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ESP: PubMed Auto Bibliography 03 Sep 2026 at 01:56 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: 2026-09-02
CmpDate: 2026-09-02
Impact of intestinal propionate metabolism on systemic metabolic homeostasis.
American journal of physiology. Endocrinology and metabolism, 331(3):E414-E424.
Propionate is an abundant short-chain fatty acid largely derived from gut microbiota in mammals. Propionate metabolism is essential to maintain systemic homeostasis, and inborn errors of essential metabolic enzymes in this pathway cause severe illness. The juxtaposition of high concentrations of propionate with the intestinal epithelium suggests a need for propionate catabolism. To understand the requirement of propionate metabolism in intestinal epithelium, we generated mice with a conditional knockout of propionyl-CoA carboxylase A (Pcca) specifically in the intestine (Pcca[Vil-Cre]). Male and female Pcca[Vil-Cre] mice were born and weaned at the expected Mendelian ratio and gained weight normally on chow and high-fat diets. Liver metabolomics of Pcca[Vil-Cre] mice suggest that propionate metabolism affects the gut-liver axis. However, the loss of Pcca in the intestine did not affect the colonic transcriptome. These data suggest that intestinal propionate metabolism is largely dispensable, and that hepatic capture and metabolism of propionate dominate systemic physiology.NEW & NOTEWORTHY Propionate generated by the microbiome is extremely high in the lumen of the gut. To determine the requirement of propionate metabolism in the gut, we generated and characterized mice with an intestine-specific knockout of propionyl-CoA carboxcylase alpha (PCCA), the first step in propionyl-CoA metabolism. Overall, mice that are unable to use propionate in the intestine are relatively normal with alterations in the gut-liver axis.
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@article {pmid42630008,
year = {2026},
author = {Encarnacion, J and Wolfgang, MJ},
title = {Impact of intestinal propionate metabolism on systemic metabolic homeostasis.},
journal = {American journal of physiology. Endocrinology and metabolism},
volume = {331},
number = {3},
pages = {E414-E424},
doi = {10.1152/ajpendo.00168.2026},
pmid = {42630008},
issn = {1522-1555},
support = {1//Propionic Acidemia Foundation (PAF)/ ; },
mesh = {Animals ; *Propionates/metabolism ; *Homeostasis ; Male ; Mice ; Female ; Liver/metabolism ; *Intestinal Mucosa/metabolism ; *Propionyl-Coenzyme A Carboxylase/genetics/metabolism ; Mice, Knockout ; Gastrointestinal Microbiome/physiology ; Colon/metabolism ; },
abstract = {Propionate is an abundant short-chain fatty acid largely derived from gut microbiota in mammals. Propionate metabolism is essential to maintain systemic homeostasis, and inborn errors of essential metabolic enzymes in this pathway cause severe illness. The juxtaposition of high concentrations of propionate with the intestinal epithelium suggests a need for propionate catabolism. To understand the requirement of propionate metabolism in intestinal epithelium, we generated mice with a conditional knockout of propionyl-CoA carboxylase A (Pcca) specifically in the intestine (Pcca[Vil-Cre]). Male and female Pcca[Vil-Cre] mice were born and weaned at the expected Mendelian ratio and gained weight normally on chow and high-fat diets. Liver metabolomics of Pcca[Vil-Cre] mice suggest that propionate metabolism affects the gut-liver axis. However, the loss of Pcca in the intestine did not affect the colonic transcriptome. These data suggest that intestinal propionate metabolism is largely dispensable, and that hepatic capture and metabolism of propionate dominate systemic physiology.NEW & NOTEWORTHY Propionate generated by the microbiome is extremely high in the lumen of the gut. To determine the requirement of propionate metabolism in the gut, we generated and characterized mice with an intestine-specific knockout of propionyl-CoA carboxcylase alpha (PCCA), the first step in propionyl-CoA metabolism. Overall, mice that are unable to use propionate in the intestine are relatively normal with alterations in the gut-liver axis.},
}
MeSH Terms:
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Animals
*Propionates/metabolism
*Homeostasis
Male
Mice
Female
Liver/metabolism
*Intestinal Mucosa/metabolism
*Propionyl-Coenzyme A Carboxylase/genetics/metabolism
Mice, Knockout
Gastrointestinal Microbiome/physiology
Colon/metabolism
RevDate: 2026-09-01
Comparative analysis of microbial communities, assembly processes, and life-history strategies in a mariculture-impacted eutrophic bay and adjacent coastal sediments.
Ecotoxicology and environmental safety, 323:120750 pii:S0147-6513(26)01080-8 [Epub ahead of print].
Coastal embayments are increasingly subjected to intensive mariculture, which delivers sustained nutrient, organic matter, and antibiotics to sediments, yet microbiome responses remain poorly understood. Here we compared sediment microbiomes of the eutrophic Xiangshan Bay (XSB) and oligotrophic East China Sea (ECS), integrating cell counts, 16S rRNA amplicon, metagenomics, and cultivation-based resistance assays. Cell counts and amplicon data showed that XSB harbored higher microbial abundance (1.28 ×10[8]-1.34 ×10[9] vs. 2.07 ×10[7]-4.43 ×10[8] cells g[-1]), Chao1 richness (10,374-16,674 vs. 8311-12,281), and Shannon diversity (6.31-7.43 vs. 5.95-6.68). Amplicon-based null and neutral models indicated that community assembly in XSB was less stochastic and more deterministically selected than in the ECS. Life-history traits inferred directly from metagenomic data were consistently elevated in XSB relative to ECS, including 16S rRNA gene copy number (3.35 vs. 2.37), codon usage bias (0.0219 vs. 0.0188), maximum growth potential (0.1208 vs. 0.0844 h[-1]), genome size (5.63 vs. 5.38 Mb), GC content (56.26% vs. 54.48%), and transposase abundance (3.91% vs. 2.55%), collectively indicating a transition from K- to r-selected life-history strategies. Moreover, metagenomic annotation revealed a similarly expanded resistome in XSB, with 4.5-fold higher antibiotic resistance gene abundance (17.40-45.37 vs. 7.96-25.96 RPM) dominated by efflux-pump mechanisms, while plate assays showed roughly two-fold higher phenotypic resistance to macrolides, tetracyclines, and sulfonamides. These findings demonstrate that microbial community, life-history strategies, and antibiotic resistance respond as a coupled system to mariculture-driven eutrophication, providing a trait-based framework for predicting microbiome trajectories under anthropogenic nutrient enrichment.
Additional Links: PMID-42679417
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@article {pmid42679417,
year = {2026},
author = {Li, H and Gao, H and Fu, J and Yang, S and Chen, L and Zhou, J},
title = {Comparative analysis of microbial communities, assembly processes, and life-history strategies in a mariculture-impacted eutrophic bay and adjacent coastal sediments.},
journal = {Ecotoxicology and environmental safety},
volume = {323},
number = {},
pages = {120750},
doi = {10.1016/j.ecoenv.2026.120750},
pmid = {42679417},
issn = {1090-2414},
abstract = {Coastal embayments are increasingly subjected to intensive mariculture, which delivers sustained nutrient, organic matter, and antibiotics to sediments, yet microbiome responses remain poorly understood. Here we compared sediment microbiomes of the eutrophic Xiangshan Bay (XSB) and oligotrophic East China Sea (ECS), integrating cell counts, 16S rRNA amplicon, metagenomics, and cultivation-based resistance assays. Cell counts and amplicon data showed that XSB harbored higher microbial abundance (1.28 ×10[8]-1.34 ×10[9] vs. 2.07 ×10[7]-4.43 ×10[8] cells g[-1]), Chao1 richness (10,374-16,674 vs. 8311-12,281), and Shannon diversity (6.31-7.43 vs. 5.95-6.68). Amplicon-based null and neutral models indicated that community assembly in XSB was less stochastic and more deterministically selected than in the ECS. Life-history traits inferred directly from metagenomic data were consistently elevated in XSB relative to ECS, including 16S rRNA gene copy number (3.35 vs. 2.37), codon usage bias (0.0219 vs. 0.0188), maximum growth potential (0.1208 vs. 0.0844 h[-1]), genome size (5.63 vs. 5.38 Mb), GC content (56.26% vs. 54.48%), and transposase abundance (3.91% vs. 2.55%), collectively indicating a transition from K- to r-selected life-history strategies. Moreover, metagenomic annotation revealed a similarly expanded resistome in XSB, with 4.5-fold higher antibiotic resistance gene abundance (17.40-45.37 vs. 7.96-25.96 RPM) dominated by efflux-pump mechanisms, while plate assays showed roughly two-fold higher phenotypic resistance to macrolides, tetracyclines, and sulfonamides. These findings demonstrate that microbial community, life-history strategies, and antibiotic resistance respond as a coupled system to mariculture-driven eutrophication, providing a trait-based framework for predicting microbiome trajectories under anthropogenic nutrient enrichment.},
}
RevDate: 2026-09-01
Localized root colonization by Trichoderma afroharzianum T22 is associated with host transcriptional reprogramming and beneficial bacterial enrichment under salinity stress in sorghum.
Microbiological research, 314:128703 pii:S0944-5013(26)00267-3 [Epub ahead of print].
Salinity is a major abiotic stress that severely restricts crop productivity. Despite considerable potential, the role of Trichoderma afroharzianum T22 in the molecular responses and root microbiome dynamics associated with salinity tolerance remains poorly understood in sorghum. In this study, T. afroharzianum inoculation alleviated salinity-induced stress by improving chlorophyll content, growth parameters, and nutrient balance, while restricting root-to-shoot Na[+] translocation. Split-root experiments showed that T. afroharzianum application to a single root compartment was insufficient to improve whole-plant performance under salinity, whereas inoculation of both compartments restored growth and chlorophyll-related traits. RNA-seq analysis showed the upregulation of genes involved in symbiosis, hormone signaling, antioxidant defense, and ion homeostasis, accompanied by repression of genes involved in ethylene biosynthesis and senescence in the roots. KEGG enrichment analysis further revealed activation of secondary metabolic pathways involved in stress adaptation. Furthermore, 16S rRNA sequencing showed that T. afroharzianum inoculation was associated with shifts in the root bacterial community without significantly altering alpha diversity, while selectively enriching putatively beneficial taxa, including Dyella mobilis, Luteibacter rhizovicinus, and Luteibacter yeojuensis under salinity. In addition, a conserved core microbiome was retained across treatments and was dominated by Streptomyces, Rhizobium, Dyella, and Labrys. Further, Janibacter was identified as a characteristic indicator taxon of T. afroharzianum inoculation, while Streptomyces showed the highest overall indicator value. Multi-omics integration analysis revealed that T. afroharzianum-associated microbial taxa were strongly associated with hormone signaling, redox homeostasis, mineral transport, and secondary metabolism under salinity stress. Particularly, Streptomyces and Luteibacter were the two genera most strongly associated with plant growth traits, whereas Rhizobium and Mucilaginibacter showed stronger positive correlations with tissue Na[+] accumulation. Collectively, these findings provide new insights into T. afroharzianum-mediated salinity tolerance in sorghum and highlight its potential as a microbial biostimulant, warranting further validation across diverse sorghum genotypes in field conditions.
Additional Links: PMID-42679497
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@article {pmid42679497,
year = {2026},
author = {Bagchi, R and Pant, B and Wang, HL and Kabir, AH},
title = {Localized root colonization by Trichoderma afroharzianum T22 is associated with host transcriptional reprogramming and beneficial bacterial enrichment under salinity stress in sorghum.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128703},
doi = {10.1016/j.micres.2026.128703},
pmid = {42679497},
issn = {1618-0623},
abstract = {Salinity is a major abiotic stress that severely restricts crop productivity. Despite considerable potential, the role of Trichoderma afroharzianum T22 in the molecular responses and root microbiome dynamics associated with salinity tolerance remains poorly understood in sorghum. In this study, T. afroharzianum inoculation alleviated salinity-induced stress by improving chlorophyll content, growth parameters, and nutrient balance, while restricting root-to-shoot Na[+] translocation. Split-root experiments showed that T. afroharzianum application to a single root compartment was insufficient to improve whole-plant performance under salinity, whereas inoculation of both compartments restored growth and chlorophyll-related traits. RNA-seq analysis showed the upregulation of genes involved in symbiosis, hormone signaling, antioxidant defense, and ion homeostasis, accompanied by repression of genes involved in ethylene biosynthesis and senescence in the roots. KEGG enrichment analysis further revealed activation of secondary metabolic pathways involved in stress adaptation. Furthermore, 16S rRNA sequencing showed that T. afroharzianum inoculation was associated with shifts in the root bacterial community without significantly altering alpha diversity, while selectively enriching putatively beneficial taxa, including Dyella mobilis, Luteibacter rhizovicinus, and Luteibacter yeojuensis under salinity. In addition, a conserved core microbiome was retained across treatments and was dominated by Streptomyces, Rhizobium, Dyella, and Labrys. Further, Janibacter was identified as a characteristic indicator taxon of T. afroharzianum inoculation, while Streptomyces showed the highest overall indicator value. Multi-omics integration analysis revealed that T. afroharzianum-associated microbial taxa were strongly associated with hormone signaling, redox homeostasis, mineral transport, and secondary metabolism under salinity stress. Particularly, Streptomyces and Luteibacter were the two genera most strongly associated with plant growth traits, whereas Rhizobium and Mucilaginibacter showed stronger positive correlations with tissue Na[+] accumulation. Collectively, these findings provide new insights into T. afroharzianum-mediated salinity tolerance in sorghum and highlight its potential as a microbial biostimulant, warranting further validation across diverse sorghum genotypes in field conditions.},
}
RevDate: 2026-09-01
Bacteriophages as emerging modulators of antitumor immunity in the tumor microenvironment.
Microbiological research, 314:128700 pii:S0944-5013(26)00264-8 [Epub ahead of print].
The tumor microenvironment (TME) is increasingly recognized as a complex ecosystem shaped by dynamic interactions among tumor cells, immune cells, and microbial components. While growing evidence has established the microbiota as a key regulator of antitumor immunity and immunotherapy response, the contribution of bacteriophages, the most abundant biological entities within microbial communities, has remained largely overlooked. Recent studies suggest that bacteriophages are not merely passive regulators of bacterial populations but can actively modulate host immune responses and influence tumor-associated immune landscapes. In this review, we summarize emerging evidence suggesting that bacteriophages may influence antitumor immunity through both direct and indirect mechanisms. Evidence from immune-cell and non-cancer experimental systems indicates that phage nucleic acids can engage TLR9-dependent sensing and, for selected phages, STING-associated inflammatory signaling; however, the relevance of these pathways within human tumors remains to be established. Indirectly, phages may alter microbial community structure and metabolic outputs, which could influence systemic immune tone and the composition of immune infiltrates within the TME. We further discuss accumulating data linking phageome features with tumor progression and responses to immune checkpoint blockade and other cancer therapies. However, much of the available evidence remains preclinical, indirect, or correlative, and causal roles for endogenous phages in human tumor immunity still require further validation. Distinct from the putative ecological and immunological roles of naturally occurring phages, engineered bacteriophages are being developed as therapeutic platforms for cancer immunotherapy, including tumor-antigen display, targeted delivery of immune agonists, cytokines or nucleic acids, and combination strategies with existing treatments. Finally, we address key methodological, mechanistic, and safety challenges that must be overcome to translate phage-based immunomodulation into clinical applications. Collectively, this review highlights the phageome as an emerging regulatory layer of tumor immunity and a promising, yet underexplored, target for therapeutic intervention.
Additional Links: PMID-42679498
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@article {pmid42679498,
year = {2026},
author = {Chen, X and Zhang, J and Gao, F and Du, H},
title = {Bacteriophages as emerging modulators of antitumor immunity in the tumor microenvironment.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128700},
doi = {10.1016/j.micres.2026.128700},
pmid = {42679498},
issn = {1618-0623},
abstract = {The tumor microenvironment (TME) is increasingly recognized as a complex ecosystem shaped by dynamic interactions among tumor cells, immune cells, and microbial components. While growing evidence has established the microbiota as a key regulator of antitumor immunity and immunotherapy response, the contribution of bacteriophages, the most abundant biological entities within microbial communities, has remained largely overlooked. Recent studies suggest that bacteriophages are not merely passive regulators of bacterial populations but can actively modulate host immune responses and influence tumor-associated immune landscapes. In this review, we summarize emerging evidence suggesting that bacteriophages may influence antitumor immunity through both direct and indirect mechanisms. Evidence from immune-cell and non-cancer experimental systems indicates that phage nucleic acids can engage TLR9-dependent sensing and, for selected phages, STING-associated inflammatory signaling; however, the relevance of these pathways within human tumors remains to be established. Indirectly, phages may alter microbial community structure and metabolic outputs, which could influence systemic immune tone and the composition of immune infiltrates within the TME. We further discuss accumulating data linking phageome features with tumor progression and responses to immune checkpoint blockade and other cancer therapies. However, much of the available evidence remains preclinical, indirect, or correlative, and causal roles for endogenous phages in human tumor immunity still require further validation. Distinct from the putative ecological and immunological roles of naturally occurring phages, engineered bacteriophages are being developed as therapeutic platforms for cancer immunotherapy, including tumor-antigen display, targeted delivery of immune agonists, cytokines or nucleic acids, and combination strategies with existing treatments. Finally, we address key methodological, mechanistic, and safety challenges that must be overcome to translate phage-based immunomodulation into clinical applications. Collectively, this review highlights the phageome as an emerging regulatory layer of tumor immunity and a promising, yet underexplored, target for therapeutic intervention.},
}
RevDate: 2026-09-01
Microplastic aging drives convergence of the plastisphere microbiome and resistome toward agricultural soils.
Journal of hazardous materials, 516:143426 pii:S0304-3894(26)02406-4 [Epub ahead of print].
The degree of microplastic (MP) aging varies substantially in agricultural soils; however, how this common aging gradient influences the plastisphere microbiome and resistome remains largely unknown. We therefore collected polyethylene MPs from long‑term mulched farmlands and classified them into low‑aged plastispheres (LAPs) and high‑aged plastispheres (HAPs). Bacterial community dissimilarity to soil decreased progressively from LAPs to HAPs, accompanied by broadening niche breadth, increasing bacterial diversity, and a shift toward more stochastic community assembly. The diversity and abundance of antibiotic resistance genes (ARGs) declined significantly along the aging gradient, with clinically relevant high-risk ARGs (e.g., vanR, ugd, and aac(6')-I) decreasing by 53.34-84.01%. Furthermore, the ARG hosts shifted from Actinomycetota in LAPs to Pseudomonadota in soils. Variance partitioning showed that the carbonyl index uniquely explained 57.03% of the variation in plastisphere ARG profile distance toward soil, identifying MP aging as the primary driver of resistome convergence. Collectively, these findings demonstrate that natural MP aging drives a progressive convergence of the plastisphere resistome toward that of the surrounding soil, indicating that aged MPs may pose a reduced risk of antibiotic resistance compared to newly formed MPs. This convergence underscores the need to incorporate plastic aging into future risk assessment frameworks for plastisphere-associated ARGs.
Additional Links: PMID-42679573
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@article {pmid42679573,
year = {2026},
author = {Liu, B and Shen, Z and Shen, Y and Ren, J and Zhang, Z and Li, T and Li, W and Zhou, Q and Wu, T and Sun, J},
title = {Microplastic aging drives convergence of the plastisphere microbiome and resistome toward agricultural soils.},
journal = {Journal of hazardous materials},
volume = {516},
number = {},
pages = {143426},
doi = {10.1016/j.jhazmat.2026.143426},
pmid = {42679573},
issn = {1873-3336},
abstract = {The degree of microplastic (MP) aging varies substantially in agricultural soils; however, how this common aging gradient influences the plastisphere microbiome and resistome remains largely unknown. We therefore collected polyethylene MPs from long‑term mulched farmlands and classified them into low‑aged plastispheres (LAPs) and high‑aged plastispheres (HAPs). Bacterial community dissimilarity to soil decreased progressively from LAPs to HAPs, accompanied by broadening niche breadth, increasing bacterial diversity, and a shift toward more stochastic community assembly. The diversity and abundance of antibiotic resistance genes (ARGs) declined significantly along the aging gradient, with clinically relevant high-risk ARGs (e.g., vanR, ugd, and aac(6')-I) decreasing by 53.34-84.01%. Furthermore, the ARG hosts shifted from Actinomycetota in LAPs to Pseudomonadota in soils. Variance partitioning showed that the carbonyl index uniquely explained 57.03% of the variation in plastisphere ARG profile distance toward soil, identifying MP aging as the primary driver of resistome convergence. Collectively, these findings demonstrate that natural MP aging drives a progressive convergence of the plastisphere resistome toward that of the surrounding soil, indicating that aged MPs may pose a reduced risk of antibiotic resistance compared to newly formed MPs. This convergence underscores the need to incorporate plastic aging into future risk assessment frameworks for plastisphere-associated ARGs.},
}
RevDate: 2026-09-01
AMPK and macrophage crosstalk in diabetes: Mechanisms, inflammation, and therapeutic perspectives.
Cytokine & growth factor reviews, 91:161-172 pii:S1359-6101(26)00062-6 [Epub ahead of print].
Diabetes mellitus, especially type 2 diabetes (T2DM), is a complex metabolic disease marked by persistent low-grade inflammation and insulin resistance. In diabetes, adipose tissue macrophages adopt a pro-inflammatory M1 phenotype, secreting cytokines including TNF-α, IL-6, and IL-1β that disrupt insulin signaling and cause metabolic dysfunction. AMP-activated protein kinase (AMPK), a cellular energy sensor, is a key regulator of macrophage polarization. It suppresses M1 responses by inhibiting NF-κB and JNK signaling, activating CREB/SIRT1 pathways, and promoting oxidative metabolism. Therefore, this review investigates the bidirectional interaction between AMPK signaling and macrophage function in diabetes, focusing on how metabolic stress affects AMPK activity, increasing inflammation and insulin resistance, whereas AMPK activation restores immune-metabolic balance. The gut microbiome further influences this axis, with short-chain fatty acids activating AMPK via GPR41/43, promoting M2 polarization and improving metabolic outcomes. Metformin, SGLT2 inhibitors, new direct AMPK activators such as PXL770, and lifestyle changes are also potential therapeutic treatments. However, considerable hurdles remain, including the prevalence of preclinical findings, a lack of macrophage-specific AMPK activators, simplicity of the M1/M2 paradigm, and uncertainty about long-term safety. Future research must focus on macrophage-targeted drug delivery, tissue-specific regulatory networks, biomarker discovery, and rigorous clinical trials with immunological outcomes. In conclusion, the AMPK-macrophage axis is a critical immune-metabolic gatekeeper in diabetes, and targeting this pathway offers a potential technique for restoring immune-metabolic balance, while significant difficulties must be overcome before practical use.
Additional Links: PMID-42679639
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PubMed:
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@article {pmid42679639,
year = {2026},
author = {Ahmad, I and Zia, MA and Tavares, RG and Spanevello, RM and Stefanello, FM},
title = {AMPK and macrophage crosstalk in diabetes: Mechanisms, inflammation, and therapeutic perspectives.},
journal = {Cytokine & growth factor reviews},
volume = {91},
number = {},
pages = {161-172},
doi = {10.1016/j.cytogfr.2026.08.002},
pmid = {42679639},
issn = {1879-0305},
abstract = {Diabetes mellitus, especially type 2 diabetes (T2DM), is a complex metabolic disease marked by persistent low-grade inflammation and insulin resistance. In diabetes, adipose tissue macrophages adopt a pro-inflammatory M1 phenotype, secreting cytokines including TNF-α, IL-6, and IL-1β that disrupt insulin signaling and cause metabolic dysfunction. AMP-activated protein kinase (AMPK), a cellular energy sensor, is a key regulator of macrophage polarization. It suppresses M1 responses by inhibiting NF-κB and JNK signaling, activating CREB/SIRT1 pathways, and promoting oxidative metabolism. Therefore, this review investigates the bidirectional interaction between AMPK signaling and macrophage function in diabetes, focusing on how metabolic stress affects AMPK activity, increasing inflammation and insulin resistance, whereas AMPK activation restores immune-metabolic balance. The gut microbiome further influences this axis, with short-chain fatty acids activating AMPK via GPR41/43, promoting M2 polarization and improving metabolic outcomes. Metformin, SGLT2 inhibitors, new direct AMPK activators such as PXL770, and lifestyle changes are also potential therapeutic treatments. However, considerable hurdles remain, including the prevalence of preclinical findings, a lack of macrophage-specific AMPK activators, simplicity of the M1/M2 paradigm, and uncertainty about long-term safety. Future research must focus on macrophage-targeted drug delivery, tissue-specific regulatory networks, biomarker discovery, and rigorous clinical trials with immunological outcomes. In conclusion, the AMPK-macrophage axis is a critical immune-metabolic gatekeeper in diabetes, and targeting this pathway offers a potential technique for restoring immune-metabolic balance, while significant difficulties must be overcome before practical use.},
}
RevDate: 2026-09-02
Maternal secretor status and human milk oligosaccharides influence the infant gut resistome.
Cell reports. Medicine pii:S2666-3791(26)00424-6 [Epub ahead of print].
