ethanol is referred as "endogenous" while the gut dysbiosis in ABS can rise from multiple fungal or bacterial species. The pathophysiology of ABS is frequently linked to shifts in gut microbiota composition often arising from antibiotics use, high carbohydrate diets, or an underlying immunological or metabolic condition. In this review, the mechanisms behind microbial endogenous ethanol production, the connection between gut, liver, brain, and microbial ethanol-producing routes are examined. Treatments for ABS have been evaluated including antifungals, low-carbohydrate diets, probiotics, and faecal-microbiota transplantation. Lastly, the social, legal, and mental impacts of ABS have been discussed. It would be wise for future studies to develop customized microbiome approaches for detection and treatment guided by omics and AI technologies.
Additional Links: PMID-42555417
PubMed:
Citation:
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@article {pmid42555417,
year = {2026},
author = {Kamaljeet, and Vijukumar, A and Shahi, A and Kumar, A and Bhatia, R},
title = {AUTO-brewery syndrome and the human microbiome: Insights into endogenous ethanol production and human diseases.},
journal = {Food science and biotechnology},
volume = {35},
number = {9},
pages = {2415-2436},
pmid = {42555417},
issn = {2092-6456},
abstract = {Auto-Brewery Syndrome (ABS) is a metabolic condition where microbiota dysbiosis undergoes ethanolic fermentation within the gastrointestinal tract. Because the microbial ethanolic fermentation of dietary carbohydrates occurs entirely within the host's gastrointestinal tract, resulting ethanol is referred as "endogenous" while the gut dysbiosis in ABS can rise from multiple fungal or bacterial species. The pathophysiology of ABS is frequently linked to shifts in gut microbiota composition often arising from antibiotics use, high carbohydrate diets, or an underlying immunological or metabolic condition. In this review, the mechanisms behind microbial endogenous ethanol production, the connection between gut, liver, brain, and microbial ethanol-producing routes are examined. Treatments for ABS have been evaluated including antifungals, low-carbohydrate diets, probiotics, and faecal-microbiota transplantation. Lastly, the social, legal, and mental impacts of ABS have been discussed. It would be wise for future studies to develop customized microbiome approaches for detection and treatment guided by omics and AI technologies.},
}
RevDate: 2026-08-05
CmpDate: 2026-08-05
Rumen mycobiome dynamics and dairy productivity: functional contributions of fungi to milk yield in bovine ruminants.
Frontiers in fungal biology, 7:1878257.
The rumen microbiome is a key factor influencing feed efficiency and milk production in ruminants. However, most studies have focused on the bacterial and archaeal components, with the fungal fraction of the rumen being relatively understudied. The unique ability of anaerobic rumen fungi of the phylum Neocallimastigomycota to colonize and degrade lignocellulosic biomass in the rumen through mechanical disruption of plant cell walls has now made them well known as important functional members of the rumen ecosystem. These fungi are armed with a plethora of carbohydrate-active enzymes degrading fiber and increase the availability of substrates for microbial fermentation. This leads to increased production of volatile fatty acids, especially acetate, which is a major precursor for milk fat production. Recent research evidence has indicated that rumen fungal communities are associated with feed efficiency, fermentation dynamics, and milk composition traits such as fat and protein content in bovine ruminants such as cattle and buffalo. However, most of the studies available are correlative, and the direct causal relationships between fungal activity and milk productivity are poorly delineated. High-throughput sequencing and multi-omics approaches have broadened our knowledge of fungal diversity and function; however, there are still limitations in reference databases and methodological biases. This review summarizes the current knowledge of the diversity, ecological roles, and functional contributions of anaerobic rumen fungi, with special reference to their association with milk production. It also highlights significant methodological and conceptual gaps and proposes future avenues for the integration of fungal ecology into microbiome-based approaches to improve dairy productivity. We need a holistic multi-kingdom view of the rumen microbiome to design efficient and sustainable dairy production systems.
Additional Links: PMID-42555451
PubMed:
Citation:
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@article {pmid42555451,
year = {2026},
author = {Singh, G and Lavika, and Nandini, and Abhay, and Deepika, and Thakur, N and Kaura, R and Kaur, S and Saini, HS and Khulape, S and Puniya, AK and Dhillon, HS},
title = {Rumen mycobiome dynamics and dairy productivity: functional contributions of fungi to milk yield in bovine ruminants.},
journal = {Frontiers in fungal biology},
volume = {7},
number = {},
pages = {1878257},
pmid = {42555451},
issn = {2673-6128},
abstract = {The rumen microbiome is a key factor influencing feed efficiency and milk production in ruminants. However, most studies have focused on the bacterial and archaeal components, with the fungal fraction of the rumen being relatively understudied. The unique ability of anaerobic rumen fungi of the phylum Neocallimastigomycota to colonize and degrade lignocellulosic biomass in the rumen through mechanical disruption of plant cell walls has now made them well known as important functional members of the rumen ecosystem. These fungi are armed with a plethora of carbohydrate-active enzymes degrading fiber and increase the availability of substrates for microbial fermentation. This leads to increased production of volatile fatty acids, especially acetate, which is a major precursor for milk fat production. Recent research evidence has indicated that rumen fungal communities are associated with feed efficiency, fermentation dynamics, and milk composition traits such as fat and protein content in bovine ruminants such as cattle and buffalo. However, most of the studies available are correlative, and the direct causal relationships between fungal activity and milk productivity are poorly delineated. High-throughput sequencing and multi-omics approaches have broadened our knowledge of fungal diversity and function; however, there are still limitations in reference databases and methodological biases. This review summarizes the current knowledge of the diversity, ecological roles, and functional contributions of anaerobic rumen fungi, with special reference to their association with milk production. It also highlights significant methodological and conceptual gaps and proposes future avenues for the integration of fungal ecology into microbiome-based approaches to improve dairy productivity. We need a holistic multi-kingdom view of the rumen microbiome to design efficient and sustainable dairy production systems.},
}
RevDate: 2026-08-05
CmpDate: 2026-08-05
Fecal microbiome transplant in food allergy in humans and mice identifies a role for bile acid metabolites in oral tolerance.
Science translational medicine, 18(861):eaee3263.
The gut microbiome has been implicated in the pathogenesis of food allergy (FA), prompting microbiome-focused interventions. We evaluated, in a phase 1 open-label trial (NCT02960074), the safety and efficacy of oral encapsulated fecal microbiome transplantation (FMT) in 15 adults with peanut allergies. An increase in the peanut reactivity threshold was noted in 3 of 10 participants not pretreated with antibiotics and 3 of 5 participants pretreated with antibiotics, without safety issues. In responders, FMT increased tolerogenic RORγt[+] regulatory T cells (Treg cells) and decreased T helper 2 cells (TH2 cells). Mice transplanted with the microbiomes of post-FMT responders were protected from FA in association with increased RORγt[+] Treg cell percentages and increased colonization with members of the gut Bacteroides. In both humans and mice, protection by FMT was associated with increased bile acid metabolites. Deletion of a bile salt hydrolase in a candidate protective Bacteroides abrogated FA suppression in mice. These results suggest that FMT is a safe and potentially promising therapeutic modality for treating FA.
Additional Links: PMID-42555752
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PubMed:
Citation:
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@article {pmid42555752,
year = {2026},
author = {Rachid, R and Martinez-Blanco, M and Kuziel, GA and Stephen-Victor, E and Groussin, M and Orakov, A and Russell, G and Nguyen, LTT and Poyet, M and Mukhatayev, Z and Yee, CSK and Albuhairi, S and Kteish, R and Rahman, EA and Farraj, FA and Wang, Z and Dahlberg, S and Ryan, M and Fitzgerald, M and Elverson, W and Lee, JJ and Schneider, L and MacGinnitie, A and Crestani, E and Queheillalt, D and Burke-Roberts, E and Watson, J and Elliott, RJ and Wong, WF and Osman, M and Voyksner, R and Hohmann, E and Huttenhower, C and Alm, E and Rakoff-Nahoum, S and Chatila, TA},
title = {Fecal microbiome transplant in food allergy in humans and mice identifies a role for bile acid metabolites in oral tolerance.},
journal = {Science translational medicine},
volume = {18},
number = {861},
pages = {eaee3263},
doi = {10.1126/scitranslmed.aee3263},
pmid = {42555752},
issn = {1946-6242},
mesh = {Animals ; Humans ; *Bile Acids and Salts/metabolism ; *Food Hypersensitivity/immunology/therapy/microbiology ; *Fecal Microbiota Transplantation ; Mice ; Adult ; T-Lymphocytes, Regulatory/immunology ; Administration, Oral ; Female ; *Immune Tolerance ; Male ; },
abstract = {The gut microbiome has been implicated in the pathogenesis of food allergy (FA), prompting microbiome-focused interventions. We evaluated, in a phase 1 open-label trial (NCT02960074), the safety and efficacy of oral encapsulated fecal microbiome transplantation (FMT) in 15 adults with peanut allergies. An increase in the peanut reactivity threshold was noted in 3 of 10 participants not pretreated with antibiotics and 3 of 5 participants pretreated with antibiotics, without safety issues. In responders, FMT increased tolerogenic RORγt[+] regulatory T cells (Treg cells) and decreased T helper 2 cells (TH2 cells). Mice transplanted with the microbiomes of post-FMT responders were protected from FA in association with increased RORγt[+] Treg cell percentages and increased colonization with members of the gut Bacteroides. In both humans and mice, protection by FMT was associated with increased bile acid metabolites. Deletion of a bile salt hydrolase in a candidate protective Bacteroides abrogated FA suppression in mice. These results suggest that FMT is a safe and potentially promising therapeutic modality for treating FA.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Humans
*Bile Acids and Salts/metabolism
*Food Hypersensitivity/immunology/therapy/microbiology
*Fecal Microbiota Transplantation
Mice
Adult
T-Lymphocytes, Regulatory/immunology
Administration, Oral
Female
*Immune Tolerance
Male
RevDate: 2026-08-05
Pharmacological prevention of second primary cancers: From chemoprevention to precision cancer interception.
Cancer treatment reviews, 149:103200 pii:S0305-7372(26)00114-3 [Epub ahead of print].
BACKGROUND: The growing population of cancer survivors is increasingly exposed to the long-term risk of second primary cancers (SPCs), which represents a major source of morbidity and mortality. While current prevention mainly relies on surveillance and screening, pharmacological and immunological strategies may offer opportunities to reduce SPC incidence in selected high-risk populations.
METHODS: This narrative review synthesises current evidence on pharmacological prevention strategies for SPCs, including endocrine therapy, aspirin and non-steroidal anti-inflammatory drugs, PARP inhibitors, metformin, GLP-1 receptor agonists, statins, nicotinamide, immune checkpoint inhibitors, cancer vaccines, and microbiome modulation. Evidence from randomised trials, observational studies, translational research, and ongoing clinical trials was reviewed, with particular attention to SPC-specific endpoints, biological rationale, safety, and clinical applicability.
RESULTS: The strongest evidence currently supports endocrine therapy for reducing contralateral breast cancer in patients with hormone receptor-positive breast cancer, and aspirin in selected populations such as Lynch syndrome carriers or patients with molecularly defined colorectal cancer. Other repurposed agents, including metformin, statins, GLP-1 receptor agonists, and nicotinamide, remain investigational, with most available data addressing incident cancer, recurrence, or surrogate endpoints rather than SPC prevention specifically. Immunological approaches are emerging as particularly promising strategies. Retrospective studies and exploratory analyses of randomised trials suggest that immune checkpoint inhibitors may reduce the occurrence of new malignancies, while neoantigen-based vaccines, especially in Lynch syndrome, provide an early proof of concept for cancer immunoprevention.
CONCLUSIONS: Pharmacological prevention of SPCs is an expanding but remains a heterogeneous field. Current evidence supports a shift from broad chemoprevention toward biologically informed, risk-adapted prevention strategies. Future progress will depend on dedicated SPC-focused trials, biomarker-driven patient selection, long-term safety evaluation, and integration of pharmacological prevention into broader cancer interception programmes.
Additional Links: PMID-42556070
Publisher:
PubMed:
Citation:
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@article {pmid42556070,
year = {2026},
author = {Wespiser, M and Rochefort, P and Gauduchon, T and Coste, C and Caux, C and Ray-Coquard, I and Perol, M and Blay, JY and Heudel, PE},
title = {Pharmacological prevention of second primary cancers: From chemoprevention to precision cancer interception.},
journal = {Cancer treatment reviews},
volume = {149},
number = {},
pages = {103200},
doi = {10.1016/j.ctrv.2026.103200},
pmid = {42556070},
issn = {1532-1967},
abstract = {BACKGROUND: The growing population of cancer survivors is increasingly exposed to the long-term risk of second primary cancers (SPCs), which represents a major source of morbidity and mortality. While current prevention mainly relies on surveillance and screening, pharmacological and immunological strategies may offer opportunities to reduce SPC incidence in selected high-risk populations.
METHODS: This narrative review synthesises current evidence on pharmacological prevention strategies for SPCs, including endocrine therapy, aspirin and non-steroidal anti-inflammatory drugs, PARP inhibitors, metformin, GLP-1 receptor agonists, statins, nicotinamide, immune checkpoint inhibitors, cancer vaccines, and microbiome modulation. Evidence from randomised trials, observational studies, translational research, and ongoing clinical trials was reviewed, with particular attention to SPC-specific endpoints, biological rationale, safety, and clinical applicability.
RESULTS: The strongest evidence currently supports endocrine therapy for reducing contralateral breast cancer in patients with hormone receptor-positive breast cancer, and aspirin in selected populations such as Lynch syndrome carriers or patients with molecularly defined colorectal cancer. Other repurposed agents, including metformin, statins, GLP-1 receptor agonists, and nicotinamide, remain investigational, with most available data addressing incident cancer, recurrence, or surrogate endpoints rather than SPC prevention specifically. Immunological approaches are emerging as particularly promising strategies. Retrospective studies and exploratory analyses of randomised trials suggest that immune checkpoint inhibitors may reduce the occurrence of new malignancies, while neoantigen-based vaccines, especially in Lynch syndrome, provide an early proof of concept for cancer immunoprevention.
CONCLUSIONS: Pharmacological prevention of SPCs is an expanding but remains a heterogeneous field. Current evidence supports a shift from broad chemoprevention toward biologically informed, risk-adapted prevention strategies. Future progress will depend on dedicated SPC-focused trials, biomarker-driven patient selection, long-term safety evaluation, and integration of pharmacological prevention into broader cancer interception programmes.},
}
RevDate: 2026-08-05
Integrated management of cyanobacterial harmful algal blooms: Coupling algaecide treatment with bioaugmentation of toxin degraders.
Journal of hazardous materials, 515:142970 pii:S0304-3894(26)01950-3 [Epub ahead of print].
Cyanobacterial harmful algal blooms (CHABs) are a growing global concern, threatening drinking water safety and complicating water treatment through cyanotoxin release, operational disruptions and increased costs. Although chemical algaecides are widely applied for rapid bloom suppression, they frequently induce cyanobacterial lysis, releasing intracellular toxins that further challenge treatment and increase risks for smaller utilities lacking advanced infrastructure. Bioaugmentation with toxin-degrading bacteria has emerged as a complementary and sustainable strategy, however, the effects of algaecides on bioaugmented bacteria remain poorly understood. This study evaluated an integrated strategy combining algaecide application with bioaugmentation for simultaneous CHAB and cyanotoxin control. Two copper-based (SeClear® and Algimycin® PWF) and two hydrogen peroxide-based (PAK®27 and Oximycin®P5) algaecides were tested in combination with a microcystin (MC)-degrading bacterium, Sphingopyxis sp. IM1 under laboratory and mesocosm conditions. Among the four algaecides and tested concentrations, PAK®27 exhibited the highest compatibility with IM1, with substantial toxin removal observed only under low-dose conditions and after sufficient oxidant decay when IM1 was introduced 24 h post-treatment. Laboratory experiments showed that medium-dose PAK®27 followed by IM1 bioaugmentation reduced chlorophyll-a by 76.7% and dissolved MC-LR by 96.6%. In lake mesocosms, maximum-dose PAK®27 with IM1 achieved 77.6% chl-a reduction and 96% cyanobacterial suppression, lowering MC concentrations below 1 µg/L within 3 days. Microbiome profiling confirmed cyanobacterial collapse accompanied by the proliferation of green algae, diatoms, and heterotrophs, with IM1 abundance negatively correlated with toxin concentrations. These findings demonstrate that hydrogen peroxide-based algaecides combined with targeted bacterial bioaugmentation can provide an effective strategy for rapid toxin mitigation and microbial community recovery in CHAB-impacted waters.
Additional Links: PMID-42556158
Publisher:
PubMed:
Citation:
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@article {pmid42556158,
year = {2026},
author = {Sharmin, A and Zalbegi, S and Bhatia, M and Siddiquee, M and Thomas, AB and Yun, TS and Bishop, WM and Kang, DW and Seo, Y},
title = {Integrated management of cyanobacterial harmful algal blooms: Coupling algaecide treatment with bioaugmentation of toxin degraders.},
journal = {Journal of hazardous materials},
volume = {515},
number = {},
pages = {142970},
doi = {10.1016/j.jhazmat.2026.142970},
pmid = {42556158},
issn = {1873-3336},
abstract = {Cyanobacterial harmful algal blooms (CHABs) are a growing global concern, threatening drinking water safety and complicating water treatment through cyanotoxin release, operational disruptions and increased costs. Although chemical algaecides are widely applied for rapid bloom suppression, they frequently induce cyanobacterial lysis, releasing intracellular toxins that further challenge treatment and increase risks for smaller utilities lacking advanced infrastructure. Bioaugmentation with toxin-degrading bacteria has emerged as a complementary and sustainable strategy, however, the effects of algaecides on bioaugmented bacteria remain poorly understood. This study evaluated an integrated strategy combining algaecide application with bioaugmentation for simultaneous CHAB and cyanotoxin control. Two copper-based (SeClear® and Algimycin® PWF) and two hydrogen peroxide-based (PAK®27 and Oximycin®P5) algaecides were tested in combination with a microcystin (MC)-degrading bacterium, Sphingopyxis sp. IM1 under laboratory and mesocosm conditions. Among the four algaecides and tested concentrations, PAK®27 exhibited the highest compatibility with IM1, with substantial toxin removal observed only under low-dose conditions and after sufficient oxidant decay when IM1 was introduced 24 h post-treatment. Laboratory experiments showed that medium-dose PAK®27 followed by IM1 bioaugmentation reduced chlorophyll-a by 76.7% and dissolved MC-LR by 96.6%. In lake mesocosms, maximum-dose PAK®27 with IM1 achieved 77.6% chl-a reduction and 96% cyanobacterial suppression, lowering MC concentrations below 1 µg/L within 3 days. Microbiome profiling confirmed cyanobacterial collapse accompanied by the proliferation of green algae, diatoms, and heterotrophs, with IM1 abundance negatively correlated with toxin concentrations. These findings demonstrate that hydrogen peroxide-based algaecides combined with targeted bacterial bioaugmentation can provide an effective strategy for rapid toxin mitigation and microbial community recovery in CHAB-impacted waters.},
}
RevDate: 2026-08-05
Niche-driven microbial assembly across the soil-root continuum of Casuarina equisetifolia under a heavy metal pollution gradient.
Ecotoxicology and environmental safety, 323:120615 pii:S0147-6513(26)00945-0 [Epub ahead of print].
Heavy metal pollution (HMP) threatens soil ecosystems and plant health. This study integrated 16S rRNA sequencing, network analysis, environmental mapping, and bacterial isolation to investigate how distinct ecological niches of Casuarina equisetifolia modulate microbial communities under metal stress. Results revealed a spatial pollution gradient, with Pb[2+], Zn[2+], and Cd[2+] decreasing with distance from the mine, while As[5+], Cr[3] [+], and Ni[2+] remained near background levels but displayed significant niche-dependent enrichment, especially for Cr[3] [+], and Ni[2+] in rhizosphere soil under medium and high pollution. Niche was the primary driver of microbial divergence, with only 0.56% of OTUs shared between the soil and root compartments. Rhizosphere soils harbored more unique OTUs and higher α-diversity than non-rhizosphere soils. Root endosphere and rhizosphere soil communities were consistently dominated by Actinobacteria across all pollution levels, whereas non-rhizosphere soil communities shifted from Proteobacteria (low pollution) to Actinobacteria (medium) and Chloroflexi (high). LEfSe identified niche-specific biomarkers from the phylum to genus levels, with high-pollution roots harboring the most diverse indicators. Heavy metals and soil properties (pH, CEC, and SOM) collectively shaped community assembly, with distinct drivers per niche: CEC and Enterobacter in non-rhizosphere soil, pH and Acidobacteriales in rhizosphere soil, and Zn as the central hub in the root endosphere network. Isolation yielded 63 metal-tolerant strains across eight genera, predominantly Bacillus cereus sensu lato group, whose niche origin shifted from the rhizosphere (low pollution) to the non-rhizosphere (medium) to the roots (high pollution), suggesting pollution-associated enrichment. These findings reveal niche-specific community assembly and pollution-driven enrichment of metal-tolerant Bacillus cereus s.l. in the root endosphere.