The infant gut resistome is established early in life and is shaped by perinatal exposures, yet the mechanisms underlying its modulation remain unclear. We combined shotgun metagenomics of fecal samples from 57 one-month-old infants and paired milk samples from 50 mothers in the MAMI cohort to investigate the influence of maternal secretor status on early-life resistome development. Longitudinal follow-up at 6 and 12 months, and also further validation in the independent Lifelines NEXT (LLNEXT) cohort, support our findings. Cesarean section (C-section) was associated with increased antibiotic resistance gene (ARG) diversity, whereas exclusive breastfeeding reduced ARG abundance and diversity. Maternal secretor status further modified resistome composition among exclusively breastfed infants. Human milk oligosaccharide profiling identified specific glycans underlying these associations, with 2'-fucosyllactose and 6'-sialyllactose showing negative correlations with distinct ARG classes. These findings identify human milk composition as a key determinant of early-life resistome assembly and a potential target for modulating antimicrobial resistance.
Additional Links: PMID-42679805
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@article {pmid42679805,
year = {2026},
author = {Samarra, A and Alcañiz, AJ and Quijada, NM and Renwick, S and George, S and Sinha, T and MartÃnez-Costa, C and Segata, N and Zhernakova, A and Bode, L and Collado, MC},
title = {Maternal secretor status and human milk oligosaccharides influence the infant gut resistome.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103007},
doi = {10.1016/j.xcrm.2026.103007},
pmid = {42679805},
issn = {2666-3791},
abstract = {The infant gut resistome is established early in life and is shaped by perinatal exposures, yet the mechanisms underlying its modulation remain unclear. We combined shotgun metagenomics of fecal samples from 57 one-month-old infants and paired milk samples from 50 mothers in the MAMI cohort to investigate the influence of maternal secretor status on early-life resistome development. Longitudinal follow-up at 6 and 12 months, and also further validation in the independent Lifelines NEXT (LLNEXT) cohort, support our findings. Cesarean section (C-section) was associated with increased antibiotic resistance gene (ARG) diversity, whereas exclusive breastfeeding reduced ARG abundance and diversity. Maternal secretor status further modified resistome composition among exclusively breastfed infants. Human milk oligosaccharide profiling identified specific glycans underlying these associations, with 2'-fucosyllactose and 6'-sialyllactose showing negative correlations with distinct ARG classes. These findings identify human milk composition as a key determinant of early-life resistome assembly and a potential target for modulating antimicrobial resistance.},
}
RevDate: 2026-09-01
The Gut Microbiota and Gut-Brain Axis in Alzheimer's Disease: From Pathogenesis to Treatment.
Ageing research reviews pii:S1568-1637(26)00337-5 [Epub ahead of print].
Alzheimer's disease (AD) is a progressive neurodegenerative disorder whose pathological course involves amyloid-β (Aβ) deposition, tau abnormalities, neuroinflammation, and neurovascular dysfunction. Interest in the microbiota-gut-brain axis does not arise because gut dysbiosis has been established as an independent initiating cause of sporadic AD, but because this axis connects modifiable peripheral factors-including diet, medication, ageing, and intestinal physiology-with barrier homeostasis, immunometabolic state, neural afferent signaling, and the brain's response to pathology. Human studies have detected microbiota differences in biomarker-positive preclinical AD and suggest that barrier abnormalities may be associated with subsequent cognitive change; patient-derived microbiota transfer, APOE-dependent tau models, and immune-vagal circuit studies further support phenotype modifiability under defined experimental conditions. This review therefore integrates barrier, immune, metabolic, and neural pathways and emphasizes that diverse microbial alterations may converge on a limited set of measurable functional nodes that could be more informative than individual genera for mechanistic validation, risk stratification, and treatment monitoring. Although clinical intervention evidence remains at an early stage, the peripheral accessibility and modifiability of the microbiota provide a rationale for investigating it as an adjunctive target alongside standard AD therapy. Future work should concurrently evaluate the microbiome, metabolites, both barriers, and immune and neural readouts in longitudinal cohorts and stratified randomized trials to determine which patients, disease stages, and intervention modalities are most likely to benefit.
Additional Links: PMID-42680070
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@article {pmid42680070,
year = {2026},
author = {Wang, J and Luo, L and Zhang, J and Yu, L and Cui, L},
title = {The Gut Microbiota and Gut-Brain Axis in Alzheimer's Disease: From Pathogenesis to Treatment.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103345},
doi = {10.1016/j.arr.2026.103345},
pmid = {42680070},
issn = {1872-9649},
abstract = {Alzheimer's disease (AD) is a progressive neurodegenerative disorder whose pathological course involves amyloid-β (Aβ) deposition, tau abnormalities, neuroinflammation, and neurovascular dysfunction. Interest in the microbiota-gut-brain axis does not arise because gut dysbiosis has been established as an independent initiating cause of sporadic AD, but because this axis connects modifiable peripheral factors-including diet, medication, ageing, and intestinal physiology-with barrier homeostasis, immunometabolic state, neural afferent signaling, and the brain's response to pathology. Human studies have detected microbiota differences in biomarker-positive preclinical AD and suggest that barrier abnormalities may be associated with subsequent cognitive change; patient-derived microbiota transfer, APOE-dependent tau models, and immune-vagal circuit studies further support phenotype modifiability under defined experimental conditions. This review therefore integrates barrier, immune, metabolic, and neural pathways and emphasizes that diverse microbial alterations may converge on a limited set of measurable functional nodes that could be more informative than individual genera for mechanistic validation, risk stratification, and treatment monitoring. Although clinical intervention evidence remains at an early stage, the peripheral accessibility and modifiability of the microbiota provide a rationale for investigating it as an adjunctive target alongside standard AD therapy. Future work should concurrently evaluate the microbiome, metabolites, both barriers, and immune and neural readouts in longitudinal cohorts and stratified randomized trials to determine which patients, disease stages, and intervention modalities are most likely to benefit.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Climate and soil shape Daqu wheat quality and seed microbiome via rhizosphere taxa and microbial assembly.
Food research international (Ottawa, Ont.), 242(Pt 3):119958.
The grain quality and seed microbiome of Daqu wheat are fundamental determinants of Daqu fermentation performance; however, the mechanisms by which cultivation environments influence these traits via rhizosphere microbial communities remain unclear. Bacterial and fungal communities across the bulk soil-rhizosphere-seed continuum of three wheat cultivars grown in four ecoregions were characterized using absolute quantitative amplicon sequencing. The rhizosphere microbiome was treated as a central intermediary, while the response variables were seed microbial diversity and grain-quality traits, including starch content, protein content, and grain hardness. Twelve physicochemical properties of soil and 11 climatic factors were integrated into a multidimensional association framework. Environmental conditions exerted stronger influences on both seed quality traits and microbial diversity than cultivar identity. Distinct regional signatures were also evident in rhizosphere microbiomes, with environmental gradients explaining community variation more effectively than geographic distance. Bacterial communities exhibited greater sensitivity to environmental fluctuations than fungi. Mantel analyses identified available nitrogen, precipitation, and atmospheric pressure as significant drivers of core rhizosphere taxa (P < 0.05). iCAMP revealed that stochastic processes predominantly governed rhizosphere bacterial assembly, whereas stochastic and deterministic mechanisms jointly shaped fungal assembly. Partial least squares path modeling further uncovered a rhizosphere-mediated environment-seed cascade, wherein sunlight intensity and duration, atmospheric pressure, and soil nitrogen directly or indirectly affected seed wet gluten content, grain hardness, and seed microbial diversity through their influences on rhizosphere microbiota. Rhizosphere bacterial diversity was negatively associated with seed bacterial diversity (path coefficient = -0.118, P < 0.05), indicating that rhizosphere communities may shape seed endophytic bacterial assemblages via environmental filtering and competitive interactions. Collectively, these findings elucidate how environments shape the quality and seed microbiomes of Daqu wheat, providing scientific guidance for optimal site selection and the standardized production of high-quality brewing wheat for industrial Baijiu.
Additional Links: PMID-42680280
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PubMed:
Citation:
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@article {pmid42680280,
year = {2026},
author = {Yu, K and Wang, S and Shi, H and Luo, R and Chen, Z and Xia, Y and Zeng, Q and Ma, Y and Han, D},
title = {Climate and soil shape Daqu wheat quality and seed microbiome via rhizosphere taxa and microbial assembly.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {119958},
doi = {10.1016/j.foodres.2026.119958},
pmid = {42680280},
issn = {1873-7145},
mesh = {*Triticum/microbiology ; *Rhizosphere ; *Soil Microbiology ; *Seeds/microbiology ; *Microbiota ; *Climate ; *Soil/chemistry ; Bacteria/classification ; Fungi/classification ; },
abstract = {The grain quality and seed microbiome of Daqu wheat are fundamental determinants of Daqu fermentation performance; however, the mechanisms by which cultivation environments influence these traits via rhizosphere microbial communities remain unclear. Bacterial and fungal communities across the bulk soil-rhizosphere-seed continuum of three wheat cultivars grown in four ecoregions were characterized using absolute quantitative amplicon sequencing. The rhizosphere microbiome was treated as a central intermediary, while the response variables were seed microbial diversity and grain-quality traits, including starch content, protein content, and grain hardness. Twelve physicochemical properties of soil and 11 climatic factors were integrated into a multidimensional association framework. Environmental conditions exerted stronger influences on both seed quality traits and microbial diversity than cultivar identity. Distinct regional signatures were also evident in rhizosphere microbiomes, with environmental gradients explaining community variation more effectively than geographic distance. Bacterial communities exhibited greater sensitivity to environmental fluctuations than fungi. Mantel analyses identified available nitrogen, precipitation, and atmospheric pressure as significant drivers of core rhizosphere taxa (P < 0.05). iCAMP revealed that stochastic processes predominantly governed rhizosphere bacterial assembly, whereas stochastic and deterministic mechanisms jointly shaped fungal assembly. Partial least squares path modeling further uncovered a rhizosphere-mediated environment-seed cascade, wherein sunlight intensity and duration, atmospheric pressure, and soil nitrogen directly or indirectly affected seed wet gluten content, grain hardness, and seed microbial diversity through their influences on rhizosphere microbiota. Rhizosphere bacterial diversity was negatively associated with seed bacterial diversity (path coefficient = -0.118, P < 0.05), indicating that rhizosphere communities may shape seed endophytic bacterial assemblages via environmental filtering and competitive interactions. Collectively, these findings elucidate how environments shape the quality and seed microbiomes of Daqu wheat, providing scientific guidance for optimal site selection and the standardized production of high-quality brewing wheat for industrial Baijiu.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Triticum/microbiology
*Rhizosphere
*Soil Microbiology
*Seeds/microbiology
*Microbiota
*Climate
*Soil/chemistry
Bacteria/classification
Fungi/classification
RevDate: 2026-09-01
CmpDate: 2026-09-01
Beyond protein source: The structure-gut microbiome axis in alternative protein digestion, fermentation, and health.
Food research international (Ottawa, Ont.), 242(Pt 3):119983.
Alternative proteins from plant, algal, fungal, and microbial sources are increasingly recognized for their potential to influence gut microbiota. However, the role of protein structure in shaping these interactions remains poorly understood. This review examines how key structural attributes of alternative proteins-including amino acid composition, folding characteristics, aggregation behavior, and enzymatic accessibility, govern gastrointestinal digestion. It also explores how these structural features affect microbial fermentation and the subsequent nutritional and functional outcomes. Structural variations influence peptide generation, microbial substrate utilization, and the production of metabolites such as short-chain fatty acids and proteolytic compounds. Current evidence indicates that protein conformation and digestibility, rather than source alone, are major determinants of microbiome responses. However, progress is hindered by limited multi-omics integration and a lack of standardized models and in-vivo validation. Collectively, current evidence supports a structure-driven framework for predicting microbiome interactions with alternative proteins. It also highlights key research priorities for developing functional protein ingredients that support gut and metabolic health.
Additional Links: PMID-42680295
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PubMed:
Citation:
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@article {pmid42680295,
year = {2026},
author = {Shafi, Z and Waheed, A and Shahid, M and Rasool, A and Ali, S},
title = {Beyond protein source: The structure-gut microbiome axis in alternative protein digestion, fermentation, and health.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {119983},
doi = {10.1016/j.foodres.2026.119983},
pmid = {42680295},
issn = {1873-7145},
mesh = {*Fermentation ; *Digestion/physiology ; Humans ; *Gastrointestinal Microbiome/physiology ; *Dietary Proteins/metabolism ; Animals ; },
abstract = {Alternative proteins from plant, algal, fungal, and microbial sources are increasingly recognized for their potential to influence gut microbiota. However, the role of protein structure in shaping these interactions remains poorly understood. This review examines how key structural attributes of alternative proteins-including amino acid composition, folding characteristics, aggregation behavior, and enzymatic accessibility, govern gastrointestinal digestion. It also explores how these structural features affect microbial fermentation and the subsequent nutritional and functional outcomes. Structural variations influence peptide generation, microbial substrate utilization, and the production of metabolites such as short-chain fatty acids and proteolytic compounds. Current evidence indicates that protein conformation and digestibility, rather than source alone, are major determinants of microbiome responses. However, progress is hindered by limited multi-omics integration and a lack of standardized models and in-vivo validation. Collectively, current evidence supports a structure-driven framework for predicting microbiome interactions with alternative proteins. It also highlights key research priorities for developing functional protein ingredients that support gut and metabolic health.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Fermentation
*Digestion/physiology
Humans
*Gastrointestinal Microbiome/physiology
*Dietary Proteins/metabolism
Animals
RevDate: 2026-09-01
CmpDate: 2026-09-01
Food-derived phenolic compounds in precision nutrition: computational and AI-assisted approaches for target identification and health intervention.
Food research international (Ottawa, Ont.), 242(Pt 3):120000.
Precision nutrition refers to nutritional interventions tailored to individual biological variability (e.g., genetics, gut microbiome, and metabolic status). Within this framework, identifying bioactive food components that modulate disease-relevant targets and pathways in an individualized manner is a central goal. Targeted interventions are increasingly used for cancer, autoimmune disorders, and metabolic diseases, but are often limited by high prices and adverse effects. Dietary phenolic compounds have therefore attracted attention as safer and more sustainable candidates for health intervention strategies, owing to their ability to interact with disease-relevant protein targets. Examples include EGCG targeting the p53-MDM2 interaction, quercetin modulating HSP90-related ferroptosis, and sesamin inhibiting Syk activation in food allergy. Their structural diversity and bioactivity make them valuable for candidate screening and personalized intervention design. However, these features also create challenges for target identification and functional evaluation. More systematic and predictive strategies are therefore needed to accelerate the identification, evaluation, and optimization of phenolic bioactives. In this context, computational and AI-assisted approaches (e.g., molecular docking, machine learning, and network pharmacology) offer new opportunities to improve target discovery, candidate prioritization, and response prediction. These approaches can integrate individual-level genetic, microbiome, metabolic, dietary, and clinical data. This integration may help predict personalized molecular targets, phenolic metabolism, bioavailability, and intervention responses, thereby supporting tailored phenolic-based nutrition strategies. This review summarizes the therapeutic potential, computational discovery strategies, molecular targets, and translational gaps in applying phenolic compounds to precision nutrition.
Additional Links: PMID-42680304
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PubMed:
Citation:
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@article {pmid42680304,
year = {2026},
author = {Li, Y and Wang, Y and Prabhakaran, P and Ouyang, F and Zhou, W and Guan, H and Chen, Y and Li, D and Sun-Waterhouse, D and Li, F},
title = {Food-derived phenolic compounds in precision nutrition: computational and AI-assisted approaches for target identification and health intervention.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {120000},
doi = {10.1016/j.foodres.2026.120000},
pmid = {42680304},
issn = {1873-7145},
mesh = {Humans ; *Phenols ; *Precision Medicine/methods ; *Artificial Intelligence ; },
abstract = {Precision nutrition refers to nutritional interventions tailored to individual biological variability (e.g., genetics, gut microbiome, and metabolic status). Within this framework, identifying bioactive food components that modulate disease-relevant targets and pathways in an individualized manner is a central goal. Targeted interventions are increasingly used for cancer, autoimmune disorders, and metabolic diseases, but are often limited by high prices and adverse effects. Dietary phenolic compounds have therefore attracted attention as safer and more sustainable candidates for health intervention strategies, owing to their ability to interact with disease-relevant protein targets. Examples include EGCG targeting the p53-MDM2 interaction, quercetin modulating HSP90-related ferroptosis, and sesamin inhibiting Syk activation in food allergy. Their structural diversity and bioactivity make them valuable for candidate screening and personalized intervention design. However, these features also create challenges for target identification and functional evaluation. More systematic and predictive strategies are therefore needed to accelerate the identification, evaluation, and optimization of phenolic bioactives. In this context, computational and AI-assisted approaches (e.g., molecular docking, machine learning, and network pharmacology) offer new opportunities to improve target discovery, candidate prioritization, and response prediction. These approaches can integrate individual-level genetic, microbiome, metabolic, dietary, and clinical data. This integration may help predict personalized molecular targets, phenolic metabolism, bioavailability, and intervention responses, thereby supporting tailored phenolic-based nutrition strategies. This review summarizes the therapeutic potential, computational discovery strategies, molecular targets, and translational gaps in applying phenolic compounds to precision nutrition.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Phenols
*Precision Medicine/methods
*Artificial Intelligence
RevDate: 2026-09-01
CmpDate: 2026-09-01
Dealcoholized muscadine wine improved skin elasticity and oxidative stress biomarkers without affecting gut microbiome in women over 40 in a randomized controlled trial.
Food research international (Ottawa, Ont.), 242(Pt 3):120042.
Muscadine wine has a unique polyphenol profile distinct from that of common wine, and limited research exists on its health benefits. This study aimed to investigate the effects of intake of dealcoholized muscadine wine (DMW) on skin health, oxidative stress, inflammatory biomarkers, and the gut microbiome. Seventeen healthy women were randomly assigned to consume 300 mL of DMW or a placebo daily for 6 weeks, separated by a 3-week washout period, in a randomized, single-blinded, crossover design. Skin health parameters were measured on the face and forearm. Oxidative stress and inflammatory biomarkers were assessed in plasma. Fecal bacterial DNA was sequenced using shotgun sequencing. DMW did not affect UVB-induced erythema compared to placebo. However, it significantly decreased transepidermal water loss and increased facial gross elasticity. Skin elasticity significantly improved on the forearm, whereas other skin parameters were not affected. DMW significantly decreased plasma levels of matrix metalloproteinase-9 and advanced glycation end products compared with placebo. However, the abundance, diversity, and functions of the gut microbiome were not affected. Polyphenol-rich DMW administered for six weeks improved certain skin health parameters and reduced oxidative and inflammatory stress, without affecting the gut microbiome in healthy women.
Additional Links: PMID-42680335
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PubMed:
Citation:
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@article {pmid42680335,
year = {2026},
author = {Christman, L and Mai, C and Gu, L},
title = {Dealcoholized muscadine wine improved skin elasticity and oxidative stress biomarkers without affecting gut microbiome in women over 40 in a randomized controlled trial.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {120042},
doi = {10.1016/j.foodres.2026.120042},
pmid = {42680335},
issn = {1873-7145},
mesh = {Humans ; *Oxidative Stress/drug effects ; Female ; Biomarkers/blood ; *Wine/analysis ; Adult ; *Gastrointestinal Microbiome/drug effects ; Single-Blind Method ; Cross-Over Studies ; *Elasticity/drug effects ; Middle Aged ; Polyphenols/pharmacology ; *Skin/drug effects ; Glycation End Products, Advanced/blood ; *Skin Physiological Phenomena/drug effects ; Vitis/chemistry ; Matrix Metalloproteinase 9/blood ; },
abstract = {Muscadine wine has a unique polyphenol profile distinct from that of common wine, and limited research exists on its health benefits. This study aimed to investigate the effects of intake of dealcoholized muscadine wine (DMW) on skin health, oxidative stress, inflammatory biomarkers, and the gut microbiome. Seventeen healthy women were randomly assigned to consume 300 mL of DMW or a placebo daily for 6 weeks, separated by a 3-week washout period, in a randomized, single-blinded, crossover design. Skin health parameters were measured on the face and forearm. Oxidative stress and inflammatory biomarkers were assessed in plasma. Fecal bacterial DNA was sequenced using shotgun sequencing. DMW did not affect UVB-induced erythema compared to placebo. However, it significantly decreased transepidermal water loss and increased facial gross elasticity. Skin elasticity significantly improved on the forearm, whereas other skin parameters were not affected. DMW significantly decreased plasma levels of matrix metalloproteinase-9 and advanced glycation end products compared with placebo. However, the abundance, diversity, and functions of the gut microbiome were not affected. Polyphenol-rich DMW administered for six weeks improved certain skin health parameters and reduced oxidative and inflammatory stress, without affecting the gut microbiome in healthy women.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Oxidative Stress/drug effects
Female
Biomarkers/blood
*Wine/analysis
Adult
*Gastrointestinal Microbiome/drug effects
Single-Blind Method
Cross-Over Studies
*Elasticity/drug effects
Middle Aged
Polyphenols/pharmacology
*Skin/drug effects
Glycation End Products, Advanced/blood
*Skin Physiological Phenomena/drug effects
Vitis/chemistry
Matrix Metalloproteinase 9/blood
RevDate: 2026-09-01
CmpDate: 2026-09-01
Drug-induced dysbiosis as a forensic biomarker: Implications for post-mortem interval estimation and forensic diagnostics.
Science & justice : journal of the Forensic Science Society, 66(5):101493.
Substance use disorders (SUDs) and drug-related deaths represent a growing global burden. Increasing evidence highlights substances ability to reshape the gut microbiome, a highly dynamic and metabolically active ecosystem that contributes to host homeostasis through interactions with neural, endocrine, and immune systems. Alterations in microbial diversity, depletion of short-chain fatty acid-producing taxa, disruption of epithelial barrier integrity, and systemic inflammation have been consistently associated with substance exposure. While these changes are increasingly characterized in living individuals, their persistence and impact after death remain less explored. In forensic contexts, drug-related fatalities are difficult to interpret due to non-specific autopsy findings, analytical limitations of toxicological methods, post-mortem redistribution, and the absence of clear lethal thresholds. The emerging study of thanatomicrobiome offers a novel avenue to address these challenges, as antemortem dysbiosis may influence post-mortem microbial succession and, consequently, post-mortem interval (PMI) estimation. This narrative review synthesises current knowledge on substance-induced microbiome alterations across antemortem and postmortem contexts, and extends this perspective to entomotoxicology, highlighting how drug-related microbial changes may influence both insect colonisation and insect-associated microbiomes. It also emphasises current methodological heterogeneity and the need for standardised approaches, outlining opportunities for future forensic applications.
Additional Links: PMID-42680466
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PubMed:
Citation:
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@article {pmid42680466,
year = {2026},
author = {Javan, GT and Di Nunzio, M and Grassi, S and Iancu, L and Procopio, N},
title = {Drug-induced dysbiosis as a forensic biomarker: Implications for post-mortem interval estimation and forensic diagnostics.},
journal = {Science & justice : journal of the Forensic Science Society},
volume = {66},
number = {5},
pages = {101493},
doi = {10.1016/j.scijus.2026.101493},
pmid = {42680466},
issn = {1876-4452},
mesh = {Humans ; *Dysbiosis/chemically induced ; *Postmortem Changes ; *Substance-Related Disorders ; Biomarkers ; *Gastrointestinal Microbiome/drug effects ; Animals ; },
abstract = {Substance use disorders (SUDs) and drug-related deaths represent a growing global burden. Increasing evidence highlights substances ability to reshape the gut microbiome, a highly dynamic and metabolically active ecosystem that contributes to host homeostasis through interactions with neural, endocrine, and immune systems. Alterations in microbial diversity, depletion of short-chain fatty acid-producing taxa, disruption of epithelial barrier integrity, and systemic inflammation have been consistently associated with substance exposure. While these changes are increasingly characterized in living individuals, their persistence and impact after death remain less explored. In forensic contexts, drug-related fatalities are difficult to interpret due to non-specific autopsy findings, analytical limitations of toxicological methods, post-mortem redistribution, and the absence of clear lethal thresholds. The emerging study of thanatomicrobiome offers a novel avenue to address these challenges, as antemortem dysbiosis may influence post-mortem microbial succession and, consequently, post-mortem interval (PMI) estimation. This narrative review synthesises current knowledge on substance-induced microbiome alterations across antemortem and postmortem contexts, and extends this perspective to entomotoxicology, highlighting how drug-related microbial changes may influence both insect colonisation and insect-associated microbiomes. It also emphasises current methodological heterogeneity and the need for standardised approaches, outlining opportunities for future forensic applications.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dysbiosis/chemically induced
*Postmortem Changes
*Substance-Related Disorders
Biomarkers
*Gastrointestinal Microbiome/drug effects
Animals
RevDate: 2026-09-01
Sperm as a multilayered epigenetic information system: encoding and transmission of paternal environmental signals.
Spermatozoa are increasingly recognized as carriers of non-genetic paternal information, rather than passive vehicles for the haploid genome. During spermatogenesis and post-testicular epididymal maturation, the paternal germline establishes a compact but functionally organized epigenome composed of DNA methylation, retained histones and histone modifications, chromatin-associated factors, and diverse small RNAs. These layers are environmentally responsive. In animal models, paternal diet, stress, toxicant exposure, and inflammatory or microbiome-related challenges can alter sperm DNA methylation, chromatin states, and small RNA cargo, with many changes mapping to loci involved in development, metabolism, and stress-response pathways. After fertilization, the paternal genome undergoes extensive epigenetic reprogramming; nevertheless, a subset of DNA methylation and chromatin features can resist erasure or be functionally relayed, while sperm-derived RNAs can influence early embryonic gene expression. Recent work, including studies of diet-induced sperm mitochondrial tRNAs, further supports the concept that defined paternal exposures may be transmitted to the embryo through discrete RNA-mediated mechanisms. In humans, lifestyle and environmental exposures are associated with measurable sperm epigenomic variation and with offspring health outcomes, but most evidence remains observational and is vulnerable to confounding by genetics, maternal factors, and shared environments. A central challenge is therefore to connect specific sperm epigenetic alterations to molecular effects in the early embryo and to subsequent offspring phenotypes. Here, we review how paternal environmental information is encoded during spermatogenesis and epididymal maturation, reshaped by environmental exposures, and interpreted by the early embryo, emphasizing multilayer integration and the evidence required to move from association to mechanism.
Additional Links: PMID-42680481
PubMed:
Citation:
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@article {pmid42680481,
year = {2026},
author = {Kim, S and Lee, HY and Kim, SY and Lee, JY},
title = {Sperm as a multilayered epigenetic information system: encoding and transmission of paternal environmental signals.},
journal = {BMB reports},
volume = {},
number = {},
pages = {},
pmid = {42680481},
issn = {1976-670X},
abstract = {Spermatozoa are increasingly recognized as carriers of non-genetic paternal information, rather than passive vehicles for the haploid genome. During spermatogenesis and post-testicular epididymal maturation, the paternal germline establishes a compact but functionally organized epigenome composed of DNA methylation, retained histones and histone modifications, chromatin-associated factors, and diverse small RNAs. These layers are environmentally responsive. In animal models, paternal diet, stress, toxicant exposure, and inflammatory or microbiome-related challenges can alter sperm DNA methylation, chromatin states, and small RNA cargo, with many changes mapping to loci involved in development, metabolism, and stress-response pathways. After fertilization, the paternal genome undergoes extensive epigenetic reprogramming; nevertheless, a subset of DNA methylation and chromatin features can resist erasure or be functionally relayed, while sperm-derived RNAs can influence early embryonic gene expression. Recent work, including studies of diet-induced sperm mitochondrial tRNAs, further supports the concept that defined paternal exposures may be transmitted to the embryo through discrete RNA-mediated mechanisms. In humans, lifestyle and environmental exposures are associated with measurable sperm epigenomic variation and with offspring health outcomes, but most evidence remains observational and is vulnerable to confounding by genetics, maternal factors, and shared environments. A central challenge is therefore to connect specific sperm epigenetic alterations to molecular effects in the early embryo and to subsequent offspring phenotypes. Here, we review how paternal environmental information is encoded during spermatogenesis and epididymal maturation, reshaped by environmental exposures, and interpreted by the early embryo, emphasizing multilayer integration and the evidence required to move from association to mechanism.},
}
RevDate: 2026-09-01
A legacy pollutant deciphered by multiomics toxicology and targeted remediation by a synthetic microbial consortium: a case study of 2-chloroacetophenone from abandoned chemical weapons.
Water research pii:S0043-1354(26)01450-8 [Epub ahead of print].
2-Chloroacetophenone (2-CA) is a typical organic poison found in abandoned Japanese chemical weapons, yet systematic research on its ecological risks and bioremediation strategies in aquatic environments remains scarce. Through a 120-day exposure experiment across three concentration gradients (10, 50, and 100 mg·L[-1]) coupled with multiomics analysis (physicochemical profiling, ionomics, 16S rRNA sequencing, metagenomics, and metabolomics), we systematically characterized the toxic effects of 2-CA on aquatic microbial communities and their molecular response mechanisms. The glutathione (GSH) metabolic pathway was identified as the core defense hub against 2-CA-induced oxidative stress, with multiomics data revealing its transition from compensatory activation to irreversible collapse. Guided by these mechanistic insights, we directionally isolated three cascade-degrading bacteria (Pseudomonas abietaniphila, Bacillus sp., and Arthrobacter agilis) harboring the key genes hapA, yjfP, and catA, which encode the three consecutive steps of Baeyer-Villiger oxidation, ester bond hydrolysis, and aromatic ring cleavage. The synthetic microbiome assembled from these three wild-type strains achieved 100% removal of 100 mg·L[-1] 2-CA within 24 h in vitro and within 10 days in simulated contaminated water, with the sequential detection of predicted intermediates (phenyl 2-chloroacetate, phenol, and pyruvic acid) confirming the operation of the cascade pathway. This study establishes a "toxicology diagnosis-functional deconstruction-synthetic reconstruction" paradigm, providing mechanistic understanding and a potential bioremediation strategy for organic toxicants at sites contaminated by relic Japanese chemical weapons, although direct ecotoxicological validation of detoxification remains to be confirmed.
Additional Links: PMID-42680679
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PubMed:
Citation:
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@article {pmid42680679,
year = {2026},
author = {Yang, X and Peng, AD and Cheng, JH and Huang, YH and Zhong, HT and Zhou, HT and Liu, PQ and Ji, XH and Li, C and Zhang, SR and Lai, JL and Luo, XG and Wen, G},
title = {A legacy pollutant deciphered by multiomics toxicology and targeted remediation by a synthetic microbial consortium: a case study of 2-chloroacetophenone from abandoned chemical weapons.},
journal = {Water research},
volume = {},
number = {},
pages = {126776},
doi = {10.1016/j.watres.2026.126776},
pmid = {42680679},
issn = {1879-2448},
abstract = {2-Chloroacetophenone (2-CA) is a typical organic poison found in abandoned Japanese chemical weapons, yet systematic research on its ecological risks and bioremediation strategies in aquatic environments remains scarce. Through a 120-day exposure experiment across three concentration gradients (10, 50, and 100 mg·L[-1]) coupled with multiomics analysis (physicochemical profiling, ionomics, 16S rRNA sequencing, metagenomics, and metabolomics), we systematically characterized the toxic effects of 2-CA on aquatic microbial communities and their molecular response mechanisms. The glutathione (GSH) metabolic pathway was identified as the core defense hub against 2-CA-induced oxidative stress, with multiomics data revealing its transition from compensatory activation to irreversible collapse. Guided by these mechanistic insights, we directionally isolated three cascade-degrading bacteria (Pseudomonas abietaniphila, Bacillus sp., and Arthrobacter agilis) harboring the key genes hapA, yjfP, and catA, which encode the three consecutive steps of Baeyer-Villiger oxidation, ester bond hydrolysis, and aromatic ring cleavage. The synthetic microbiome assembled from these three wild-type strains achieved 100% removal of 100 mg·L[-1] 2-CA within 24 h in vitro and within 10 days in simulated contaminated water, with the sequential detection of predicted intermediates (phenyl 2-chloroacetate, phenol, and pyruvic acid) confirming the operation of the cascade pathway. This study establishes a "toxicology diagnosis-functional deconstruction-synthetic reconstruction" paradigm, providing mechanistic understanding and a potential bioremediation strategy for organic toxicants at sites contaminated by relic Japanese chemical weapons, although direct ecotoxicological validation of detoxification remains to be confirmed.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-01
Microbiome features associated with persistent intestinal carriages of Escherichia coli ST131 in a Southeast Asian cohort study.
Nature communications, 17(1):.
Escherichia coli sequence-type 131 (ST131) is the dominant global extraintestinal pathogen capable of asymptomatic intestinal carriage and sustained household transmission, challenging infection control. Despite its clinical significance, the ecological determinants of gut persistence remain poorly understood. We performed shotgun metagenomics on fecal samples to investigate gut microbiome features associated with ST131-positive samples, distinct host carrier statuses (persistent, intermittent and non-carriers) and household risks in a study of a Southeast Asian cohort. Here, we show that ST131 carriage was associated with compositional shifts without reducing species alpha-diversity. Regression analyses identified depletion of commensal taxa and the 1,5-anhydrofructose degradation pathway in ST131-positive samples. Persistent carriers exhibited highly perturbed microbiome enriched with pathobionts, aerobactin- and lipopolysaccharide (LPS)-biosynthesis pathways. Comparing household risk groups to control, revealed that biotin biosynthesis and 1,5-anhydrofructose degradation may influence ST131 co-colonization through both direct and indirect mechanisms. Machine learning analyses identified metabolic pathways as stronger discriminators of persistent carriage than taxonomic features. Genomic-resolved analysis of clinical ST131 isolates revealed conserved genes for iron-acquisition, LPS and antibiotic resistance determinants. Overall, while commensals and metabolism may influence initial ST131 colonization, persistent carriage is associated with specific microbial and metabolic adaptations, providing potential targets to limit intestinal ST131 persistence.
Additional Links: PMID-42680742
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Citation:
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@article {pmid42680742,
year = {2026},
author = {Low, A and Yang, Z and Anantaya, KT and Zhao, S and Tan, WC and Perez, RL and Chung The, H and Lim, SZY and Liu, L and Gounot, JS and Kwah, JS and Ong, RT and Nagarajan, N and Lee, JWJ and Mo, Y},
title = {Microbiome features associated with persistent intestinal carriages of Escherichia coli ST131 in a Southeast Asian cohort study.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42680742},
issn = {2041-1723},
mesh = {Humans ; *Escherichia coli/genetics/isolation & purification/classification ; *Escherichia coli Infections/microbiology/epidemiology ; Feces/microbiology ; *Gastrointestinal Microbiome/genetics ; Cohort Studies ; Metagenomics ; *Carrier State/microbiology ; Asia, Southeastern/epidemiology ; Intestines/microbiology ; },
abstract = {Escherichia coli sequence-type 131 (ST131) is the dominant global extraintestinal pathogen capable of asymptomatic intestinal carriage and sustained household transmission, challenging infection control. Despite its clinical significance, the ecological determinants of gut persistence remain poorly understood. We performed shotgun metagenomics on fecal samples to investigate gut microbiome features associated with ST131-positive samples, distinct host carrier statuses (persistent, intermittent and non-carriers) and household risks in a study of a Southeast Asian cohort. Here, we show that ST131 carriage was associated with compositional shifts without reducing species alpha-diversity. Regression analyses identified depletion of commensal taxa and the 1,5-anhydrofructose degradation pathway in ST131-positive samples. Persistent carriers exhibited highly perturbed microbiome enriched with pathobionts, aerobactin- and lipopolysaccharide (LPS)-biosynthesis pathways. Comparing household risk groups to control, revealed that biotin biosynthesis and 1,5-anhydrofructose degradation may influence ST131 co-colonization through both direct and indirect mechanisms. Machine learning analyses identified metabolic pathways as stronger discriminators of persistent carriage than taxonomic features. Genomic-resolved analysis of clinical ST131 isolates revealed conserved genes for iron-acquisition, LPS and antibiotic resistance determinants. Overall, while commensals and metabolism may influence initial ST131 colonization, persistent carriage is associated with specific microbial and metabolic adaptations, providing potential targets to limit intestinal ST131 persistence.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Escherichia coli/genetics/isolation & purification/classification
*Escherichia coli Infections/microbiology/epidemiology
Feces/microbiology
*Gastrointestinal Microbiome/genetics
Cohort Studies
Metagenomics
*Carrier State/microbiology
Asia, Southeastern/epidemiology
Intestines/microbiology
RevDate: 2026-09-02
Early-life fentanyl exposure, microbiome-brain axis and neurodevelopment.
Pediatric research [Epub ahead of print].
Additional Links: PMID-42680796
PubMed:
Citation:
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@article {pmid42680796,
year = {2026},
author = {Mu, C and Yusuf, K and Hasan, SU},
title = {Early-life fentanyl exposure, microbiome-brain axis and neurodevelopment.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42680796},
issn = {1530-0447},
}
RevDate: 2026-09-02
Antifungal therapy improves microbiome dynamics in inflammatory bowel disease.
Nature medicine [Epub ahead of print].
Gut fungal dysbiosis has been implicated in inflammatory bowel disease (IBD), yet strategies for targeting the gut mycobiota in IBD remain unexplored. Here we leveraged the observation that Candida albicans strains are shared between the oral cavity and gut in patients with IBD with mild oral thrush, a condition caused by Candida overgrowth, to design a prospective observational study comparing oral antifungal therapy (swish-and-spit nystatin; oral nystatin fungal targeting (ORNT); n = 18) with orogastrointestinal antifungal therapy (fluconazole; gastrointestinal and oral fluconazole fungal targeting (GIFT); n = 35). Among 53 patients with mild-to-moderate ulcerative colitis or Crohn's disease, fluconazole, but not nystatin, effectively reduced intestinal Candida burden and reshaped gut fungal-community composition. Fluconazole treatment was accompanied by increased bacterial diversity, expansion of short-chain fatty-acid-producing taxa, restoration of anti-inflammatory microbial metabolites and durable shifts in cross-kingdom microbial networks. These microbiome and metabolomic changes coincided with improved disease activity indices and a decreased risk of disease progression over the 8-week follow-up period. These findings demonstrate the feasibility of mycobiome-based patient stratification, provide evidence that targeted antifungal therapy can reshape the intestinal microbiota in IBD and establish a framework for implementing antifungal cotherapy in patients with fungal-associated disease manifestations.
Additional Links: PMID-42680951
PubMed:
Citation:
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@article {pmid42680951,
year = {2026},
author = {Pan, X and Conroy, A and Ngima, TS and Mesko, M and Morzhanaeva, O and Li, A and Marino, J and Westblade, LF and Grier, A and Bacher, P and Longman, RS and Scherl, EJ and Iliev, ID},
title = {Antifungal therapy improves microbiome dynamics in inflammatory bowel disease.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {42680951},
issn = {1546-170X},
abstract = {Gut fungal dysbiosis has been implicated in inflammatory bowel disease (IBD), yet strategies for targeting the gut mycobiota in IBD remain unexplored. Here we leveraged the observation that Candida albicans strains are shared between the oral cavity and gut in patients with IBD with mild oral thrush, a condition caused by Candida overgrowth, to design a prospective observational study comparing oral antifungal therapy (swish-and-spit nystatin; oral nystatin fungal targeting (ORNT); n = 18) with orogastrointestinal antifungal therapy (fluconazole; gastrointestinal and oral fluconazole fungal targeting (GIFT); n = 35). Among 53 patients with mild-to-moderate ulcerative colitis or Crohn's disease, fluconazole, but not nystatin, effectively reduced intestinal Candida burden and reshaped gut fungal-community composition. Fluconazole treatment was accompanied by increased bacterial diversity, expansion of short-chain fatty-acid-producing taxa, restoration of anti-inflammatory microbial metabolites and durable shifts in cross-kingdom microbial networks. These microbiome and metabolomic changes coincided with improved disease activity indices and a decreased risk of disease progression over the 8-week follow-up period. These findings demonstrate the feasibility of mycobiome-based patient stratification, provide evidence that targeted antifungal therapy can reshape the intestinal microbiota in IBD and establish a framework for implementing antifungal cotherapy in patients with fungal-associated disease manifestations.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Induction of Ustilago maydis Appressorium and Filamentation.
Methods in molecular biology (Clifton, N.J.), 3050:17-27.
Ustilago maydis is a model smut-causing fungus infecting maize. Two compatible mating-type isolates of the fungus must form the infectious dikaryotic filaments that form infection. However, several laboratory techniques and strains have been developed that can induce this phenotype under controlled conditions, in order to study the pathogen outside the complexities of the host and microbiome. Three such methods are described here, which cover the use of charcoal-supplemented agar to induce filamentation, appressorium formation on hydrophic surfaces with 16-hydroxyhexadecanoic acid, as well as inducing b-dependent filamentation in liquid culture with engineered strains.
Additional Links: PMID-42681027
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Citation:
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@article {pmid42681027,
year = {2026},
author = {John, E and Kuan, JE and Djamei, A},
title = {Induction of Ustilago maydis Appressorium and Filamentation.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3050},
number = {},
pages = {17-27},
pmid = {42681027},
issn = {1940-6029},
mesh = {*Zea mays/microbiology ; *Ustilago/growth & development ; *Plant Diseases/microbiology ; *Hyphae/growth & development ; Culture Media/chemistry ; Basidiomycota ; },
abstract = {Ustilago maydis is a model smut-causing fungus infecting maize. Two compatible mating-type isolates of the fungus must form the infectious dikaryotic filaments that form infection. However, several laboratory techniques and strains have been developed that can induce this phenotype under controlled conditions, in order to study the pathogen outside the complexities of the host and microbiome. Three such methods are described here, which cover the use of charcoal-supplemented agar to induce filamentation, appressorium formation on hydrophic surfaces with 16-hydroxyhexadecanoic acid, as well as inducing b-dependent filamentation in liquid culture with engineered strains.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Zea mays/microbiology
*Ustilago/growth & development
*Plant Diseases/microbiology
*Hyphae/growth & development
Culture Media/chemistry
Basidiomycota
RevDate: 2026-09-02
CmpDate: 2026-09-02
Extraction and Quantification of Skin Immune Cells and Skin Lipids.
Methods in molecular biology (Clifton, N.J.), 3053:785-797.
We have recently shown that the immune system, specifically T cells stimulated by the skin-derived cytokine thymic stromal lymphopoietin, can promote total body adipose loss. This effect is caused by the regulation of lipid metabolism in the skin, whereby T cells induce the release of a lipid-rich substance called sebum. The adoptive transfer of thymic stromal lymphopoietin-stimulated T cells can also induce adipose loss and sebum secretion, making this approach applicable to cellular therapies for metabolic and dermatologic diseases. The skin is the body's largest organ system and provides a critical barrier surface that senses and protects the host from the outside environment. Sebocytes within the skin secrete sebum, a lipid-rich substance that coats the skin and protects it against water, pathogens, and sun damage while also regulating the skin immune landscape and microbiome. Methods to quantify and characterize sebum production are needed to better investigate the role of sebum in skin immunobiology. Here, we describe a protocol that we developed to extract lipids from mouse fur followed by thin layer chromatography analysis of the various lipid classes. We also describe a protocol to maximally extract immune cells from the skin for flow cytometric analysis, which has previously been limited by low cell numbers. These methods will be useful to study skin immunobiology including, but not limited to, its impact on sebum secretion.
Additional Links: PMID-42681450
PubMed:
Citation:
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@article {pmid42681450,
year = {2026},
author = {Choa, R and Sun, L and Kambayashi, T},
title = {Extraction and Quantification of Skin Immune Cells and Skin Lipids.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3053},
number = {},
pages = {785-797},
pmid = {42681450},
issn = {1940-6029},
mesh = {Animals ; *Skin/immunology/cytology/metabolism/chemistry ; Mice ; *Lipids/isolation & purification/analysis ; Chromatography, Thin Layer/methods ; Sebum/metabolism/immunology/chemistry ; T-Lymphocytes/immunology/metabolism ; Flow Cytometry/methods ; Lipid Metabolism ; },
abstract = {We have recently shown that the immune system, specifically T cells stimulated by the skin-derived cytokine thymic stromal lymphopoietin, can promote total body adipose loss. This effect is caused by the regulation of lipid metabolism in the skin, whereby T cells induce the release of a lipid-rich substance called sebum. The adoptive transfer of thymic stromal lymphopoietin-stimulated T cells can also induce adipose loss and sebum secretion, making this approach applicable to cellular therapies for metabolic and dermatologic diseases. The skin is the body's largest organ system and provides a critical barrier surface that senses and protects the host from the outside environment. Sebocytes within the skin secrete sebum, a lipid-rich substance that coats the skin and protects it against water, pathogens, and sun damage while also regulating the skin immune landscape and microbiome. Methods to quantify and characterize sebum production are needed to better investigate the role of sebum in skin immunobiology. Here, we describe a protocol that we developed to extract lipids from mouse fur followed by thin layer chromatography analysis of the various lipid classes. We also describe a protocol to maximally extract immune cells from the skin for flow cytometric analysis, which has previously been limited by low cell numbers. These methods will be useful to study skin immunobiology including, but not limited to, its impact on sebum secretion.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Skin/immunology/cytology/metabolism/chemistry
Mice
*Lipids/isolation & purification/analysis
Chromatography, Thin Layer/methods
Sebum/metabolism/immunology/chemistry
T-Lymphocytes/immunology/metabolism
Flow Cytometry/methods
Lipid Metabolism
RevDate: 2026-09-02
CmpDate: 2026-09-02
Human milk microbiome as a modulator of the early-life gut-brain axis: mechanisms and translational opportunities for neurodevelopment.
Journal of translational medicine, 24(1):.
The first 1000 days of life represent a critical developmental window during which early microbial colonization contributes to immune, metabolic, and neurodevelopmental programming. Human milk is increasingly recognized as a biologically active fluid that shapes infant gut microbiome assembly through microorganisms, human milk oligosaccharides (HMOs), immune factors, and microbial metabolites. Within this framework, the human milk microbiome has emerged as a potential contributor to the milk-gut-brain axis (MGBA), a bidirectional communication network linking the gut microbiota with neural, immune, endocrine, and metabolic pathways involved in brain development. This review summarizes current evidence regarding the origins, determinants, and functional relevance of the human milk microbiome and its potential role in early-life neurodevelopment. Proposed microbial sources include maternal skin, the infant oral cavity, environmental exposure, and the entero-mammary pathway, while key determinants include lactational stage, delivery mode, antibiotic exposure, maternal diet, obesity, and prematurity. Mechanistic pathways linking milk-associated microbes with neurodevelopment are discussed, including microbial colonization, immune and barrier maturation, vagal and neuroendocrine signalling, and production of short-chain fatty acids (SCFAs) and tryptophan-derived metabolites. We further evaluate evidence relating breastfeeding and milk-associated microbial exposures to cognitive, behavioural, and neurodevelopmental outcomes, particularly in preterm and medically vulnerable infants. Although experimental and observational evidence supports biologically plausible links between the human milk microbiome and the developing microbiota-gut-brain axis, major uncertainties remain regarding microbial viability, sustained colonization, causality, and long-term functional significance. Methodological limitations, including low microbial biomass, contamination susceptibility, and heterogeneity in analytical approaches, continue to complicate interpretation across studies. Future progress will require longitudinal, mechanistically informed studies integrating microbiome profiling with metabolomics, immune phenotyping, neuroimaging, and validated neurodevelopmental outcomes.
Additional Links: PMID-42681656
PubMed:
Citation:
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@article {pmid42681656,
year = {2026},
author = {Alnuaimi, F and Yassin, LK and Alketbi, S and Skrabulyte-Barbulescu, J and Almazrouei, S and Alremeithi, D and Alahbabi, N and Almarzooqi, S and Shamma, H and Hamad, MIK},
title = {Human milk microbiome as a modulator of the early-life gut-brain axis: mechanisms and translational opportunities for neurodevelopment.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {42681656},
issn = {1479-5876},
mesh = {Humans ; *Milk, Human/microbiology ; *Neurodevelopment ; *Brain/growth & development ; *Gastrointestinal Microbiome ; *Translational Research, Biomedical ; *Microbiota ; Infant, Newborn ; *Translational Science, Biomedical ; },
abstract = {The first 1000 days of life represent a critical developmental window during which early microbial colonization contributes to immune, metabolic, and neurodevelopmental programming. Human milk is increasingly recognized as a biologically active fluid that shapes infant gut microbiome assembly through microorganisms, human milk oligosaccharides (HMOs), immune factors, and microbial metabolites. Within this framework, the human milk microbiome has emerged as a potential contributor to the milk-gut-brain axis (MGBA), a bidirectional communication network linking the gut microbiota with neural, immune, endocrine, and metabolic pathways involved in brain development. This review summarizes current evidence regarding the origins, determinants, and functional relevance of the human milk microbiome and its potential role in early-life neurodevelopment. Proposed microbial sources include maternal skin, the infant oral cavity, environmental exposure, and the entero-mammary pathway, while key determinants include lactational stage, delivery mode, antibiotic exposure, maternal diet, obesity, and prematurity. Mechanistic pathways linking milk-associated microbes with neurodevelopment are discussed, including microbial colonization, immune and barrier maturation, vagal and neuroendocrine signalling, and production of short-chain fatty acids (SCFAs) and tryptophan-derived metabolites. We further evaluate evidence relating breastfeeding and milk-associated microbial exposures to cognitive, behavioural, and neurodevelopmental outcomes, particularly in preterm and medically vulnerable infants. Although experimental and observational evidence supports biologically plausible links between the human milk microbiome and the developing microbiota-gut-brain axis, major uncertainties remain regarding microbial viability, sustained colonization, causality, and long-term functional significance. Methodological limitations, including low microbial biomass, contamination susceptibility, and heterogeneity in analytical approaches, continue to complicate interpretation across studies. Future progress will require longitudinal, mechanistically informed studies integrating microbiome profiling with metabolomics, immune phenotyping, neuroimaging, and validated neurodevelopmental outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Milk, Human/microbiology
*Neurodevelopment
*Brain/growth & development
*Gastrointestinal Microbiome
*Translational Research, Biomedical
*Microbiota
Infant, Newborn
*Translational Science, Biomedical
RevDate: 2026-09-02
CmpDate: 2026-09-02
Pathogens in rheumatoid arthritis: epidemiological, mechanistic, and clinical insights.
Biomarker research, 14(1):.