Additional Links: PMID-42556226
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PubMed:
Citation:
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@article {pmid42556226,
year = {2026},
author = {Zhang, H and Shen, J and Bai, G and Ma, Y and Chu, R and Zhang, N and Zhang, G and Zuo, L and Li, L},
title = {Niche-driven microbial assembly across the soil-root continuum of Casuarina equisetifolia under a heavy metal pollution gradient.},
journal = {Ecotoxicology and environmental safety},
volume = {323},
number = {},
pages = {120615},
doi = {10.1016/j.ecoenv.2026.120615},
pmid = {42556226},
issn = {1090-2414},
abstract = {Heavy metal pollution (HMP) threatens soil ecosystems and plant health. This study integrated 16S rRNA sequencing, network analysis, environmental mapping, and bacterial isolation to investigate how distinct ecological niches of Casuarina equisetifolia modulate microbial communities under metal stress. Results revealed a spatial pollution gradient, with Pb[2+], Zn[2+], and Cd[2+] decreasing with distance from the mine, while As[5+], Cr[3] [+], and Ni[2+] remained near background levels but displayed significant niche-dependent enrichment, especially for Cr[3] [+], and Ni[2+] in rhizosphere soil under medium and high pollution. Niche was the primary driver of microbial divergence, with only 0.56% of OTUs shared between the soil and root compartments. Rhizosphere soils harbored more unique OTUs and higher α-diversity than non-rhizosphere soils. Root endosphere and rhizosphere soil communities were consistently dominated by Actinobacteria across all pollution levels, whereas non-rhizosphere soil communities shifted from Proteobacteria (low pollution) to Actinobacteria (medium) and Chloroflexi (high). LEfSe identified niche-specific biomarkers from the phylum to genus levels, with high-pollution roots harboring the most diverse indicators. Heavy metals and soil properties (pH, CEC, and SOM) collectively shaped community assembly, with distinct drivers per niche: CEC and Enterobacter in non-rhizosphere soil, pH and Acidobacteriales in rhizosphere soil, and Zn as the central hub in the root endosphere network. Isolation yielded 63 metal-tolerant strains across eight genera, predominantly Bacillus cereus sensu lato group, whose niche origin shifted from the rhizosphere (low pollution) to the non-rhizosphere (medium) to the roots (high pollution), suggesting pollution-associated enrichment. These findings reveal niche-specific community assembly and pollution-driven enrichment of metal-tolerant Bacillus cereus s.l. in the root endosphere.},
}
RevDate: 2026-08-05
Coordinated microbial-inflammatory associations in never-smoking lung cancer.
Lung cancer (Amsterdam, Netherlands), 219:109561 pii:S0169-5002(26)00622-7 [Epub ahead of print].
BACKGROUND: While smoking is the leading cause of lung cancer, the increasing incidence among never-smokers is a growing concern, highlighting non-tobacco-related mechanisms of carcinogenesis. Emerging evidence suggests that respiratory microbial dysbiosis and associated inflammatory responses may contribute to lung tumorigenesis. We previously showed that elevated abundances of Selenomonas, Streptococcus, and Veillonella are correlated with lung cancer independent of smoking history. Here, we examine whether circulating microbial and inflammatory profiles are linked to lung cancer in never-smokers.
METHODS: Circulating bacterial DNA representing the three genera was quantified by droplet digital PCR, and seven systemic inflammatory cytokines were measured by ELISA in plasma of 56 ever-smoker lung cancer patients, 56 never-smoker lung cancer patients, and 78 healthy controls. Integrative statistical modeling was performed to evaluate relationships among bacterial DNA burden, inflammatory activation, smoking history, and cancer status.
RESULTS: Plasma DNA levels of Selenomonas, Streptococcus, and Veillonella, together with IL-6, TNF-α, IL-1β, IL-8, and IL-17A, were elevated in lung cancer patients compared with controls (all p < 0.05). No significant differences were observed between smoking and never-smoking lung cancer patients for bacterial DNA levels, IL-6, TNF-α, or IL-17A (all > 0.05), whereas modest but statistically significant differences were observed for IL-8 (P = 0.036) and IL-1β (P = 0.048). Bacterial DNA burden was correlated with systemic inflammatory cytokine activation independent of smoking history (all p < 0.05).
CONCLUSIONS: A smoking-independent microbial-inflammatory signature is associated with lung cancer and provides a foundation for future studies evaluating its biological significance and clinical utility for diagnosis and management.
Additional Links: PMID-42556260
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PubMed:
Citation:
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@article {pmid42556260,
year = {2026},
author = {Dhilipkannah, P and Jiang, F},
title = {Coordinated microbial-inflammatory associations in never-smoking lung cancer.},
journal = {Lung cancer (Amsterdam, Netherlands)},
volume = {219},
number = {},
pages = {109561},
doi = {10.1016/j.lungcan.2026.109561},
pmid = {42556260},
issn = {1872-8332},
abstract = {BACKGROUND: While smoking is the leading cause of lung cancer, the increasing incidence among never-smokers is a growing concern, highlighting non-tobacco-related mechanisms of carcinogenesis. Emerging evidence suggests that respiratory microbial dysbiosis and associated inflammatory responses may contribute to lung tumorigenesis. We previously showed that elevated abundances of Selenomonas, Streptococcus, and Veillonella are correlated with lung cancer independent of smoking history. Here, we examine whether circulating microbial and inflammatory profiles are linked to lung cancer in never-smokers.
METHODS: Circulating bacterial DNA representing the three genera was quantified by droplet digital PCR, and seven systemic inflammatory cytokines were measured by ELISA in plasma of 56 ever-smoker lung cancer patients, 56 never-smoker lung cancer patients, and 78 healthy controls. Integrative statistical modeling was performed to evaluate relationships among bacterial DNA burden, inflammatory activation, smoking history, and cancer status.
RESULTS: Plasma DNA levels of Selenomonas, Streptococcus, and Veillonella, together with IL-6, TNF-α, IL-1β, IL-8, and IL-17A, were elevated in lung cancer patients compared with controls (all p < 0.05). No significant differences were observed between smoking and never-smoking lung cancer patients for bacterial DNA levels, IL-6, TNF-α, or IL-17A (all > 0.05), whereas modest but statistically significant differences were observed for IL-8 (P = 0.036) and IL-1β (P = 0.048). Bacterial DNA burden was correlated with systemic inflammatory cytokine activation independent of smoking history (all p < 0.05).
CONCLUSIONS: A smoking-independent microbial-inflammatory signature is associated with lung cancer and provides a foundation for future studies evaluating its biological significance and clinical utility for diagnosis and management.},
}
RevDate: 2026-08-05
Paenibacillus polymyxa drives root fatty acyl metabolites-rhizosphere Pseudomonas abundance interaction to suppress root-knot nematode disease in tomato.
Microbiological research, 312:128662 pii:S0944-5013(26)00226-0 [Epub ahead of print].
Root-knot nematodes (RKNs) pose a severe threat to global agricultural production, highlighting the urgent need for effective biocontrol agents. However, the mechanisms by which biocontrol agents suppress RKNs in complex soil environments remain poorly understood, which hinders the development and practical application of these agents. In the present study, the application of Paenibacillus polymyxa KM2501-1 significantly reduced RKN disease, with a control efficacy of 69.89%. Metabolomics analysis revealed that the biocontrol agent P. polymyxa altered the composition of tomato root exudates, leading to the identification of a key fatty acyl metabolite 8-methylnon-6-enoic acid. Specifically, P. polymyxa increased the abundance of 8-methylnon-6-enoic acid, which exhibited repellent activity against RKNs in vitro and suppressed RKN infection in situ. Metagenomic analysis further demonstrated that P. polymyxa reshaped the tomato rhizosphere microbial community and promoted the enrichment of Pseudomonas putida, particularly its representative strains PR035 and PR036. Both strains exhibited significant biocontrol efficacy against Meloidogyne incognita. A significant positive correlation was observed between the levels of key metabolite 8-methylnon-6-enoic acid and the abundance of P. putida, and their combined application exhibited effective control against M. incognita. Overall, this study demonstrates that the suppression of RKNs by P. polymyxa is associated with triggering the exudation of fatty acyl metabolites from tomato roots and enriching rhizosphere Pseudomonas populations. These findings provide valuable insights into the interplay between root metabolites and the rhizosphere microbiome in mediating synergistic plant disease control, offering a theoretical basis for the development of next-generation microbial nematicides.
Additional Links: PMID-42556262
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PubMed:
Citation:
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@article {pmid42556262,
year = {2026},
author = {Dai, W and Yang, F and Chen, W and Liu, C and Henawy, AR and Liu, X and Huang, F and Cai, M and Zheng, L and Yu, Z and Gong, Y and van Huis, A and Zhang, J and Cheng, W},
title = {Paenibacillus polymyxa drives root fatty acyl metabolites-rhizosphere Pseudomonas abundance interaction to suppress root-knot nematode disease in tomato.},
journal = {Microbiological research},
volume = {312},
number = {},
pages = {128662},
doi = {10.1016/j.micres.2026.128662},
pmid = {42556262},
issn = {1618-0623},
abstract = {Root-knot nematodes (RKNs) pose a severe threat to global agricultural production, highlighting the urgent need for effective biocontrol agents. However, the mechanisms by which biocontrol agents suppress RKNs in complex soil environments remain poorly understood, which hinders the development and practical application of these agents. In the present study, the application of Paenibacillus polymyxa KM2501-1 significantly reduced RKN disease, with a control efficacy of 69.89%. Metabolomics analysis revealed that the biocontrol agent P. polymyxa altered the composition of tomato root exudates, leading to the identification of a key fatty acyl metabolite 8-methylnon-6-enoic acid. Specifically, P. polymyxa increased the abundance of 8-methylnon-6-enoic acid, which exhibited repellent activity against RKNs in vitro and suppressed RKN infection in situ. Metagenomic analysis further demonstrated that P. polymyxa reshaped the tomato rhizosphere microbial community and promoted the enrichment of Pseudomonas putida, particularly its representative strains PR035 and PR036. Both strains exhibited significant biocontrol efficacy against Meloidogyne incognita. A significant positive correlation was observed between the levels of key metabolite 8-methylnon-6-enoic acid and the abundance of P. putida, and their combined application exhibited effective control against M. incognita. Overall, this study demonstrates that the suppression of RKNs by P. polymyxa is associated with triggering the exudation of fatty acyl metabolites from tomato roots and enriching rhizosphere Pseudomonas populations. These findings provide valuable insights into the interplay between root metabolites and the rhizosphere microbiome in mediating synergistic plant disease control, offering a theoretical basis for the development of next-generation microbial nematicides.},
}
RevDate: 2026-08-05
Translating the gut microbiome: where are we?.
The lancet. Gastroenterology & hepatology, 11(9):750-752.
Additional Links: PMID-42556364
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PubMed:
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@article {pmid42556364,
year = {2026},
author = {Raes, J},
title = {Translating the gut microbiome: where are we?.},
journal = {The lancet. Gastroenterology & hepatology},
volume = {11},
number = {9},
pages = {750-752},
doi = {10.1016/S2468-1253(26)00181-0},
pmid = {42556364},
issn = {2468-1253},
}
RevDate: 2026-08-05
Dietary carboxymethyl starch improves glycemic control and enhances barrier function via Bifidobacterium-mediated galactose metabolism in vivo and in organoids.
International journal of biological macromolecules pii:S0141-8130(26)03871-7 [Epub ahead of print].
Etherified resistant starches (ERS), including hydroxypropyl starch (HPS), carboxymethyl starch (CMS), and hydroxyethyl starch (HES), are emerging as functional food ingredients with potential to modulate glycemic responses and gut health. However, their comparative efficacy and underlying gut-mediated mechanisms remain poorly defined. This study systematically evaluated their digestive properties and effects on gut microbiota. In vitro digestion demonstrated that etherification substantially increased resistant starch content, with CMS exhibiting approximately 70% resistant starch content and the lowest estimated glycemic index (GI = 53) among the tested starches. In vivo evaluation further showed that CMS significantly attenuated the peak postprandial glucose level (9.6 mmol/L) compared with native starch (17.4 mmol/L). Microbiome analysis revealed that CMS intervention was associated with specific remodeling of the gut microbiota, notably enriching beneficial Bifidobacterium pseudocatenulatum and Bifidobacterium adolescentis. Functionally, integrated KEGG pathway analysis and metabolomics consistently indicated that CMS markedly downregulated galactose metabolism, evidenced by reduced concentrations of galactose-related metabolites such as galactonic acid and galactitol. Furthermore, Spearman correlation analysis highlighted a strong mechanistic link between B. adolescentis abundance and galactose metabolic shifts. Crucially, utilizing, CMS-derived microbiota enhanced intestinal barrier function and galactose metabolism via co-culture model of gut microbiota and colonic organoids. Overall, CMS as a promising functional food ingredient that not only mitigates postprandial glycemia but also improves gut health by regulating microbiota-dependent galactose metabolism.
Additional Links: PMID-42556662
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PubMed:
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@article {pmid42556662,
year = {2026},
author = {Fan, Y and Xu, Z and Zheng, H and Han, J and Hu, S and Pan, X and Ma, R and Liu, C and Tian, Y},
title = {Dietary carboxymethyl starch improves glycemic control and enhances barrier function via Bifidobacterium-mediated galactose metabolism in vivo and in organoids.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {153925},
doi = {10.1016/j.ijbiomac.2026.153925},
pmid = {42556662},
issn = {1879-0003},
abstract = {Etherified resistant starches (ERS), including hydroxypropyl starch (HPS), carboxymethyl starch (CMS), and hydroxyethyl starch (HES), are emerging as functional food ingredients with potential to modulate glycemic responses and gut health. However, their comparative efficacy and underlying gut-mediated mechanisms remain poorly defined. This study systematically evaluated their digestive properties and effects on gut microbiota. In vitro digestion demonstrated that etherification substantially increased resistant starch content, with CMS exhibiting approximately 70% resistant starch content and the lowest estimated glycemic index (GI = 53) among the tested starches. In vivo evaluation further showed that CMS significantly attenuated the peak postprandial glucose level (9.6 mmol/L) compared with native starch (17.4 mmol/L). Microbiome analysis revealed that CMS intervention was associated with specific remodeling of the gut microbiota, notably enriching beneficial Bifidobacterium pseudocatenulatum and Bifidobacterium adolescentis. Functionally, integrated KEGG pathway analysis and metabolomics consistently indicated that CMS markedly downregulated galactose metabolism, evidenced by reduced concentrations of galactose-related metabolites such as galactonic acid and galactitol. Furthermore, Spearman correlation analysis highlighted a strong mechanistic link between B. adolescentis abundance and galactose metabolic shifts. Crucially, utilizing, CMS-derived microbiota enhanced intestinal barrier function and galactose metabolism via co-culture model of gut microbiota and colonic organoids. Overall, CMS as a promising functional food ingredient that not only mitigates postprandial glycemia but also improves gut health by regulating microbiota-dependent galactose metabolism.},
}
RevDate: 2026-08-05
Gut microbiome composition in Huntington's disease: Stage-dependent differences between premanifest and manifest patients.
Life sciences pii:S0024-3205(26)00426-1 [Epub ahead of print].
BACKGROUND: Huntington's disease (HD) is a progressive neurodegenerative disorder with substantial clinical heterogeneity. The gut microbiome has been proposed as a potential modulator of neurodegeneration, but its role in HD and across disease stages remains unclear.
METHODS: This cross-sectional case-control study included 50 individuals with HD (35 manifest, 15 pre-manifest) and 36 age- and sex-matched cohabiting controls. Stool samples were analysed using 16S rRNA sequencing. Clinical, lifestyle, and dietary variables were recorded. Microbial diversity and differential taxonomic abundance were assessed, accounting for relevant covariates.
RESULTS: No significant differences in global microbial diversity were observed between HD and controls. Age was the main factor associated with both alpha and beta diversity. However, HD was associated with discrete taxonomic differences. More pronounced alterations were identified between manifest and pre-manifest stages, with exploratory genus-level compositional differences identified between disease stages. Antibiotic exposure significantly reduced microbial richness and influenced community structure.
CONCLUSIONS: Gut microbiome alterations in HD may differ across clinical stages rather than reflecting global dysbiosis. These exploratory findings suggest that microbiome composition may contribute to disease heterogeneity, although confirmation in larger longitudinal and independent cohorts is required before considering its potential as a biomarker or therapeutic target.
Additional Links: PMID-42556710
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PubMed:
Citation:
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@article {pmid42556710,
year = {2026},
author = {Simón-Vicente, L and Lafont, MO and Franch, MA and Menéndez-Trillo, P and Rivadeneyra-Posadas, J and Miguel-Pérez, I and Aguado, L and Siscart, IM and Piñeiro, DD and Mariscal, N and Megías-Lobón, G and Calvo, S and Cubo, E and Saiz-Rodríguez, M},
title = {Gut microbiome composition in Huntington's disease: Stage-dependent differences between premanifest and manifest patients.},
journal = {Life sciences},
volume = {},
number = {},
pages = {124617},
doi = {10.1016/j.lfs.2026.124617},
pmid = {42556710},
issn = {1879-0631},
abstract = {BACKGROUND: Huntington's disease (HD) is a progressive neurodegenerative disorder with substantial clinical heterogeneity. The gut microbiome has been proposed as a potential modulator of neurodegeneration, but its role in HD and across disease stages remains unclear.
METHODS: This cross-sectional case-control study included 50 individuals with HD (35 manifest, 15 pre-manifest) and 36 age- and sex-matched cohabiting controls. Stool samples were analysed using 16S rRNA sequencing. Clinical, lifestyle, and dietary variables were recorded. Microbial diversity and differential taxonomic abundance were assessed, accounting for relevant covariates.
RESULTS: No significant differences in global microbial diversity were observed between HD and controls. Age was the main factor associated with both alpha and beta diversity. However, HD was associated with discrete taxonomic differences. More pronounced alterations were identified between manifest and pre-manifest stages, with exploratory genus-level compositional differences identified between disease stages. Antibiotic exposure significantly reduced microbial richness and influenced community structure.
CONCLUSIONS: Gut microbiome alterations in HD may differ across clinical stages rather than reflecting global dysbiosis. These exploratory findings suggest that microbiome composition may contribute to disease heterogeneity, although confirmation in larger longitudinal and independent cohorts is required before considering its potential as a biomarker or therapeutic target.},
}
RevDate: 2026-08-05
CmpDate: 2026-08-05
Microbiota, fermentation, and metabolite biotransformation: Pathways to functional foods and personalised nutrition.
Advances in food and nutrition research, 121:79-130.
Fermentation is among the oldest biotechnological processes and a modern platform for precision metabolic engineering, enabling the targeted production of health-promoting metabolites. The human gut microbiota, with its complex enzymatic potential, converts dietary substrates into a wide range of bioactive molecules, including short-chain fatty acids, vitamins, neuroactive compounds, and polyphenol-derived metabolites that influence host metabolism, immunity, and neurological functions. Advances in microbial genomics, systems biology, and synthetic biology now allow the design of fermentation processes and engineered microbial strains capable of producing specific metabolites with improved bioavailability and tailored health effects. Precision fermentation integrates traditional microbial fermentation with genome editing, metabolic flux optimisation, and AI-assisted pathway design to achieve predictable yields of vitamins, polyphenols, bioactive peptides, and long-chain polyunsaturated fatty acids. These innovations create opportunities to develop functional foods, nutraceuticals, and personalized nutrition strategies that match metabolite profiles to an individual's microbiome composition. This chapter explores the mechanistic links between microbial metabolism and host health, reviews emerging fermentation technologies for targeted metabolite production, and highlights industrial case studies demonstrating the transition of precision fermentation from research to commercial applications.
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@article {pmid42556887,
year = {2026},
author = {Mitrea, L and Martău, GA and Călinoiu, LF and Vodnar, DC},
title = {Microbiota, fermentation, and metabolite biotransformation: Pathways to functional foods and personalised nutrition.},
journal = {Advances in food and nutrition research},
volume = {121},
number = {},
pages = {79-130},
doi = {10.1016/bs.afnr.2026.02.001},
pmid = {42556887},
issn = {1043-4526},
mesh = {*Fermentation ; Humans ; *Functional Food ; *Biotransformation ; *Gastrointestinal Microbiome/physiology ; *Precision Medicine ; },
abstract = {Fermentation is among the oldest biotechnological processes and a modern platform for precision metabolic engineering, enabling the targeted production of health-promoting metabolites. The human gut microbiota, with its complex enzymatic potential, converts dietary substrates into a wide range of bioactive molecules, including short-chain fatty acids, vitamins, neuroactive compounds, and polyphenol-derived metabolites that influence host metabolism, immunity, and neurological functions. Advances in microbial genomics, systems biology, and synthetic biology now allow the design of fermentation processes and engineered microbial strains capable of producing specific metabolites with improved bioavailability and tailored health effects. Precision fermentation integrates traditional microbial fermentation with genome editing, metabolic flux optimisation, and AI-assisted pathway design to achieve predictable yields of vitamins, polyphenols, bioactive peptides, and long-chain polyunsaturated fatty acids. These innovations create opportunities to develop functional foods, nutraceuticals, and personalized nutrition strategies that match metabolite profiles to an individual's microbiome composition. This chapter explores the mechanistic links between microbial metabolism and host health, reviews emerging fermentation technologies for targeted metabolite production, and highlights industrial case studies demonstrating the transition of precision fermentation from research to commercial applications.},
}
MeSH Terms:
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*Fermentation
Humans
*Functional Food
*Biotransformation
*Gastrointestinal Microbiome/physiology
*Precision Medicine
RevDate: 2026-08-06
First poo transplant to treat food allergy in people has 'exciting' results.
Additional Links: PMID-42557497
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Citation:
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@article {pmid42557497,
year = {2026},
author = {Chen, E},
title = {First poo transplant to treat food allergy in people has 'exciting' results.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42557497},
issn = {1476-4687},
}
RevDate: 2026-08-06
Diurnal dynamics of maize gene expression is associated with phyllosphere microbiome composition.
International microbiology : the official journal of the Spanish Society for Microbiology [Epub ahead of print].