Rheumatoid arthritis is a chronic systemic autoimmune disease characterized by synovial inflammation, joint destruction, and systemic comorbidities. Emerging evidence highlights the critical involvement of the microbiome in disease pathogenesis, encompassing bacteria, viruses, fungi, and mycoplasmas. This review synthesizes recent findings on microbiome alterations, summarizing epidemiological, molecular, and mechanistic data. Among the evaluated pathogens, Porphyromonas gingivalis and Prevotella copri currently demonstrate the strongest causal evidence for initiating autoimmunity. Porphyromonas gingivalis directly catalyzes host protein citrullination via its unique peptidylarginine deiminase, driving anti-citrullinated protein antibody production, while Prevotella copri expands during the preclinical phase to drive T helper 17 cell polarization. Furthermore, chronic Hepatitis C virus infection presents compelling causal links, as continuous viral stimulation triggers robust autoantibody production in atypical memory B cells. Other infectious agents, including Epstein-Barr virus and Proteus mirabilis, act as environmental triggers through molecular mimicry, whereas opportunistic pathogens like Pneumocystis jirovecii emerge as severe secondary complications resulting from profound pharmacological immunosuppression. In terms of immediate clinical translation, several microbiome-targeted strategies are poised for routine practice. These include non-surgical periodontal therapy and oral hygiene optimization to reduce systemic disease activity, the utilization of direct-acting antivirals for Hepatitis C virus to concurrently resolve joint inflammation, and targeted prophylaxis using sulfasalazine to prevent Pneumocystis jirovecii pneumonia in highly immunosuppressed populations. Additionally, the immunomodulatory application of Ganoderma lucidum polysaccharides for symptomatic pain relief and the preclinical development of bacterial virulence factor inhibitors represent promising therapeutic avenues. Together, these findings confirm that the microbiome acts as a critical modifier of the inflammatory milieu. Future studies integrating longitudinal cohorts and precision interventional trials will further solidify causality and refine these microbiome-targeted therapies.
Additional Links: PMID-42681689
PubMed:
Citation:
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@article {pmid42681689,
year = {2026},
author = {Feng, F and Wu, Z and Xu, H and Li, Z and Wu, H and Zhang, J and Xu, Z and Zhang, S and Li, Y},
title = {Pathogens in rheumatoid arthritis: epidemiological, mechanistic, and clinical insights.},
journal = {Biomarker research},
volume = {14},
number = {1},
pages = {},
pmid = {42681689},
issn = {2050-7771},
abstract = {Rheumatoid arthritis is a chronic systemic autoimmune disease characterized by synovial inflammation, joint destruction, and systemic comorbidities. Emerging evidence highlights the critical involvement of the microbiome in disease pathogenesis, encompassing bacteria, viruses, fungi, and mycoplasmas. This review synthesizes recent findings on microbiome alterations, summarizing epidemiological, molecular, and mechanistic data. Among the evaluated pathogens, Porphyromonas gingivalis and Prevotella copri currently demonstrate the strongest causal evidence for initiating autoimmunity. Porphyromonas gingivalis directly catalyzes host protein citrullination via its unique peptidylarginine deiminase, driving anti-citrullinated protein antibody production, while Prevotella copri expands during the preclinical phase to drive T helper 17 cell polarization. Furthermore, chronic Hepatitis C virus infection presents compelling causal links, as continuous viral stimulation triggers robust autoantibody production in atypical memory B cells. Other infectious agents, including Epstein-Barr virus and Proteus mirabilis, act as environmental triggers through molecular mimicry, whereas opportunistic pathogens like Pneumocystis jirovecii emerge as severe secondary complications resulting from profound pharmacological immunosuppression. In terms of immediate clinical translation, several microbiome-targeted strategies are poised for routine practice. These include non-surgical periodontal therapy and oral hygiene optimization to reduce systemic disease activity, the utilization of direct-acting antivirals for Hepatitis C virus to concurrently resolve joint inflammation, and targeted prophylaxis using sulfasalazine to prevent Pneumocystis jirovecii pneumonia in highly immunosuppressed populations. Additionally, the immunomodulatory application of Ganoderma lucidum polysaccharides for symptomatic pain relief and the preclinical development of bacterial virulence factor inhibitors represent promising therapeutic avenues. Together, these findings confirm that the microbiome acts as a critical modifier of the inflammatory milieu. Future studies integrating longitudinal cohorts and precision interventional trials will further solidify causality and refine these microbiome-targeted therapies.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Dietary green tea residue improves growth and antioxidant capacity via rumen microbiota and glutathione modulation in finishing beef cattle.
Journal of animal science and biotechnology, 17(1):.
BACKGROUND: Green tea residue (GTR) is an abundant by-product rich in polyphenols. This study aimed to investigate the effects of GTR on growth performance, rumen microbiota, and systemic metabolism in finishing beef cattle.
RESULTS: Forty-five 18‑month‑old finishing Angus steers with an average initial body weight of 474.44 ± 14.03 kg (mean ± SD) were individually housed and randomly assigned to three dietary treatments (n = 15 per group) using stratified randomization by initial body weight: control group (CG group, 150 g rice straw), low-dose GTR group (LG group, 75 g rice straw +75 g GTR), and high-dose GTR group (HG group, 150 g GTR). The feeding trial lasted 70 d with a 10-day adaptation period. To elucidate the regulatory mechanisms of GTR on beef cattle growth, we thoroughly assessed growth performance, nutrient digestibility, ruminal fermentation parameters, conducted bacterial 16S rRNA sequencing, analysed plasma biochemical and antioxidant markers, and executed an untargeted plasma metabolomic analysis. The LG group tended to increase average daily gain (ADG). Meanwhile, the LG group exhibited elevated plasma concentrations of β-hydroxybutyrate and glucose, increased activities of superoxide dismutase and glutathione S-transferase, an increased glutathione (GSH)/glutathione disulfide (GSSG) ratio, and reduced GSSG content. GTR treatment decreased reactive oxygen species and oxidative stress index. Furthermore, dietary GTR significantly modified the rumen microbial community structure, enriching Xylanibacter and Prevotellaceae_UCG-003, while reducing the abundance of Rikenellaceae_RC9_gut_group. Plasma metabolomics revealed that GTR treatment enriched GSH Metabolism and the Pentose Phosphate Pathway. Notably, gamma-glutamylcysteine was identified as a key mediator of the association between Xylanibacter and ADG in fattening beef cattle supplemented with GTR.
CONCLUSIONS: Dietary supplementation with 75 g/steer/d GTR improved growth performance and systemic antioxidant capacity in finishing beef cattle by modulating the rumen microbiota and activating the glutathione system. GTR represents a promising functional feed additive that simultaneously valorizes tea by‑products and enhances livestock productivity.
Additional Links: PMID-42681694
PubMed:
Citation:
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@article {pmid42681694,
year = {2026},
author = {Shi, C and Deng, J and Zhang, H and Li, Y and Zhang, S and Wang, H and Min, S and Luo, Y and Zhang, Z and Hao, J and Wang, Y and Cao, B and He, Y and Su, H},
title = {Dietary green tea residue improves growth and antioxidant capacity via rumen microbiota and glutathione modulation in finishing beef cattle.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42681694},
issn = {1674-9782},
support = {CARS-37//China Agriculture Research Systems of MOF and MARA/ ; 2023YFD1300904//the National Key R&D Program of China/ ; },
abstract = {BACKGROUND: Green tea residue (GTR) is an abundant by-product rich in polyphenols. This study aimed to investigate the effects of GTR on growth performance, rumen microbiota, and systemic metabolism in finishing beef cattle.
RESULTS: Forty-five 18‑month‑old finishing Angus steers with an average initial body weight of 474.44 ± 14.03 kg (mean ± SD) were individually housed and randomly assigned to three dietary treatments (n = 15 per group) using stratified randomization by initial body weight: control group (CG group, 150 g rice straw), low-dose GTR group (LG group, 75 g rice straw +75 g GTR), and high-dose GTR group (HG group, 150 g GTR). The feeding trial lasted 70 d with a 10-day adaptation period. To elucidate the regulatory mechanisms of GTR on beef cattle growth, we thoroughly assessed growth performance, nutrient digestibility, ruminal fermentation parameters, conducted bacterial 16S rRNA sequencing, analysed plasma biochemical and antioxidant markers, and executed an untargeted plasma metabolomic analysis. The LG group tended to increase average daily gain (ADG). Meanwhile, the LG group exhibited elevated plasma concentrations of β-hydroxybutyrate and glucose, increased activities of superoxide dismutase and glutathione S-transferase, an increased glutathione (GSH)/glutathione disulfide (GSSG) ratio, and reduced GSSG content. GTR treatment decreased reactive oxygen species and oxidative stress index. Furthermore, dietary GTR significantly modified the rumen microbial community structure, enriching Xylanibacter and Prevotellaceae_UCG-003, while reducing the abundance of Rikenellaceae_RC9_gut_group. Plasma metabolomics revealed that GTR treatment enriched GSH Metabolism and the Pentose Phosphate Pathway. Notably, gamma-glutamylcysteine was identified as a key mediator of the association between Xylanibacter and ADG in fattening beef cattle supplemented with GTR.
CONCLUSIONS: Dietary supplementation with 75 g/steer/d GTR improved growth performance and systemic antioxidant capacity in finishing beef cattle by modulating the rumen microbiota and activating the glutathione system. GTR represents a promising functional feed additive that simultaneously valorizes tea by‑products and enhances livestock productivity.},
}
RevDate: 2026-09-02
Oligosaccharides With Defined Glycosidic Bonds Shape Gut Microbial Succession and Metabolism Via Bond-Specific Microbial Responders.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Functional oligosaccharides are important prebiotic ingredients, but the structure-function relationships and mechanisms by which defined glycosidic bonds shape microbial responses remain unclear. Five glucose disaccharides, trehalose (α-1,1), maltose (α-1,4), isomaltose (α-1,6), cellobiose (β-1,4), and gentiobiose (β-1,6), were used as minimal oligosaccharide models to isolate glycosidic bond effects. Absolute time-series profiling combined with Bayesian generalized Lotka-Volterra modeling identified bond-specific microbial responders, operationally defined as taxa with statistically supported substrate-associated growth advantages beyond endpoint dominance. α-Linked disaccharides mainly recruited Bifidobacterium pseudocatenulatum and Megamonas funiformis, cellobiose enriched Faecalibacterium prausnitzii, and gentiobiose enriched B. pseudocatenulatum. Monoculture assays confirmed direct cognate disaccharide utilization. Metaproteomics revealed linkage-matched modules: isomaltose responders upregulated GanO/ChvE and oligo-1,6-glucosidase; cellobiose responders expressed CebE/ChvE, ABC.MS.S, CelB, cellobiose phosphorylase, and β-glucosidases; whereas the molecular evidence for gentiobiose was based mainly on ABC.MS.S and general β-glucosidases. Metabolically, gentiobiose favored acetic acid accumulation, cellobiose yielded the highest butyric acid concentration, and isomaltose elevated trans-4-hydroxy-L-proline and 7,8-dihydroneopterin associated with redox and immune-related cofactor pathways. Guided by these ecological and molecular observations, microbial responder-centered synthetic microbial communities utilized cognate disaccharides, recapitulated glycosidic bond-specific ecological succession, showed greater net short-chain fatty acid (SCFA) accumulation than matched complex communities under equal initial substrate input in vitro, and elevated fecal SCFAs in mice, with cellobiose increasing butyric acid by 2.1-fold. These results support a mechanistically informed pathway linking glycosidic bond structure, microbial succession, and metabolic outputs, providing a basis for structure‑guided microbiome modulation.
Additional Links: PMID-42681814
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PubMed:
Citation:
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@article {pmid42681814,
year = {2026},
author = {Lu, X and Zou, J and Han, G and Zhao, M and Luo, T and Feng, X and Zhu, L and Chen, Y and Ji, X and Jin, J and Zhao, L},
title = {Oligosaccharides With Defined Glycosidic Bonds Shape Gut Microbial Succession and Metabolism Via Bond-Specific Microbial Responders.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e77488},
doi = {10.1002/advs.77488},
pmid = {42681814},
issn = {2198-3844},
support = {32302102//National Natural Science Foundation of China/ ; 23ZR1415400//Natural Science Foundation of Shanghai/ ; 23YF1409800//Shanghai Sailing Program/ ; //Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism (Shanghai Municipal Education Commission)/ ; },
abstract = {Functional oligosaccharides are important prebiotic ingredients, but the structure-function relationships and mechanisms by which defined glycosidic bonds shape microbial responses remain unclear. Five glucose disaccharides, trehalose (α-1,1), maltose (α-1,4), isomaltose (α-1,6), cellobiose (β-1,4), and gentiobiose (β-1,6), were used as minimal oligosaccharide models to isolate glycosidic bond effects. Absolute time-series profiling combined with Bayesian generalized Lotka-Volterra modeling identified bond-specific microbial responders, operationally defined as taxa with statistically supported substrate-associated growth advantages beyond endpoint dominance. α-Linked disaccharides mainly recruited Bifidobacterium pseudocatenulatum and Megamonas funiformis, cellobiose enriched Faecalibacterium prausnitzii, and gentiobiose enriched B. pseudocatenulatum. Monoculture assays confirmed direct cognate disaccharide utilization. Metaproteomics revealed linkage-matched modules: isomaltose responders upregulated GanO/ChvE and oligo-1,6-glucosidase; cellobiose responders expressed CebE/ChvE, ABC.MS.S, CelB, cellobiose phosphorylase, and β-glucosidases; whereas the molecular evidence for gentiobiose was based mainly on ABC.MS.S and general β-glucosidases. Metabolically, gentiobiose favored acetic acid accumulation, cellobiose yielded the highest butyric acid concentration, and isomaltose elevated trans-4-hydroxy-L-proline and 7,8-dihydroneopterin associated with redox and immune-related cofactor pathways. Guided by these ecological and molecular observations, microbial responder-centered synthetic microbial communities utilized cognate disaccharides, recapitulated glycosidic bond-specific ecological succession, showed greater net short-chain fatty acid (SCFA) accumulation than matched complex communities under equal initial substrate input in vitro, and elevated fecal SCFAs in mice, with cellobiose increasing butyric acid by 2.1-fold. These results support a mechanistically informed pathway linking glycosidic bond structure, microbial succession, and metabolic outputs, providing a basis for structure‑guided microbiome modulation.},
}
RevDate: 2026-09-02
Quantitative metabarcoding for invertebrate pest monitoring and management.
Journal of economic entomology pii:8779444 [Epub ahead of print].
Invertebrate pests pose one of the most significant threats to global agriculture. Trap-based surveillance is widely used to monitor the presence and abundance of pests, beneficial taxa and broader agroecosystem communities; however nonselective traps often collect hundreds or even thousands of individuals per sample, making conventional sorting and morphological identification labor-intensive and delaying the delivery of actionable information. Metabarcoding offers a scalable alternative for rapidly identifying agriculturally significant taxa in mixed trap samples, while providing more precise identifications (i.e. to species level). However, metabarcoding currently only provides semiquantitative estimates of relative abundance, rather than the accurate absolute abundance information required for many pest-monitoring and management decisions. Improving the quantitative capacity of metabarcoding is therefore an important and rapidly developing area of research across ecological, medical, microbiome, and environmental DNA research. This review summarizes progress toward quantitative metabarcoding of bulk invertebrate samples, highlighting key sources of bias, emerging correction methods, and the opportunities and challenges associated with their translation into agricultural monitoring systems. By consolidating insights from diverse ecological applications, we present a practical roadmap for improving the quantitative outputs and interpretation of metabarcoding data and integrating these novel approaches into agricultural pest monitoring and management.
Additional Links: PMID-42681862
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PubMed:
Citation:
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@article {pmid42681862,
year = {2026},
author = {Gretgrix, LJ and Scanlan, JL and Martoni, F and Blacket, MJ and Rodoni, BC and Piper, AM},
title = {Quantitative metabarcoding for invertebrate pest monitoring and management.},
journal = {Journal of economic entomology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jee/toag264},
pmid = {42681862},
issn = {1938-291X},
support = {//Agriculture Victoria/ ; DEE2305-004RTX//National Grains Diagnostic and Surveillance Initiative/ ; //Grains Research and Development Corporation (GRDC)/ ; ULA2601-003RSX//Australian Government Research Training Program Scholarship and GRDC/ ; },
abstract = {Invertebrate pests pose one of the most significant threats to global agriculture. Trap-based surveillance is widely used to monitor the presence and abundance of pests, beneficial taxa and broader agroecosystem communities; however nonselective traps often collect hundreds or even thousands of individuals per sample, making conventional sorting and morphological identification labor-intensive and delaying the delivery of actionable information. Metabarcoding offers a scalable alternative for rapidly identifying agriculturally significant taxa in mixed trap samples, while providing more precise identifications (i.e. to species level). However, metabarcoding currently only provides semiquantitative estimates of relative abundance, rather than the accurate absolute abundance information required for many pest-monitoring and management decisions. Improving the quantitative capacity of metabarcoding is therefore an important and rapidly developing area of research across ecological, medical, microbiome, and environmental DNA research. This review summarizes progress toward quantitative metabarcoding of bulk invertebrate samples, highlighting key sources of bias, emerging correction methods, and the opportunities and challenges associated with their translation into agricultural monitoring systems. By consolidating insights from diverse ecological applications, we present a practical roadmap for improving the quantitative outputs and interpretation of metabarcoding data and integrating these novel approaches into agricultural pest monitoring and management.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Microbiome-Derived Tryptophan Metabolites Regulate AhR Signaling to Restore Epithelial Barrier Integrity in Inflammatory Bowel Disease.
MicrobiologyOpen, 15(5):e70386.
Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation and compromised epithelial barrier integrity. Emerging evidence demonstrates that gut microbiota-derived tryptophan metabolites serve as endogenous ligands for the aryl hydrocarbon receptor (AhR), initiating protective signaling cascades that restore mucosal homeostasis. This review synthesizes current mechanistic insights into how microbial tryptophan catabolites including indole-3-aldehyde, indole-3-propionic acid, indole-3-lactic acid, and indole-3-acetic acid activate AhR to enhance epithelial barrier function. However, this protective capacity is specific to activation by physiological, low-affinity microbial ligands and should not be generalized to AhR signaling irrespective of ligand identity, dose, or duration of exposure. Key bacterial producers include Lactobacillus species (L. reuteri and L. plantarum), Clostridium sporogenes, and Allobaculum species. AhR activation by these metabolites triggers multiple downstream pathways, including AMP-activated protein kinase (AMPK) activation, which promotes autophagy and mitochondrial homeostasis; nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant responses; nuclear factor-κB (NF-κB) inhibition, which reduces pro-inflammatory cytokine production; and interleukin-22 (IL-22) induction, which supports epithelial regeneration. These signaling events converge to upregulate tight junction proteins, preserve mucus layer integrity, and reduce actomyosin-mediated permeability through decreased myosin light chain phosphorylation. Preclinical studies demonstrate AhR-dependent barrier restoration, with protective effects abolished by AhR antagonists. Despite these preclinical findings, their therapeutic utility in IBD remains to be established in human interventional studies. Importantly, the protective effects of AhR are highly context-dependent, as kynurenine pathway ligands and sustained receptor activation may exert immunosuppressive or pro-tumorigenic effects, highlighting the importance of ligand selectivity in therapeutic development.
Additional Links: PMID-42681875
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PubMed:
Citation:
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@article {pmid42681875,
year = {2026},
author = {Mahdiabadi, MA and Moghaddam, A and Erfanian, N},
title = {Microbiome-Derived Tryptophan Metabolites Regulate AhR Signaling to Restore Epithelial Barrier Integrity in Inflammatory Bowel Disease.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70386},
doi = {10.1002/mbo3.70386},
pmid = {42681875},
issn = {2045-8827},
mesh = {*Receptors, Aryl Hydrocarbon/metabolism ; Humans ; *Inflammatory Bowel Diseases/metabolism/microbiology ; *Tryptophan/metabolism ; *Signal Transduction ; Intestinal Barrier Function ; Animals ; *Intestinal Mucosa/metabolism ; *Gastrointestinal Microbiome ; Indoles/metabolism ; Basic Helix-Loop-Helix Proteins ; },
abstract = {Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation and compromised epithelial barrier integrity. Emerging evidence demonstrates that gut microbiota-derived tryptophan metabolites serve as endogenous ligands for the aryl hydrocarbon receptor (AhR), initiating protective signaling cascades that restore mucosal homeostasis. This review synthesizes current mechanistic insights into how microbial tryptophan catabolites including indole-3-aldehyde, indole-3-propionic acid, indole-3-lactic acid, and indole-3-acetic acid activate AhR to enhance epithelial barrier function. However, this protective capacity is specific to activation by physiological, low-affinity microbial ligands and should not be generalized to AhR signaling irrespective of ligand identity, dose, or duration of exposure. Key bacterial producers include Lactobacillus species (L. reuteri and L. plantarum), Clostridium sporogenes, and Allobaculum species. AhR activation by these metabolites triggers multiple downstream pathways, including AMP-activated protein kinase (AMPK) activation, which promotes autophagy and mitochondrial homeostasis; nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant responses; nuclear factor-κB (NF-κB) inhibition, which reduces pro-inflammatory cytokine production; and interleukin-22 (IL-22) induction, which supports epithelial regeneration. These signaling events converge to upregulate tight junction proteins, preserve mucus layer integrity, and reduce actomyosin-mediated permeability through decreased myosin light chain phosphorylation. Preclinical studies demonstrate AhR-dependent barrier restoration, with protective effects abolished by AhR antagonists. Despite these preclinical findings, their therapeutic utility in IBD remains to be established in human interventional studies. Importantly, the protective effects of AhR are highly context-dependent, as kynurenine pathway ligands and sustained receptor activation may exert immunosuppressive or pro-tumorigenic effects, highlighting the importance of ligand selectivity in therapeutic development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Receptors, Aryl Hydrocarbon/metabolism
Humans
*Inflammatory Bowel Diseases/metabolism/microbiology
*Tryptophan/metabolism
*Signal Transduction
Intestinal Barrier Function
Animals
*Intestinal Mucosa/metabolism
*Gastrointestinal Microbiome
Indoles/metabolism
Basic Helix-Loop-Helix Proteins
RevDate: 2026-09-02
CmpDate: 2026-09-02
Gut Microbiome Diversity, Functional Potential, and Ecological Relevance of Hottentotta tamulus.
MicrobiologyOpen, 15(5):e70373.
Scorpions are ancient arachnids of medical and ecological importance; they prey on insects and other arthropods while serving as prey to birds and reptiles. In this study, we reported for the first time on the characterization of the gut intestinal microbiome of Hottentotta tamulus native to northeastern Pakistan. The scorpions were identified on a morphological basis and the Cytochrome c oxidase subunit 1 gene sequence, while the gut microbiome was characterized through full-length 16S rRNA (V1-V9) Nanopore sequencing. The gut microbiota exhibited low to moderate alpha diversity with Chao1 and Shannon indices of 126 ± 90.54 and 0.85 ± 0.21, respectively. The intestinal microbial community was dominated by the phyla Firmicutes (79.48%-90.43%), followed by Proteobacteria (9.46%-20.48%), whereas Actinobacteriota (0.03%-0.11%) and Bacteroidota (0.00%-0.01%) were present at very low relative abundance. The functional profiling identified 23 notable pathways involved in energy metabolism, biomolecule synthesis, the biodegradation of various xenobiotics, and nucleotide metabolism, highlighting the role of the gut microbiome in metabolic homeostasis. The dominance of Bacillus and Mycoplasma in gut microbial communities may enhance host adaptation to low-resource environments.
Additional Links: PMID-42681893
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PubMed:
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@article {pmid42681893,
year = {2026},
author = {Khan, KU and Zahid, MT and Mustafa, G and Tanpure, RS and Tahir, HM and Kumar, R and Kim, DW and Park, HK and Jeon, BH},
title = {Gut Microbiome Diversity, Functional Potential, and Ecological Relevance of Hottentotta tamulus.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70373},
doi = {10.1002/mbo3.70373},
pmid = {42681893},
issn = {2045-8827},
support = {2026-RISE-01-027-01//Regional Innovation System & Education (RISE)"/ ; RS-2025-00520940//National Research Foundation of Korea (NRF)/ ; },
mesh = {Animals ; RNA, Ribosomal, 16S/genetics ; *Bacteria/classification/genetics/isolation & purification ; *Gastrointestinal Microbiome ; Phylogeny ; DNA, Bacterial/genetics ; Biodiversity ; Sequence Analysis, DNA ; Animals, Poisonous ; Scorpions ; },
abstract = {Scorpions are ancient arachnids of medical and ecological importance; they prey on insects and other arthropods while serving as prey to birds and reptiles. In this study, we reported for the first time on the characterization of the gut intestinal microbiome of Hottentotta tamulus native to northeastern Pakistan. The scorpions were identified on a morphological basis and the Cytochrome c oxidase subunit 1 gene sequence, while the gut microbiome was characterized through full-length 16S rRNA (V1-V9) Nanopore sequencing. The gut microbiota exhibited low to moderate alpha diversity with Chao1 and Shannon indices of 126 ± 90.54 and 0.85 ± 0.21, respectively. The intestinal microbial community was dominated by the phyla Firmicutes (79.48%-90.43%), followed by Proteobacteria (9.46%-20.48%), whereas Actinobacteriota (0.03%-0.11%) and Bacteroidota (0.00%-0.01%) were present at very low relative abundance. The functional profiling identified 23 notable pathways involved in energy metabolism, biomolecule synthesis, the biodegradation of various xenobiotics, and nucleotide metabolism, highlighting the role of the gut microbiome in metabolic homeostasis. The dominance of Bacillus and Mycoplasma in gut microbial communities may enhance host adaptation to low-resource environments.},
}
MeSH Terms:
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hide MeSH Terms
Animals
RNA, Ribosomal, 16S/genetics
*Bacteria/classification/genetics/isolation & purification
*Gastrointestinal Microbiome
Phylogeny
DNA, Bacterial/genetics
Biodiversity
Sequence Analysis, DNA
Animals, Poisonous
Scorpions
RevDate: 2026-09-02
Bacterial composition of Polygenis (Polygenis) bohlsi bohlsi (Wagner, 1901) (Siphonaptera: Rhopalopsyllidae) associated with Thrichomys fosteri (Rodentia: Echimyidae) in the Brazilian Pantanal wetland.
Medical and veterinary entomology [Epub ahead of print].
Fleas (Insecta: Siphonaptera) are important vectors of zoonotic bacterial pathogens. However, the bacterial communities hosted by fleas remain poorly understood, especially regarding the interactions between nonpathogenic bacteria and pathogens, as well as the factors shaping these bacterial communities. This study aimed to explore the bacterial composition and diversity between female and male Polygenis (Polygenis) bohlsi bohlsi fleas collected from free-living Thrichomys fosteri (Rodentia: Echimyidae) in the Nhecolândia region of central-western Brazil. Here, bacterial profiling of fleas was performed using a Next-Generation Sequencing approach targeting the V3-V4 hypervariable region of the 16S rRNA gene to assess community structure. Bacterial diversity in P. (P.) bohlsi bohlsi fleas varied by sex, as indicated by significant differences in alpha diversity, while beta diversity showed a trend toward separation between sexes. Pseudomonadota was the predominant phylum in the flea microbiome. Ten bacterial genera showed differentially abundance between male and female fleas, including Bartonella spp., which was detected exclusively in males, and Wolbachia spp., which was more abundant in females than in males. Phylogenetic analysis positioned Bartonella gltA sequences detected in two fleas within the same clade as Bartonella harrusi. While the Wolbachia wsp and 16S rRNA sequences detected in P. (P.) bohlsi bohlsi grouped within the supergroups S (associated with pseudoscorpions), gatB sequences grouped with V (cat flea-related). These findings suggest sex-associated differences in the microbiome of P. (P.) bohlsi bohlsi fleas and highlight the need for further investigation into the potential role of Wolbachia spp. in shaping flea-associated microbial communities and their interactions with Bartonella spp.
Additional Links: PMID-42681944
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PubMed:
Citation:
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@article {pmid42681944,
year = {2026},
author = {Funnicelli, MIG and do Amaral, RB and de Mello, VVC and Bassini-Silva, R and Micolta, LFB and Buysse, M and de Assis, WO and da Silva, AR and Herrera, HM and Machado, RZ and Barros-Battesti, DM and Pinheiro, DG and Duron, O and André, MR},
title = {Bacterial composition of Polygenis (Polygenis) bohlsi bohlsi (Wagner, 1901) (Siphonaptera: Rhopalopsyllidae) associated with Thrichomys fosteri (Rodentia: Echimyidae) in the Brazilian Pantanal wetland.},
journal = {Medical and veterinary entomology},
volume = {},
number = {},
pages = {},
doi = {10.1111/mve.70111},
pmid = {42681944},
issn = {1365-2915},
support = {2022/05615-2//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2023/16710-9//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2024/20336-8//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 303701/2021-8//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; },
abstract = {Fleas (Insecta: Siphonaptera) are important vectors of zoonotic bacterial pathogens. However, the bacterial communities hosted by fleas remain poorly understood, especially regarding the interactions between nonpathogenic bacteria and pathogens, as well as the factors shaping these bacterial communities. This study aimed to explore the bacterial composition and diversity between female and male Polygenis (Polygenis) bohlsi bohlsi fleas collected from free-living Thrichomys fosteri (Rodentia: Echimyidae) in the Nhecolândia region of central-western Brazil. Here, bacterial profiling of fleas was performed using a Next-Generation Sequencing approach targeting the V3-V4 hypervariable region of the 16S rRNA gene to assess community structure. Bacterial diversity in P. (P.) bohlsi bohlsi fleas varied by sex, as indicated by significant differences in alpha diversity, while beta diversity showed a trend toward separation between sexes. Pseudomonadota was the predominant phylum in the flea microbiome. Ten bacterial genera showed differentially abundance between male and female fleas, including Bartonella spp., which was detected exclusively in males, and Wolbachia spp., which was more abundant in females than in males. Phylogenetic analysis positioned Bartonella gltA sequences detected in two fleas within the same clade as Bartonella harrusi. While the Wolbachia wsp and 16S rRNA sequences detected in P. (P.) bohlsi bohlsi grouped within the supergroups S (associated with pseudoscorpions), gatB sequences grouped with V (cat flea-related). These findings suggest sex-associated differences in the microbiome of P. (P.) bohlsi bohlsi fleas and highlight the need for further investigation into the potential role of Wolbachia spp. in shaping flea-associated microbial communities and their interactions with Bartonella spp.},
}
RevDate: 2026-09-02
Gut microbiota-derived indole-3-propionic acid attenuates Arsenic trioxide-induced cognitive impairment by inhibiting ubiquitination and degradation of BRD4.
British journal of pharmacology [Epub ahead of print].
BACKGROUND AND PURPOSE: Arsenic trioxide (ATO) therapy for acute promyelocytic leukaemia (APL) can induce neurological disorders, including cognitive impairment (CI) and depression, severely impacting patient quality of life, yet effective interventions are lacking. Clinical observations indicate ATO treatment is associated with gut microbiota dysbiosis. Given the crucial role of gut microbes and their metabolites in neurological health, this study investigated indole-3-propionic acid (IPA), a neuroprotective microbiota-derived metabolite capable of crossing the blood-brain barrier.
RESULTS: In ATO-treated mice, behavioural tests confirmed significant cognitive decline. 16S rRNA genotyping revealed a reduction in Bifidobacterium abundance, and metabolomics identified a concomitant decrease in its metabolite, IPA, alongside disruptions in the tricarboxylic acid cycle and glycolysis. IPA supplementation alleviated ATO-induced intestinal inflammation and behavioural deficits. Mechanistically, IPA inhibited ATO-induced BRD4 degradation and the associated reduction in H4 acetylation, thereby restoring the expression of the metabolic enzyme PFKM and the synaptic protein PSD95.
CONCLUSION: IPA mitigates ATO-induced intestinal injury and glycolytic dysfunction via the 'BRD4-H4ac-PFKM' axis, providing novel insights for preventing and treating ATO-induced neurotoxicity.
Additional Links: PMID-42681956
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PubMed:
Citation:
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@article {pmid42681956,
year = {2026},
author = {Ren, K and Zhao, T and Li, L and Lin, L and Ren, S and Ni, X and Gao, Z and Zhang, W and Duan, X and Hai, X},
title = {Gut microbiota-derived indole-3-propionic acid attenuates Arsenic trioxide-induced cognitive impairment by inhibiting ubiquitination and degradation of BRD4.},
journal = {British journal of pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bph.70632},
pmid = {42681956},
issn = {1476-5381},
support = {82274028//National Natural Science Foundation of China/ ; 320.6750.2024-18-37//Scientific Research Project of Wu Jieping Medical Foundation/ ; LH2023H032//Natural Science Foundation of Heilongjiang Province/ ; PL2025H098//Natural Science Foundation of Heilongjiang Province/ ; ZL2024H005//Key Project of Natural Science Foundation of Heilongjiang Province/ ; 2025M781968//China Postdoctoral Science Foundation/ ; 2025//provincial universities in heilongjiang province/ ; },
abstract = {BACKGROUND AND PURPOSE: Arsenic trioxide (ATO) therapy for acute promyelocytic leukaemia (APL) can induce neurological disorders, including cognitive impairment (CI) and depression, severely impacting patient quality of life, yet effective interventions are lacking. Clinical observations indicate ATO treatment is associated with gut microbiota dysbiosis. Given the crucial role of gut microbes and their metabolites in neurological health, this study investigated indole-3-propionic acid (IPA), a neuroprotective microbiota-derived metabolite capable of crossing the blood-brain barrier.
RESULTS: In ATO-treated mice, behavioural tests confirmed significant cognitive decline. 16S rRNA genotyping revealed a reduction in Bifidobacterium abundance, and metabolomics identified a concomitant decrease in its metabolite, IPA, alongside disruptions in the tricarboxylic acid cycle and glycolysis. IPA supplementation alleviated ATO-induced intestinal inflammation and behavioural deficits. Mechanistically, IPA inhibited ATO-induced BRD4 degradation and the associated reduction in H4 acetylation, thereby restoring the expression of the metabolic enzyme PFKM and the synaptic protein PSD95.
CONCLUSION: IPA mitigates ATO-induced intestinal injury and glycolytic dysfunction via the 'BRD4-H4ac-PFKM' axis, providing novel insights for preventing and treating ATO-induced neurotoxicity.},
}
RevDate: 2026-09-02
Nutrition support in gastroenterology: opinion on current literature.
Current opinion in gastroenterology pii:00001574-990000000-00260 [Epub ahead of print].
PURPOSE OF REVIEW: Historically, enteral nutrition has been the preferred therapy due to its physiologic benefits, with parenteral nutrition selected if enteral nutrition was contraindicated or insufficient; however, recent advances in nutrition support have prompted reevaluation of this process. This review summarizes the current evidence regarding enteral nutrition and parenteral nutrition in gastrointestinal oncology, inflammatory bowel disease (IBD), critical care, and gastrointestinal surgery.
RECENT FINDINGS: In gastric cancer, parenteral nutrition may improve the nutritional status and clinical outcomes of treatment-related gastrointestinal dysfunction. In IBD, exclusive enteral nutrition may be effective for inducing remission and promoting mucosal healing, whereas parenteral nutrition is preferred in intestinal failure and severe complications. Studies have shown the value of early parenteral nutrition when enteral nutrition is contraindicated or insufficient, specifically for improving nutrient delivery and reducing complications in critically ill and surgical patients. Additional areas of interest include caloric and protein dosing, indirect calorimetry, and the effect of nutrition support on the gut microbiome.
SUMMARY: Current evidence supports a patient-centered approach to nutrition support with enteral nutrition remaining as the preference when the gastrointestinal tract can be utilized and parenteral nutrition as an important alternative or adjunct in select populations. Future research should focus on the refinement of supplemental parenteral nutrition practices and the development of evidence-based approaches for specific disease states.
Additional Links: PMID-42681978
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PubMed:
Citation:
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@article {pmid42681978,
year = {2026},
author = {Deringer, R and Silva, CS and Klein, D},
title = {Nutrition support in gastroenterology: opinion on current literature.},
journal = {Current opinion in gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1097/MOG.0000000000001194},
pmid = {42681978},
issn = {1531-7056},
abstract = {PURPOSE OF REVIEW: Historically, enteral nutrition has been the preferred therapy due to its physiologic benefits, with parenteral nutrition selected if enteral nutrition was contraindicated or insufficient; however, recent advances in nutrition support have prompted reevaluation of this process. This review summarizes the current evidence regarding enteral nutrition and parenteral nutrition in gastrointestinal oncology, inflammatory bowel disease (IBD), critical care, and gastrointestinal surgery.
RECENT FINDINGS: In gastric cancer, parenteral nutrition may improve the nutritional status and clinical outcomes of treatment-related gastrointestinal dysfunction. In IBD, exclusive enteral nutrition may be effective for inducing remission and promoting mucosal healing, whereas parenteral nutrition is preferred in intestinal failure and severe complications. Studies have shown the value of early parenteral nutrition when enteral nutrition is contraindicated or insufficient, specifically for improving nutrient delivery and reducing complications in critically ill and surgical patients. Additional areas of interest include caloric and protein dosing, indirect calorimetry, and the effect of nutrition support on the gut microbiome.
SUMMARY: Current evidence supports a patient-centered approach to nutrition support with enteral nutrition remaining as the preference when the gastrointestinal tract can be utilized and parenteral nutrition as an important alternative or adjunct in select populations. Future research should focus on the refinement of supplemental parenteral nutrition practices and the development of evidence-based approaches for specific disease states.},
}
RevDate: 2026-09-02
Vaginal microbiome metabolite shifts as early predictors of premature ovarian insufficiency in adolescents with novel gene variants.
Turkish journal of obstetrics and gynecology [Epub ahead of print].
Additional Links: PMID-42682004
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PubMed:
Citation:
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@article {pmid42682004,
year = {2026},
author = {Sufiyan, R and Nadeem, M and Bokhari, SMS and Khan, BS and Fatima, M},
title = {Vaginal microbiome metabolite shifts as early predictors of premature ovarian insufficiency in adolescents with novel gene variants.},
journal = {Turkish journal of obstetrics and gynecology},
volume = {},
number = {},
pages = {},
doi = {10.4274/tjod.galenos.2026.72418},
pmid = {42682004},
issn = {2149-9322},
}
RevDate: 2026-09-02
A Critical Synthesis of Machine Learning in Autism Spectrum Disorder Genomic Research: From Transcriptomics to Microbiome.
Medeniyet medical journal [Epub ahead of print].
Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by persistent impairments in social communication, restricted interests, and repetitive behaviors. This narrative review synthesizes advances in machine learning applications to ASD genomic research through May 2026, spanning gene expression analysis, whole-exome sequencing (WES), non-coding variant interpretation, multi-omics integration, single-cell transcriptomics, epigenetic profiling, and gut microbiome analysis. A purposive, thematic literature synthesis approach was employed, allowing broad coverage of emerging methodological innovations and biological insights. We critically evaluate state-of-the-art deep learning architectures-including the Separate Translated Autism Research Neural Network and SHapley Additive exPlanations-based explainable artificial intelligence frameworks. Reported discrimination across the field varies widely, from receiver operating characteristic-area under the curve (ROC-AUC) values near 0.66 to implausibly perfect values of 1.00; the best-validated specialized genomic architecture achieves only modest discrimination (ROC-AUC≈0.73). We emphasize that interpretability and predictive performance are orthogonal properties: specialized architectures yield biologically interpretable feature attributions despite modest discriminative power; and several extreme AUC values in the literature are, in our assessment, more consistent with overfitting or data leakage than with genuine signal, although the primary reports did not always provide the information needed to definitively attribute them. Key themes include: (1) identification of differentially expressed genes through meta-analysis of transcriptomic data; (2) validation of predictive gene features from large-scale WES; (3) detection of non-coding regulatory mutations affecting synaptic transmission pathways; (4) discovery of gut microbiome signatures associated with ASD classification; and (5) discovery of data-driven subtypes enabling precision medicine stratification. Critical challenges include population bias toward European ancestry, socioeconomic ascertainment bias, modest predictive effect sizes, conflation of association with causation, and gaps between computational prediction and clinical utility. Future directions emphasize multi-modal data integration, diverse cohort expansion, engagement with neurodiversity perspectives, and regulatory science development.
Additional Links: PMID-42682077
Publisher:
PubMed:
Citation:
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@article {pmid42682077,
year = {2026},
author = {Sadr, Z and Fallahpour, B and Dastgheib, AA and Bahrami, R and Tafti, MG and Shiri, A and Masoudi, A and Nematzadeh, F and Neamatzadeh, H},
title = {A Critical Synthesis of Machine Learning in Autism Spectrum Disorder Genomic Research: From Transcriptomics to Microbiome.},
journal = {Medeniyet medical journal},
volume = {},
number = {},
pages = {},
doi = {10.4274/MMJ.galenos.2026.69259},
pmid = {42682077},
issn = {2149-2042},
abstract = {Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by persistent impairments in social communication, restricted interests, and repetitive behaviors. This narrative review synthesizes advances in machine learning applications to ASD genomic research through May 2026, spanning gene expression analysis, whole-exome sequencing (WES), non-coding variant interpretation, multi-omics integration, single-cell transcriptomics, epigenetic profiling, and gut microbiome analysis. A purposive, thematic literature synthesis approach was employed, allowing broad coverage of emerging methodological innovations and biological insights. We critically evaluate state-of-the-art deep learning architectures-including the Separate Translated Autism Research Neural Network and SHapley Additive exPlanations-based explainable artificial intelligence frameworks. Reported discrimination across the field varies widely, from receiver operating characteristic-area under the curve (ROC-AUC) values near 0.66 to implausibly perfect values of 1.00; the best-validated specialized genomic architecture achieves only modest discrimination (ROC-AUC≈0.73). We emphasize that interpretability and predictive performance are orthogonal properties: specialized architectures yield biologically interpretable feature attributions despite modest discriminative power; and several extreme AUC values in the literature are, in our assessment, more consistent with overfitting or data leakage than with genuine signal, although the primary reports did not always provide the information needed to definitively attribute them. Key themes include: (1) identification of differentially expressed genes through meta-analysis of transcriptomic data; (2) validation of predictive gene features from large-scale WES; (3) detection of non-coding regulatory mutations affecting synaptic transmission pathways; (4) discovery of gut microbiome signatures associated with ASD classification; and (5) discovery of data-driven subtypes enabling precision medicine stratification. Critical challenges include population bias toward European ancestry, socioeconomic ascertainment bias, modest predictive effect sizes, conflation of association with causation, and gaps between computational prediction and clinical utility. Future directions emphasize multi-modal data integration, diverse cohort expansion, engagement with neurodiversity perspectives, and regulatory science development.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Comment on "Global clinical trial landscape of microbiome modulator therapy in sepsis: gut microbiota interventions and challenges".
International journal of surgery (London, England), 112(6):12987-12988.
Additional Links: PMID-42682281
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@article {pmid42682281,
year = {2026},
author = {You, G and Ren, Y and Du, Y},
title = {Comment on "Global clinical trial landscape of microbiome modulator therapy in sepsis: gut microbiota interventions and challenges".},
journal = {International journal of surgery (London, England)},
volume = {112},
number = {6},
pages = {12987-12988},
pmid = {42682281},
issn = {1743-9159},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Metronidazole-mediated gut anaerobe remodeling is associated with transplant rejection.
Frontiers in cellular and infection microbiology, 16:1874387.
BACKGROUND: The gut microbiome has emerged as a potential modulator of transplant rejection. However, the relevance of anaerobe-associated gut microbial communities to transplant rejection responses remains unclear.
METHODS: In a murine islet transplantation model, we assessed the effects of metronidazole pretreatment on allograft survival and function. 16S rRNA sequencing was performed to characterize treatment-associated changes in gut microbial composition. Separately, an exploratory two-sample MR analysis using human GWAS data was performed to prioritize gut microbial taxa associated with a composite outcome of transplant failure or rejection. Biological annotation was subsequently used to prioritize candidate host pathways. Immunohistochemistry and flow cytometry were used to evaluate post-transplant immune responses after metronidazole pretreatment.
RESULTS: Metronidazole treatment remodeled gut microbiota composition and significantly delayed islet allograft rejection. MR analyses identified several anaerobe-associated gut microbial taxa potentially relevant to transplant rejection risk, including the family Defluviitaleaceae and the genera Intestinibacter, Bilophila, Ruminococcus and Eubacterium fissicatena. Integrative biological annotation highlighted glycosylation-related pathways and prioritized ST3GAL4 for subsequent expression assessment in the murine transplant model. Furthermore, metronidazole treatment reduced CD4[+] T-cell infiltration around the allograft and Th17-related inflammatory responses.
CONCLUSION: Altogether, our findings document gut microbial remodeling and delayed allograft rejection following metronidazole pretreatment. These findings are hypothesis-generating and warrant further mechanistic investigation.
Additional Links: PMID-42682404
PubMed:
Citation:
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@article {pmid42682404,
year = {2026},
author = {Liu, Y and Tian, Y and Pu, C and Yang, Y and Peng, X and Zhu, H and Fan, J and Zhang, R and Yuan, H and Zhang, J and Liu, J and Zhao, G},
title = {Metronidazole-mediated gut anaerobe remodeling is associated with transplant rejection.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1874387},
pmid = {42682404},
issn = {2235-2988},
mesh = {*Metronidazole/pharmacology/administration & dosage ; Animals ; *Graft Rejection/prevention & control/microbiology/immunology ; Mice ; *Gastrointestinal Microbiome/drug effects ; RNA, Ribosomal, 16S/genetics ; Humans ; *Bacteria, Anaerobic/drug effects/classification/genetics ; *Islets of Langerhans Transplantation/adverse effects ; Graft Survival/drug effects ; Mice, Inbred C57BL ; Disease Models, Animal ; Male ; },
abstract = {BACKGROUND: The gut microbiome has emerged as a potential modulator of transplant rejection. However, the relevance of anaerobe-associated gut microbial communities to transplant rejection responses remains unclear.
METHODS: In a murine islet transplantation model, we assessed the effects of metronidazole pretreatment on allograft survival and function. 16S rRNA sequencing was performed to characterize treatment-associated changes in gut microbial composition. Separately, an exploratory two-sample MR analysis using human GWAS data was performed to prioritize gut microbial taxa associated with a composite outcome of transplant failure or rejection. Biological annotation was subsequently used to prioritize candidate host pathways. Immunohistochemistry and flow cytometry were used to evaluate post-transplant immune responses after metronidazole pretreatment.
RESULTS: Metronidazole treatment remodeled gut microbiota composition and significantly delayed islet allograft rejection. MR analyses identified several anaerobe-associated gut microbial taxa potentially relevant to transplant rejection risk, including the family Defluviitaleaceae and the genera Intestinibacter, Bilophila, Ruminococcus and Eubacterium fissicatena. Integrative biological annotation highlighted glycosylation-related pathways and prioritized ST3GAL4 for subsequent expression assessment in the murine transplant model. Furthermore, metronidazole treatment reduced CD4[+] T-cell infiltration around the allograft and Th17-related inflammatory responses.
CONCLUSION: Altogether, our findings document gut microbial remodeling and delayed allograft rejection following metronidazole pretreatment. These findings are hypothesis-generating and warrant further mechanistic investigation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Metronidazole/pharmacology/administration & dosage
Animals
*Graft Rejection/prevention & control/microbiology/immunology
Mice
*Gastrointestinal Microbiome/drug effects
RNA, Ribosomal, 16S/genetics
Humans
*Bacteria, Anaerobic/drug effects/classification/genetics
*Islets of Langerhans Transplantation/adverse effects
Graft Survival/drug effects
Mice, Inbred C57BL
Disease Models, Animal
Male
RevDate: 2026-09-02
CmpDate: 2026-09-02
Temporal changes in circulating metabolites after metabolic and bariatric surgery and risk of incident coronary heart disease: evidence from prospective cohort and nested case-control studies.
International journal of surgery (London, England), 112(7):13105-13115.
BACKGROUND: Metabolic and bariatric surgery (MBS) has notable cardiovascular benefits beyond weight loss.
METHODS: The Gut Microbiome in Metabolic Surgery Study (GUMMY) enrolled patients who underwent first-time Roux-en-Y gastric bypass or sleeve gastrectomy, with blood samples collected at pre- and 3- and 12-month post-surgery. Significant metabolite changes were identified using paired Wilcoxon signed-rank tests with a false discovery rate (FDR) < 0.05 and |log2 fold change| > log21.5, comparing 3-month post- vs. pre-surgery (early phase) and 12- vs. 3-month post-surgery (late phase). Significantly changed metabolites were classified into three patterns: early changed, late sustained; early changed, late reversed; and early unchanged, late changed. Subsequently, a nested case-control study within the Southern Community Cohort Study (SCCS) assessed the associations between surgery-altered metabolites and incident coronary heart disease (CHD) risk using conditional logistic regression. The same untargeted metabolomic assay was conducted in GUMMY and SCCS plasma samples.
RESULTS: Among 115 surgical patients, the mean (SD) age was 44.9 (9.5) years, and 90 (78%) were women. Significant changes were observed in 224 metabolites, mainly encompassing sustained increases in bile acids and decreases in branched-chain amino acids, lactoyl, and lysine amino acids; reversed changes in some ketone bodies, phospholipids, lysophospholipids, and glycogen metabolites; late increases in taurine, caffeine, benzoate, and some tryptophan metabolites; and late decreases in ceramide metabolites and certain fatty acids. In the SCCS (n = 1194; 597 case-control pairs), 37 surgery-altered metabolites were significantly associated with incident CHD (FDR < 0.1), 28 with concordant effects, i.e., post-surgical increases were associated with reduced CHD risk and vice versa.
CONCLUSIONS: MBS elicits substantial metabolomic alterations, with many altered metabolites associated with incident CHD. These findings provide mechanistic insights into the cardiovascular benefits of MBS and suggest potential therapeutic targets for CHD prevention.
Additional Links: PMID-42682435
PubMed:
Citation:
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@article {pmid42682435,
year = {2026},
author = {Zheng, Y and Wang, Z and Wang, L and Flynn, CR and Shu, XO and English, WJ and Samuels, JM and Chen, Y and Lipworth, L and Gupta, D and Cai, Q and Zheng, W and Yu, D},
title = {Temporal changes in circulating metabolites after metabolic and bariatric surgery and risk of incident coronary heart disease: evidence from prospective cohort and nested case-control studies.},
journal = {International journal of surgery (London, England)},
volume = {112},
number = {7},
pages = {13105-13115},
pmid = {42682435},
issn = {1743-9159},
abstract = {BACKGROUND: Metabolic and bariatric surgery (MBS) has notable cardiovascular benefits beyond weight loss.
METHODS: The Gut Microbiome in Metabolic Surgery Study (GUMMY) enrolled patients who underwent first-time Roux-en-Y gastric bypass or sleeve gastrectomy, with blood samples collected at pre- and 3- and 12-month post-surgery. Significant metabolite changes were identified using paired Wilcoxon signed-rank tests with a false discovery rate (FDR) < 0.05 and |log2 fold change| > log21.5, comparing 3-month post- vs. pre-surgery (early phase) and 12- vs. 3-month post-surgery (late phase). Significantly changed metabolites were classified into three patterns: early changed, late sustained; early changed, late reversed; and early unchanged, late changed. Subsequently, a nested case-control study within the Southern Community Cohort Study (SCCS) assessed the associations between surgery-altered metabolites and incident coronary heart disease (CHD) risk using conditional logistic regression. The same untargeted metabolomic assay was conducted in GUMMY and SCCS plasma samples.