Bacterial communities play important roles in the plant phyllosphere. Both microbial communities and their hosts exhibit endogenous circadian rhythms while simultaneously responding to environmental changes across the diurnal cycle. However, the interaction between the host and microbiome is still poorly understood. Here, we exploit paired sequencing data of host transcriptome and microbiome derived from diverse maize genotypes in field conditions and under two contrasting diurnal periods. Expression patterns of known maize circadian clock genes were consistent with the expected sampling phases. Groups of co-expressed genes that responded to diurnal periods were associated with nucleic acid-binding, heat stress responses, and photosynthesis. Microbiome analysis revealed only modest differences in alpha diversity between midday and midnight samples. However, beta diversity indicated a significant shift in community composition. Co-occurrence network analysis identified keystone taxa specific to each time point, suggesting time-dependent ecological roles within the phyllosphere microbiome. Cross-correlation analyses between host gene expression and bacterial taxon abundance revealed a greater number of host-microbe associations during the night. Several canonical circadian clock genes significantly correlated with microbial taxa. Our findings provide initial evidence for diurnal associations between host gene expression and leaf-associated bacteriome, suggesting that maize diurnal transcriptional dynamics, including the activity of circadian clock genes, may contribute to shaping the composition and functional potential of the phyllosphere microbiome.
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@article {pmid42557505,
year = {2026},
author = {Dos Santos, RAC and Hidalgo-Martinez, K and Muñoz-Perez, JM and Laspisa, DJ and Li, C and Mendes, LW and Riaño-Pachón, DM and Wallace, JG},
title = {Diurnal dynamics of maize gene expression is associated with phyllosphere microbiome composition.},
journal = {International microbiology : the official journal of the Spanish Society for Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42557505},
issn = {1618-1905},
abstract = {Bacterial communities play important roles in the plant phyllosphere. Both microbial communities and their hosts exhibit endogenous circadian rhythms while simultaneously responding to environmental changes across the diurnal cycle. However, the interaction between the host and microbiome is still poorly understood. Here, we exploit paired sequencing data of host transcriptome and microbiome derived from diverse maize genotypes in field conditions and under two contrasting diurnal periods. Expression patterns of known maize circadian clock genes were consistent with the expected sampling phases. Groups of co-expressed genes that responded to diurnal periods were associated with nucleic acid-binding, heat stress responses, and photosynthesis. Microbiome analysis revealed only modest differences in alpha diversity between midday and midnight samples. However, beta diversity indicated a significant shift in community composition. Co-occurrence network analysis identified keystone taxa specific to each time point, suggesting time-dependent ecological roles within the phyllosphere microbiome. Cross-correlation analyses between host gene expression and bacterial taxon abundance revealed a greater number of host-microbe associations during the night. Several canonical circadian clock genes significantly correlated with microbial taxa. Our findings provide initial evidence for diurnal associations between host gene expression and leaf-associated bacteriome, suggesting that maize diurnal transcriptional dynamics, including the activity of circadian clock genes, may contribute to shaping the composition and functional potential of the phyllosphere microbiome.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Genomic characteristics and geographical distribution of uncultivated soil prokaryotes.
BMC genomics, 27(1):.
Most soil prokaryotic species remain uncultivated, limiting our understanding of the terrestrial microbiome. Metagenomic sequencing, and particularly the study of metagenome-assembled genomes (MAGs), represents an unprecedented opportunity to characterize the genomic features and biogeography of uncultivated prokaryotic taxa at the large scale. Here, we analyze 40,039 genomic bins from cultivated and uncultivated soil taxa within the SMAG catalog, and examine the occurrence of uncultivated prokaryotes in 9,012 metagenomic samples from the Sandpiper resource. Compared to genera with cultivated representatives, uncultivated soil prokaryotes show smaller genomes, lower G + C content, tendency to acidophilic, non-alkaline, thermophilic and host-associated lifestyles, and slower growth rates, with the latter having the highest predictive power for cultivation status. Uncultivated soil microbes also show unique gene repertoires, characterized by a depletion of biosynthetic and motility genes. We also show that completely uncultivated genera are more abundant in tropical and arctic soils, indicating substantial hidden diversity in these regions. Our work emphasizes that current cultivation efforts systematically fail to capture a particular fraction of soil prokaryotic diversity, and provides guidelines for future cultivation strategies.
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@article {pmid42557545,
year = {2026},
author = {Rodríguez Del Río, Á and Cui, Y and Mansour, I and Rillig, MC},
title = {Genomic characteristics and geographical distribution of uncultivated soil prokaryotes.},
journal = {BMC genomics},
volume = {27},
number = {1},
pages = {},
pmid = {42557545},
issn = {1471-2164},
mesh = {*Soil Microbiology ; Metagenomics ; Metagenome ; *Bacteria/genetics/classification ; *Genome, Bacterial ; *Genomics ; Phylogeography ; Phylogeny ; *Prokaryotic Cells ; *Archaea/genetics/classification ; },
abstract = {Most soil prokaryotic species remain uncultivated, limiting our understanding of the terrestrial microbiome. Metagenomic sequencing, and particularly the study of metagenome-assembled genomes (MAGs), represents an unprecedented opportunity to characterize the genomic features and biogeography of uncultivated prokaryotic taxa at the large scale. Here, we analyze 40,039 genomic bins from cultivated and uncultivated soil taxa within the SMAG catalog, and examine the occurrence of uncultivated prokaryotes in 9,012 metagenomic samples from the Sandpiper resource. Compared to genera with cultivated representatives, uncultivated soil prokaryotes show smaller genomes, lower G + C content, tendency to acidophilic, non-alkaline, thermophilic and host-associated lifestyles, and slower growth rates, with the latter having the highest predictive power for cultivation status. Uncultivated soil microbes also show unique gene repertoires, characterized by a depletion of biosynthetic and motility genes. We also show that completely uncultivated genera are more abundant in tropical and arctic soils, indicating substantial hidden diversity in these regions. Our work emphasizes that current cultivation efforts systematically fail to capture a particular fraction of soil prokaryotic diversity, and provides guidelines for future cultivation strategies.},
}
MeSH Terms:
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hide MeSH Terms
*Soil Microbiology
Metagenomics
Metagenome
*Bacteria/genetics/classification
*Genome, Bacterial
*Genomics
Phylogeography
Phylogeny
*Prokaryotic Cells
*Archaea/genetics/classification
RevDate: 2026-08-06
CmpDate: 2026-08-06
Temperature and Ultraviolet Radiation Influence the Skin Microbiome of Humpback Whales.
Molecular ecology, 35(15):e70500.
The skin microbiome of humpback whales harbours diverse microbial communities that play a crucial role in host skin protection and environmental interaction. However, studies on cetacean skin microbiomes in the Southern Hemisphere focus on feeding grounds, with limited information on microbiome dynamics at breeding grounds and during migration across contrasting habitats. We characterised the skin microbiome of 46 humpback whales from two seasonal habitats: the Magellan Strait feeding ground and the Ecuadorian coast breeding ground, comparing age, sex, environmental conditions, and seawater. Amplicon sequencing of the 16S rRNA gene revealed no differences in alpha diversity, but habitat-specific compositional shifts were found. Psychrobacter was detected in both regions, with higher abundance in the feeding ground, while Tenacibaculum remained abundant across sites. Additional taxa exhibited habitat-specific patterns, including bacteria associated with thermal sensitivity and ultraviolet radiation-tolerance in the Magellan Strait, and lactic acid bacteria in Ecuador. Skin microbiomes were similar between age classes and sexes, but distinct from seawater. Our findings show that geographic and environmental factors, such as superficial seawater temperature and maximum ultraviolet B radiation, shape the skin microbiome of humpback whales, with certain taxa reflecting migratory behaviour across seasonal habitats.
Additional Links: PMID-42557733
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PubMed:
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@article {pmid42557733,
year = {2026},
author = {Murillo-Herrera, AI and Eguiarte, LE and Acuña Gómez, EP and Castro, C and Acevedo, J and Castrillon, J and Oyarzún-Galaz, L and Valenzuela, P and Aguayo-Lobo, A and Pastene, LA and Souza, V},
title = {Temperature and Ultraviolet Radiation Influence the Skin Microbiome of Humpback Whales.},
journal = {Molecular ecology},
volume = {35},
number = {15},
pages = {e70500},
doi = {10.1111/mec.70500},
pmid = {42557733},
issn = {1365-294X},
support = {R20F0009//Agencia Nacional de Investigación y Desarrollo/ ; },
mesh = {Animals ; *Ultraviolet Rays ; RNA, Ribosomal, 16S/genetics ; Female ; *Humpback Whale/microbiology ; *Skin Microbiome ; Male ; *Temperature ; *Bacteria/classification/genetics ; *Skin/microbiology ; Ecuador ; Ecosystem ; *Microbiota ; Seawater ; Sequence Analysis, DNA ; Seasons ; DNA, Bacterial/genetics ; },
abstract = {The skin microbiome of humpback whales harbours diverse microbial communities that play a crucial role in host skin protection and environmental interaction. However, studies on cetacean skin microbiomes in the Southern Hemisphere focus on feeding grounds, with limited information on microbiome dynamics at breeding grounds and during migration across contrasting habitats. We characterised the skin microbiome of 46 humpback whales from two seasonal habitats: the Magellan Strait feeding ground and the Ecuadorian coast breeding ground, comparing age, sex, environmental conditions, and seawater. Amplicon sequencing of the 16S rRNA gene revealed no differences in alpha diversity, but habitat-specific compositional shifts were found. Psychrobacter was detected in both regions, with higher abundance in the feeding ground, while Tenacibaculum remained abundant across sites. Additional taxa exhibited habitat-specific patterns, including bacteria associated with thermal sensitivity and ultraviolet radiation-tolerance in the Magellan Strait, and lactic acid bacteria in Ecuador. Skin microbiomes were similar between age classes and sexes, but distinct from seawater. Our findings show that geographic and environmental factors, such as superficial seawater temperature and maximum ultraviolet B radiation, shape the skin microbiome of humpback whales, with certain taxa reflecting migratory behaviour across seasonal habitats.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Ultraviolet Rays
RNA, Ribosomal, 16S/genetics
Female
*Humpback Whale/microbiology
*Skin Microbiome
Male
*Temperature
*Bacteria/classification/genetics
*Skin/microbiology
Ecuador
Ecosystem
*Microbiota
Seawater
Sequence Analysis, DNA
Seasons
DNA, Bacterial/genetics
RevDate: 2026-08-06
Microbial mediation of invasion: Effects of environmental microbiota on the development and physiology of Aedes albopictus.
Medical and veterinary entomology [Epub ahead of print].
Global invasions by the mosquito Aedes albopictus pose serious threats to biodiversity and public health due to its capacity to vector multiple emerging infectious diseases. As a highly invasive species, its success is closely linked to environmental conditions during its complex life cycle. In this study, we investigated how compositionally distinct environmental microbiomes influence A. albopictus development, physiology and starvation resistance. Larvae were reared in mesocosms containing water from three sources-laboratory, plastic buckets and bromeliad tanks-each filtered at three levels (30-50 μm, 10 μm and 0.1 μm) to manipulate microbial diversity. We found that microbial community composition significantly affected larval development time and pupation success. Larvae reared in water with reduced microbial diversity developed faster and had higher pupation success than those exposed to more complex communities. Although lipid concentrations and time to adult eclosion were unaffected across habitat types, adult survival under starvation conditions varied significantly by microbial exposure and sex. Females from low-diversity habitat types exhibited the highest survival, suggesting early-life microbial environments influence adult fitness traits critical to invasion success. These results highlight the ecological importance of environmental microbiomes in shaping mosquito life history and suggest that microbial diversity in larval habitat types may influence the establishment and spread of A. albopictus in novel environments.
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PubMed:
Citation:
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@article {pmid42557796,
year = {2026},
author = {Griffin, CD and Schreiber, J and Bierwert, A and Olaso, CM and Medeiros, MCI},
title = {Microbial mediation of invasion: Effects of environmental microbiota on the development and physiology of Aedes albopictus.},
journal = {Medical and veterinary entomology},
volume = {},
number = {},
pages = {},
doi = {10.1111/mve.70106},
pmid = {42557796},
issn = {1365-2915},
support = {/NH/NIH HHS/United States ; //University of Hawai'i at Mānoa Undergraduate Research Opportunities Program/ ; },
abstract = {Global invasions by the mosquito Aedes albopictus pose serious threats to biodiversity and public health due to its capacity to vector multiple emerging infectious diseases. As a highly invasive species, its success is closely linked to environmental conditions during its complex life cycle. In this study, we investigated how compositionally distinct environmental microbiomes influence A. albopictus development, physiology and starvation resistance. Larvae were reared in mesocosms containing water from three sources-laboratory, plastic buckets and bromeliad tanks-each filtered at three levels (30-50 μm, 10 μm and 0.1 μm) to manipulate microbial diversity. We found that microbial community composition significantly affected larval development time and pupation success. Larvae reared in water with reduced microbial diversity developed faster and had higher pupation success than those exposed to more complex communities. Although lipid concentrations and time to adult eclosion were unaffected across habitat types, adult survival under starvation conditions varied significantly by microbial exposure and sex. Females from low-diversity habitat types exhibited the highest survival, suggesting early-life microbial environments influence adult fitness traits critical to invasion success. These results highlight the ecological importance of environmental microbiomes in shaping mosquito life history and suggest that microbial diversity in larval habitat types may influence the establishment and spread of A. albopictus in novel environments.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Work-Influenced Circadian Disruption Connected to Disease Risk but Not Microbiomes in a Cohort of Philadelphia Nurses.
American journal of human biology : the official journal of the Human Biology Council, 38(8):e70314.
OBJECTIVES: Circadian rhythms influence activity cycles in humans, and circadian rhythm disruption (CRD) can negatively impact cardiometabolic disease risk and microbiome composition. This study documented CRD in a sample of nurses in Philadelphia, examining connections between CRD, disease risk, and work environment factors, proposing the concept of work-influenced circadian disruption (WICD).
MATERIALS AND METHODS: A total of 75 nurses were recruited for the study. Disease risk indicators included triglycerides (TRG), C-reactive protein (hs-CRP), blood pressure (BP), and fecal gut microbiome composition. Surveys recorded CRD via sleep/exhaustion levels, weekly exercise, mealtime timing/length, shift diet, and night shift work. Work environment variables included staff/resources, physician-nurse relations, break times, and patient care assignments. Mixed multiple regression models assessed CRD's associations with cardiometabolic disease risk indicators (H1) and work environment variables (H2). Microbiome similarity by CRD variables was tested using PERMANOVAs.
RESULTS: Lower exercise levels were associated with higher hs-CRP (β = -4.2, p = 0.05), TRG (β = -9.8, p = 0.03), BP (β = -3.6, p = 0.01), and less break time (β = 0.1, p = 0.01). Higher exhaustion was linked to elevated hs-CRP (β = 6.0, p = 0.02) and fewer staff/resources (β = -0.7, p = 0.01). Less mealtime was associated with higher BP (β = -0.2, p = 0.05) and shorter breaks (β = 0.2, p = 0.04). Night shifts were linked to higher BP (β = 6.3, p = 0.01). CRD variables were not significantly associated with microbiome profiles.
CONCLUSIONS: CRD is associated with disease risk indicators and with work environment variables but not with microbiome profiles, suggesting these relationships may operate through other pathways. Further studies should explore biobehavioral networks in WICD.
Additional Links: PMID-42557889
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@article {pmid42557889,
year = {2026},
author = {Super, C and Asif, M and Compher, C and Schurr, TG and Hoke, MK},
title = {Work-Influenced Circadian Disruption Connected to Disease Risk but Not Microbiomes in a Cohort of Philadelphia Nurses.},
journal = {American journal of human biology : the official journal of the Human Biology Council},
volume = {38},
number = {8},
pages = {e70314},
doi = {10.1002/ajhb.70314},
pmid = {42557889},
issn = {1520-6300},
support = {BCS-2147647//National Science Foundation/ ; DFG 584233//Wenner-Gren Foundation/ ; },
mesh = {Humans ; *Nurses/statistics & numerical data ; *Circadian Rhythm ; Philadelphia/epidemiology ; Adult ; Working Conditions ; Female ; Male ; Middle Aged ; *Gastrointestinal Microbiome ; Risk Factors ; Cohort Studies ; *Chronobiology Disorders/epidemiology ; *Cardiometabolic Risk Factors ; },
abstract = {OBJECTIVES: Circadian rhythms influence activity cycles in humans, and circadian rhythm disruption (CRD) can negatively impact cardiometabolic disease risk and microbiome composition. This study documented CRD in a sample of nurses in Philadelphia, examining connections between CRD, disease risk, and work environment factors, proposing the concept of work-influenced circadian disruption (WICD).
MATERIALS AND METHODS: A total of 75 nurses were recruited for the study. Disease risk indicators included triglycerides (TRG), C-reactive protein (hs-CRP), blood pressure (BP), and fecal gut microbiome composition. Surveys recorded CRD via sleep/exhaustion levels, weekly exercise, mealtime timing/length, shift diet, and night shift work. Work environment variables included staff/resources, physician-nurse relations, break times, and patient care assignments. Mixed multiple regression models assessed CRD's associations with cardiometabolic disease risk indicators (H1) and work environment variables (H2). Microbiome similarity by CRD variables was tested using PERMANOVAs.
RESULTS: Lower exercise levels were associated with higher hs-CRP (β = -4.2, p = 0.05), TRG (β = -9.8, p = 0.03), BP (β = -3.6, p = 0.01), and less break time (β = 0.1, p = 0.01). Higher exhaustion was linked to elevated hs-CRP (β = 6.0, p = 0.02) and fewer staff/resources (β = -0.7, p = 0.01). Less mealtime was associated with higher BP (β = -0.2, p = 0.05) and shorter breaks (β = 0.2, p = 0.04). Night shifts were linked to higher BP (β = 6.3, p = 0.01). CRD variables were not significantly associated with microbiome profiles.
CONCLUSIONS: CRD is associated with disease risk indicators and with work environment variables but not with microbiome profiles, suggesting these relationships may operate through other pathways. Further studies should explore biobehavioral networks in WICD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Nurses/statistics & numerical data
*Circadian Rhythm
Philadelphia/epidemiology
Adult
Working Conditions
Female
Male
Middle Aged
*Gastrointestinal Microbiome
Risk Factors
Cohort Studies
*Chronobiology Disorders/epidemiology
*Cardiometabolic Risk Factors
RevDate: 2026-08-06
Pain syndromes in transplantation: the role of the gut microbiome.
Current opinion in organ transplantation pii:00075200-990000000-00240 [Epub ahead of print].
PURPOSE OF REVIEW: The purpose of this review is to discuss common pain phenotypes in transplantation, summarize known gut microbiome features associated with chronic pain, and to map known gut microbiome features in transplantation with diagnosis-independent pain features.
RECENT FINDINGS: Persistent pain is common across solid organ and hematopoietic stem cell transplantation, arises from diverse mechanisms, and often extends well beyond the perioperative period. Growing evidence supports the gut microbiome as a biologically plausible modulator of chronic pain across disease states, including transplantation. Alterations in microbial diversity, microbial metabolites, intestinal barrier integrity, and neuroimmune signaling have been linked to pain amplification and central sensitization across multiple chronic pain conditions. In transplant populations, exposure to immunosuppressive therapies, antibiotics, metabolic comorbidities, and other transplant-related stressors creates a unique environment for sustained microbiome disruption that may contribute to persistent symptom burden.
SUMMARY: Collectively, these data highlight the importance to systematically assess and manage pain as a core transplant outcome rather than a secondary concern, and to highlight the potential role of the gut microbiome as a risk screening tool or a therapeutic target for pain interventions. Although mechanistic and observational data support biologic plausibility, transplant-specific microbiome-pain evidence remains preliminary and warrants longitudinal investigation.
Additional Links: PMID-42557943
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PubMed:
Citation:
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@article {pmid42557943,
year = {2026},
author = {Lockwood, MB and Gallon, L and Kortan, E and Tussing-Humphreys, L},
title = {Pain syndromes in transplantation: the role of the gut microbiome.},
journal = {Current opinion in organ transplantation},
volume = {},
number = {},
pages = {},
doi = {10.1097/MOT.0000000000001308},
pmid = {42557943},
issn = {1531-7013},
abstract = {PURPOSE OF REVIEW: The purpose of this review is to discuss common pain phenotypes in transplantation, summarize known gut microbiome features associated with chronic pain, and to map known gut microbiome features in transplantation with diagnosis-independent pain features.
RECENT FINDINGS: Persistent pain is common across solid organ and hematopoietic stem cell transplantation, arises from diverse mechanisms, and often extends well beyond the perioperative period. Growing evidence supports the gut microbiome as a biologically plausible modulator of chronic pain across disease states, including transplantation. Alterations in microbial diversity, microbial metabolites, intestinal barrier integrity, and neuroimmune signaling have been linked to pain amplification and central sensitization across multiple chronic pain conditions. In transplant populations, exposure to immunosuppressive therapies, antibiotics, metabolic comorbidities, and other transplant-related stressors creates a unique environment for sustained microbiome disruption that may contribute to persistent symptom burden.
SUMMARY: Collectively, these data highlight the importance to systematically assess and manage pain as a core transplant outcome rather than a secondary concern, and to highlight the potential role of the gut microbiome as a risk screening tool or a therapeutic target for pain interventions. Although mechanistic and observational data support biologic plausibility, transplant-specific microbiome-pain evidence remains preliminary and warrants longitudinal investigation.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Microbiota in cholestatic diseases: crosstalk among bile composition, the biliary microbiome, and host immunity.
Frontiers in immunology, 17:1884030.