RESULTS: Among 115 surgical patients, the mean (SD) age was 44.9 (9.5) years, and 90 (78%) were women. Significant changes were observed in 224 metabolites, mainly encompassing sustained increases in bile acids and decreases in branched-chain amino acids, lactoyl, and lysine amino acids; reversed changes in some ketone bodies, phospholipids, lysophospholipids, and glycogen metabolites; late increases in taurine, caffeine, benzoate, and some tryptophan metabolites; and late decreases in ceramide metabolites and certain fatty acids. In the SCCS (n = 1194; 597 case-control pairs), 37 surgery-altered metabolites were significantly associated with incident CHD (FDR < 0.1), 28 with concordant effects, i.e., post-surgical increases were associated with reduced CHD risk and vice versa.
CONCLUSIONS: MBS elicits substantial metabolomic alterations, with many altered metabolites associated with incident CHD. These findings provide mechanistic insights into the cardiovascular benefits of MBS and suggest potential therapeutic targets for CHD prevention.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Gut microbiome-immune-metabolic mechanisms in cerebrovascular disease: evidence-graded insights from cerebral small vessel disease, ischemic stroke, and intracerebral hemorrhage.
Frontiers in microbiology, 17:1927904.
Cerebrovascular disease is increasingly being examined in relation to the gut microbiome, but the field has not advanced evenly across disease phenotypes. A central challenge is to distinguish broad dysbiosis-based associations from microbial functions, host-facing metabolites, epithelial barrier injury, and immune pathways that may plausibly influence neurovascular vulnerability or recovery. This distinction is particularly important because cerebral small vessel disease, acute ischemic stroke, and intracerebral hemorrhage differ in time scale, vascular pathology, clinical exposure, and available microbiome evidence. This review evaluates gut microbiome-immune-metabolic mechanisms across these cerebrovascular contexts with a focus on microbial ecology, intestinal barrier dysfunction, microbial translocation, short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), bile acid derivatives, tryptophan-linked metabolites, lipopolysaccharide (LPS)-related inflammatory signaling, and emerging multi-kingdom signals, including the gut virome and mycobiome. Current evidence is most convincing in acute ischemic stroke, where human cohort studies and experimental perturbation models link microbiome disruption, microbial metabolites, immune programming, and functional outcome. Evidence for imaging-defined cerebral small vessel disease remains more limited and is largely cross-sectional, whereas intracerebral hemorrhage is an emerging but mechanistically distinct domain. Virome- and mycobiome-related mechanisms remain exploratory and require longitudinal, multi-omics, and perturbation-based validation. This review argues that cerebrovascular microbiome research should move beyond taxonomic association toward time-resolved microbial function, host-facing metabolites, disease-specific host-microbe interfaces, and experimentally testable mechanisms. Candidate microbiome-directed interventions-including dietary, prebiotic, probiotic, postbiotic, fecal microbiota transplantation, defined microbial consortia, metabolite-targeted, and phage-based approaches-remain investigational. Their translation will require disease- and time-window-specific evaluation of biological target engagement, safety, and clinically meaningful outcomes. Longitudinal multi-omics cohorts, disease-specific models, and careful control of diet, antibiotics, vascular medications, hospitalization, and frailty will be essential for determining which gut microbiome-related pathways are causal, context-specific, modifiable, and therapeutically actionable.
Additional Links: PMID-42682509
PubMed:
Citation:
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@article {pmid42682509,
year = {2026},
author = {Ren, C and Xiu, Y and Zhang, Y and Wang, X and Zhao, H and Tang, J and Li, Q and Zhang, S and Zhao, F},
title = {Gut microbiome-immune-metabolic mechanisms in cerebrovascular disease: evidence-graded insights from cerebral small vessel disease, ischemic stroke, and intracerebral hemorrhage.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1927904},
pmid = {42682509},
issn = {1664-302X},
abstract = {Cerebrovascular disease is increasingly being examined in relation to the gut microbiome, but the field has not advanced evenly across disease phenotypes. A central challenge is to distinguish broad dysbiosis-based associations from microbial functions, host-facing metabolites, epithelial barrier injury, and immune pathways that may plausibly influence neurovascular vulnerability or recovery. This distinction is particularly important because cerebral small vessel disease, acute ischemic stroke, and intracerebral hemorrhage differ in time scale, vascular pathology, clinical exposure, and available microbiome evidence. This review evaluates gut microbiome-immune-metabolic mechanisms across these cerebrovascular contexts with a focus on microbial ecology, intestinal barrier dysfunction, microbial translocation, short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), bile acid derivatives, tryptophan-linked metabolites, lipopolysaccharide (LPS)-related inflammatory signaling, and emerging multi-kingdom signals, including the gut virome and mycobiome. Current evidence is most convincing in acute ischemic stroke, where human cohort studies and experimental perturbation models link microbiome disruption, microbial metabolites, immune programming, and functional outcome. Evidence for imaging-defined cerebral small vessel disease remains more limited and is largely cross-sectional, whereas intracerebral hemorrhage is an emerging but mechanistically distinct domain. Virome- and mycobiome-related mechanisms remain exploratory and require longitudinal, multi-omics, and perturbation-based validation. This review argues that cerebrovascular microbiome research should move beyond taxonomic association toward time-resolved microbial function, host-facing metabolites, disease-specific host-microbe interfaces, and experimentally testable mechanisms. Candidate microbiome-directed interventions-including dietary, prebiotic, probiotic, postbiotic, fecal microbiota transplantation, defined microbial consortia, metabolite-targeted, and phage-based approaches-remain investigational. Their translation will require disease- and time-window-specific evaluation of biological target engagement, safety, and clinically meaningful outcomes. Longitudinal multi-omics cohorts, disease-specific models, and careful control of diet, antibiotics, vascular medications, hospitalization, and frailty will be essential for determining which gut microbiome-related pathways are causal, context-specific, modifiable, and therapeutically actionable.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Gut microbiota dysbiosis and aromatic amino acid metabolism alterations: a multi-omics analysis of cognitive impairment following aneurysmal subarachnoid hemorrhage.
Frontiers in microbiology, 17:1870309.
BACKGROUND: Aneurysmal subarachnoid hemorrhage (aSAH) is frequently followed by persistent cognitive impairment, characterized by a complex and multifactorial pathological mechanism. While the role of the "microbiota-gut-brain axis" in neurocognition has garnered increasing attention, the specific ways in which gut microbiota and their derived metabolites might be associated with the development and progression of post-aSAH cognitive impairment remain largely undefined. Consequently, there remains a lack of systematic multi-omics evidence to elucidate these potential underlying associations.
METHODS: In this prospective observational study, we enrolled 48 patients with intracranial aneurysms. Among them, patients with aSAH (n = 33) were divided into a cognitive impairment group (aSAH-CI, n = 18) and a group without cognitive impairment (aSAH-WCI, n = 15) based on a 6-month longitudinal neurocognitive assessment. Patients with unruptured intracranial aneurysms (UIA, n = 15) served as the control group. We integrated a multi-omics approach encompassing fecal metagenomics, untargeted metabolomics, and serological profiles of inflammation, oxidative stress, and apoptosis to explore the potential correlations between the host and the microbiome, as well as to identify early diagnostic biomarkers.
RESULTS: Fecal metagenomics revealed distinct gut dysbiosis in aSAH-CI patients, characterized by reduced alpha diversity, depletion of beneficial commensals (e.g., Agathobacter), and expansion of opportunistic pathogens (e.g., Enterococcus). Functional and metabolomic analyses identified a significant alteration in aromatic amino acid biosynthesis. Specifically, tyrosine metabolism was altered, marked by reduced levels of neurotransmitter precursors and elevated neurotoxic trace amines (tyramine and phenylethylamine). Serologically, aSAH-CI patients exhibited heightened systemic inflammation, oxidative stress, and apoptosis. Integrated multi-omics network analysis underscored a strong correlation between elevated trace amines, depleted Agathobacter, and systemic pathological indices. Notably, Agathobacter rectalis and tyramine demonstrated robust potential as early diagnostic biomarkers for cognitive impairment following aSAH.
CONCLUSION: Our findings suggest a potential dual-hit correlative signature via the microbiota-gut-brain axis in cognitive impairment following aSAH. We hypothesize that the depletion of aromatic amino acid-producing microbiota correlates with reduced neurotransmitter precursors, theoretically impairing synaptic repair. Concurrently, observed associations among opportunistic pathogens, trace amines, and systemic inflammatory and oxidative stress markers suggest a synergistic effect potentially linked to further neuronal damage.
Additional Links: PMID-42682513
PubMed:
Citation:
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@article {pmid42682513,
year = {2026},
author = {Zhang, W and Chen, M and Guo, T and Kuang, G and Ma, N},
title = {Gut microbiota dysbiosis and aromatic amino acid metabolism alterations: a multi-omics analysis of cognitive impairment following aneurysmal subarachnoid hemorrhage.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1870309},
pmid = {42682513},
issn = {1664-302X},
abstract = {BACKGROUND: Aneurysmal subarachnoid hemorrhage (aSAH) is frequently followed by persistent cognitive impairment, characterized by a complex and multifactorial pathological mechanism. While the role of the "microbiota-gut-brain axis" in neurocognition has garnered increasing attention, the specific ways in which gut microbiota and their derived metabolites might be associated with the development and progression of post-aSAH cognitive impairment remain largely undefined. Consequently, there remains a lack of systematic multi-omics evidence to elucidate these potential underlying associations.
METHODS: In this prospective observational study, we enrolled 48 patients with intracranial aneurysms. Among them, patients with aSAH (n = 33) were divided into a cognitive impairment group (aSAH-CI, n = 18) and a group without cognitive impairment (aSAH-WCI, n = 15) based on a 6-month longitudinal neurocognitive assessment. Patients with unruptured intracranial aneurysms (UIA, n = 15) served as the control group. We integrated a multi-omics approach encompassing fecal metagenomics, untargeted metabolomics, and serological profiles of inflammation, oxidative stress, and apoptosis to explore the potential correlations between the host and the microbiome, as well as to identify early diagnostic biomarkers.
RESULTS: Fecal metagenomics revealed distinct gut dysbiosis in aSAH-CI patients, characterized by reduced alpha diversity, depletion of beneficial commensals (e.g., Agathobacter), and expansion of opportunistic pathogens (e.g., Enterococcus). Functional and metabolomic analyses identified a significant alteration in aromatic amino acid biosynthesis. Specifically, tyrosine metabolism was altered, marked by reduced levels of neurotransmitter precursors and elevated neurotoxic trace amines (tyramine and phenylethylamine). Serologically, aSAH-CI patients exhibited heightened systemic inflammation, oxidative stress, and apoptosis. Integrated multi-omics network analysis underscored a strong correlation between elevated trace amines, depleted Agathobacter, and systemic pathological indices. Notably, Agathobacter rectalis and tyramine demonstrated robust potential as early diagnostic biomarkers for cognitive impairment following aSAH.
CONCLUSION: Our findings suggest a potential dual-hit correlative signature via the microbiota-gut-brain axis in cognitive impairment following aSAH. We hypothesize that the depletion of aromatic amino acid-producing microbiota correlates with reduced neurotransmitter precursors, theoretically impairing synaptic repair. Concurrently, observed associations among opportunistic pathogens, trace amines, and systemic inflammatory and oxidative stress markers suggest a synergistic effect potentially linked to further neuronal damage.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
16S rRNA sequencing and conventional culture provide complementary information in hospitalized patients with chronic lower-limb wounds.
Frontiers in cellular and infection microbiology, 16:1865385.
Chronic lower-limb wounds are polymicrobial and difficult to characterize using conventional culture alone. We compared baseline wound microbiota assessed by 16S rRNA sequencing and conventional culture in 62 hospitalized adults with chronic lower-limb wounds and examined associations with subsequent length of stay. Sequencing detected a mean of 11.62 taxa per sample versus 2.24 by culture, with an overall concordance of 51.35%. In sequencing-based analyses, alpha diversity was not associated with length of stay, whereas beta diversity differed significantly according to hospitalization duration (PERMANOVA, R[2] = 0.030, p = 0.005), and six genera were associated with length of stay. Conventional culture showed no significant association with length of stay. No significant associations were found between sequencing-derived baseline microbiota and wound thermal parameters or 12-week healing. These findings indicate that 16S rRNA sequencing and conventional culture provide distinct yet complementary views of chronic wound microbiology.
Additional Links: PMID-42682564
PubMed:
Citation:
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@article {pmid42682564,
year = {2026},
author = {Molasy, B and Rachuna, J and Wawszczak-Kasza, M and Dulębska, J and Kuszewska, K and Adamus-Białek, W},
title = {16S rRNA sequencing and conventional culture provide complementary information in hospitalized patients with chronic lower-limb wounds.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1865385},
pmid = {42682564},
issn = {2235-2988},
mesh = {Humans ; *RNA, Ribosomal, 16S/genetics ; Sequence Analysis, DNA ; Female ; Male ; Aged ; Middle Aged ; *Bacteria/classification/genetics/isolation & purification ; Microbiota ; Length of Stay ; DNA, Bacterial/genetics/chemistry ; Aged, 80 and over ; *Wound Infection/microbiology ; DNA, Ribosomal/genetics/chemistry ; Adult ; Hospitalization ; *Wounds and Injuries/microbiology ; },
abstract = {Chronic lower-limb wounds are polymicrobial and difficult to characterize using conventional culture alone. We compared baseline wound microbiota assessed by 16S rRNA sequencing and conventional culture in 62 hospitalized adults with chronic lower-limb wounds and examined associations with subsequent length of stay. Sequencing detected a mean of 11.62 taxa per sample versus 2.24 by culture, with an overall concordance of 51.35%. In sequencing-based analyses, alpha diversity was not associated with length of stay, whereas beta diversity differed significantly according to hospitalization duration (PERMANOVA, R[2] = 0.030, p = 0.005), and six genera were associated with length of stay. Conventional culture showed no significant association with length of stay. No significant associations were found between sequencing-derived baseline microbiota and wound thermal parameters or 12-week healing. These findings indicate that 16S rRNA sequencing and conventional culture provide distinct yet complementary views of chronic wound microbiology.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*RNA, Ribosomal, 16S/genetics
Sequence Analysis, DNA
Female
Male
Aged
Middle Aged
*Bacteria/classification/genetics/isolation & purification
Microbiota
Length of Stay
DNA, Bacterial/genetics/chemistry
Aged, 80 and over
*Wound Infection/microbiology
DNA, Ribosomal/genetics/chemistry
Adult
Hospitalization
*Wounds and Injuries/microbiology
RevDate: 2026-09-02
CmpDate: 2026-09-02
Predictive, Preventive and Personalized Medicine Approaches in Periodontitis: Emerging Technologies from Biomarkers to Artificial Intelligence-Driven Integrated Strategies.
The EPMA journal, 17(3):585-609.
RATIONALE AND PURPOSE: Periodontitis is a chronic multifactorial inflammatory disease linked to systemic conditions including cardiovascular disease and diabetes, underscoring the need for a holistic diagnostic approach. Current diagnostics rely on clinical probing and radiography, which detect accumulated damage rather than early biological activity or individual progression risk. This reactive paradigm delays intervention and limits personalization. Within predictive, preventive and personalized medicine (PPPM), this review examines emerging diagnostic technologies and evaluates their potential to enable a paradigm shift toward early prediction, targeted prevention, and individualized periodontal management.
WORKING HYPOTHESIS: The convergence of molecular biomarkers, advanced imaging, microbiome profiling, artificial intelligence, and smart oral technologies into a multimodal framework can support the transition from reactive care to PPPM by enabling detection of suboptimal health states before irreversible damage, continuous digital health monitoring beyond episodic visits, and AI-driven patient stratification for individualized protection against health-to-disease transition and disease progression.
Salivary and gingival crevicular fluid biomarkers detect inflammatory activity prior to clinical attachment loss, supporting early risk identification. Optical coherence tomography and Raman spectroscopy capture structural and biochemical tissue changes non-invasively. Next-generation sequencing reveals early dysbiotic shifts preceding clinical deterioration. Artificial intelligence integrates these heterogeneous datasets into patient-specific risk signatures, with recent PPPM-oriented studies confirming feasibility of automated oral health assessment. Smart oral devices extend monitoring into daily life, enabling continuous surveillance of behavioral and biochemical risk parameters.
For predictive diagnostics, biomarker panels and AI-driven analysis enable identification of preclinical disease activity and individual risk stratification. For targeted prevention, digital monitoring and wearable technologies support continuous risk surveillance and timely individualized interventions. For personalization of medical services, multimodal data integration through AI facilitates patient-specific treatment planning and adaptive care pathways. This integrative framework goes beyond technology-focused reviews by positioning emerging periodontal diagnostics within a unified PPPM paradigm, contributing to the shift from reactive care toward predictive, preventive and personalized disease management.
Additional Links: PMID-42682580
PubMed:
Citation:
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@article {pmid42682580,
year = {2026},
author = {Yaliniz, G and Tas, Z and Tasdemir, I and Unal, M},
title = {Predictive, Preventive and Personalized Medicine Approaches in Periodontitis: Emerging Technologies from Biomarkers to Artificial Intelligence-Driven Integrated Strategies.},
journal = {The EPMA journal},
volume = {17},
number = {3},
pages = {585-609},
pmid = {42682580},
issn = {1878-5077},
abstract = {RATIONALE AND PURPOSE: Periodontitis is a chronic multifactorial inflammatory disease linked to systemic conditions including cardiovascular disease and diabetes, underscoring the need for a holistic diagnostic approach. Current diagnostics rely on clinical probing and radiography, which detect accumulated damage rather than early biological activity or individual progression risk. This reactive paradigm delays intervention and limits personalization. Within predictive, preventive and personalized medicine (PPPM), this review examines emerging diagnostic technologies and evaluates their potential to enable a paradigm shift toward early prediction, targeted prevention, and individualized periodontal management.
WORKING HYPOTHESIS: The convergence of molecular biomarkers, advanced imaging, microbiome profiling, artificial intelligence, and smart oral technologies into a multimodal framework can support the transition from reactive care to PPPM by enabling detection of suboptimal health states before irreversible damage, continuous digital health monitoring beyond episodic visits, and AI-driven patient stratification for individualized protection against health-to-disease transition and disease progression.
Salivary and gingival crevicular fluid biomarkers detect inflammatory activity prior to clinical attachment loss, supporting early risk identification. Optical coherence tomography and Raman spectroscopy capture structural and biochemical tissue changes non-invasively. Next-generation sequencing reveals early dysbiotic shifts preceding clinical deterioration. Artificial intelligence integrates these heterogeneous datasets into patient-specific risk signatures, with recent PPPM-oriented studies confirming feasibility of automated oral health assessment. Smart oral devices extend monitoring into daily life, enabling continuous surveillance of behavioral and biochemical risk parameters.
For predictive diagnostics, biomarker panels and AI-driven analysis enable identification of preclinical disease activity and individual risk stratification. For targeted prevention, digital monitoring and wearable technologies support continuous risk surveillance and timely individualized interventions. For personalization of medical services, multimodal data integration through AI facilitates patient-specific treatment planning and adaptive care pathways. This integrative framework goes beyond technology-focused reviews by positioning emerging periodontal diagnostics within a unified PPPM paradigm, contributing to the shift from reactive care toward predictive, preventive and personalized disease management.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Evidence-based recommendations for advancing the chronic pelvic pain syndrome management by the paradigm change from reactive symptom suppression to proactive 3PM-guided patient-centered care.
The EPMA journal, 17(3):715-734.
Chronic pelvic pain syndrome (CPPS) encompasses a heterogeneous group of debilitating conditions including interstitial cystitis/bladder pain syndrome (IC/BPS), chronic abacterial prostatitis, endometriosis, and pelvic congestion syndrome, among others. Despite advances in symptomatic management, CPPS remains challenging due to its multifactorial etiology, complex phenotypes, and poor response to conventional reactive treatments. On the other hand, sympathetic overdrive phenotype (SOP) carriers frequently suffer from increased stress sensitivity, chronic sterile inflammation, pain chronification, and mitochondrial stress - all considered the key CPPS/SOP shared pathomechanisms. Further, the dominant vasoconstriction, altered sense regulation (e.g. the reduced feeling of thirst potentially resulting in systemic dehydration) as well as altered multi-drug resistance protein profiles characteristic for SOP (e.g. exemplified by the Flammer syndrome) may predispose affected individuals to the therapy resistance such as CPPS patients with vulvar-vaginal dryness and abacterial prostatitis. This review article highlights the central role of SOP, systemic mitochondrial stress as well as gut and urinary microbiome alterations - all, per evidence, are considered systemic modifiable risk factors of the CPPS manifestation, disease progression, and therapy resistance. The article introduces 3PM-guided patient-centered solutions aiming to improve life quality and individual outcomes in the CPPS patient cohort. Non-invasive mitochondria-based biosensorics, e.g. applied via the tear fluid analysis, and digital health monitoring, per evidence, enable early health risk assessment and patient stratification at the level of reversible damage to health. Recommended targeted preventive strategies encompass individually adapted lifestyle modifications, modulation of the stress-associated mitochondrial homeostasis, and application of supportive nutraceuticals. Personalized 3PM-guided treatment algorithms transform CPPS management into the patient-centered, cause-oriented and cost-effective proactive care, protecting vulnerable individuals against health-to-disease transition and preventing disease progression in stratified patients.
Additional Links: PMID-42682645
PubMed:
Citation:
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@article {pmid42682645,
year = {2026},
author = {Bajinka, O and Jallow, L and Li, N and Kuhn, C and Kuhn, W and Stetkarova, I and Golubnitschaja, O and Zhan, X},
title = {Evidence-based recommendations for advancing the chronic pelvic pain syndrome management by the paradigm change from reactive symptom suppression to proactive 3PM-guided patient-centered care.},
journal = {The EPMA journal},
volume = {17},
number = {3},
pages = {715-734},
pmid = {42682645},
issn = {1878-5077},
abstract = {Chronic pelvic pain syndrome (CPPS) encompasses a heterogeneous group of debilitating conditions including interstitial cystitis/bladder pain syndrome (IC/BPS), chronic abacterial prostatitis, endometriosis, and pelvic congestion syndrome, among others. Despite advances in symptomatic management, CPPS remains challenging due to its multifactorial etiology, complex phenotypes, and poor response to conventional reactive treatments. On the other hand, sympathetic overdrive phenotype (SOP) carriers frequently suffer from increased stress sensitivity, chronic sterile inflammation, pain chronification, and mitochondrial stress - all considered the key CPPS/SOP shared pathomechanisms. Further, the dominant vasoconstriction, altered sense regulation (e.g. the reduced feeling of thirst potentially resulting in systemic dehydration) as well as altered multi-drug resistance protein profiles characteristic for SOP (e.g. exemplified by the Flammer syndrome) may predispose affected individuals to the therapy resistance such as CPPS patients with vulvar-vaginal dryness and abacterial prostatitis. This review article highlights the central role of SOP, systemic mitochondrial stress as well as gut and urinary microbiome alterations - all, per evidence, are considered systemic modifiable risk factors of the CPPS manifestation, disease progression, and therapy resistance. The article introduces 3PM-guided patient-centered solutions aiming to improve life quality and individual outcomes in the CPPS patient cohort. Non-invasive mitochondria-based biosensorics, e.g. applied via the tear fluid analysis, and digital health monitoring, per evidence, enable early health risk assessment and patient stratification at the level of reversible damage to health. Recommended targeted preventive strategies encompass individually adapted lifestyle modifications, modulation of the stress-associated mitochondrial homeostasis, and application of supportive nutraceuticals. Personalized 3PM-guided treatment algorithms transform CPPS management into the patient-centered, cause-oriented and cost-effective proactive care, protecting vulnerable individuals against health-to-disease transition and preventing disease progression in stratified patients.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Fermented fruit waste as a microbiome-active soil amendment: a review of field and greenhouse evidence (2009-2025).
Frontiers in microbiology, 17:1928844.
Fruit residues generated across the global food supply chain constitute a rapidly growing, biologically reactive waste stream that, when left unmanaged, degrades environmental and agricultural quality, whereas controlled microbial fermentation offers a practical means of transforming this waste into stabilized, biologically active soil amendments. This review synthesizes evidence from field trials, greenhouse experiments, and microbiome studies published between 2009 and 2025 to evaluate the agronomic and microbiome-level effects of fermented fruit waste (FFW) as a soil amendment within circular waste-management frameworks. FFW application has been associated with increases in soil organic carbon of 12-24%, microbial biomass carbon of 38-64%, and plant biomass accumulation of 15-35% relative to unamended controls, with the magnitude of these effects varying substantially across studies according to feedstock composition, soil type, crop species, and fermentation method, rather than reflecting a single generalisable effect size. At the rhizosphere level, fermentation-derived substrates selectively recruit plant-growth-promoting rhizobacteria and phosphorus-solubilizing taxa, enhancing nutrient-use efficiency and microbial network resilience. These findings indicate that FFW functions not merely as a recycled nutrient input but as a biologically transformed amendment that actively restructures soil microbial communities and reinforces plant-soil feedback networks, while practical constraints such as phytotoxicity, salinity accumulation, pathogen survival, and feedstock contamination require evidence-based mitigation. However, standardized fermentation protocols, quantitative process-parameter thresholds, and long-term field validation remain limited, underscoring the need for future research integrating process optimization with multi-site field trials to enable reliable, microbiome-guided FFW application at scale.