Cholestatic liver diseases are a heterogeneous group of hepatobiliary disorders caused by impaired bile formation, secretion, or excretion, leading to hepatocyte injury, biliary inflammation, fibrosis, and eventually cirrhosis. Traditional studies have largely focused on isolated mechanisms, including bile acid toxicity, immune dysregulation, and genetic susceptibility. However, recent advances in metagenomics, metabolomics, and immunology have highlighted the critical role of the gut and biliary microbiota in disease pathogenesis. This review proposes the core concept of a "tripartite interplay among bile composition, biliary microbiome, and host immunity," integrating the dynamic crosstalk among these three axes in cholestatic liver diseases. Bile composition shapes microbial communities and modulates immune responses through receptors such as FXR and TGR5. In turn, the biliary microbiome regulates bile acid metabolism and immune activity through microbial metabolites. Meanwhile, the host immune system senses microbial signals via pattern-recognition receptors, triggering inflammatory pathways and influencing microbial colonization and metabolism. These reciprocal interactions form complex feedback loops that drive disease progression from early inflammation to chronic fibrosis and cirrhosis. Based on this framework, emerging diagnostic approaches combine microbial signatures, bile acid profiles, and immune markers into multidimensional biomarker systems. Therapeutically, integrated strategies targeting the microbiome, bile acid metabolism, and immune pathways may offer synergistic benefits. Despite challenges including sampling difficulty, interindividual variability, and limitations of current models, future technologies such as single-cell sequencing, spatial transcriptomics, and multi-omics integration may enable precision diagnosis and targeted therapy.
Additional Links: PMID-42558207
PubMed:
Citation:
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@article {pmid42558207,
year = {2026},
author = {Yang, Y and Ren, L and Zhang, Y and Wang, X and Shang, J and Zhang, L},
title = {Microbiota in cholestatic diseases: crosstalk among bile composition, the biliary microbiome, and host immunity.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1884030},
pmid = {42558207},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Microbiota/immunology ; Bile Acids and Salts/metabolism ; *Cholestasis/microbiology/immunology/metabolism ; *Bile/metabolism/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; },
abstract = {Cholestatic liver diseases are a heterogeneous group of hepatobiliary disorders caused by impaired bile formation, secretion, or excretion, leading to hepatocyte injury, biliary inflammation, fibrosis, and eventually cirrhosis. Traditional studies have largely focused on isolated mechanisms, including bile acid toxicity, immune dysregulation, and genetic susceptibility. However, recent advances in metagenomics, metabolomics, and immunology have highlighted the critical role of the gut and biliary microbiota in disease pathogenesis. This review proposes the core concept of a "tripartite interplay among bile composition, biliary microbiome, and host immunity," integrating the dynamic crosstalk among these three axes in cholestatic liver diseases. Bile composition shapes microbial communities and modulates immune responses through receptors such as FXR and TGR5. In turn, the biliary microbiome regulates bile acid metabolism and immune activity through microbial metabolites. Meanwhile, the host immune system senses microbial signals via pattern-recognition receptors, triggering inflammatory pathways and influencing microbial colonization and metabolism. These reciprocal interactions form complex feedback loops that drive disease progression from early inflammation to chronic fibrosis and cirrhosis. Based on this framework, emerging diagnostic approaches combine microbial signatures, bile acid profiles, and immune markers into multidimensional biomarker systems. Therapeutically, integrated strategies targeting the microbiome, bile acid metabolism, and immune pathways may offer synergistic benefits. Despite challenges including sampling difficulty, interindividual variability, and limitations of current models, future technologies such as single-cell sequencing, spatial transcriptomics, and multi-omics integration may enable precision diagnosis and targeted therapy.},
}
MeSH Terms:
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Humans
Animals
*Microbiota/immunology
Bile Acids and Salts/metabolism
*Cholestasis/microbiology/immunology/metabolism
*Bile/metabolism/immunology/microbiology
*Gastrointestinal Microbiome/immunology
RevDate: 2026-08-06
CmpDate: 2026-08-06
Targeting the gut microbiota: emerging strategies to enhance healing of diabetic foot ulcers.
Frontiers in endocrinology, 17:1865273.
Diabetic foot ulcer (DFU) affects up to 34% of diabetic patients, with a 1-year recurrence rate of approximately 40%. This review primarily focuses on type 2 diabetes mellitus (T2DM), the most common form of diabetes associated with DFUs. Emerging evidence shows that gut microbiota critically influences DFUs healing through immune modulation (e.g., Treg/Th17 balance), regulation of inflammatory responses via short-chain fatty acids (SCFAs) that inhibit NF-κB, the gut-immune-skin axis, and systemic effects of microbial metabolites. Microbiota-targeted interventions-probiotics, prebiotics, fecal microbiota transplantation, and dietary strategies-can restore microbial balance and reduce inflammation, thereby promoting DFUs healing. These findings provide a mechanistic foundation for microbiome-based therapies and guide future clinical research.
Additional Links: PMID-42558256
PubMed:
Citation:
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@article {pmid42558256,
year = {2026},
author = {Chen, Z and Wu, W and Chen, Y and Li, F and Xie, X and Lin, Y and Zhang, X and Ye, Q},
title = {Targeting the gut microbiota: emerging strategies to enhance healing of diabetic foot ulcers.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1865273},
pmid = {42558256},
issn = {1664-2392},
mesh = {Humans ; *Diabetic Foot/microbiology/therapy ; *Wound Healing/physiology ; *Gastrointestinal Microbiome/physiology ; Animals ; *Diabetes Mellitus, Type 2/complications/microbiology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Prebiotics/administration & dosage ; },
abstract = {Diabetic foot ulcer (DFU) affects up to 34% of diabetic patients, with a 1-year recurrence rate of approximately 40%. This review primarily focuses on type 2 diabetes mellitus (T2DM), the most common form of diabetes associated with DFUs. Emerging evidence shows that gut microbiota critically influences DFUs healing through immune modulation (e.g., Treg/Th17 balance), regulation of inflammatory responses via short-chain fatty acids (SCFAs) that inhibit NF-κB, the gut-immune-skin axis, and systemic effects of microbial metabolites. Microbiota-targeted interventions-probiotics, prebiotics, fecal microbiota transplantation, and dietary strategies-can restore microbial balance and reduce inflammation, thereby promoting DFUs healing. These findings provide a mechanistic foundation for microbiome-based therapies and guide future clinical research.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetic Foot/microbiology/therapy
*Wound Healing/physiology
*Gastrointestinal Microbiome/physiology
Animals
*Diabetes Mellitus, Type 2/complications/microbiology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Prebiotics/administration & dosage
RevDate: 2026-08-06
CmpDate: 2026-08-06
Dietary index for gut microbiota score is inversely associated with carotid calcified plaque score in ischemic stroke patients.
Frontiers in nutrition, 13:1811243.
BACKGROUND: Diet influences gut microbiota-derived metabolites, which may affect vascular inflammation and calcification. The Dietary Index for Gut Microbiota (DI-GM) captures dietary patterns hypothesized to support favorable microbial metabolite profiles. In this study, we examined whether higher DI-GM scores are associated with lower carotid calcification burden in ischemic stroke patients and whether trimethylamine N-oxide (TMAO) is statistically associated with this relationship, without implying causality.
METHOD: In this cross-sectional study of 788 ischemic stroke patients from Central Hospital Affiliated to Shandong First Medical University, we calculated DI-GM scores from validated food frequency questionnaires and quantified carotid calcification using the Agatston method via computed tomography angiography. Plasma TMAO levels were measured by enzyme-linked immunosorbent assay (ELISA) ELISA.
RESULTS: Our findings revealed that participants in the highest DI-GM tertile had significantly lower calcification scores (76.07 ± 14.55) compared to the lowest tertile (316.00 ± 75.33, p < 0.001). Higher DI-GM scores correlated with lower TMAO, and decreased inflammatory markers (all p < 0.001). Each one-unit increase in DI-GM was independently associated with lower calcification odds (adjusted OR = 0.60, p = 0.02). Mediation analysis confirmed that TMAO significantly mediated these associations, accounting for substantial proportions of the total effects of DI-GM score on inflammatory markers, plaque thickness, and calcification score.
CONCLUSION: Higher DI-GM score is cross-sectionally associated with lower carotid calcification and TMAO-mediated pathways, but causality remains unproven without longitudinal and microbiome-sequencing data.
Additional Links: PMID-42558262
PubMed:
Citation:
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@article {pmid42558262,
year = {2026},
author = {Guan, Y and Chang, D},
title = {Dietary index for gut microbiota score is inversely associated with carotid calcified plaque score in ischemic stroke patients.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1811243},
pmid = {42558262},
issn = {2296-861X},
abstract = {BACKGROUND: Diet influences gut microbiota-derived metabolites, which may affect vascular inflammation and calcification. The Dietary Index for Gut Microbiota (DI-GM) captures dietary patterns hypothesized to support favorable microbial metabolite profiles. In this study, we examined whether higher DI-GM scores are associated with lower carotid calcification burden in ischemic stroke patients and whether trimethylamine N-oxide (TMAO) is statistically associated with this relationship, without implying causality.
METHOD: In this cross-sectional study of 788 ischemic stroke patients from Central Hospital Affiliated to Shandong First Medical University, we calculated DI-GM scores from validated food frequency questionnaires and quantified carotid calcification using the Agatston method via computed tomography angiography. Plasma TMAO levels were measured by enzyme-linked immunosorbent assay (ELISA) ELISA.
RESULTS: Our findings revealed that participants in the highest DI-GM tertile had significantly lower calcification scores (76.07 ± 14.55) compared to the lowest tertile (316.00 ± 75.33, p < 0.001). Higher DI-GM scores correlated with lower TMAO, and decreased inflammatory markers (all p < 0.001). Each one-unit increase in DI-GM was independently associated with lower calcification odds (adjusted OR = 0.60, p = 0.02). Mediation analysis confirmed that TMAO significantly mediated these associations, accounting for substantial proportions of the total effects of DI-GM score on inflammatory markers, plaque thickness, and calcification score.
CONCLUSION: Higher DI-GM score is cross-sectionally associated with lower carotid calcification and TMAO-mediated pathways, but causality remains unproven without longitudinal and microbiome-sequencing data.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Morphology-defined bacterial vaginosis and HPV-related cervical screening abnormalities: a two-year real-world study with histopathologic correlation.
Frontiers in cellular and infection microbiology, 16:1890650.
BACKGROUND: Bacterial vaginosis (BV) is characterized by reduced Lactobacillus dominance and enrichment of anaerobic bacteria. Although BV has been associated with human papillomavirus (HPV) infection, its relationship with cytologic abnormalities and biopsy-confirmed cervical lesions remains incompletely defined in real-world laboratory settings.
METHODS: We conducted a retrospective real-world study integrating vaginal fluorescence microscopy, 21-genotype HPV genotyping, thin-prep cytology (TCT), and cervical histopathology records from January 2024 through December 2025 at a tertiary hospital in China. Morphology-defined BV was defined by clue cells or Gardnerella-like anaerobic bacteria on vaginal fluorescence microscopy and was not equivalent to Nugent scoring, Amsel criteria, culture-based diagnosis, or molecular microbiome profiling. HPV and TCT records were matched within a prespecified 30-day window after patient-level deduplication. Multivariable logistic regression adjusted for year, age, and vaginal microecological covariates. A 90-day sensitivity analysis was performed. The histopathology cohort was clinically selected and was analyzed as a correlation subgroup rather than as a random sample of the screening cohort.
RESULTS: The main 30-day analysis included 4,492 unique patients, of whom 587 (13.07%) had morphology-defined BV. After multivariable adjustment, morphology-defined BV remained associated with overall HPV positivity (adjusted odds ratio [aOR] 1.560; 95% confidence interval [CI] 1.293-1.883), high-risk HPV positivity (aOR 1.611; 95% CI 1.327-1.957), HPV multiple infection (aOR 1.976; 95% CI 1.526-2.559), TCT abnormality (aOR 1.465; 95% CI 1.125-1.907), and concurrent high-risk HPV positivity plus TCT abnormality (aOR 1.558; 95% CI 1.174-2.066). After additional adjustment for high-risk HPV, the BV-TCT association was attenuated and non-significant. Among 825 patients with cervical histopathology records, BV was not independently associated with any histologic lesion grade, whereas high-risk HPV, HPV16/18, and TCT abnormality were the principal predictors of histopathologic disease.
CONCLUSION: Morphology-defined BV was associated with HPV infection and HPV-related cytologic abnormalities, but not with histologic cervical lesions in the clinically selected biopsy subgroup. These findings suggest that routine morphologic evidence of BV marks an HPV-related screening-positive phenotype rather than an independent histopathologic lesion predictor.
Additional Links: PMID-42558303
PubMed:
Citation:
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@article {pmid42558303,
year = {2026},
author = {Li, Z and Duan, Z and Liu, R and Yu, S and Wang, N and Chen, H and Xu, Q},
title = {Morphology-defined bacterial vaginosis and HPV-related cervical screening abnormalities: a two-year real-world study with histopathologic correlation.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1890650},
pmid = {42558303},
issn = {2235-2988},
mesh = {Humans ; Female ; *Vaginosis, Bacterial/microbiology/pathology/diagnosis ; *Papillomavirus Infections/pathology/diagnosis/virology/complications ; Retrospective Studies ; Adult ; *Human Papillomavirus Viruses/genetics ; *Cervix Uteri/pathology/virology/microbiology ; *Papillomaviridae/genetics/classification ; Middle Aged ; China ; Genotype ; Vagina/microbiology/pathology/virology ; Uterine Cervical Neoplasms/virology/pathology ; Early Detection of Cancer ; },
abstract = {BACKGROUND: Bacterial vaginosis (BV) is characterized by reduced Lactobacillus dominance and enrichment of anaerobic bacteria. Although BV has been associated with human papillomavirus (HPV) infection, its relationship with cytologic abnormalities and biopsy-confirmed cervical lesions remains incompletely defined in real-world laboratory settings.
METHODS: We conducted a retrospective real-world study integrating vaginal fluorescence microscopy, 21-genotype HPV genotyping, thin-prep cytology (TCT), and cervical histopathology records from January 2024 through December 2025 at a tertiary hospital in China. Morphology-defined BV was defined by clue cells or Gardnerella-like anaerobic bacteria on vaginal fluorescence microscopy and was not equivalent to Nugent scoring, Amsel criteria, culture-based diagnosis, or molecular microbiome profiling. HPV and TCT records were matched within a prespecified 30-day window after patient-level deduplication. Multivariable logistic regression adjusted for year, age, and vaginal microecological covariates. A 90-day sensitivity analysis was performed. The histopathology cohort was clinically selected and was analyzed as a correlation subgroup rather than as a random sample of the screening cohort.
RESULTS: The main 30-day analysis included 4,492 unique patients, of whom 587 (13.07%) had morphology-defined BV. After multivariable adjustment, morphology-defined BV remained associated with overall HPV positivity (adjusted odds ratio [aOR] 1.560; 95% confidence interval [CI] 1.293-1.883), high-risk HPV positivity (aOR 1.611; 95% CI 1.327-1.957), HPV multiple infection (aOR 1.976; 95% CI 1.526-2.559), TCT abnormality (aOR 1.465; 95% CI 1.125-1.907), and concurrent high-risk HPV positivity plus TCT abnormality (aOR 1.558; 95% CI 1.174-2.066). After additional adjustment for high-risk HPV, the BV-TCT association was attenuated and non-significant. Among 825 patients with cervical histopathology records, BV was not independently associated with any histologic lesion grade, whereas high-risk HPV, HPV16/18, and TCT abnormality were the principal predictors of histopathologic disease.
CONCLUSION: Morphology-defined BV was associated with HPV infection and HPV-related cytologic abnormalities, but not with histologic cervical lesions in the clinically selected biopsy subgroup. These findings suggest that routine morphologic evidence of BV marks an HPV-related screening-positive phenotype rather than an independent histopathologic lesion predictor.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Vaginosis, Bacterial/microbiology/pathology/diagnosis
*Papillomavirus Infections/pathology/diagnosis/virology/complications
Retrospective Studies
Adult
*Human Papillomavirus Viruses/genetics
*Cervix Uteri/pathology/virology/microbiology
*Papillomaviridae/genetics/classification
Middle Aged
China
Genotype
Vagina/microbiology/pathology/virology
Uterine Cervical Neoplasms/virology/pathology
Early Detection of Cancer
RevDate: 2026-08-06
CmpDate: 2026-08-06
Bile acid signaling at the gut-vascular interface: a novel modulator of hantavirus endothelial barrier dysfunction.
Frontiers in cellular and infection microbiology, 16:1883162.
Hantavirus infection triggers life-threatening hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), driven by severe endothelial barrier breakdown and systemic capillary leakage. Clinical severity varies widely with undefined host regulators, and no targeted endothelial-protective treatments exist. Recent data link hantaviruses to gut microbiome remodeling, while bile acid (BA) receptors FXR and TGR5 potently inhibit NF-κB-mediated endothelial inflammation. We synthesize four core lines of evidence. First, metagenomic reports confirm hantavirus reshapes gut/lung microbiota in rodent reservoirs. Second, we re-analyzed three public GEO datasets via standardized RNA-seq/microarray pipelines: (i) GSE245916: SEOV-infected human/rat lung ECs show conserved VCAM1/ICAM1 upregulation (human VCAM1 log2FC=+1.17, P = 0.023; rat Icam1 log2FC=+0.32, padj=0.016) with unaltered FXR; (ii) GSE7271: SEOV-infected rat lung displays sustained Nfkb1 suppression (all timepoints, P<0.05) and day-15 Slc10a2 downregulation (P = 0.028); (iii) GSE270172: PUUV 3D vessel chips feature robust IL6 elevation (log2FC=+1.22, P = 3.1×10[-8]) and disrupted BA transporters (ABCC3 log2FC=-1.44, P = 7.4×10[-][12]). TGR5 (GPBAR1) was undetectable in endothelial cells across all datasets. Third, FXR/TGR5 agonists repress NF-κB inflammation and mitigate lung vascular injury. Fourth, HTNV upregulates CH25H to block HMGCR-dependent cholesterol synthesis, depleting BA precursor substrates. We propose a unified pathogenic model: hantavirus-triggered gut dysbiosis plus virus-impaired cholesterol metabolism deplete circulating FXR/TGR5 agonistic BAs, relieving constitutive inhibition of endothelial NF-κB and monocyte NLRP3 inflammasomes to exacerbate capillary leakage. We define tiered testable predictions covering clinical multi-omics cohorts, in vitro receptor modulation assays and in vivo pharmacological interventions. This gut microbiota-BA-FXR/TGR5 axis represents a repurposable therapeutic target for hantavirus diseases, though direct causal evidence connecting BA signaling to viral vascular damage remains absent; our framework offers a rigorous testable roadmap for subsequent validation.
Additional Links: PMID-42558343
PubMed:
Citation:
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@article {pmid42558343,
year = {2026},
author = {Liu, L and Lin, J and Sang, K and Lai, J and Huang, N and Zhong, P and Liu, Y and Chen, S},
title = {Bile acid signaling at the gut-vascular interface: a novel modulator of hantavirus endothelial barrier dysfunction.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1883162},
pmid = {42558343},
issn = {2235-2988},
mesh = {Animals ; Humans ; *Orthohantavirus/pathogenicity/physiology ; *Bile Acids and Salts/metabolism ; *Signal Transduction ; Receptor, Farnesoid X-Activated ; Rats ; *Endothelial Cells/virology/metabolism ; Gastrointestinal Microbiome ; *Hantavirus Infections/virology/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; NF-kappa B/metabolism ; Lung/virology/microbiology ; Vascular Cell Adhesion Molecule-1/metabolism/genetics ; },
abstract = {Hantavirus infection triggers life-threatening hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), driven by severe endothelial barrier breakdown and systemic capillary leakage. Clinical severity varies widely with undefined host regulators, and no targeted endothelial-protective treatments exist. Recent data link hantaviruses to gut microbiome remodeling, while bile acid (BA) receptors FXR and TGR5 potently inhibit NF-κB-mediated endothelial inflammation. We synthesize four core lines of evidence. First, metagenomic reports confirm hantavirus reshapes gut/lung microbiota in rodent reservoirs. Second, we re-analyzed three public GEO datasets via standardized RNA-seq/microarray pipelines: (i) GSE245916: SEOV-infected human/rat lung ECs show conserved VCAM1/ICAM1 upregulation (human VCAM1 log2FC=+1.17, P = 0.023; rat Icam1 log2FC=+0.32, padj=0.016) with unaltered FXR; (ii) GSE7271: SEOV-infected rat lung displays sustained Nfkb1 suppression (all timepoints, P<0.05) and day-15 Slc10a2 downregulation (P = 0.028); (iii) GSE270172: PUUV 3D vessel chips feature robust IL6 elevation (log2FC=+1.22, P = 3.1×10[-8]) and disrupted BA transporters (ABCC3 log2FC=-1.44, P = 7.4×10[-][12]). TGR5 (GPBAR1) was undetectable in endothelial cells across all datasets. Third, FXR/TGR5 agonists repress NF-κB inflammation and mitigate lung vascular injury. Fourth, HTNV upregulates CH25H to block HMGCR-dependent cholesterol synthesis, depleting BA precursor substrates. We propose a unified pathogenic model: hantavirus-triggered gut dysbiosis plus virus-impaired cholesterol metabolism deplete circulating FXR/TGR5 agonistic BAs, relieving constitutive inhibition of endothelial NF-κB and monocyte NLRP3 inflammasomes to exacerbate capillary leakage. We define tiered testable predictions covering clinical multi-omics cohorts, in vitro receptor modulation assays and in vivo pharmacological interventions. This gut microbiota-BA-FXR/TGR5 axis represents a repurposable therapeutic target for hantavirus diseases, though direct causal evidence connecting BA signaling to viral vascular damage remains absent; our framework offers a rigorous testable roadmap for subsequent validation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Humans
*Orthohantavirus/pathogenicity/physiology
*Bile Acids and Salts/metabolism
*Signal Transduction
Receptor, Farnesoid X-Activated
Rats
*Endothelial Cells/virology/metabolism
Gastrointestinal Microbiome
*Hantavirus Infections/virology/metabolism
Receptors, G-Protein-Coupled/metabolism
Receptors, Cytoplasmic and Nuclear/metabolism
NF-kappa B/metabolism
Lung/virology/microbiology
Vascular Cell Adhesion Molecule-1/metabolism/genetics
RevDate: 2026-08-06
CmpDate: 2026-08-06
Hyperglycemia during the first 1000 days as a driver of metabolic programming.
Frontiers in endocrinology, 17:1899593.
The first 1000 days of life, spanning from conception to the end of the second postnatal year, represent a critical developmental window during which environmental and metabolic exposures exert long-lasting effects on offspring health. Among these exposures, maternal and early-life hyperglycemia have emerged as major determinants of metabolic programming and future cardiometabolic disease risk. Increasing evidence suggests that hyperglycemic exposure during this vulnerable period induces complex alterations in placental function, fetal endocrine adaptation, epigenetic regulation, and postnatal metabolic homeostasis, thereby predisposing offspring to obesity, insulin resistance, type 2 diabetes mellitus, and neurodevelopmental disturbances later in life. This review summarizes current evidence regarding the mechanistic pathways linking hyperglycemia during the first 1000 days to adverse metabolic outcomes. We discuss the role of maternal hyperglycemia in placental dysfunction, oxidative stress, inflammation, and altered nutrient transport, as well as its effects on fetal pancreatic development, adipogenesis, and insulin signaling. Particular emphasis is placed on emerging evidence implicating epigenetic modifications, mitochondrial dysfunction, microbiome alterations, and endocrine dysregulation in developmental programming. We further examine the impact of neonatal and early infant metabolic exposures on growth trajectories, adiposity, neurodevelopment, and long-term cardiometabolic health. Finally, we highlight current knowledge gaps and potential opportunities for early intervention, including optimized glycemic control during pregnancy, nutritional modulation, breastfeeding promotion, and precision prevention strategies targeting high-risk mother-infant dyads. A deeper understanding of the biological mechanisms underlying hyperglycemia-induced metabolic programming may facilitate the development of preventive approaches aimed at reducing the intergenerational transmission of metabolic disease.
Additional Links: PMID-42558395
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Citation:
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@article {pmid42558395,
year = {2026},
author = {Schandl, M and Ertl, T and Vass, RA},
title = {Hyperglycemia during the first 1000 days as a driver of metabolic programming.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1899593},
pmid = {42558395},
issn = {1664-2392},
mesh = {Humans ; Pregnancy ; Female ; *Hyperglycemia/metabolism/complications ; Developmental Origins of Health and Disease ; Animals ; *Prenatal Exposure Delayed Effects/metabolism ; Infant, Newborn ; *Fetal Development ; Epigenesis, Genetic ; Metabolic Reprogramming ; },
abstract = {The first 1000 days of life, spanning from conception to the end of the second postnatal year, represent a critical developmental window during which environmental and metabolic exposures exert long-lasting effects on offspring health. Among these exposures, maternal and early-life hyperglycemia have emerged as major determinants of metabolic programming and future cardiometabolic disease risk. Increasing evidence suggests that hyperglycemic exposure during this vulnerable period induces complex alterations in placental function, fetal endocrine adaptation, epigenetic regulation, and postnatal metabolic homeostasis, thereby predisposing offspring to obesity, insulin resistance, type 2 diabetes mellitus, and neurodevelopmental disturbances later in life. This review summarizes current evidence regarding the mechanistic pathways linking hyperglycemia during the first 1000 days to adverse metabolic outcomes. We discuss the role of maternal hyperglycemia in placental dysfunction, oxidative stress, inflammation, and altered nutrient transport, as well as its effects on fetal pancreatic development, adipogenesis, and insulin signaling. Particular emphasis is placed on emerging evidence implicating epigenetic modifications, mitochondrial dysfunction, microbiome alterations, and endocrine dysregulation in developmental programming. We further examine the impact of neonatal and early infant metabolic exposures on growth trajectories, adiposity, neurodevelopment, and long-term cardiometabolic health. Finally, we highlight current knowledge gaps and potential opportunities for early intervention, including optimized glycemic control during pregnancy, nutritional modulation, breastfeeding promotion, and precision prevention strategies targeting high-risk mother-infant dyads. A deeper understanding of the biological mechanisms underlying hyperglycemia-induced metabolic programming may facilitate the development of preventive approaches aimed at reducing the intergenerational transmission of metabolic disease.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Pregnancy
Female
*Hyperglycemia/metabolism/complications
Developmental Origins of Health and Disease
Animals
*Prenatal Exposure Delayed Effects/metabolism
Infant, Newborn
*Fetal Development
Epigenesis, Genetic
Metabolic Reprogramming
RevDate: 2026-08-06
CmpDate: 2026-08-06
Recombinant Bacillus subtilis spores expressing cholera toxin B and ovalbumin prevent ovalbumin-specific food allergy in mice by upregulating regulatory T cells and modulating gut microbiome flora.
Frontiers in immunology, 17:1872151.
BACKGROUND: Although oral immunotherapy has shown clinical efficacy in treating food allergies, its broader implementation is constrained by the occurrence of adverse effects. Consequently, inducing allergen-specific immune tolerance during early life can be a preventive strategy to reduce the development of food allergy.
OBJECTIVE: Here, we developed a novel fusion protein cholera toxin B (CTB)-ovalbumin (OVA) expressed on Bacillus subtilis (B.s-CotC-CTB-OVA) spore surface and investigated whether B.s-CotC-CTB-OVA spores prevent OVA-induced food allergy in a mouse model and explored the potential underlying mechanisms.
METHOD: Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot were used to confirm that CTB-OVA was expressed on B. subtilis spores. Female BALB/c mice were orally administered with B.s-CotC-CTB-OVA spores and B. subtilis spore control (B.s-CotC and B.s-CotC-CTB) for 4 weeks. Then, sensitization and challenge with OVA were performed on mice. Fecal OVA-secretory IgA (sIgA) and serum OVA-IgE, IgG1, and IgG2a levels were measured by enzyme-linked immunosorbent assay (ELISA). The gut microbiome was analyzed by 16S rDNA sequencing. After challenge, diarrhea score, anaphylactic reactions score, splenocyte interleukin (IL)-10, IL-4, and interferon-γ (IFN-γ), and Treg levels were measured. mRNA of IL-10, IL-4, IFN-γ, and Foxp3 were measured. Fecal microbiota transplant (FMT) was used to explore the mechanisms of microbiome in B. subtilis on food allergy.
RESULTS: Recombinant CTB-OVA was successfully expressed on the surface of B. subtilis. Oral administration of B.s-CotC-CTB-OVA can increase fecal OVA-sIgA, alleviate food allergy symptoms, and decrease serum OVA-IgE in mice with significance (p < 0.05). Moreover, oral administration of B.s-CotC-CTB-OVA can significantly reduce serum OVA-IgG1, OVA-IgG2, IL-4, spleen mast cells, and eosinophil levels and significantly increase serum IL-10 and Treg levels (p < 0.05). Additionally, microbiome analysis shows that oral administration of B.s-CotC-CTB-OVA can significantly increase the relative abundance of Muribaculaceae and significantly decrease the relative abundance of Alistipes. FMT partially reproduced the reduction in serum OVA-specific IgE, but did not significantly improve allergic symptom or diarrhea scores, suggesting that gut microbiota alterations may partially contribute to the immunological effects of B.s-CotC-CTB-OVA.
CONCLUSION: These findings suggest that B.s-CotC-CTB-OVA spores may serve as a preventive oral antigen-delivery strategy to promote antigen-specific immune regulation and partially modulate microbiota-associated immune responses in OVA-induced food allergy.
Additional Links: PMID-42558510
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Citation:
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@article {pmid42558510,
year = {2026},
author = {Xiong, Z and Liu, X and Deng, X and Zhang, C and Yang, K and Zhao, Z and Ding, T and Liu, S and Zhou, Z},
title = {Recombinant Bacillus subtilis spores expressing cholera toxin B and ovalbumin prevent ovalbumin-specific food allergy in mice by upregulating regulatory T cells and modulating gut microbiome flora.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1872151},
pmid = {42558510},
issn = {1664-3224},
mesh = {Animals ; *Bacillus subtilis/genetics/immunology ; *Ovalbumin/immunology/genetics ; *Food Hypersensitivity/immunology/prevention & control/microbiology ; *T-Lymphocytes, Regulatory/immunology/metabolism ; *Cholera Toxin/genetics/immunology ; Mice ; Female ; Mice, Inbred BALB C ; *Gastrointestinal Microbiome/immunology ; *Spores, Bacterial/genetics/immunology ; Immunoglobulin E/blood ; Disease Models, Animal ; Cytokines/metabolism ; Allergens/immunology ; Immune Tolerance ; },
abstract = {BACKGROUND: Although oral immunotherapy has shown clinical efficacy in treating food allergies, its broader implementation is constrained by the occurrence of adverse effects. Consequently, inducing allergen-specific immune tolerance during early life can be a preventive strategy to reduce the development of food allergy.
OBJECTIVE: Here, we developed a novel fusion protein cholera toxin B (CTB)-ovalbumin (OVA) expressed on Bacillus subtilis (B.s-CotC-CTB-OVA) spore surface and investigated whether B.s-CotC-CTB-OVA spores prevent OVA-induced food allergy in a mouse model and explored the potential underlying mechanisms.
METHOD: Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot were used to confirm that CTB-OVA was expressed on B. subtilis spores. Female BALB/c mice were orally administered with B.s-CotC-CTB-OVA spores and B. subtilis spore control (B.s-CotC and B.s-CotC-CTB) for 4 weeks. Then, sensitization and challenge with OVA were performed on mice. Fecal OVA-secretory IgA (sIgA) and serum OVA-IgE, IgG1, and IgG2a levels were measured by enzyme-linked immunosorbent assay (ELISA). The gut microbiome was analyzed by 16S rDNA sequencing. After challenge, diarrhea score, anaphylactic reactions score, splenocyte interleukin (IL)-10, IL-4, and interferon-γ (IFN-γ), and Treg levels were measured. mRNA of IL-10, IL-4, IFN-γ, and Foxp3 were measured. Fecal microbiota transplant (FMT) was used to explore the mechanisms of microbiome in B. subtilis on food allergy.
RESULTS: Recombinant CTB-OVA was successfully expressed on the surface of B. subtilis. Oral administration of B.s-CotC-CTB-OVA can increase fecal OVA-sIgA, alleviate food allergy symptoms, and decrease serum OVA-IgE in mice with significance (p < 0.05). Moreover, oral administration of B.s-CotC-CTB-OVA can significantly reduce serum OVA-IgG1, OVA-IgG2, IL-4, spleen mast cells, and eosinophil levels and significantly increase serum IL-10 and Treg levels (p < 0.05). Additionally, microbiome analysis shows that oral administration of B.s-CotC-CTB-OVA can significantly increase the relative abundance of Muribaculaceae and significantly decrease the relative abundance of Alistipes. FMT partially reproduced the reduction in serum OVA-specific IgE, but did not significantly improve allergic symptom or diarrhea scores, suggesting that gut microbiota alterations may partially contribute to the immunological effects of B.s-CotC-CTB-OVA.
CONCLUSION: These findings suggest that B.s-CotC-CTB-OVA spores may serve as a preventive oral antigen-delivery strategy to promote antigen-specific immune regulation and partially modulate microbiota-associated immune responses in OVA-induced food allergy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Bacillus subtilis/genetics/immunology
*Ovalbumin/immunology/genetics
*Food Hypersensitivity/immunology/prevention & control/microbiology
*T-Lymphocytes, Regulatory/immunology/metabolism
*Cholera Toxin/genetics/immunology
Mice
Female
Mice, Inbred BALB C
*Gastrointestinal Microbiome/immunology
*Spores, Bacterial/genetics/immunology
Immunoglobulin E/blood
Disease Models, Animal
Cytokines/metabolism
Allergens/immunology
Immune Tolerance
RevDate: 2026-08-06
CmpDate: 2026-08-06
Inflammation, infection, and immune dysregulation in chronic kidney disease: translational and epidemiological perspectives.
Frontiers in nephrology, 6:1919658.
Chronic kidney disease (CKD) represents a growing global health challenge associated with substantial morbidity, mortality, and healthcare burden. Although metabolic and haemodynamic factors, particularly diabetes mellitus and hypertension, remain major contributors, increasing evidence demonstrates that persistent inflammation and immune dysregulation are central mechanisms influencing CKD initiation, progression, and complications. The renal immune microenvironment consists of complex interactions among resident kidney cells, infiltrating immune cells, inflammatory mediators, and molecular signalling networks that regulate tissue repair, fibrosis, and disease outcomes. Persistent activation of innate and adaptive immune responses promotes cytokine release, oxidative stress, endothelial dysfunction, and maladaptive tissue remodelling, contributing to progressive loss of kidney function. Infectious diseases and altered host-microbiome interactions may further amplify systemic inflammation and immune imbalance, particularly in vulnerable populations. Advances in immunology and molecular medicine have identified inflammatory biomarkers and immune-related pathways with potential applications in early detection, risk stratification, and targeted interventions. This Mini Review synthesizes current evidence linking inflammation, infection, and immune dysregulation with CKD progression, highlighting translational opportunities and epidemiological perspectives. Integrating mechanistic insights with population-level evidence may accelerate precision approaches for improving CKD prevention, monitoring, and therapeutic outcomes.
Additional Links: PMID-42558570
PubMed:
Citation:
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@article {pmid42558570,
year = {2026},
author = {Shittu, A},
title = {Inflammation, infection, and immune dysregulation in chronic kidney disease: translational and epidemiological perspectives.},
journal = {Frontiers in nephrology},
volume = {6},
number = {},
pages = {1919658},
pmid = {42558570},
issn = {2813-0626},
abstract = {Chronic kidney disease (CKD) represents a growing global health challenge associated with substantial morbidity, mortality, and healthcare burden. Although metabolic and haemodynamic factors, particularly diabetes mellitus and hypertension, remain major contributors, increasing evidence demonstrates that persistent inflammation and immune dysregulation are central mechanisms influencing CKD initiation, progression, and complications. The renal immune microenvironment consists of complex interactions among resident kidney cells, infiltrating immune cells, inflammatory mediators, and molecular signalling networks that regulate tissue repair, fibrosis, and disease outcomes. Persistent activation of innate and adaptive immune responses promotes cytokine release, oxidative stress, endothelial dysfunction, and maladaptive tissue remodelling, contributing to progressive loss of kidney function. Infectious diseases and altered host-microbiome interactions may further amplify systemic inflammation and immune imbalance, particularly in vulnerable populations. Advances in immunology and molecular medicine have identified inflammatory biomarkers and immune-related pathways with potential applications in early detection, risk stratification, and targeted interventions. This Mini Review synthesizes current evidence linking inflammation, infection, and immune dysregulation with CKD progression, highlighting translational opportunities and epidemiological perspectives. Integrating mechanistic insights with population-level evidence may accelerate precision approaches for improving CKD prevention, monitoring, and therapeutic outcomes.},
}
RevDate: 2026-08-06
Maternal and infant gut microbiome.
iMeta [Epub ahead of print].
Early-life gut microbiome assembly is a pivotal determinant of lifelong health; however, the integrated frameworks governing this process across developmental milestones remain insufficiently defined. This review establishes a multidimensional framework by delineating the crosstalk between the gut microbiome and the host throughout the preconception, prenatal, postpartum, and early childhood stages. We first highlight the emerging paradigm of biparental microbial contributions during the preconception period, detailing how paternal and maternal niches jointly prime offspring development. Moving into pregnancy, we examine the maternal reservoir, integrating the role of gut microbiota-derived metabolites across multiple trimesters in prenatal priming and vertical transmission. For the postpartum period, we discuss the development of the multikingdom gut microbiome and address the impacts of delivery modes and clinical interventions. Here, we articulate a critical knowledge gap: the discrepancy between taxonomic "catch-up" and true functional restoration, particularly in vulnerable cohorts such as preterm infants. Furthermore, we propose a "developmental synchronization" model within the maternal-infant-microbiome continuum. This model posits that early-life "windows of opportunity" are defined by the obligate temporal coupling of host physiological maturation with stage-specific microbial metabolic signals. From a translational perspective, we discuss how this framework informs the development of precision interventions, such as stage-specific probiotics, prebiotics, or metabolic modulators. These therapies aim to restore not only the microbial composition but also the synchronized functional dialog between the microbiome and host development. By mapping the "microbiota-metabolite-host target-physiological phenotype" network, we provide a systematic roadmap for precision-targeted interventions during the first 1000 days of life.
Additional Links: PMID-42558572
PubMed:
Citation:
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@article {pmid42558572,
year = {2026},
author = {Wang, H and Tin, F and Chen, H and Jiao, F and Wu, M and Sun, S and Lin, L and Li, D and Zheng, H and Niu, Z and Lan, M and Yilmaz, B and Eriksson, JG and Wang, M and Macpherson, A and Clemente, JC and Xu, J and Xie, RH and Zheng, X and Zhou, T and Wang, J and Shen, W and Huang, B and Chen, X and Li, H and He, Y},
title = {Maternal and infant gut microbiome.},
journal = {iMeta},
volume = {},
number = {},
pages = {e70151},
pmid = {42558572},
issn = {2770-596X},
abstract = {Early-life gut microbiome assembly is a pivotal determinant of lifelong health; however, the integrated frameworks governing this process across developmental milestones remain insufficiently defined. This review establishes a multidimensional framework by delineating the crosstalk between the gut microbiome and the host throughout the preconception, prenatal, postpartum, and early childhood stages. We first highlight the emerging paradigm of biparental microbial contributions during the preconception period, detailing how paternal and maternal niches jointly prime offspring development. Moving into pregnancy, we examine the maternal reservoir, integrating the role of gut microbiota-derived metabolites across multiple trimesters in prenatal priming and vertical transmission. For the postpartum period, we discuss the development of the multikingdom gut microbiome and address the impacts of delivery modes and clinical interventions. Here, we articulate a critical knowledge gap: the discrepancy between taxonomic "catch-up" and true functional restoration, particularly in vulnerable cohorts such as preterm infants. Furthermore, we propose a "developmental synchronization" model within the maternal-infant-microbiome continuum. This model posits that early-life "windows of opportunity" are defined by the obligate temporal coupling of host physiological maturation with stage-specific microbial metabolic signals. From a translational perspective, we discuss how this framework informs the development of precision interventions, such as stage-specific probiotics, prebiotics, or metabolic modulators. These therapies aim to restore not only the microbial composition but also the synchronized functional dialog between the microbiome and host development. By mapping the "microbiota-metabolite-host target-physiological phenotype" network, we provide a systematic roadmap for precision-targeted interventions during the first 1000 days of life.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Bacteria-related signals in brain metastases: evidence boundaries, tumor-microenvironment remodeling, and translational prospects.
Frontiers in cell and developmental biology, 14:1893882.
Brain metastases (BrM) develop within a highly specialized central nervous system niche shaped by the blood-brain barrier/blood-tumor barrier, brain-resident stromal cells, myeloid populations, and distinct metabolic constraints. Emerging studies suggest that bacteria-related signals can be detected in primary and metastatic brain tumors; however, their biological meaning remains incompletely defined. In particular, low-biomass brain tissues are highly vulnerable to reagent contamination, environmental carry-over, batch effects, and bioinformatic misclassification, making it essential to distinguish molecular bacterial traces from viable intratumoral bacteria or a bona fide tumor microbiome. In this review, we propose a graded conceptual framework that separates bacterial signals/elements, intratumoral bacteria, and intratumoral microbiota/microbiome according to evidentiary strength. We summarize current evidence for the spatial and cellular localization of bacteria-related signals in BrM and discuss potential source models, including primary-tumor carry-over, hematogenous dissemination, gut microbiota-derived metabolites, oral microbial input, and bacterial extracellular vesicles. We further examine how these signals may interact with the BrM tumor microenvironment by influencing tumor-cell stress adaptation, myeloid inflammatory niches, antigen-presentation pathways, vascular-barrier remodeling, and metabolic reprogramming. Particular attention is given to the emerging gut-brain-metastasis axis and to cancer-type-specific contexts in breast cancer, lung cancer, and melanoma brain metastases. From a translational perspective, bacteria-related signals in BrM may eventually contribute to biomarker development, patient stratification, and therapeutic modulation of the microbe-host axis. Nevertheless, current evidence remains insufficient to conclude that BrM broadly harbor stable, active, and clinically actionable microbial communities. Future progress will require multi-source matched cohorts, longitudinal sampling, stringent low-biomass contamination control, absolute quantification, spatial validation, functional models, and explicit separation of microbial presence, viability, and causality. A rigorous evidence-based approach will be essential for moving this field from intriguing associations toward biologically interpretable and clinically meaningful applications.