Additional Links: PMID-42682646
PubMed:
Citation:
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@article {pmid42682646,
year = {2026},
author = {Kanjana, N and Zhao, Z and Fan, A and Shah, I and Ahmed, MA and Poonsawat, T},
title = {Fermented fruit waste as a microbiome-active soil amendment: a review of field and greenhouse evidence (2009-2025).},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1928844},
pmid = {42682646},
issn = {1664-302X},
abstract = {Fruit residues generated across the global food supply chain constitute a rapidly growing, biologically reactive waste stream that, when left unmanaged, degrades environmental and agricultural quality, whereas controlled microbial fermentation offers a practical means of transforming this waste into stabilized, biologically active soil amendments. This review synthesizes evidence from field trials, greenhouse experiments, and microbiome studies published between 2009 and 2025 to evaluate the agronomic and microbiome-level effects of fermented fruit waste (FFW) as a soil amendment within circular waste-management frameworks. FFW application has been associated with increases in soil organic carbon of 12-24%, microbial biomass carbon of 38-64%, and plant biomass accumulation of 15-35% relative to unamended controls, with the magnitude of these effects varying substantially across studies according to feedstock composition, soil type, crop species, and fermentation method, rather than reflecting a single generalisable effect size. At the rhizosphere level, fermentation-derived substrates selectively recruit plant-growth-promoting rhizobacteria and phosphorus-solubilizing taxa, enhancing nutrient-use efficiency and microbial network resilience. These findings indicate that FFW functions not merely as a recycled nutrient input but as a biologically transformed amendment that actively restructures soil microbial communities and reinforces plant-soil feedback networks, while practical constraints such as phytotoxicity, salinity accumulation, pathogen survival, and feedstock contamination require evidence-based mitigation. However, standardized fermentation protocols, quantitative process-parameter thresholds, and long-term field validation remain limited, underscoring the need for future research integrating process optimization with multi-site field trials to enable reliable, microbiome-guided FFW application at scale.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Diet-gut microbiota-immune-brain interactions in aging: mechanistic pathways and clinical implications.
Frontiers in molecular neuroscience, 19:1847644.
With rising life expectancy and global population aging, cognitive decline has become a major and growing public health challenge. Advances in nutritional neuroscience highlight the gut microbiota-immune-brain axis as a key biological pathway through which diet may influence cognitive function during aging. The gut microbiota, a metabolically active ecosystem, responds dynamically to habitual dietary patterns and produces bioactive metabolites capable of modulating immune signaling, neuroinflammation, and neuronal function. Diets rich in microbiota-modulating foods (e.g., dietary fiber, polyphenols, prebiotics, and probiotics) promote beneficial microbial communities. These communities support short-chain fatty acid production, maintain intestinal barrier integrity, and regulate systemic immune responses, processes increasingly associated with cognitive resilience in aging populations. In contrast, Western-style dietary patterns characterized by high intakes of saturated fats and refined sugars are linked to microbial dysbiosis, impaired gut barrier function, metabolic endotoxemia, and chronic low-grade inflammation, which may contribute to neuroinflammatory pathways involved in cognitive decline. This narrative review synthesizes evidence from observational studies, dietary intervention trials, and mechanistic animal models to examine how diet-driven alterations in gut microbiota composition and microbial metabolites interact with and modulate immune pathways to influence brain function in aging populations. Although emerging evidence supports the biological plausibility of this axis in cognitive health, current evidence remains constrained by methodological heterogeneity, short intervention durations, limited functional insight, and substantial inter-individual variability in microbiota responsiveness. In particular, much of the mechanistic understanding derives from preclinical research, while human evidence remains largely associative and insufficient to establish causal pathways. Future research should integrate longitudinal cohort designs, harmonized cognitive assessment tools, and repeated profiling of microbial and host metabolites to clarify the functional and causal links between diet, microbial metabolism, immune regulation, and brain aging. A more integrated understanding of these interactions may help inform targeted, microbiome-informed nutritional strategies for supporting healthy cognitive aging, while maintaining appropriate caution in clinical interpretation.
Additional Links: PMID-42682873
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Citation:
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@article {pmid42682873,
year = {2026},
author = {Jarfan, MA and Vimaleswaran, KS and Wijeyesekera, A},
title = {Diet-gut microbiota-immune-brain interactions in aging: mechanistic pathways and clinical implications.},
journal = {Frontiers in molecular neuroscience},
volume = {19},
number = {},
pages = {1847644},
pmid = {42682873},
issn = {1662-5099},
abstract = {With rising life expectancy and global population aging, cognitive decline has become a major and growing public health challenge. Advances in nutritional neuroscience highlight the gut microbiota-immune-brain axis as a key biological pathway through which diet may influence cognitive function during aging. The gut microbiota, a metabolically active ecosystem, responds dynamically to habitual dietary patterns and produces bioactive metabolites capable of modulating immune signaling, neuroinflammation, and neuronal function. Diets rich in microbiota-modulating foods (e.g., dietary fiber, polyphenols, prebiotics, and probiotics) promote beneficial microbial communities. These communities support short-chain fatty acid production, maintain intestinal barrier integrity, and regulate systemic immune responses, processes increasingly associated with cognitive resilience in aging populations. In contrast, Western-style dietary patterns characterized by high intakes of saturated fats and refined sugars are linked to microbial dysbiosis, impaired gut barrier function, metabolic endotoxemia, and chronic low-grade inflammation, which may contribute to neuroinflammatory pathways involved in cognitive decline. This narrative review synthesizes evidence from observational studies, dietary intervention trials, and mechanistic animal models to examine how diet-driven alterations in gut microbiota composition and microbial metabolites interact with and modulate immune pathways to influence brain function in aging populations. Although emerging evidence supports the biological plausibility of this axis in cognitive health, current evidence remains constrained by methodological heterogeneity, short intervention durations, limited functional insight, and substantial inter-individual variability in microbiota responsiveness. In particular, much of the mechanistic understanding derives from preclinical research, while human evidence remains largely associative and insufficient to establish causal pathways. Future research should integrate longitudinal cohort designs, harmonized cognitive assessment tools, and repeated profiling of microbial and host metabolites to clarify the functional and causal links between diet, microbial metabolism, immune regulation, and brain aging. A more integrated understanding of these interactions may help inform targeted, microbiome-informed nutritional strategies for supporting healthy cognitive aging, while maintaining appropriate caution in clinical interpretation.},
}
RevDate: 2026-09-02
Metal oxide nanoparticles for acne vulgaris: mechanisms, synthesis, formulation, and translational prospects.
RSC advances [Epub ahead of print].
Acne vulgaris is a chronic inflammatory condition of the pilosebaceous unit resulting from follicular hyperkeratinization, increased sebum production, overgrowth of Cutibacterium acnes, and immune activation, with subsequent activation of Toll-like receptor signalling and increased expression of IL-1β, IL-8, and matrix metalloproteinases, leading to scarring and hyperpigmentation. Conventional treatments such as topical retinoids, benzoyl peroxide, antibiotics, oral isotretinoin, and hormonal therapies are often associated with limited efficacy, slow response, irritation, photosensitivity, and poor tolerability, prompting the search for non-antibiotic strategies that preserve the microbiome. This review evaluates metal oxide nanoparticles as multifunctional agents with acne-targeted, anti-inflammatory, antioxidant, and photocatalytic activities suitable for the follicular microenvironment. The emphasis is placed on zinc oxide, titanium dioxide, copper oxide, iron oxide, magnesium oxide, cerium oxide, aluminium oxide and manganese oxide nanoparticles. The review further examines synthesis methods (physical, wet-chemical, and green plant/microbial synthesis), formulation platforms (hydrogels/nanogels, electrospun fibers, lipid carriers, microneedles, and near-infrared (NIR)-responsive nanomotors), as well as safety and regulatory aspects. Available evidence suggests that primary particle size (typically 20-70 nm), hydrodynamic aggregation (200-700 nm for follicular depots), zeta potential (-10 to -30 mV), and surface coatings (e.g., hyaluronic acid, polysaccharides, and polyethylene glycol (PEG)) significantly influence dermal fate. Metal oxide nanoparticles represent promising adjuvants and potential alternatives for the treatment of mild-to-moderate acne vulgaris and maintenance therapy, provided they are synthesized using standardized protocols, formulated through microbiome-friendly approaches, toxicologically evaluated using harmonized assessment frameworks, and validated through rigorous, adequately powered clinical trials.
Additional Links: PMID-42682944
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Citation:
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@article {pmid42682944,
year = {2026},
author = {Nair, A and S M, S and Rai, SD and Netto, G and Mutalik, S and Prabhu, PP},
title = {Metal oxide nanoparticles for acne vulgaris: mechanisms, synthesis, formulation, and translational prospects.},
journal = {RSC advances},
volume = {},
number = {},
pages = {},
pmid = {42682944},
issn = {2046-2069},
abstract = {Acne vulgaris is a chronic inflammatory condition of the pilosebaceous unit resulting from follicular hyperkeratinization, increased sebum production, overgrowth of Cutibacterium acnes, and immune activation, with subsequent activation of Toll-like receptor signalling and increased expression of IL-1β, IL-8, and matrix metalloproteinases, leading to scarring and hyperpigmentation. Conventional treatments such as topical retinoids, benzoyl peroxide, antibiotics, oral isotretinoin, and hormonal therapies are often associated with limited efficacy, slow response, irritation, photosensitivity, and poor tolerability, prompting the search for non-antibiotic strategies that preserve the microbiome. This review evaluates metal oxide nanoparticles as multifunctional agents with acne-targeted, anti-inflammatory, antioxidant, and photocatalytic activities suitable for the follicular microenvironment. The emphasis is placed on zinc oxide, titanium dioxide, copper oxide, iron oxide, magnesium oxide, cerium oxide, aluminium oxide and manganese oxide nanoparticles. The review further examines synthesis methods (physical, wet-chemical, and green plant/microbial synthesis), formulation platforms (hydrogels/nanogels, electrospun fibers, lipid carriers, microneedles, and near-infrared (NIR)-responsive nanomotors), as well as safety and regulatory aspects. Available evidence suggests that primary particle size (typically 20-70 nm), hydrodynamic aggregation (200-700 nm for follicular depots), zeta potential (-10 to -30 mV), and surface coatings (e.g., hyaluronic acid, polysaccharides, and polyethylene glycol (PEG)) significantly influence dermal fate. Metal oxide nanoparticles represent promising adjuvants and potential alternatives for the treatment of mild-to-moderate acne vulgaris and maintenance therapy, provided they are synthesized using standardized protocols, formulated through microbiome-friendly approaches, toxicologically evaluated using harmonized assessment frameworks, and validated through rigorous, adequately powered clinical trials.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Severity-stratified gut microbiome dysbiosis and systemic neuroinflammation in acute traumatic brain injury: a metagenomic and cytokine profiling study.
Frontiers in microbiology, 17:1845360.
BACKGROUND: The gut-brain axis has increasingly been implicated in the pathophysiology of traumatic brain injury (TBI). However, few human studies have simultaneously examined gut functional metagenomics and peripheral cytokine profiles across mild to moderate-to-severe TBI, which limits our understanding of how gut health may influence recovery outcomes in TBI patients.
METHODS: This cross-sectional case-control investigation involved the collection of fecal and matched serum samples within 7 days post-injury from 60 mild TBI patients (MT; GCS 13-15), 45 moderate-to-severe TBI patients (MST; GCS ≤ 12), and 113 healthy controls (HC). Shotgun metagenomic sequencing examined gut microbiota. Serum IL-1β, IL-6, IL-8, and TNF-α were measured using a 4-plex Luminex test. Spearman correlation was utilized to construct a hypothesis relating cytokine levels to microbial severity-stratified abundance patterns.
RESULTS: TBI was associated with severity-dependent remodeling of the gut microbiota. Alpha diversity decreased from HC to MST (p < 10[-6]), and community structure varied significantly among all three groups (PERMANOVA, p = 0.001). Serum TNF-α increased in a severity-associated manner (MST vs. HC and MT, p adj < 0.015). Among 332 differentially abundant species, butyrate-producing commensals fell abruptly at MT with no additional decline in MST, suggesting an apparent floor-like pattern rather than confirming a true biological floor effect. For example, Faecalibacterium prausnitzii dropped from 9.02% in HC to 4.29% in MT. In terms of function, metagenomic inference indicated that pathways for fermentative metabolism and short-chain fatty acid (SCFA) biosynthesis were largely suppressed, suggesting a predicted reduction in microbial SCFA production capacity. On the other hand, secondary bile acid synthesis was specifically increased in MST-dominant KOs (85%). Systemically, reduced commensals showed weak, directionally consistent correlations with pro-inflammatory cytokines (|ρ| = 0.16-0.25), although none of the species-cytokine associations survived FDR correction.
CONCLUSION: Acute TBI is associated with severity-specific gut dysbiosis, which is accompanied by systemic neuroinflammation. The early reduction of butyrate-producing taxa in mild TBI suggests that the early post-injury period may represent a potential window for future gut-targeted intervention studies.
Additional Links: PMID-42682993
PubMed:
Citation:
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@article {pmid42682993,
year = {2026},
author = {Wang, Y and Zhang, Y and Li, C and Liu, R and Zhang, S},
title = {Severity-stratified gut microbiome dysbiosis and systemic neuroinflammation in acute traumatic brain injury: a metagenomic and cytokine profiling study.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1845360},
pmid = {42682993},
issn = {1664-302X},
abstract = {BACKGROUND: The gut-brain axis has increasingly been implicated in the pathophysiology of traumatic brain injury (TBI). However, few human studies have simultaneously examined gut functional metagenomics and peripheral cytokine profiles across mild to moderate-to-severe TBI, which limits our understanding of how gut health may influence recovery outcomes in TBI patients.
METHODS: This cross-sectional case-control investigation involved the collection of fecal and matched serum samples within 7 days post-injury from 60 mild TBI patients (MT; GCS 13-15), 45 moderate-to-severe TBI patients (MST; GCS ≤ 12), and 113 healthy controls (HC). Shotgun metagenomic sequencing examined gut microbiota. Serum IL-1β, IL-6, IL-8, and TNF-α were measured using a 4-plex Luminex test. Spearman correlation was utilized to construct a hypothesis relating cytokine levels to microbial severity-stratified abundance patterns.
RESULTS: TBI was associated with severity-dependent remodeling of the gut microbiota. Alpha diversity decreased from HC to MST (p < 10[-6]), and community structure varied significantly among all three groups (PERMANOVA, p = 0.001). Serum TNF-α increased in a severity-associated manner (MST vs. HC and MT, p adj < 0.015). Among 332 differentially abundant species, butyrate-producing commensals fell abruptly at MT with no additional decline in MST, suggesting an apparent floor-like pattern rather than confirming a true biological floor effect. For example, Faecalibacterium prausnitzii dropped from 9.02% in HC to 4.29% in MT. In terms of function, metagenomic inference indicated that pathways for fermentative metabolism and short-chain fatty acid (SCFA) biosynthesis were largely suppressed, suggesting a predicted reduction in microbial SCFA production capacity. On the other hand, secondary bile acid synthesis was specifically increased in MST-dominant KOs (85%). Systemically, reduced commensals showed weak, directionally consistent correlations with pro-inflammatory cytokines (|ρ| = 0.16-0.25), although none of the species-cytokine associations survived FDR correction.
CONCLUSION: Acute TBI is associated with severity-specific gut dysbiosis, which is accompanied by systemic neuroinflammation. The early reduction of butyrate-producing taxa in mild TBI suggests that the early post-injury period may represent a potential window for future gut-targeted intervention studies.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Molecular mechanism of gut microbiota regulation in skeletal muscle metabolic remodeling and meat quality trait formation in livestock and poultry: a review.
Frontiers in microbiology, 17:1896270.
Meat quality is a major determinant of consumer acceptance and economic value, as meat serves as a primary source of high quality protein and essential micronutrients. The formation of meat is a highly complex biological process orchestrated by genetic background, nutritional regulation, and microbial modulation. Recent advances in sequencing technologies and microbiome research have elucidated the regulatory role of the gut microbiota in skeletal muscle metabolism and meat quality via the gut-muscle axis. This review comprehensively synthesizes variations in the gut microbiota of livestock and poultry, highlighting their associations with key meat quality traits such as color, water-holding capacity, tenderness, flavor, and fat deposition. We critically examine how the gut microbiota influences skeletal muscle metabolism and meat formation through the modulation of lipid, glucose, and protein metabolism, alongside muscle fiber characteristics. Furthermore, we review major microbial-derived mediators and signaling pathways integral to gut-muscle crosstalk-specifically short-chain fatty acids, bile acids, amino acids, and vitamins-and discuss how microbial homeostasis or dysbiosis impacts muscle mass and function via inflammatory, oxidative, and hormonal mechanisms. Collectively, these insights clarify potential mechanisms underlying the gut microbiota and muscle axis in animals. Consequently, this review provides a robust theoretical framework for future mechanistic studies and offers practical guidance for developing microbiota-targeted strategies to enhance muscle health and meat quality in livestock and poultry production systems.
Additional Links: PMID-42683199
PubMed:
Citation:
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@article {pmid42683199,
year = {2026},
author = {Han, L and Huang, X and Chen, Q and Zhi, R and Li, S and Peng, Q and Li, H and Peng, Z and Qi, M and Fu, R and Qiao, Y},
title = {Molecular mechanism of gut microbiota regulation in skeletal muscle metabolic remodeling and meat quality trait formation in livestock and poultry: a review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1896270},
pmid = {42683199},
issn = {1664-302X},
abstract = {Meat quality is a major determinant of consumer acceptance and economic value, as meat serves as a primary source of high quality protein and essential micronutrients. The formation of meat is a highly complex biological process orchestrated by genetic background, nutritional regulation, and microbial modulation. Recent advances in sequencing technologies and microbiome research have elucidated the regulatory role of the gut microbiota in skeletal muscle metabolism and meat quality via the gut-muscle axis. This review comprehensively synthesizes variations in the gut microbiota of livestock and poultry, highlighting their associations with key meat quality traits such as color, water-holding capacity, tenderness, flavor, and fat deposition. We critically examine how the gut microbiota influences skeletal muscle metabolism and meat formation through the modulation of lipid, glucose, and protein metabolism, alongside muscle fiber characteristics. Furthermore, we review major microbial-derived mediators and signaling pathways integral to gut-muscle crosstalk-specifically short-chain fatty acids, bile acids, amino acids, and vitamins-and discuss how microbial homeostasis or dysbiosis impacts muscle mass and function via inflammatory, oxidative, and hormonal mechanisms. Collectively, these insights clarify potential mechanisms underlying the gut microbiota and muscle axis in animals. Consequently, this review provides a robust theoretical framework for future mechanistic studies and offers practical guidance for developing microbiota-targeted strategies to enhance muscle health and meat quality in livestock and poultry production systems.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Significant impact of threshold adjustments on microbiome characterization following Nanopore sequencing.
ISME communications, 6(1):ycag219.
Sequencing the full-length 16S rRNA gene is essential for improving the taxonomic resolution of bacterial identification. Long-read Oxford Nanopore Technologies (ONT) sequencing, coupled with its real-time analysis platform EPI2ME, has become increasingly competitive in microbial community profiling studies. However, the impact of threshold settings in EPI2ME Agent on the alignment-based confidence (hereafter "Alignment accuracy") and the proportion of reads successfully assigned to a taxon (hereafter "Classification success") has not yet been systematically evaluated. In this study, we performed ONT-based full-length 16S rRNA gene sequencing on samples collected from eggshells of wild Oriental Tits (Parus minor). By adjusting different threshold settings in the EPI2ME Agent, we examined how filtering conditions affect Alignment accuracy, Classification success, and downstream microbiome diversity analysis. Our results revealed that filtering thresholds had substantial effects on these outputs. These findings highlight the importance of carefully selecting filtering parameters in the EPI2ME Agent to balance alignment accuracy and classification success, and to improve the interpretability and consistency of taxonomic profiles generated from ONT sequencing data.
Additional Links: PMID-42683226
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Citation:
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@article {pmid42683226,
year = {2026},
author = {Fu, M and Yoon, Y and Cho, H and Jablonski, PG and Lee, SI and Choe, JC},
title = {Significant impact of threshold adjustments on microbiome characterization following Nanopore sequencing.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag219},
pmid = {42683226},
issn = {2730-6151},
abstract = {Sequencing the full-length 16S rRNA gene is essential for improving the taxonomic resolution of bacterial identification. Long-read Oxford Nanopore Technologies (ONT) sequencing, coupled with its real-time analysis platform EPI2ME, has become increasingly competitive in microbial community profiling studies. However, the impact of threshold settings in EPI2ME Agent on the alignment-based confidence (hereafter "Alignment accuracy") and the proportion of reads successfully assigned to a taxon (hereafter "Classification success") has not yet been systematically evaluated. In this study, we performed ONT-based full-length 16S rRNA gene sequencing on samples collected from eggshells of wild Oriental Tits (Parus minor). By adjusting different threshold settings in the EPI2ME Agent, we examined how filtering conditions affect Alignment accuracy, Classification success, and downstream microbiome diversity analysis. Our results revealed that filtering thresholds had substantial effects on these outputs. These findings highlight the importance of carefully selecting filtering parameters in the EPI2ME Agent to balance alignment accuracy and classification success, and to improve the interpretability and consistency of taxonomic profiles generated from ONT sequencing data.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Non-nutritive sweeteners, the gut microbiome, and tumor immunity: evidence hierarchy and a sucralose-centered translational model.
Frontiers in nutrition, 13:1868431.
Non-nutritive sweeteners (NNS) are widely used sugar substitutes and constitute heterogeneous dietary and non-dietary exposures. Human gut microbiota findings vary by sweetener identity, purified compound versus commercial formulation, carrier ingredients, dose, duration, host background, and analytical method. Purified compounds and commercial formulations are therefore biologically non-equivalent. A structured narrative search of PubMed, Embase, and the Web of Science Core Collection was conducted from database inception through 17 July 2026 without language restrictions. Evidence was organized by directness to the clinical question and translational distance. Direct human evidence relating NNS exposure to immune checkpoint inhibitor (ICI) outcomes remains observational and sucralose-centered. Experimental evidence for gut microbiota involvement, arginine-related mediation, and reversibility derives mainly from preclinical models; comparable class-wide evidence is lacking. No prospective evidence currently supports NNS-specific dietary modification during immune checkpoint inhibitor therapy. Validation requires prospective, sweetener-specific exposure assessment integrated with gut microbiota, metabolomic, and immune profiling.
Additional Links: PMID-42683394
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Citation:
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@article {pmid42683394,
year = {2026},
author = {Li, J and Li, DH and Liu, YH and Zhang, YP and Guo, QQ and Zhu, XJ and Wang, YR and Shi, YQ},
title = {Non-nutritive sweeteners, the gut microbiome, and tumor immunity: evidence hierarchy and a sucralose-centered translational model.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1868431},
pmid = {42683394},
issn = {2296-861X},
abstract = {Non-nutritive sweeteners (NNS) are widely used sugar substitutes and constitute heterogeneous dietary and non-dietary exposures. Human gut microbiota findings vary by sweetener identity, purified compound versus commercial formulation, carrier ingredients, dose, duration, host background, and analytical method. Purified compounds and commercial formulations are therefore biologically non-equivalent. A structured narrative search of PubMed, Embase, and the Web of Science Core Collection was conducted from database inception through 17 July 2026 without language restrictions. Evidence was organized by directness to the clinical question and translational distance. Direct human evidence relating NNS exposure to immune checkpoint inhibitor (ICI) outcomes remains observational and sucralose-centered. Experimental evidence for gut microbiota involvement, arginine-related mediation, and reversibility derives mainly from preclinical models; comparable class-wide evidence is lacking. No prospective evidence currently supports NNS-specific dietary modification during immune checkpoint inhibitor therapy. Validation requires prospective, sweetener-specific exposure assessment integrated with gut microbiota, metabolomic, and immune profiling.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Integrating metagenome-scale metabolic models and metabolomics to explore candidate biochemical interactions in cultivated Microcystis phycospheres.
ISME communications, 6(1):ycag226.
Favored by global changes, freshwater cyanobacterial harmful blooms generate major ecological, economic, and public health challenges. Microcystis, one of the most widespread cyanobacterial genera, grows within a phycosphere where specialized interactions with its microbiome occur, that are suspected to influence bloom appearance and its potential toxicity. Using a combination of metagenomics, metabolomics, and metabolic modeling, we characterized the culture-associated phycospheres of 12 Microcystis strains isolated from a French pond. The distribution of metabolic reactions within Microcystis was consistent with their genospecies, whereas the metabolic landscape at the community level diverged from cyanobacterial phylogeny, indicating partial functional decoupling between cyanobacteria and their associated microbiomes. Bacteria associated with the simplified phycospheres substantially expanded the metabolic repertoire of the system, while maintaining functional redundancy within and across communities. On the other hand, endometabolomic profiles were largely driven by cyanobacterial metabolic outputs, whereas exometabolomic analysis did not reveal metabolites involved in exchange processes. Metabolic modeling, together with the identification of toxic specialized metabolites produced by specific biosynthetic gene clusters, further highlighted differences in metabolic potential among phycospheres. Together, these findings deepen the understanding of Microcystis' phycosphere functioning and demonstrate the value of multi-omics systems biology approaches, while suggesting that metabolic complementarity between species and across phycospheres could play a role in bloom-associated microbiome structure.