Additional Links: PMID-42558585
PubMed:
Citation:
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@article {pmid42558585,
year = {2026},
author = {Kuang, G and Qiu, Z and Li, L and Bai, J and Ji, H and Liu, Y},
title = {Bacteria-related signals in brain metastases: evidence boundaries, tumor-microenvironment remodeling, and translational prospects.},
journal = {Frontiers in cell and developmental biology},
volume = {14},
number = {},
pages = {1893882},
pmid = {42558585},
issn = {2296-634X},
abstract = {Brain metastases (BrM) develop within a highly specialized central nervous system niche shaped by the blood-brain barrier/blood-tumor barrier, brain-resident stromal cells, myeloid populations, and distinct metabolic constraints. Emerging studies suggest that bacteria-related signals can be detected in primary and metastatic brain tumors; however, their biological meaning remains incompletely defined. In particular, low-biomass brain tissues are highly vulnerable to reagent contamination, environmental carry-over, batch effects, and bioinformatic misclassification, making it essential to distinguish molecular bacterial traces from viable intratumoral bacteria or a bona fide tumor microbiome. In this review, we propose a graded conceptual framework that separates bacterial signals/elements, intratumoral bacteria, and intratumoral microbiota/microbiome according to evidentiary strength. We summarize current evidence for the spatial and cellular localization of bacteria-related signals in BrM and discuss potential source models, including primary-tumor carry-over, hematogenous dissemination, gut microbiota-derived metabolites, oral microbial input, and bacterial extracellular vesicles. We further examine how these signals may interact with the BrM tumor microenvironment by influencing tumor-cell stress adaptation, myeloid inflammatory niches, antigen-presentation pathways, vascular-barrier remodeling, and metabolic reprogramming. Particular attention is given to the emerging gut-brain-metastasis axis and to cancer-type-specific contexts in breast cancer, lung cancer, and melanoma brain metastases. From a translational perspective, bacteria-related signals in BrM may eventually contribute to biomarker development, patient stratification, and therapeutic modulation of the microbe-host axis. Nevertheless, current evidence remains insufficient to conclude that BrM broadly harbor stable, active, and clinically actionable microbial communities. Future progress will require multi-source matched cohorts, longitudinal sampling, stringent low-biomass contamination control, absolute quantification, spatial validation, functional models, and explicit separation of microbial presence, viability, and causality. A rigorous evidence-based approach will be essential for moving this field from intriguing associations toward biologically interpretable and clinically meaningful applications.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Dose-dependent supplementation of Schizochytrium in the biofloc system modulates dual microbiomes to enhance growth and survival in Pacific white shrimp (Litopenaeus vannamei).
Frontiers in microbiology, 17:1867320.
Integrating microalgae into biofloc system is a promising yet debated strategy in Pacific white shrimp (Litopenaeus vannamei) aquaculture, due to its inconsistent efficacy even for the same microalgal species. Such inconsistent performances are likely dose-dependent and the underlying microbial mechanisms remain elusive. Here, we investigated the impacts of supplementing microalga strain, Schizochytrium sp. ATCC 20888, at low (10[3] cells/mL, M1) and high (10[6] cells/mL, M2) levels compared with a clear water (CLW) system. Schizochytrium supplementation improved growth performance and feed efficiency and the M2 treatment further increased shrimp survival. Transcriptional profiling revealed the M2 treatment upregulated the expression of genes relevant to hepatopancreatic lipid and protein digestion (trypsin and lipase) and intestinal amino acid transportation (peptide transporter 1). Concurrently, M2 fortified the intestinal defense against pathogenic microbes by enhancing antimicrobial genes (lysozyme and penaeidin 3a). Redundancy analysis further supported the growth promotion was closely associated with improved lipid and a corresponding protein-sparing effect. Notably, Schizochytrium persisted at an extremely low abundance, whilst 16S rRNA sequencing revealed its disproportionate impact as a rare taxon on the microbiota in both biofloc and gut. High-dose supplementation enriched beneficial genera such as Aureispira, Marivita, Neptuniibacter, and Phaeodactylibacter in bioflocs, which are vital for nutrient recycling. Meanwhile, the intestinal microbiota was characterized by enrichment of the probiotic Fusibacter and the suppression of the opportunistic pathogen Shewanella. Overall, Schizochytrium orchestrates a dose-dependent reshaping of biofloc and gut microbiomes, effectively boosting the growth, feed efficiency, and specifically reinforcing antimicrobial activity of L. vannamei.
Additional Links: PMID-42558610
PubMed:
Citation:
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@article {pmid42558610,
year = {2026},
author = {Li, Z and Li, X and Sun, B and Wu, H and Zhang, J and Wan, X and Zhao, B and Xiao, N and Qi, Z and Li, Q and Liu, H},
title = {Dose-dependent supplementation of Schizochytrium in the biofloc system modulates dual microbiomes to enhance growth and survival in Pacific white shrimp (Litopenaeus vannamei).},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1867320},
pmid = {42558610},
issn = {1664-302X},
abstract = {Integrating microalgae into biofloc system is a promising yet debated strategy in Pacific white shrimp (Litopenaeus vannamei) aquaculture, due to its inconsistent efficacy even for the same microalgal species. Such inconsistent performances are likely dose-dependent and the underlying microbial mechanisms remain elusive. Here, we investigated the impacts of supplementing microalga strain, Schizochytrium sp. ATCC 20888, at low (10[3] cells/mL, M1) and high (10[6] cells/mL, M2) levels compared with a clear water (CLW) system. Schizochytrium supplementation improved growth performance and feed efficiency and the M2 treatment further increased shrimp survival. Transcriptional profiling revealed the M2 treatment upregulated the expression of genes relevant to hepatopancreatic lipid and protein digestion (trypsin and lipase) and intestinal amino acid transportation (peptide transporter 1). Concurrently, M2 fortified the intestinal defense against pathogenic microbes by enhancing antimicrobial genes (lysozyme and penaeidin 3a). Redundancy analysis further supported the growth promotion was closely associated with improved lipid and a corresponding protein-sparing effect. Notably, Schizochytrium persisted at an extremely low abundance, whilst 16S rRNA sequencing revealed its disproportionate impact as a rare taxon on the microbiota in both biofloc and gut. High-dose supplementation enriched beneficial genera such as Aureispira, Marivita, Neptuniibacter, and Phaeodactylibacter in bioflocs, which are vital for nutrient recycling. Meanwhile, the intestinal microbiota was characterized by enrichment of the probiotic Fusibacter and the suppression of the opportunistic pathogen Shewanella. Overall, Schizochytrium orchestrates a dose-dependent reshaping of biofloc and gut microbiomes, effectively boosting the growth, feed efficiency, and specifically reinforcing antimicrobial activity of L. vannamei.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Gut metabolites: key factors in the cross-talk between the gut microbiota and tumor immunotherapy.
Frontiers in immunology, 17:1882542.
This review synthesizes recent research findings and proposes an integrated "microbiota-metabolite-immune-oncology" framework, highlighting how gut-derived metabolites regulate the dynamics of tumor immunity and informing the development of next-generation immunotherapies. Key metabolites-including short-chain fatty acids (SCFAs), bile acids (BAs), trimethylamine N-oxide (TMAO), indole-3-propionic acid (IPA), and urolithin A-exert bidirectional effects on antitumor immunity through multiple mechanisms. These include histone acetylation-driven epigenetic reprogramming, aryl hydrocarbon receptor (AhR)- and farnesoid X receptor (FXR)-mediated metabolic reprogramming, and direct regulation of immune effectors such as CD8[+] T cells and myeloid-derived suppressor cells. Emerging evidence highlights specific roles of these metabolites within the tumor microenvironment (TME): microbial dysbiosis can amplify immunosuppressive circuits, whereas targeted enrichment of certain metabolites may enhance the efficacy of immune checkpoint blockade. Integrative multi-omics analyses have revealed the vascular remodeling effect of TMAO and the spatiotemporal heterogeneity of BAs, thereby connecting the gut-liver-tumor axis and achieving overall immune regulation. By mapping a precision-oriented metabolic roadmap, this review identifies underexplored therapeutic avenues-such as metabolite-targeted interventions and engineered probiotics-that, when combined with immune checkpoint inhibitors, may enable personalized, microbiome-based strategies with the potential to improve outcomes in cancer immunotherapy.
Additional Links: PMID-42558660
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Citation:
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@article {pmid42558660,
year = {2026},
author = {Zeng, L and Ren, Y and Huang, H and Wang, Q and Li, H and Song, J and He, F and Li, J},
title = {Gut metabolites: key factors in the cross-talk between the gut microbiota and tumor immunotherapy.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1882542},
pmid = {42558660},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Neoplasms/therapy/immunology/metabolism ; Animals ; *Immunotherapy/methods ; Tumor Microenvironment/immunology ; },
abstract = {This review synthesizes recent research findings and proposes an integrated "microbiota-metabolite-immune-oncology" framework, highlighting how gut-derived metabolites regulate the dynamics of tumor immunity and informing the development of next-generation immunotherapies. Key metabolites-including short-chain fatty acids (SCFAs), bile acids (BAs), trimethylamine N-oxide (TMAO), indole-3-propionic acid (IPA), and urolithin A-exert bidirectional effects on antitumor immunity through multiple mechanisms. These include histone acetylation-driven epigenetic reprogramming, aryl hydrocarbon receptor (AhR)- and farnesoid X receptor (FXR)-mediated metabolic reprogramming, and direct regulation of immune effectors such as CD8[+] T cells and myeloid-derived suppressor cells. Emerging evidence highlights specific roles of these metabolites within the tumor microenvironment (TME): microbial dysbiosis can amplify immunosuppressive circuits, whereas targeted enrichment of certain metabolites may enhance the efficacy of immune checkpoint blockade. Integrative multi-omics analyses have revealed the vascular remodeling effect of TMAO and the spatiotemporal heterogeneity of BAs, thereby connecting the gut-liver-tumor axis and achieving overall immune regulation. By mapping a precision-oriented metabolic roadmap, this review identifies underexplored therapeutic avenues-such as metabolite-targeted interventions and engineered probiotics-that, when combined with immune checkpoint inhibitors, may enable personalized, microbiome-based strategies with the potential to improve outcomes in cancer immunotherapy.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Gastrointestinal Microbiome/immunology
*Neoplasms/therapy/immunology/metabolism
Animals
*Immunotherapy/methods
Tumor Microenvironment/immunology
RevDate: 2026-08-06
CmpDate: 2026-08-06
Mapping research trends in irritable bowel syndrome and the gut microbiome: a cross-database bibliometric analysis.
Frontiers in microbiology, 17:1900159.
BACKGROUND/OBJECTIVES: Research on irritable bowel syndrome (IBS) and the gut microbiome has expanded rapidly. However, the structural evolution of this literature has not been systematically characterized across major indexing platforms.
METHODS: We performed a parallel bibliometric analysis of the Web of Science Core Collection (WoSCC, n = 1,502), Scopus (n = 1,163), and PubMed (n = 975). The analysis included English-language articles and reviews published from January 2000 to December 2025. WoSCC served as the primary dataset, and Scopus and PubMed were analyzed in parallel for cross-database comparison. Bibliometric mapping and visualization were performed using VOSviewer, CiteSpace, and bibliometrix.
RESULTS: Annual output increased from fewer than 10 articles per year before 2010 to 162 in 2025. This acceleration became marked after 2014 and was reproduced across all three databases. The United States and China led publication volume, whereas the UK output was concentrated in a small number of flagship centers. Our analysis suggests three developmental phases: compositional profiling and culture-dependent benchmarks (2000-2012), community-level characterization and interventional consolidation (2012-2017), and neuroendocrine and short-chain fatty acid mechanisms (2017-2025). Visceral hyperalgesia and hypothalamic-pituitary-adrenal axis dysregulation showed the strongest currently active keyword bursts. Diet-related and precision-oriented approaches also gained visibility.
CONCLUSION: IBS-gut microbiome research has shifted from descriptive profiling toward mechanistic, diet-related, and precision-medicine themes. These findings provide a structured overview of the field and help clarify priorities for its next phase.
Additional Links: PMID-42558675
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Citation:
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@article {pmid42558675,
year = {2026},
author = {Mo, W and Cai, F and Li, L and Liang, J and Zhang, J and Yao, L and Mo, S and Liao, Y and Tang, S and Liu, Z and Chen, Z and Qin, M and Liu, S and Zou, J and Huang, J},
title = {Mapping research trends in irritable bowel syndrome and the gut microbiome: a cross-database bibliometric analysis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1900159},
pmid = {42558675},
issn = {1664-302X},
abstract = {BACKGROUND/OBJECTIVES: Research on irritable bowel syndrome (IBS) and the gut microbiome has expanded rapidly. However, the structural evolution of this literature has not been systematically characterized across major indexing platforms.
METHODS: We performed a parallel bibliometric analysis of the Web of Science Core Collection (WoSCC, n = 1,502), Scopus (n = 1,163), and PubMed (n = 975). The analysis included English-language articles and reviews published from January 2000 to December 2025. WoSCC served as the primary dataset, and Scopus and PubMed were analyzed in parallel for cross-database comparison. Bibliometric mapping and visualization were performed using VOSviewer, CiteSpace, and bibliometrix.
RESULTS: Annual output increased from fewer than 10 articles per year before 2010 to 162 in 2025. This acceleration became marked after 2014 and was reproduced across all three databases. The United States and China led publication volume, whereas the UK output was concentrated in a small number of flagship centers. Our analysis suggests three developmental phases: compositional profiling and culture-dependent benchmarks (2000-2012), community-level characterization and interventional consolidation (2012-2017), and neuroendocrine and short-chain fatty acid mechanisms (2017-2025). Visceral hyperalgesia and hypothalamic-pituitary-adrenal axis dysregulation showed the strongest currently active keyword bursts. Diet-related and precision-oriented approaches also gained visibility.
CONCLUSION: IBS-gut microbiome research has shifted from descriptive profiling toward mechanistic, diet-related, and precision-medicine themes. These findings provide a structured overview of the field and help clarify priorities for its next phase.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Editorial: Natural products: a microecological perspective for treating diabetes and its complications.
Frontiers in nutrition, 13:1896973.
Additional Links: PMID-42558707
PubMed:
Citation:
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@article {pmid42558707,
year = {2026},
author = {Khan, I},
title = {Editorial: Natural products: a microecological perspective for treating diabetes and its complications.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1896973},
pmid = {42558707},
issn = {2296-861X},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Relationship Between Vaginal Microbiome and Preterm Birth During Pregnancy: In Different Ethnic Populations.
Women's health reports (New Rochelle, N.Y.), 7:26884844261471777.
The incidence of preterm birth (PTB) varies and remains stubbornly high across different countries and regions. Besides, PTB can lead to a wide range of maternal and infant complications and even death in severe cases. Despite the severity of the consequences of PTB, the exact causes of morbidity remain unclear. In the past few years, with the development of the microbiome, a growing body of research focuses on the impact of vaginal microbiome (VMB) on PTB. Moreover, accumulating studies have suggested that the VMB plays a crucial role in the development of PTB. In addition, the VMB varies greatly in different populations. Therefore, in this review, we describe the normal VMB in women with or without pregnancy. Subsequently, we highlight differences in the VMB among ethnically diverse PTB populations. Overall, understanding the relationship between the VMB and PTB in different populations is essential for developing targeted interventions and personalized approaches to reduce the risk of PTB. Further research is needed to fully elucidate the specific microbial patterns and mechanisms underlying this association.
Additional Links: PMID-42558754
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@article {pmid42558754,
year = {2026},
author = {Fan, C and Zhang, Y and Zhang, J and Xu, C and Wang, X and Fan, Y},
title = {Relationship Between Vaginal Microbiome and Preterm Birth During Pregnancy: In Different Ethnic Populations.},
journal = {Women's health reports (New Rochelle, N.Y.)},
volume = {7},
number = {},
pages = {26884844261471777},
pmid = {42558754},
issn = {2688-4844},
abstract = {The incidence of preterm birth (PTB) varies and remains stubbornly high across different countries and regions. Besides, PTB can lead to a wide range of maternal and infant complications and even death in severe cases. Despite the severity of the consequences of PTB, the exact causes of morbidity remain unclear. In the past few years, with the development of the microbiome, a growing body of research focuses on the impact of vaginal microbiome (VMB) on PTB. Moreover, accumulating studies have suggested that the VMB plays a crucial role in the development of PTB. In addition, the VMB varies greatly in different populations. Therefore, in this review, we describe the normal VMB in women with or without pregnancy. Subsequently, we highlight differences in the VMB among ethnically diverse PTB populations. Overall, understanding the relationship between the VMB and PTB in different populations is essential for developing targeted interventions and personalized approaches to reduce the risk of PTB. Further research is needed to fully elucidate the specific microbial patterns and mechanisms underlying this association.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.
Frontiers in microbiology, 17:1834439.
Gastric cancer is one of the most prevalent gastrointestinal malignancies worldwide, with Helicobacter pylori infection, host genetic susceptibility and environmental exposure serving as major driving risk factors. Accumulating studies have demonstrated that host genetics, the microbiome and epigenetic modifications collectively govern gastric cancer initiation and progression. These three components form a bidirectional regulatory axis: host genetic profiles and epigenetic remodeling shape the composition of endogenous microbial communities, while the microbiome and its metabolites trigger epigenetic reprogramming to modulate transcription of oncogenes and tumor suppressors. Deciphering this intricate tripartite regulatory network holds great potential to facilitate the development of precise therapeutic interventions for gastric cancer. This review delineates the respective roles of host genetics, the microbiome and epigenetic modifications throughout gastric cancer evolution and summarizes corresponding prospective intervention strategies. We elaborate on the reciprocal interplay between the microbiome and host genetic/epigenetic factors, and highlight the vital clinical significance of this crosstalk for gastric cancer prevention and treatment.
Additional Links: PMID-42558801
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@article {pmid42558801,
year = {2026},
author = {Zhou, T and Li, G and Ye, W and Wu, L and Liu, H and Guo, J and Wen, Y and Li, J and Wu, M and Li, W and Wu, H},
title = {The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1834439},
pmid = {42558801},
issn = {1664-302X},
abstract = {Gastric cancer is one of the most prevalent gastrointestinal malignancies worldwide, with Helicobacter pylori infection, host genetic susceptibility and environmental exposure serving as major driving risk factors. Accumulating studies have demonstrated that host genetics, the microbiome and epigenetic modifications collectively govern gastric cancer initiation and progression. These three components form a bidirectional regulatory axis: host genetic profiles and epigenetic remodeling shape the composition of endogenous microbial communities, while the microbiome and its metabolites trigger epigenetic reprogramming to modulate transcription of oncogenes and tumor suppressors. Deciphering this intricate tripartite regulatory network holds great potential to facilitate the development of precise therapeutic interventions for gastric cancer. This review delineates the respective roles of host genetics, the microbiome and epigenetic modifications throughout gastric cancer evolution and summarizes corresponding prospective intervention strategies. We elaborate on the reciprocal interplay between the microbiome and host genetic/epigenetic factors, and highlight the vital clinical significance of this crosstalk for gastric cancer prevention and treatment.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Neurocognitive and neurophysiological consequences of sleep-disordered breathing in bronchiectasis: the role of respiratory rehabilitation.
Frontiers in rehabilitation sciences, 7:1846233.
Bronchiectasis (BE) is a chronic respiratory disease characterized by a vicious cycle of irreversible bronchial dilatation and persistent respiratory infections which results in progressive functional impairment and reduced quality of life. Increasing attention has been directed toward comorbidities that may aggravate disease burden, including sleep-disordered breathing (SDB), which remains underrecognized in this population. Emerging evidence suggests that SDB, particularly obstructive sleep apnea (OSA), is highly prevalent in BE and may contribute to adverse outcomes through mechanisms such as intermittent hypoxia, systemic inflammation, microbiome alterations, and ventilatory instability. This narrative review synthesizes current evidence on the relationship between BE and SDB, with a focus on the underlying pathophysiological mechanisms, the neurophysiological and cognitive consequences and the implications for rehabilitation. A comprehensive literature search was conducted using PubMed, Embase, and the Cochrane Library, supplemented by evidence from related chronic respiratory diseases. Available data indicate that sleep disturbances are common in BE and are associated with impaired daytime functioning, reduced quality of life as well as increased symptom burden, independent of disease severity. Rehabilitation interventions, in particular pulmonary rehabilitation, positive airway pressure (PAP), and non-invasive ventilation (NIV), may offer clinically meaningful benefits by enhancing gas exchange, improving sleep quality and patient-reported outcomes. However, high-quality evidence specific to BE populations remains limited. In conclusion, we consider that recognizing SDB as a potentially modifiable trait in bronchiectasis highlights the need for integrated, multidisciplinary management strategies. Future research should prioritize prospective studies to clarify the role of targeted rehabilitation interventions and to support evidence-based clinical practice.
Additional Links: PMID-42558826
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@article {pmid42558826,
year = {2026},
author = {Battaglia, EG and Leonardi, G and Banfi, PI and Volpato, E},
title = {Neurocognitive and neurophysiological consequences of sleep-disordered breathing in bronchiectasis: the role of respiratory rehabilitation.},
journal = {Frontiers in rehabilitation sciences},
volume = {7},
number = {},
pages = {1846233},
pmid = {42558826},
issn = {2673-6861},
abstract = {Bronchiectasis (BE) is a chronic respiratory disease characterized by a vicious cycle of irreversible bronchial dilatation and persistent respiratory infections which results in progressive functional impairment and reduced quality of life. Increasing attention has been directed toward comorbidities that may aggravate disease burden, including sleep-disordered breathing (SDB), which remains underrecognized in this population. Emerging evidence suggests that SDB, particularly obstructive sleep apnea (OSA), is highly prevalent in BE and may contribute to adverse outcomes through mechanisms such as intermittent hypoxia, systemic inflammation, microbiome alterations, and ventilatory instability. This narrative review synthesizes current evidence on the relationship between BE and SDB, with a focus on the underlying pathophysiological mechanisms, the neurophysiological and cognitive consequences and the implications for rehabilitation. A comprehensive literature search was conducted using PubMed, Embase, and the Cochrane Library, supplemented by evidence from related chronic respiratory diseases. Available data indicate that sleep disturbances are common in BE and are associated with impaired daytime functioning, reduced quality of life as well as increased symptom burden, independent of disease severity. Rehabilitation interventions, in particular pulmonary rehabilitation, positive airway pressure (PAP), and non-invasive ventilation (NIV), may offer clinically meaningful benefits by enhancing gas exchange, improving sleep quality and patient-reported outcomes. However, high-quality evidence specific to BE populations remains limited. In conclusion, we consider that recognizing SDB as a potentially modifiable trait in bronchiectasis highlights the need for integrated, multidisciplinary management strategies. Future research should prioritize prospective studies to clarify the role of targeted rehabilitation interventions and to support evidence-based clinical practice.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
The Microbiome-Mitochondria Axis in aging: a self-reinforcing vicious cycle linking metabolic dysregulation, mitochondrial quality control failure, and inflammaging.
Frontiers in microbiology, 17:1874222.
Aging is a progressive degenerative process of cellular and systemic homeostasis in organisms, with mitochondrial dysfunction and altered intercellular communication as core hallmarks of this process. During aging, the gut microbiome and mitochondria exhibit a highly synchronized degenerative trajectory: this is characterized by decreased microbial diversity, reduced abundance of beneficial short-chain fatty acid (SCFA)-producing bacteria, and expansion of pro-inflammatory pathobionts in the gut, alongside impaired oxidative phosphorylation efficiency, excessive reactive oxygen species (ROS) production, and compromised quality control in mitochondria. Built on the evolutionary cornerstone of endosymbiotic theory, this review establishes a theoretical framework for the Microbiome-Mitochondria Axis (MMA) and proposes that the ancient molecular homology between mitochondria and modern gut bacteria has preserved a sensitive cross-species signal crosstalk mechanism. This review systematically dissects the bidirectional communication mechanisms of the MMA. First, microbial metabolites-including SCFAs, tryptophan-derived indole metabolites, and secondary bile acids-regulate mitochondrial energy metabolism, oxidative stress responses, and dynamic homeostasis via key signaling pathways such as AMPK-PGC-1α, AhR-Nrf2, and FXR/TGR5. Conversely, dysfunctional mitochondria actively reshape the gut microenvironment and propagate sterile inflammation through multiple pathways: mitochondrial ROS (mtROS)-mediated intestinal barrier disruption, metabolic reprogramming of immune cells toward a pro-inflammatory phenotype, and activation of the cGAS-STING innate immune pathway triggered by mitochondrial DNA (mtDNA) release. Here, we propose a unified theoretical framework centered on the MMA as a self-reinforcing pathological loop. In this model, gut dysbiosis drives depletion of beneficial microbial metabolites, which triggers mitochondrial quality control failure, mtDNA leakage, and inflammaging; in turn, inflammaging exacerbates gut dysbiosis by remodeling the intestinal microenvironment, thus forming a closed, self-amplifying vicious cycle. The MMA links multiple hallmarks of aging, including epigenetic alterations, immunosenescence, and stem cell exhaustion, providing a unifying pathological basis for age-related disorders such as neurodegenerative diseases, cardiovascular diseases, sarcopenia, and osteoarthritis. It also offers a systematic entry point for anti-aging interventions targeting the bidirectional metabolic-immune crosstalk between the microbiome and mitochondria.
Additional Links: PMID-42558902
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@article {pmid42558902,
year = {2026},
author = {Liu, E and Jia, J and Liu, Q and Li, C and Li, S and Cai, T},
title = {The Microbiome-Mitochondria Axis in aging: a self-reinforcing vicious cycle linking metabolic dysregulation, mitochondrial quality control failure, and inflammaging.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1874222},
pmid = {42558902},
issn = {1664-302X},
abstract = {Aging is a progressive degenerative process of cellular and systemic homeostasis in organisms, with mitochondrial dysfunction and altered intercellular communication as core hallmarks of this process. During aging, the gut microbiome and mitochondria exhibit a highly synchronized degenerative trajectory: this is characterized by decreased microbial diversity, reduced abundance of beneficial short-chain fatty acid (SCFA)-producing bacteria, and expansion of pro-inflammatory pathobionts in the gut, alongside impaired oxidative phosphorylation efficiency, excessive reactive oxygen species (ROS) production, and compromised quality control in mitochondria. Built on the evolutionary cornerstone of endosymbiotic theory, this review establishes a theoretical framework for the Microbiome-Mitochondria Axis (MMA) and proposes that the ancient molecular homology between mitochondria and modern gut bacteria has preserved a sensitive cross-species signal crosstalk mechanism. This review systematically dissects the bidirectional communication mechanisms of the MMA. First, microbial metabolites-including SCFAs, tryptophan-derived indole metabolites, and secondary bile acids-regulate mitochondrial energy metabolism, oxidative stress responses, and dynamic homeostasis via key signaling pathways such as AMPK-PGC-1α, AhR-Nrf2, and FXR/TGR5. Conversely, dysfunctional mitochondria actively reshape the gut microenvironment and propagate sterile inflammation through multiple pathways: mitochondrial ROS (mtROS)-mediated intestinal barrier disruption, metabolic reprogramming of immune cells toward a pro-inflammatory phenotype, and activation of the cGAS-STING innate immune pathway triggered by mitochondrial DNA (mtDNA) release. Here, we propose a unified theoretical framework centered on the MMA as a self-reinforcing pathological loop. In this model, gut dysbiosis drives depletion of beneficial microbial metabolites, which triggers mitochondrial quality control failure, mtDNA leakage, and inflammaging; in turn, inflammaging exacerbates gut dysbiosis by remodeling the intestinal microenvironment, thus forming a closed, self-amplifying vicious cycle. The MMA links multiple hallmarks of aging, including epigenetic alterations, immunosenescence, and stem cell exhaustion, providing a unifying pathological basis for age-related disorders such as neurodegenerative diseases, cardiovascular diseases, sarcopenia, and osteoarthritis. It also offers a systematic entry point for anti-aging interventions targeting the bidirectional metabolic-immune crosstalk between the microbiome and mitochondria.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Habitat environment is associated with the microbiota of the human terminal airway.
Frontiers in microbiology, 17:1887778.
While environmental exposures are closely associated with the human microbiome, the microbial landscape of the terminal airways remains largely uncharacterized due to the ethical challenges of tissue sampling. To address this gap, we analyzed surgically resected idiopathic lung bullae (localized developmental anomalies surrounded by otherwise normal tissue) to establish a baseline microbiome atlas. We performed ultra-deep metagenomic sequencing on terminal airway tissues from 60 subjects residing in two climatically distinct Chinese cities: Zhuhai (a subtropical coastal region) and Yinchuan (an arid, high-altitude industrial area on the Qinghai-Tibet Plateau). Our analysis revealed that the high-altitude Yinchuan cohort exhibited significantly higher microbial loads and alpha diversity compared to the coastal Zhuhai cohort. Functionally, the Yinchuan microbiome was enriched in taxa associated with fatty acid beta-oxidation, alongside a markedly higher burden of virulence factors and antibiotic resistance genes. These compositional and functional differences may be associated with regional variation in climate, altitude, and local antibiotic usage patterns, whereas the Zhuhai cohort exhibited greater fungal diversity. Ultimately, this study provides the tissue-resolved microbial atlas of the human terminal respiratory tract and reveals substantial differences in microbial composition and function across distinct habitat environments. Furthermore, these findings suggest a potential association between environmental conditions and variation in resident microbiota, providing a basis for future investigations into how environmental change may influence respiratory microecology and human health.
Additional Links: PMID-42559032
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Citation:
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@article {pmid42559032,
year = {2026},
author = {Sun, Y and Li, X and Zheng, X and Sun, X and Liu, J and Zhang, S and Zhang, G and He, W and Huo, W and Zuo, J},
title = {Habitat environment is associated with the microbiota of the human terminal airway.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1887778},
pmid = {42559032},
issn = {1664-302X},
abstract = {While environmental exposures are closely associated with the human microbiome, the microbial landscape of the terminal airways remains largely uncharacterized due to the ethical challenges of tissue sampling. To address this gap, we analyzed surgically resected idiopathic lung bullae (localized developmental anomalies surrounded by otherwise normal tissue) to establish a baseline microbiome atlas. We performed ultra-deep metagenomic sequencing on terminal airway tissues from 60 subjects residing in two climatically distinct Chinese cities: Zhuhai (a subtropical coastal region) and Yinchuan (an arid, high-altitude industrial area on the Qinghai-Tibet Plateau). Our analysis revealed that the high-altitude Yinchuan cohort exhibited significantly higher microbial loads and alpha diversity compared to the coastal Zhuhai cohort. Functionally, the Yinchuan microbiome was enriched in taxa associated with fatty acid beta-oxidation, alongside a markedly higher burden of virulence factors and antibiotic resistance genes. These compositional and functional differences may be associated with regional variation in climate, altitude, and local antibiotic usage patterns, whereas the Zhuhai cohort exhibited greater fungal diversity. Ultimately, this study provides the tissue-resolved microbial atlas of the human terminal respiratory tract and reveals substantial differences in microbial composition and function across distinct habitat environments. Furthermore, these findings suggest a potential association between environmental conditions and variation in resident microbiota, providing a basis for future investigations into how environmental change may influence respiratory microecology and human health.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Filtration-enriched metabolites and their association with salivary microbiota: a combined two-cohort analysis.
Journal of oral microbiology, 18(1):2711156.
OBJECTIVE: We aimed to identify significantly reduced metabolites (SRMs) in saliva by filtration and to analyze their associations with oral microorganisms.
METHODS: A total of 423 volunteers were assigned into two cohorts. Paired saliva samples were collected from cohort 1 (n = 60) and underwent metabolomics analysis before and after filtration. SRMs were identified based on the following thresholds: variable importance in projection ≥1, false discovery rate <0.05, and fold change ≥10. The pre-filtration samples from Cohort 1 were subjected to microbiome analysis. Saliva samples collected from cohort 2 (n = 334) underwent metabolomic and microbiome analyses, but were not filtered.
RESULTS: Principal coordinates analysis revealed a clear separation between pre- and post-filtration samples. The filtered saliva samples had approximately 5.8% fewer detectable metabolites. Notably, over half of the SRMs had an unknown origin, indicating significant knowledge gaps in oral metabolites. Prevotella melaninogenica and Veillonella parvula were core species associated with the SRMs (hypoxanthine and phosphatidylcholine), with purine metabolism identified as enriched pathway for Prevotella melaninogenica.
CONCLUSIONS: Filtration can reshape saliva metabolite profiles. This study combined key metabolite filtration with integrated multi-omics and functional analyses, providing new insights into saliva metabolism and microbe-metabolite interactions.
Additional Links: PMID-42559081
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Citation:
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@article {pmid42559081,
year = {2026},
author = {Zhang, Y and Wang, Q and Zhai, Y and Wang, Q and Li, Z and Liu, Y and Liu, S},
title = {Filtration-enriched metabolites and their association with salivary microbiota: a combined two-cohort analysis.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2711156},
pmid = {42559081},
issn = {2000-2297},
abstract = {OBJECTIVE: We aimed to identify significantly reduced metabolites (SRMs) in saliva by filtration and to analyze their associations with oral microorganisms.
METHODS: A total of 423 volunteers were assigned into two cohorts. Paired saliva samples were collected from cohort 1 (n = 60) and underwent metabolomics analysis before and after filtration. SRMs were identified based on the following thresholds: variable importance in projection ≥1, false discovery rate <0.05, and fold change ≥10. The pre-filtration samples from Cohort 1 were subjected to microbiome analysis. Saliva samples collected from cohort 2 (n = 334) underwent metabolomic and microbiome analyses, but were not filtered.
RESULTS: Principal coordinates analysis revealed a clear separation between pre- and post-filtration samples. The filtered saliva samples had approximately 5.8% fewer detectable metabolites. Notably, over half of the SRMs had an unknown origin, indicating significant knowledge gaps in oral metabolites. Prevotella melaninogenica and Veillonella parvula were core species associated with the SRMs (hypoxanthine and phosphatidylcholine), with purine metabolism identified as enriched pathway for Prevotella melaninogenica.
CONCLUSIONS: Filtration can reshape saliva metabolite profiles. This study combined key metabolite filtration with integrated multi-omics and functional analyses, providing new insights into saliva metabolism and microbe-metabolite interactions.},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Exploring the Role of Microbiota-Mediated Gut-Kidney Axis in Acute Kidney Injury: Immunomodulation and Therapy.
Kidney diseases (Basel, Switzerland), 12(1):722-733.
BACKGROUND: Acute kidney injury (AKI) remains a major clinical problem characterized by high morbidity and an increased risk of progression to chronic kidney disease (CKD). Immune cell infiltration and activation are important features of AKI; however, the upstream mechanisms that shape this inflammatory response are not fully understood. Emerging evidence suggests that gut microbiota dysbiosis and systemic immune activation may contribute to renal injury, but the functional significance of the gut-kidney axis in AKI pathogenesis remains to be further clarified.
SUMMARY: This review synthesizes current evidence regarding gut-kidney crosstalk in AKI, with a focus on the immunometabolic impact of microbiota-derived metabolites. We discuss the potential roles of short-chain fatty acids, indole derivatives, indoxyl sulfate (IS), p-cresol sulfate (PCS), and trimethylamine-N-oxide (TMAO) in regulating T and B lymphocytes, macrophages, neutrophils, and other immune cell populations. Importantly, we distinguish direct AKI-related evidence from findings extrapolated from CKD, uremic conditions, or broader microbiome-immunity studies. Potential therapeutic interventions, including pharmacological modulation and probiotic strategies aimed at restoring gut-kidney homeostasis, are also highlighted.
KEY MESSAGES: The gut-kidney axis is increasingly recognized as a potential contributor to immune-mediated injury and repair in AKI. However, the causal roles and temporal dynamics of several gut-derived uremic toxins, including IS, PCS, and TMAO, remain incompletely defined in AKI. By integrating direct AKI evidence with indirect evidence from CKD and broader microbiome-immunity studies, this review provides a more balanced conceptual framework for understanding renal immunopathology and identifying potential microbiome-targeted strategies to mitigate AKI and its progression to CKD.
Additional Links: PMID-42559590
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@article {pmid42559590,
year = {2026},
author = {Zhu, L and Jiang, S and Yan, Q and Zhou, Y and Zhang, Y and Peng, H and Zhou, L},
title = {Exploring the Role of Microbiota-Mediated Gut-Kidney Axis in Acute Kidney Injury: Immunomodulation and Therapy.},
journal = {Kidney diseases (Basel, Switzerland)},
volume = {12},
number = {1},
pages = {722-733},
pmid = {42559590},
issn = {2296-9381},
abstract = {BACKGROUND: Acute kidney injury (AKI) remains a major clinical problem characterized by high morbidity and an increased risk of progression to chronic kidney disease (CKD). Immune cell infiltration and activation are important features of AKI; however, the upstream mechanisms that shape this inflammatory response are not fully understood. Emerging evidence suggests that gut microbiota dysbiosis and systemic immune activation may contribute to renal injury, but the functional significance of the gut-kidney axis in AKI pathogenesis remains to be further clarified.
SUMMARY: This review synthesizes current evidence regarding gut-kidney crosstalk in AKI, with a focus on the immunometabolic impact of microbiota-derived metabolites. We discuss the potential roles of short-chain fatty acids, indole derivatives, indoxyl sulfate (IS), p-cresol sulfate (PCS), and trimethylamine-N-oxide (TMAO) in regulating T and B lymphocytes, macrophages, neutrophils, and other immune cell populations. Importantly, we distinguish direct AKI-related evidence from findings extrapolated from CKD, uremic conditions, or broader microbiome-immunity studies. Potential therapeutic interventions, including pharmacological modulation and probiotic strategies aimed at restoring gut-kidney homeostasis, are also highlighted.
KEY MESSAGES: The gut-kidney axis is increasingly recognized as a potential contributor to immune-mediated injury and repair in AKI. However, the causal roles and temporal dynamics of several gut-derived uremic toxins, including IS, PCS, and TMAO, remain incompletely defined in AKI. By integrating direct AKI evidence with indirect evidence from CKD and broader microbiome-immunity studies, this review provides a more balanced conceptual framework for understanding renal immunopathology and identifying potential microbiome-targeted strategies to mitigate AKI and its progression to CKD.},
}
RevDate: 2026-08-06
Long-term stability at -80°C of oral wash and saliva samples for microbiome analyses.
Microbiology spectrum [Epub ahead of print].
Large-scale prospective biological studies necessitate the storage of oral samples for numerous years to accrue adequate sample sizes. However, there is minimal research on the impact of long-term storage of oral samples on the oral microbiome. We investigated the freezer stability over 5 years of the oral microbiome measured from oral wash and saliva samples to provide insight for future microbiome analyses of stored oral samples. Healthy participants provided oral wash and saliva samples using Scope mouthwash and the OMNIgene ORAL collection device, respectively. DNA was extracted from an aliquot of each sample type at baseline, the V4 region of the 16S rRNA gene sequenced, and additional aliquots were then similarly extracted and sequenced after being stored for approximately 1 month, 12 months, and 5 years after collection. Intraclass correlation coefficients (ICC) and 95% confidence intervals (CI) were calculated for 4 alpha-diversity metrics, the first 2 principal coordinates of four beta-diversity matrices, and the 14 most abundant genera. The alpha diversity and beta diversity ICCs for both sample types remained stable over 5 years. For example, the 5-year Shannon index ICCs were 0.94 (95% CI: 0.88, 0.98) and 0.90 (95% CI: 0.72, 0.95) for oral wash and saliva samples, respectively. The ICCs for the relative abundances of the examined genera during the 5 years of freezer storage were also generally stable. Both oral wash and saliva samples were relatively stable for diversity metrics and relative abundance after 5 years when stored at -80°C.IMPORTANCELarge, prospective studies will likely need to store biospecimens for many years in the freezer prior to DNA extraction and sequencing for analyses considering the association between the microbiome and specific health conditions. In this study, we demonstrated that oral wash using Scope mouthwash and saliva specimens in the OMNIgene ORAL kit have generally stable microbiome communities for up to 5 years at -80°C.
Additional Links: PMID-42560044
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@article {pmid42560044,
year = {2026},
author = {Slack, J and Wilcher, E and Hua, X and Wan, Y and Liu, J and Dagnall, CL and Jones, K and Hicks, BD and Hutchinson, A and Shi, J and Abnet, CC and Vogtmann, E},
title = {Long-term stability at -80°C of oral wash and saliva samples for microbiome analyses.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0057326},
doi = {10.1128/spectrum.00573-26},
pmid = {42560044},
issn = {2165-0497},
abstract = {Large-scale prospective biological studies necessitate the storage of oral samples for numerous years to accrue adequate sample sizes. However, there is minimal research on the impact of long-term storage of oral samples on the oral microbiome. We investigated the freezer stability over 5 years of the oral microbiome measured from oral wash and saliva samples to provide insight for future microbiome analyses of stored oral samples. Healthy participants provided oral wash and saliva samples using Scope mouthwash and the OMNIgene ORAL collection device, respectively. DNA was extracted from an aliquot of each sample type at baseline, the V4 region of the 16S rRNA gene sequenced, and additional aliquots were then similarly extracted and sequenced after being stored for approximately 1 month, 12 months, and 5 years after collection. Intraclass correlation coefficients (ICC) and 95% confidence intervals (CI) were calculated for 4 alpha-diversity metrics, the first 2 principal coordinates of four beta-diversity matrices, and the 14 most abundant genera. The alpha diversity and beta diversity ICCs for both sample types remained stable over 5 years. For example, the 5-year Shannon index ICCs were 0.94 (95% CI: 0.88, 0.98) and 0.90 (95% CI: 0.72, 0.95) for oral wash and saliva samples, respectively. The ICCs for the relative abundances of the examined genera during the 5 years of freezer storage were also generally stable. Both oral wash and saliva samples were relatively stable for diversity metrics and relative abundance after 5 years when stored at -80°C.IMPORTANCELarge, prospective studies will likely need to store biospecimens for many years in the freezer prior to DNA extraction and sequencing for analyses considering the association between the microbiome and specific health conditions. In this study, we demonstrated that oral wash using Scope mouthwash and saliva specimens in the OMNIgene ORAL kit have generally stable microbiome communities for up to 5 years at -80°C.},
}
RevDate: 2026-08-06
A functionally selected Acinetobacter sp. phosphoethanolamine transferase gene from the goose fecal microbiome confers colistin resistance in E. coli.
Applied and environmental microbiology [Epub ahead of print].
Polymyxins are last-resort antibiotics for infections caused by multidrug-resistant gram-negative bacteria such as Enterobacteriaceae, Pseudomonas aeruginosa, and Acinetobacter baumannii. This makes the rise of bacteria exhibiting polymyxin E (colistin) resistance, largely through modification of lipid A moieties, concerning and suggests that it is important to document the potential sources of the corresponding resistance genes. This study searched for potential emerging colistin resistance genes from the environment by investigating a previously performed functional metagenomic selection for colistin resistance of a goose fecal microbiome. We found that the selection captured Acinetobacter sp. DNA fragments that all contained eptA genes. We confirmed their ability to confer significant colistin resistance in Escherichia coli via modification of lipid A in the outer membrane. Furthermore, we found evidence for mobilization of closely related eptA genes in Acinetobacter genomes, marking them as potential mcr genes or their precursors. This study highlights the potential for functional metagenomic selections for colistin resistance to capture genes from unexpected environmental sources such as the goose fecal microbiome.IMPORTANCEColistin is an important antibiotic of last resort, and increasing resistance to this drug via mobile phosphoethanolamine transferase genes, such as mcr-1, threatens its clinical utility. Given the discovery of mcr-1 in pigs, the ability of animals to act as vectors in the spread of colistin resistance is alarming. We show here that functionally selected Acinetobacter phosphoethanolamine transferase genes from the goose microbiome have the ability to confer clinical levels of colistin resistance when transferred into E. coli. While the genes are annotated as eptA homologs, closer study of these genes suggests that they may be mobilized within the Acinetobacter genus, suggesting that they may be mcr genes of concern instead.
Additional Links: PMID-42560056
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42560056,
year = {2026},
author = {Bernate, E and Shi, Y and Franck, E and Crofts, TS},
title = {A functionally selected Acinetobacter sp. phosphoethanolamine transferase gene from the goose fecal microbiome confers colistin resistance in E. coli.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0246825},
doi = {10.1128/aem.02468-25},
pmid = {42560056},
issn = {1098-5336},
abstract = {Polymyxins are last-resort antibiotics for infections caused by multidrug-resistant gram-negative bacteria such as Enterobacteriaceae, Pseudomonas aeruginosa, and Acinetobacter baumannii. This makes the rise of bacteria exhibiting polymyxin E (colistin) resistance, largely through modification of lipid A moieties, concerning and suggests that it is important to document the potential sources of the corresponding resistance genes. This study searched for potential emerging colistin resistance genes from the environment by investigating a previously performed functional metagenomic selection for colistin resistance of a goose fecal microbiome. We found that the selection captured Acinetobacter sp. DNA fragments that all contained eptA genes. We confirmed their ability to confer significant colistin resistance in Escherichia coli via modification of lipid A in the outer membrane. Furthermore, we found evidence for mobilization of closely related eptA genes in Acinetobacter genomes, marking them as potential mcr genes or their precursors. This study highlights the potential for functional metagenomic selections for colistin resistance to capture genes from unexpected environmental sources such as the goose fecal microbiome.IMPORTANCEColistin is an important antibiotic of last resort, and increasing resistance to this drug via mobile phosphoethanolamine transferase genes, such as mcr-1, threatens its clinical utility. Given the discovery of mcr-1 in pigs, the ability of animals to act as vectors in the spread of colistin resistance is alarming. We show here that functionally selected Acinetobacter phosphoethanolamine transferase genes from the goose microbiome have the ability to confer clinical levels of colistin resistance when transferred into E. coli. While the genes are annotated as eptA homologs, closer study of these genes suggests that they may be mobilized within the Acinetobacter genus, suggesting that they may be mcr genes of concern instead.},
}
RevDate: 2026-08-06
Rice-crayfish farming mode drives distinct soil properties and ecological assembly of soil microbiome.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: Rice-crayfish farming (RCF) system represents an effective ecological agricultural model characterized by the cyclical spatiotemporal integration of rice farming and crayfish aquaculture. However, the effects of farming mode and stage on soil microbial community structure over time remain insufficiently explored. In this study, we investigated taxonomic and functional changes in soil microbiomes and their associations with soil nutrient fertility in both RCF and rice monoculture (RM) systems. Our findings demonstrated that RCF significantly increased soil pH, total nitrogen (TN), and soil organic carbon (SOC) compared to RM across multiple growth stages (P < 0.05). Two-way analysis of variance showed that both mode and stage affected the Chao1 index, while the Shannon index was only affected by stage. Microbial community analysis revealed clear structural differences between the two systems (P < 0.001). Functional prediction indicated lower chemoheterotrophy but higher photoheterotrophy, aromatic degradation, and sulfur cycling in RCF, along with reduced nitrogen cycling function. Co-occurrence network analysis further showed a longer average path length and higher modularity in RCF than in RM. Modules 3 and 6 in RCF were positively correlated with pH, TN, and SOC. Overall, RCF stabilizes the soil environment and selects for specific functionally sensitive taxa, thereby promoting the formation of a highly modular microbial network, which ultimately maintains the synergistic stability of soil nutrients and the microbial community.
IMPORTANCE: The present study comprehensively compared two different farming modes in terms of their soil microbiome structures and the associations between the microbiomes and soil nutrient fertility. Rice-crayfish farming (RCF) model-specific microbial taxa were identified, and their modularity was found in RCF. These findings provide valuable insights into microbial community responses and regulation in ecological agriculture, establishing a robust microbiological foundation for optimizing rice-aquatic animal integrated farming management and advancing sustainable agricultural practices.
Additional Links: PMID-42560063
Publisher:
PubMed:
Citation:
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@article {pmid42560063,
year = {2026},
author = {Peng, L and Dai, L-l and Tao, L and Li, G and Zhu, J-q and Zhang, H},
title = {Rice-crayfish farming mode drives distinct soil properties and ecological assembly of soil microbiome.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0383225},
doi = {10.1128/spectrum.03832-25},
pmid = {42560063},
issn = {2165-0497},
abstract = {UNLABELLED: Rice-crayfish farming (RCF) system represents an effective ecological agricultural model characterized by the cyclical spatiotemporal integration of rice farming and crayfish aquaculture. However, the effects of farming mode and stage on soil microbial community structure over time remain insufficiently explored. In this study, we investigated taxonomic and functional changes in soil microbiomes and their associations with soil nutrient fertility in both RCF and rice monoculture (RM) systems. Our findings demonstrated that RCF significantly increased soil pH, total nitrogen (TN), and soil organic carbon (SOC) compared to RM across multiple growth stages (P < 0.05). Two-way analysis of variance showed that both mode and stage affected the Chao1 index, while the Shannon index was only affected by stage. Microbial community analysis revealed clear structural differences between the two systems (P < 0.001). Functional prediction indicated lower chemoheterotrophy but higher photoheterotrophy, aromatic degradation, and sulfur cycling in RCF, along with reduced nitrogen cycling function. Co-occurrence network analysis further showed a longer average path length and higher modularity in RCF than in RM. Modules 3 and 6 in RCF were positively correlated with pH, TN, and SOC. Overall, RCF stabilizes the soil environment and selects for specific functionally sensitive taxa, thereby promoting the formation of a highly modular microbial network, which ultimately maintains the synergistic stability of soil nutrients and the microbial community.
IMPORTANCE: The present study comprehensively compared two different farming modes in terms of their soil microbiome structures and the associations between the microbiomes and soil nutrient fertility. Rice-crayfish farming (RCF) model-specific microbial taxa were identified, and their modularity was found in RCF. These findings provide valuable insights into microbial community responses and regulation in ecological agriculture, establishing a robust microbiological foundation for optimizing rice-aquatic animal integrated farming management and advancing sustainable agricultural practices.},
}
RevDate: 2026-08-06
Defunctioning stomas and the effect of oral antibiotic bowel preparation in colorectal surgery: a microbiome-based hypothesis.
The British journal of surgery pii:8753190 [Epub ahead of print].
Additional Links: PMID-42560133
Publisher:
PubMed:
Citation:
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@article {pmid42560133,
year = {2026},
author = {Helliwell, JA and Kirby, A and Chilton, C and Wood, H and Quirke, P and Jayne, DG},
title = {Defunctioning stomas and the effect of oral antibiotic bowel preparation in colorectal surgery: a microbiome-based hypothesis.},
journal = {The British journal of surgery},
volume = {},
number = {},
pages = {},
doi = {10.1093/bjs/znag102},
pmid = {42560133},
issn = {1365-2168},
}
RevDate: 2026-08-06
CmpDate: 2026-08-06
Distinct Gut Microbiome and Metabolome Profiles Associate with Differential Responses to Immunotherapy in Colorectal Cancer.
Polish journal of microbiology, 75(2):168-194.
The composition of the intestinal microbiome has been identified as a key factor influencing the efficacy of immune checkpoint inhibitors. This study aimed to systematically evaluate the potential associations among gut microbiota, metabolic profiles, and clinical outcomes in patients with MSI-H advanced colorectal cancer (CRC) treated with immunotherapy. Twenty advanced CRC patients receiving immunotherapy were enrolled and categorized into clinical benefit response (CBR) and non-benefit (NCB) groups based on treatment efficacy. Fecal samples were analyzed using metagenomic sequencing and untargeted metabolomics. The results revealed significant enrichments of s_Clostridium unclassified and metabolites such as guanosine, 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid, and quercetin 3-(6"-malonyl-glucoside) in the CBR group, suggesting their potential positive predictive value for immunotherapy response. Conversely, the NCB group showed significant enrichments of s_Roseburia hominis, s_Marseilla massiliensis, and metabolites including pyrophosphate, riboflavin, and PC(22:5(4Z,7Z,10Z,13Z,16Z)/14:0), indicating a possible association with treatment resistance. By integrating fecal metagenomics and metabolomics, this study reveals distinctive "flora-metabolite" interactions linked to therapeutic response in advanced CRC patients undergoing immunotherapy. Specific microbial and metabolic profiles were positively or negatively correlated with immunotherapy outcomes, highlighting their potential not only as predictive biomarkers but also as a theoretical foundation for developing individualized immunotherapy strategies based on microecological modulation.
Additional Links: PMID-42560299
PubMed:
Citation:
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@article {pmid42560299,
year = {2026},
author = {Liang, F and Li, J and Yue, Y and Pan, J and Liu, C and Cheng, D and Zhang, N and Li, K and Chu, F and Wu, H},
title = {Distinct Gut Microbiome and Metabolome Profiles Associate with Differential Responses to Immunotherapy in Colorectal Cancer.},
journal = {Polish journal of microbiology},
volume = {75},
number = {2},
pages = {168-194},
pmid = {42560299},
issn = {2544-4646},
mesh = {Humans ; *Colorectal Neoplasms/therapy/microbiology/metabolism ; *Metabolome ; *Immunotherapy ; *Gastrointestinal Microbiome ; Female ; Feces/microbiology ; Male ; Middle Aged ; Aged ; Metabolomics ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {The composition of the intestinal microbiome has been identified as a key factor influencing the efficacy of immune checkpoint inhibitors. This study aimed to systematically evaluate the potential associations among gut microbiota, metabolic profiles, and clinical outcomes in patients with MSI-H advanced colorectal cancer (CRC) treated with immunotherapy. Twenty advanced CRC patients receiving immunotherapy were enrolled and categorized into clinical benefit response (CBR) and non-benefit (NCB) groups based on treatment efficacy. Fecal samples were analyzed using metagenomic sequencing and untargeted metabolomics. The results revealed significant enrichments of s_Clostridium unclassified and metabolites such as guanosine, 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid, and quercetin 3-(6"-malonyl-glucoside) in the CBR group, suggesting their potential positive predictive value for immunotherapy response. Conversely, the NCB group showed significant enrichments of s_Roseburia hominis, s_Marseilla massiliensis, and metabolites including pyrophosphate, riboflavin, and PC(22:5(4Z,7Z,10Z,13Z,16Z)/14:0), indicating a possible association with treatment resistance. By integrating fecal metagenomics and metabolomics, this study reveals distinctive "flora-metabolite" interactions linked to therapeutic response in advanced CRC patients undergoing immunotherapy. Specific microbial and metabolic profiles were positively or negatively correlated with immunotherapy outcomes, highlighting their potential not only as predictive biomarkers but also as a theoretical foundation for developing individualized immunotherapy strategies based on microecological modulation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Colorectal Neoplasms/therapy/microbiology/metabolism
*Metabolome
*Immunotherapy
*Gastrointestinal Microbiome
Female
Feces/microbiology
Male
Middle Aged
Aged
Metabolomics
Bacteria/classification/genetics/isolation & purification
RevDate: 2026-08-06
CmpDate: 2026-08-06
Microbial Signatures in Head and Neck versus Gastrointestinal Tumors: Identification and Prognostic Modeling.
Polish journal of microbiology, 75(2):123-138.
This study identified key intra-tumor microbial signatures distinguishing head and neck cancers from gastrointestinal cancers and explored their diagnostic and prognostic potential. Intra-tumor microbial data of five cancer types were obtained from the Cancer Microbiome Atlas, and corresponding clinical data were retrieved from the Cancer Genome Atlas. The Wilcoxon test was used to analyze differences in microbial populations. Univariate logistic regression, least absolute shrinkage and selection operator, and recursive feature elimination were sequentially applied to screen optimal microbial markers, and a support vector machine classification model was constructed. A nomogram model and Kaplan-Meier curves were used to validate the predictive and prognostic value of the optimal microbes, respectively. Overall, 463 tumor samples and 47 controls were included. Twenty-three microbes showed significant differences in distribution between head and neck and gastrointestinal tumors; among these, eight overlapping microbes were selected as optimal markers. The SVM model based on these eight microbes achieved AUCs of 0.937 and 0.856 in the training and validation datasets, respectively. The nomogram model constructed with these markers showed high predictive accuracy (C-index = 0.8944 in training, 0.8023 in validation). Kaplan-Meier analysis revealed that high abundance of Capnocytophaga, Lachnospiraceae, and Bacteroidales was significantly associated with longer overall survival in both head and neck tumors and gastrointestinal tumors (all P < 0.05). The eight intra-tumor microbial communities serve as a robust signature for distinguishing head and neck tumors from gastrointestinal tumors. Among these, Capnocytophaga, Lachnospiraceae, and Bacteroidales have potential as prognostic biomarkers to improve survival prediction in cancers.
Additional Links: PMID-42560302
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42560302,
year = {2026},
author = {Guo, H and Wang, J and Niu, Y and Liu, F},
title = {Microbial Signatures in Head and Neck versus Gastrointestinal Tumors: Identification and Prognostic Modeling.},
journal = {Polish journal of microbiology},
volume = {75},
number = {2},
pages = {123-138},
pmid = {42560302},
issn = {2544-4646},
mesh = {Humans ; *Head and Neck Neoplasms/microbiology/diagnosis ; *Gastrointestinal Neoplasms/microbiology/diagnosis ; Prognosis ; *Bacteria/classification/isolation & purification/genetics ; Nomograms ; *Microbiota ; },
abstract = {This study identified key intra-tumor microbial signatures distinguishing head and neck cancers from gastrointestinal cancers and explored their diagnostic and prognostic potential. Intra-tumor microbial data of five cancer types were obtained from the Cancer Microbiome Atlas, and corresponding clinical data were retrieved from the Cancer Genome Atlas. The Wilcoxon test was used to analyze differences in microbial populations. Univariate logistic regression, least absolute shrinkage and selection operator, and recursive feature elimination were sequentially applied to screen optimal microbial markers, and a support vector machine classification model was constructed. A nomogram model and Kaplan-Meier curves were used to validate the predictive and prognostic value of the optimal microbes, respectively. Overall, 463 tumor samples and 47 controls were included. Twenty-three microbes showed significant differences in distribution between head and neck and gastrointestinal tumors; among these, eight overlapping microbes were selected as optimal markers. The SVM model based on these eight microbes achieved AUCs of 0.937 and 0.856 in the training and validation datasets, respectively. The nomogram model constructed with these markers showed high predictive accuracy (C-index = 0.8944 in training, 0.8023 in validation). Kaplan-Meier analysis revealed that high abundance of Capnocytophaga, Lachnospiraceae, and Bacteroidales was significantly associated with longer overall survival in both head and neck tumors and gastrointestinal tumors (all P < 0.05). The eight intra-tumor microbial communities serve as a robust signature for distinguishing head and neck tumors from gastrointestinal tumors. Among these, Capnocytophaga, Lachnospiraceae, and Bacteroidales have potential as prognostic biomarkers to improve survival prediction in cancers.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Head and Neck Neoplasms/microbiology/diagnosis
*Gastrointestinal Neoplasms/microbiology/diagnosis
Prognosis
*Bacteria/classification/isolation & purification/genetics
Nomograms
*Microbiota
RevDate: 2026-08-06
CmpDate: 2026-08-06
A Pilot Longitudinal 16S rRNA Gene Sequencing Study Exploring the Relationship Between Gut Microbiota and Body Composition in Healthy Adults.
Polish journal of microbiology, 75(2):157-167.
The gut microbiome is linked to body composition, yet most studies involve probiotic or dietary interventions. This study explored relationships between changes in body composition and the fecal microbiota under natural lifestyle conditions. A repeated-measures design involved 15 adults completing four body composition assessments at 3-month intervals. Fecal samples from each time point underwent 16S rRNA gene sequencing. Participants were stratified by body composition parameters, and microbial profiles from initial and final measurements were compared to assess longitudinal patterns. Overweight participants showed lower alpha diversity. Linear mixed models revealed fecal microbiota remained stable across all four time points, with no statistically significant continuous trends observed longitudinally. Exploratory baseline-to-endpoint comparisons across stratified groups and Spearman correlation analyses suggested potential microbiota shifts, though these associations remained statistically non-significant. Preliminary observations exhibited that the OTU identified as Parasutterella excrementihominis tended to associate with higher body fat, whereas the putative species Akkermansia muciniphila showed a potential inverse association. Representative taxa, such as Dialister invisus, appeared enriched in individuals with higher skeletal muscle percentages, whereas the OTU assigned to Bifidobacterium pseudocatenulatum showed the opposite trend. Several associations differed by sex, suggesting modulation by host factors. These preliminary findings suggest possible fecal microbiota patterns associated with body composition, even without targeted interventions. While lacking robust linear associations in this small pilot cohort, the observed directional consistency across statistical approaches highlights the potential of fecal microbes as candidate indicators of metabolic health. These exploratory results require further validation in larger, longitudinal studies with sufficient statistical power.
Additional Links: PMID-42560303
PubMed:
Citation:
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@article {pmid42560303,
year = {2026},
author = {Shih, MY and Yang, YC and Liu, YR},
title = {A Pilot Longitudinal 16S rRNA Gene Sequencing Study Exploring the Relationship Between Gut Microbiota and Body Composition in Healthy Adults.},
journal = {Polish journal of microbiology},
volume = {75},
number = {2},
pages = {157-167},
pmid = {42560303},
issn = {2544-4646},
mesh = {Humans ; *Body Composition ; *RNA, Ribosomal, 16S/genetics ; Male ; Female ; Pilot Projects ; Feces/microbiology ; Adult ; *Gastrointestinal Microbiome ; Longitudinal Studies ; *Bacteria/classification/genetics/isolation & purification ; Middle Aged ; },
abstract = {The gut microbiome is linked to body composition, yet most studies involve probiotic or dietary interventions. This study explored relationships between changes in body composition and the fecal microbiota under natural lifestyle conditions. A repeated-measures design involved 15 adults completing four body composition assessments at 3-month intervals. Fecal samples from each time point underwent 16S rRNA gene sequencing. Participants were stratified by body composition parameters, and microbial profiles from initial and final measurements were compared to assess longitudinal patterns. Overweight participants showed lower alpha diversity. Linear mixed models revealed fecal microbiota remained stable across all four time points, with no statistically significant continuous trends observed longitudinally. Exploratory baseline-to-endpoint comparisons across stratified groups and Spearman correlation analyses suggested potential microbiota shifts, though these associations remained statistically non-significant. Preliminary observations exhibited that the OTU identified as Parasutterella excrementihominis tended to associate with higher body fat, whereas the putative species Akkermansia muciniphila showed a potential inverse association. Representative taxa, such as Dialister invisus, appeared enriched in individuals with higher skeletal muscle percentages, whereas the OTU assigned to Bifidobacterium pseudocatenulatum showed the opposite trend. Several associations differed by sex, suggesting modulation by host factors. These preliminary findings suggest possible fecal microbiota patterns associated with body composition, even without targeted interventions. While lacking robust linear associations in this small pilot cohort, the observed directional consistency across statistical approaches highlights the potential of fecal microbes as candidate indicators of metabolic health. These exploratory results require further validation in larger, longitudinal studies with sufficient statistical power.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Body Composition
*RNA, Ribosomal, 16S/genetics
Male
Female
Pilot Projects
Feces/microbiology
Adult
*Gastrointestinal Microbiome
Longitudinal Studies
*Bacteria/classification/genetics/isolation & purification
Middle Aged
RevDate: 2026-08-06
CmpDate: 2026-08-06
Toward Meta-Omics Governance of the Urban Microbiome Commons.
Annals of the New York Academy of Sciences, 1562(1):e70361.
Urban microbial communities are undergoing directional homogenization across soils, wildlife gut microbiota, and human exposure pathways, yet no monitoring framework exists to track this loss or govern the probiotic city interventions now scaling without ecological oversight. I argue that the urban microbiome constitutes an "invisible commons": a shared, depletable resource whose depletion goes unaccounted for because it has never been made measurable. The meta-omics community has the tools to change this. I propose five monitoring priorities and six immediately deployable indicators and show that the governance architecture required to convert these measurements into decisions already exists in conservation biology. What is missing is not new science but the decision to apply existing methods to this domain. With antibiotic resistance causing over one million deaths annually and probiotic city interventions advancing without resistance gene screening, that decision is overdue.
Additional Links: PMID-42560340
PubMed:
Citation:
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hide bibtex listing
@article {pmid42560340,
year = {2026},
author = {Zheng, B},
title = {Toward Meta-Omics Governance of the Urban Microbiome Commons.},
journal = {Annals of the New York Academy of Sciences},
volume = {1562},
number = {1},
pages = {e70361},
pmid = {42560340},
issn = {1749-6632},
support = {JAT220336//Fujian Provincial Young and Middle-aged Teachers' Education and Research Project/ ; 2024I0043//Fujian International Cooperation Project/ ; 3502Z202372040//Xiamen Natural Science Foundation Youth Project/ ; },
mesh = {Humans ; *Microbiota/physiology ; Animals ; Cities ; Multiomics ; Probiotics ; },
abstract = {Urban microbial communities are undergoing directional homogenization across soils, wildlife gut microbiota, and human exposure pathways, yet no monitoring framework exists to track this loss or govern the probiotic city interventions now scaling without ecological oversight. I argue that the urban microbiome constitutes an "invisible commons": a shared, depletable resource whose depletion goes unaccounted for because it has never been made measurable. The meta-omics community has the tools to change this. I propose five monitoring priorities and six immediately deployable indicators and show that the governance architecture required to convert these measurements into decisions already exists in conservation biology. What is missing is not new science but the decision to apply existing methods to this domain. With antibiotic resistance causing over one million deaths annually and probiotic city interventions advancing without resistance gene screening, that decision is overdue.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota/physiology
Animals
Cities
Multiomics
Probiotics
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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.