Additional Links: PMID-42683437
PubMed:
Citation:
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@article {pmid42683437,
year = {2026},
author = {Audemard, J and Creusot, N and Leloup, J and Duval, C and Halary, S and Mary, L and Eon, M and Forjonel, T and Mouffok, M and Puppo, R and Belmonte, E and Gautier, V and Got, J and Lefebvre, M and Markov, GV and Muller, C and Marie, B and Diémé, B and Frioux, C},
title = {Integrating metagenome-scale metabolic models and metabolomics to explore candidate biochemical interactions in cultivated Microcystis phycospheres.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag226},
pmid = {42683437},
issn = {2730-6151},
abstract = {Favored by global changes, freshwater cyanobacterial harmful blooms generate major ecological, economic, and public health challenges. Microcystis, one of the most widespread cyanobacterial genera, grows within a phycosphere where specialized interactions with its microbiome occur, that are suspected to influence bloom appearance and its potential toxicity. Using a combination of metagenomics, metabolomics, and metabolic modeling, we characterized the culture-associated phycospheres of 12 Microcystis strains isolated from a French pond. The distribution of metabolic reactions within Microcystis was consistent with their genospecies, whereas the metabolic landscape at the community level diverged from cyanobacterial phylogeny, indicating partial functional decoupling between cyanobacteria and their associated microbiomes. Bacteria associated with the simplified phycospheres substantially expanded the metabolic repertoire of the system, while maintaining functional redundancy within and across communities. On the other hand, endometabolomic profiles were largely driven by cyanobacterial metabolic outputs, whereas exometabolomic analysis did not reveal metabolites involved in exchange processes. Metabolic modeling, together with the identification of toxic specialized metabolites produced by specific biosynthetic gene clusters, further highlighted differences in metabolic potential among phycospheres. Together, these findings deepen the understanding of Microcystis' phycosphere functioning and demonstrate the value of multi-omics systems biology approaches, while suggesting that metabolic complementarity between species and across phycospheres could play a role in bloom-associated microbiome structure.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Protease-serpin-microbiome interactions in inflammatory bowel disease: toward integrated biomarkers of gut health.
Gut microbes, 18(1):2726641.
Proteolytic imbalance involving host and microbial serine proteases and their inhibitors (serpins) contributes to intestinal barrier disruption and chronic inflammation in inflammatory bowel disease (IBD). However, the interplay among these components remains insufficiently characterized. Here, we survey 13,304 publications over five decades, to map protease-serpin-microbiome literature in IBD. Our analysis reveals a fragmented literature structure, with uneven coverage and limited cross-domain integration among host proteases, microbial proteases, and inhibitory pathways. We synthesize evidence linking these components to intestinal barrier integrity, mucosal immunity, extracellular-matrix remodeling, and microbial ecology. Considering the protease-serpin-microbiome axis may provide an integrative direction for future studies of IBD pathogenesis, including the investigation of mechanisms underlying disease heterogeneity, prioritizing future biomarker and therapeutic studies.
Additional Links: PMID-42683650
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PubMed:
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@article {pmid42683650,
year = {2026},
author = {Almalki, M and De Pierri, CR and Méric, T and Mkaouar, H and Slimani, D and Mariaule, V and Tebassi, S and Akermi, N and Maguin, E and Hernandez, J and Raittz, RT and Rhimi, M and Asnicar, F},
title = {Protease-serpin-microbiome interactions in inflammatory bowel disease: toward integrated biomarkers of gut health.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2726641},
doi = {10.1080/19490976.2026.2726641},
pmid = {42683650},
issn = {1949-0984},
mesh = {Humans ; *Inflammatory Bowel Diseases/microbiology/metabolism/immunology ; *Serpins/metabolism ; Biomarkers/metabolism ; Intestinal Barrier Function ; *Gastrointestinal Microbiome ; Animals ; *Peptide Hydrolases/metabolism ; Intestinal Mucosa/microbiology/metabolism/immunology ; Bacteria/enzymology/classification/genetics/metabolism/isolation & purification ; *Serine Proteases/metabolism ; Immunity, Mucosal ; },
abstract = {Proteolytic imbalance involving host and microbial serine proteases and their inhibitors (serpins) contributes to intestinal barrier disruption and chronic inflammation in inflammatory bowel disease (IBD). However, the interplay among these components remains insufficiently characterized. Here, we survey 13,304 publications over five decades, to map protease-serpin-microbiome literature in IBD. Our analysis reveals a fragmented literature structure, with uneven coverage and limited cross-domain integration among host proteases, microbial proteases, and inhibitory pathways. We synthesize evidence linking these components to intestinal barrier integrity, mucosal immunity, extracellular-matrix remodeling, and microbial ecology. Considering the protease-serpin-microbiome axis may provide an integrative direction for future studies of IBD pathogenesis, including the investigation of mechanisms underlying disease heterogeneity, prioritizing future biomarker and therapeutic studies.},
}
MeSH Terms:
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Humans
*Inflammatory Bowel Diseases/microbiology/metabolism/immunology
*Serpins/metabolism
Biomarkers/metabolism
Intestinal Barrier Function
*Gastrointestinal Microbiome
Animals
*Peptide Hydrolases/metabolism
Intestinal Mucosa/microbiology/metabolism/immunology
Bacteria/enzymology/classification/genetics/metabolism/isolation & purification
*Serine Proteases/metabolism
Immunity, Mucosal
RevDate: 2026-09-02
CmpDate: 2026-09-02
Metagenome-scale modeling to assess microbiome metabolic complementarity for precision microbiota transplantation therapies.
Gut microbes, 18(1):2725403.
Fecal microbiota transplantation (FMT) holds therapeutic promise beyond recurrent Clostridioides difficile infection, but clinical outcomes remain unpredictable and donor-selection strategies remain limited, in part because the role of donor‒recipient metabolic interactions in shaping the post-FMT community remains poorly understood. Here, we leverage metagenome-scale metabolic modeling to quantify metabolic niche complementarity between donor and recipient microbiomes and predict post-FMT community composition. Using MICOM-derived metabolic models, we show that donor genomes whose metabolic flux profiles are more dissimilar from the recipient community colonize at significantly higher rates in a murine FMT model. In a human IBS trial, the same metric predicted post-FMT community composition via leave-one-out cross-validation and captured known disease-associated alterations in short-chain fatty acid, sulfur, and gas metabolism. We then performed 2,548 in silico FMT simulations between IBS-D/M patients and donors from the OpenBiome biobank to evaluate personalized donor screening, identifying super-donors characterized by high taxonomic diversity, broad metabolic niche coverage, and community interaction networks dominated by cross-feeding rather than competition. Together, these results support metabolic niche complementarity as a potential determinant of post-FMT community composition and provide a mechanistic basis for evaluating donor-recipient metabolic compatibility. This framework offers a scalable approach for generating testable hypotheses for personalized donor selection.
Additional Links: PMID-42683728
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PubMed:
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@article {pmid42683728,
year = {2026},
author = {Zhang, Z and Holton, M and Ferrer, DM and Tripp, AD and Richter, A and Dixit, PD and Urtecho, G},
title = {Metagenome-scale modeling to assess microbiome metabolic complementarity for precision microbiota transplantation therapies.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2725403},
doi = {10.1080/19490976.2026.2725403},
pmid = {42683728},
issn = {1949-0984},
mesh = {*Fecal Microbiota Transplantation ; Humans ; Animals ; *Metagenome ; Mice ; *Gastrointestinal Microbiome ; *Bacteria/classification/genetics/metabolism/isolation & purification ; Feces/microbiology ; Irritable Bowel Syndrome/therapy/microbiology ; Computer Simulation ; },
abstract = {Fecal microbiota transplantation (FMT) holds therapeutic promise beyond recurrent Clostridioides difficile infection, but clinical outcomes remain unpredictable and donor-selection strategies remain limited, in part because the role of donor‒recipient metabolic interactions in shaping the post-FMT community remains poorly understood. Here, we leverage metagenome-scale metabolic modeling to quantify metabolic niche complementarity between donor and recipient microbiomes and predict post-FMT community composition. Using MICOM-derived metabolic models, we show that donor genomes whose metabolic flux profiles are more dissimilar from the recipient community colonize at significantly higher rates in a murine FMT model. In a human IBS trial, the same metric predicted post-FMT community composition via leave-one-out cross-validation and captured known disease-associated alterations in short-chain fatty acid, sulfur, and gas metabolism. We then performed 2,548 in silico FMT simulations between IBS-D/M patients and donors from the OpenBiome biobank to evaluate personalized donor screening, identifying super-donors characterized by high taxonomic diversity, broad metabolic niche coverage, and community interaction networks dominated by cross-feeding rather than competition. Together, these results support metabolic niche complementarity as a potential determinant of post-FMT community composition and provide a mechanistic basis for evaluating donor-recipient metabolic compatibility. This framework offers a scalable approach for generating testable hypotheses for personalized donor selection.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Fecal Microbiota Transplantation
Humans
Animals
*Metagenome
Mice
*Gastrointestinal Microbiome
*Bacteria/classification/genetics/metabolism/isolation & purification
Feces/microbiology
Irritable Bowel Syndrome/therapy/microbiology
Computer Simulation
RevDate: 2026-09-02
Microbiome and Metabolomics in Obesity: Advances in Understanding and Interventions Across the Lifespan.
Obesity reviews : an official journal of the International Association for the Study of Obesity [Epub ahead of print].
Obesity arises from intertwined and reciprocal diet-microbiome-host pathways that reshape energy balance, insulin sensitivity, and inflammation. This review synthesizes mechanistic links between microbial functions and metabolic control, charts lifestyle-related lifecourse dynamics from birth to older age, examines how GLP-1-based therapies may perturb gut ecology and metabolite output and surveys AI/ML frameworks for multi-omics integration. Plant-based, fiber-rich dietary patterns generally enrich saccharolytic guilds, boost SCFAs production, and modulate bile acid signaling, whereas Westernized patterns favor bile-tolerant, amino acid-fermenting consortia and proinflammatory metabolites. Preclinical data suggest that incretin-based therapies remodel the microbiome-metabolome axis, but human causal mediation remains unproven and observed changes may partly reflect weight loss or metabolic improvement. Function-centered metrics outperform phylum-level ratios for translation. Harmonized longitudinal cohorts and explainable ML-derived microbial and metabolomic signatures are now pivotal to identify responder subtypes and actionable microbe-metabolite targets, enabling precision nutrition alongside pharmacotherapy across the lifespan.
Additional Links: PMID-42683734
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PubMed:
Citation:
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@article {pmid42683734,
year = {2026},
author = {Kalafati, IP and Krongauz, D and Bosco, A and Noto, A and Piras, C and Kafyra, M and Dessì, A and Mauri, M and Atzori, L and Weinberger, A and Fanos, V and Dedoussis, GV and , },
title = {Microbiome and Metabolomics in Obesity: Advances in Understanding and Interventions Across the Lifespan.},
journal = {Obesity reviews : an official journal of the International Association for the Study of Obesity},
volume = {},
number = {},
pages = {e70220},
doi = {10.1111/obr.70220},
pmid = {42683734},
issn = {1467-789X},
support = {101080117//European Union's Horizon Europe Research and Innovation programme/ ; 10093560//UK Research and Innovation/ ; 10106435//UK Research and Innovation/ ; //Swiss State Secretariat for Education, Research and Innovation/ ; },
abstract = {Obesity arises from intertwined and reciprocal diet-microbiome-host pathways that reshape energy balance, insulin sensitivity, and inflammation. This review synthesizes mechanistic links between microbial functions and metabolic control, charts lifestyle-related lifecourse dynamics from birth to older age, examines how GLP-1-based therapies may perturb gut ecology and metabolite output and surveys AI/ML frameworks for multi-omics integration. Plant-based, fiber-rich dietary patterns generally enrich saccharolytic guilds, boost SCFAs production, and modulate bile acid signaling, whereas Westernized patterns favor bile-tolerant, amino acid-fermenting consortia and proinflammatory metabolites. Preclinical data suggest that incretin-based therapies remodel the microbiome-metabolome axis, but human causal mediation remains unproven and observed changes may partly reflect weight loss or metabolic improvement. Function-centered metrics outperform phylum-level ratios for translation. Harmonized longitudinal cohorts and explainable ML-derived microbial and metabolomic signatures are now pivotal to identify responder subtypes and actionable microbe-metabolite targets, enabling precision nutrition alongside pharmacotherapy across the lifespan.},
}
RevDate: 2026-09-02
Penicillium-mediated toxicity and microbial dysbiosis are associated with fruiting body abortion in artificially cultivated Chinese cordyceps.
Virulence [Epub ahead of print].
Chinese cordyceps consists of fruiting body and sclerotia (larvae part) formed through the parasitism of the insect Hepialidae by the fungus Ophiocordyceps sinensis, but artificial cultivation is hindered by fruiting body abortion, severely impacting yield and quality. The interactions between the fungus, its host insects, and soil are critical for its development. Multi-omics analyses were conducted to compare normally and abnormally developing samples, examining microbial communities and metabolites in fungus-colonized host larvae and the mycosphere soil. Abnormal fruiting body development was associated with profound shifts in microbial ecology: fungal diversity increased significantly in both endophytic larvae and mycosphere soil, whereas bacterial diversity decreased within host larvae. The microbial composition in and around abnormal samples was markedly altered, characterized by a high enrichment of Penicillium fungi and a depletion of Bacillus bacteria. Cross-kingdom microbial network analysis showed fewer connections and lower stability in abnormally developing samples. Untargeted metabolomic profiling revealed significant accumulation of the antibiotics N1-hydroxy-roquefortine C and glandicoline A, both roquefortine C derivatives characteristic of Penicillium metabolism, along with enriched pathways involved in antibiotic biosynthesis. Exploratory Partial Least Squares Structural Equation Modeling (PLS-SEM) analysis supported an associative pathway in which Penicillium-mediated toxicity is correlated with microbial dysbiosis, which in turn is associated with fruiting body abortion. Conversely, Bacillus may play a critical role in suppressing Penicillium overgrowth and maintaining microbial homeostasis, representing a promising target for biocontrol strategies. This study is the first to reveal potential links between Penicillium‑mediated toxicity, microbial imbalance, and developmental disorders of Chinese cordyceps.
Additional Links: PMID-42683775
Publisher:
PubMed:
Citation:
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@article {pmid42683775,
year = {2026},
author = {Bao, X and Wang, R and Qian, X and Wang, Y and Li, T and Wang, Q and Liu, S and Niu, S and Guo, J},
title = {Penicillium-mediated toxicity and microbial dysbiosis are associated with fruiting body abortion in artificially cultivated Chinese cordyceps.},
journal = {Virulence},
volume = {},
number = {},
pages = {2728527},
doi = {10.1080/21505594.2026.2728527},
pmid = {42683775},
issn = {2150-5608},
abstract = {Chinese cordyceps consists of fruiting body and sclerotia (larvae part) formed through the parasitism of the insect Hepialidae by the fungus Ophiocordyceps sinensis, but artificial cultivation is hindered by fruiting body abortion, severely impacting yield and quality. The interactions between the fungus, its host insects, and soil are critical for its development. Multi-omics analyses were conducted to compare normally and abnormally developing samples, examining microbial communities and metabolites in fungus-colonized host larvae and the mycosphere soil. Abnormal fruiting body development was associated with profound shifts in microbial ecology: fungal diversity increased significantly in both endophytic larvae and mycosphere soil, whereas bacterial diversity decreased within host larvae. The microbial composition in and around abnormal samples was markedly altered, characterized by a high enrichment of Penicillium fungi and a depletion of Bacillus bacteria. Cross-kingdom microbial network analysis showed fewer connections and lower stability in abnormally developing samples. Untargeted metabolomic profiling revealed significant accumulation of the antibiotics N1-hydroxy-roquefortine C and glandicoline A, both roquefortine C derivatives characteristic of Penicillium metabolism, along with enriched pathways involved in antibiotic biosynthesis. Exploratory Partial Least Squares Structural Equation Modeling (PLS-SEM) analysis supported an associative pathway in which Penicillium-mediated toxicity is correlated with microbial dysbiosis, which in turn is associated with fruiting body abortion. Conversely, Bacillus may play a critical role in suppressing Penicillium overgrowth and maintaining microbial homeostasis, representing a promising target for biocontrol strategies. This study is the first to reveal potential links between Penicillium‑mediated toxicity, microbial imbalance, and developmental disorders of Chinese cordyceps.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Non-antibiotic treatments for the management of recurrent urinary tract infection in the multidrug resistance era: A narrative review.
Investigative and clinical urology, 67(5):403-412.
Recurrent urinary tract infections (UTIs) are a significant global health burden, increasingly complicated by antibiotic resistance. Traditional approaches with antibiotics increase the risk of multidrug-resistant (MDR) strains, emphasizing the need for new non-antibiotic treatments. Several promising approaches have emerged during the last decade. Microbiome-based therapies, including probiotics, asymptomatic bacteriuria strains, and fecal microbiota transplantation, aim to restore microbial balance. Immunomodulation, through cytokine targeting and bacterial vaccines, shows potential for boosting host defenses. Bacteriophage therapy offers precision targeting of MDR pathogens and biofilms. Nanoparticles enable targeted delivery and biofilm disruption through both organic and inorganic carriers. Additionally, agents like methenamine hippurate, D-mannose, estrogen, and cranberry extracts have shown varying degrees of efficacy and safety. These strategies represent essential steps toward sustainable UTI management, but most will require further clinical validation before their use in the general population.
Additional Links: PMID-42683852
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PubMed:
Citation:
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@article {pmid42683852,
year = {2026},
author = {Kim, DS and Choi, CI and Choi, JB and Choi, T and Lee, JW},
title = {Non-antibiotic treatments for the management of recurrent urinary tract infection in the multidrug resistance era: A narrative review.},
journal = {Investigative and clinical urology},
volume = {67},
number = {5},
pages = {403-412},
doi = {10.4111/icu.20250655},
pmid = {42683852},
issn = {2466-054X},
mesh = {Humans ; *Urinary Tract Infections/therapy/microbiology ; Recurrence ; *Drug Resistance, Multiple, Bacterial ; Phage Therapy ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Vaccinium macrocarpon ; Biofilms ; Mannose/therapeutic use ; Microbiota ; Plant Extracts/therapeutic use ; Nanoparticles/therapeutic use ; Estrogens/therapeutic use ; },
abstract = {Recurrent urinary tract infections (UTIs) are a significant global health burden, increasingly complicated by antibiotic resistance. Traditional approaches with antibiotics increase the risk of multidrug-resistant (MDR) strains, emphasizing the need for new non-antibiotic treatments. Several promising approaches have emerged during the last decade. Microbiome-based therapies, including probiotics, asymptomatic bacteriuria strains, and fecal microbiota transplantation, aim to restore microbial balance. Immunomodulation, through cytokine targeting and bacterial vaccines, shows potential for boosting host defenses. Bacteriophage therapy offers precision targeting of MDR pathogens and biofilms. Nanoparticles enable targeted delivery and biofilm disruption through both organic and inorganic carriers. Additionally, agents like methenamine hippurate, D-mannose, estrogen, and cranberry extracts have shown varying degrees of efficacy and safety. These strategies represent essential steps toward sustainable UTI management, but most will require further clinical validation before their use in the general population.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Urinary Tract Infections/therapy/microbiology
Recurrence
*Drug Resistance, Multiple, Bacterial
Phage Therapy
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Vaccinium macrocarpon
Biofilms
Mannose/therapeutic use
Microbiota
Plant Extracts/therapeutic use
Nanoparticles/therapeutic use
Estrogens/therapeutic use
RevDate: 2026-09-02
CmpDate: 2026-09-02
Perioperative Modulation of the Gut-Liver Axis in Liver Surgery: Clinical Evidence and Future Directions.
Journal of visualized experiments : JoVE.
Liver resection and liver transplantation remain cornerstone treatments for many hepatobiliary diseases, yet postoperative infection, impaired liver regeneration, and post-hepatectomy liver failure (PHLF) remain serious complications. Perioperative stressors can disrupt the gut-liver axis by altering the intestinal microbiota, epithelial barrier integrity, microbial metabolites, bile acid signaling, and host immunity. This review examines how these alterations relate to clinical outcomes and evaluates evidence for microbiota-targeted interventions, including probiotics, synbiotics, nutritional optimization, antibiotic stewardship, bile acid modulation, and emerging multiomics strategies. We distinguish liver resection from living-donor and deceased-donor liver transplantation because the patient populations, graft or remnant anatomy, ischemia-reperfusion exposures, immune status, and outcome definitions differ. Clinical evidence most consistently supports selected pro-/synbiotic strategies for reducing postoperative infection in higher-risk settings, whereas microbiome-based prediction of PHLF, fecal microbiota transplantation (FMT), bile acid-directed therapy, and precision multiomics-guided pathways remain investigational. Future work should use transparent literature identification, standardized perioperative protocols, risk-defined populations, external validation, and prospective multicenter trials. A better understanding of gut-liver interactions may help preserve beneficial host-microbial signals while limiting translocation and inflammation during recovery.
Additional Links: PMID-42683887
Publisher:
PubMed:
Citation:
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@article {pmid42683887,
year = {2026},
author = {Sun, Y and Jiao, Y and Liu, WC},
title = {Perioperative Modulation of the Gut-Liver Axis in Liver Surgery: Clinical Evidence and Future Directions.},
journal = {Journal of visualized experiments : JoVE},
volume = {},
number = {235},
pages = {},
doi = {10.3791/73747},
pmid = {42683887},
issn = {1940-087X},
mesh = {Humans ; *Liver/surgery/microbiology/metabolism ; *Gastrointestinal Microbiome/physiology ; *Hepatectomy/methods ; Liver Transplantation/methods ; *Perioperative Care/methods ; Multiomics ; },
abstract = {Liver resection and liver transplantation remain cornerstone treatments for many hepatobiliary diseases, yet postoperative infection, impaired liver regeneration, and post-hepatectomy liver failure (PHLF) remain serious complications. Perioperative stressors can disrupt the gut-liver axis by altering the intestinal microbiota, epithelial barrier integrity, microbial metabolites, bile acid signaling, and host immunity. This review examines how these alterations relate to clinical outcomes and evaluates evidence for microbiota-targeted interventions, including probiotics, synbiotics, nutritional optimization, antibiotic stewardship, bile acid modulation, and emerging multiomics strategies. We distinguish liver resection from living-donor and deceased-donor liver transplantation because the patient populations, graft or remnant anatomy, ischemia-reperfusion exposures, immune status, and outcome definitions differ. Clinical evidence most consistently supports selected pro-/synbiotic strategies for reducing postoperative infection in higher-risk settings, whereas microbiome-based prediction of PHLF, fecal microbiota transplantation (FMT), bile acid-directed therapy, and precision multiomics-guided pathways remain investigational. Future work should use transparent literature identification, standardized perioperative protocols, risk-defined populations, external validation, and prospective multicenter trials. A better understanding of gut-liver interactions may help preserve beneficial host-microbial signals while limiting translocation and inflammation during recovery.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Liver/surgery/microbiology/metabolism
*Gastrointestinal Microbiome/physiology
*Hepatectomy/methods
Liver Transplantation/methods
*Perioperative Care/methods
Multiomics
RevDate: 2026-09-02
Functional metatranscriptomics of the rhizosphere: Towards an understanding of metabolic processes of the microbial carbon pump.
FEMS microbiology ecology pii:8779974 [Epub ahead of print].
The soil microbiome drives soil organic carbon (SOC) transformation, shaped and impacted by plant growth stage and soil management such as tillage. The soil microbial carbon pump conceptually links the degradation of plant- and microbe-derived compounds and the neosynthesis of microbial biomass, as driver of SOC buildup. Using metatranscriptomic sequencing, we characterized actively expressed microbial functions associated with the microbial carbon pump in the Brassica napus rhizosphere across growth stages and under simulated erosion, using a tailored KEGG Orthology (KO) approach complemented by CAZy analysis of carbohydrate-active enzyme transcripts. A clear growth stage effect emerged with higher transcript abundances at flowering. Transcripts for substrate-binding proteins and permeases of ABC transporters (e.g. xylose, trehalose, phospholipids) increased at flowering, while plant polymer-degrading transcripts remained unaffected. Elevated transcripts for chitin synthase, glmS (peptidoglycan precursor), and EPS-related genes (ExoY, algF, cysE) at flowering suggested enhanced microbial activity. Simulated soil erosion impacted only two KO transcripts. CAZy results show the same pattern with GH related to sugars and plant polymers increased at flowering. Despite functional shifts, taxonomic composition stayed stable for most affected transcripts. Our study uncovered metabolic pathways associated with SOC transformation and microbial-derived SOC neosynthesis, offering insights into microbial contributions to SOC formation and persistence.
Additional Links: PMID-42684041
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PubMed:
Citation:
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@article {pmid42684041,
year = {2026},
author = {Ruggaber, J and Wende, S and Yang, S and Keiluweit, M and Kolb, S},
title = {Functional metatranscriptomics of the rhizosphere: Towards an understanding of metabolic processes of the microbial carbon pump.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag097},
pmid = {42684041},
issn = {1574-6941},
abstract = {The soil microbiome drives soil organic carbon (SOC) transformation, shaped and impacted by plant growth stage and soil management such as tillage. The soil microbial carbon pump conceptually links the degradation of plant- and microbe-derived compounds and the neosynthesis of microbial biomass, as driver of SOC buildup. Using metatranscriptomic sequencing, we characterized actively expressed microbial functions associated with the microbial carbon pump in the Brassica napus rhizosphere across growth stages and under simulated erosion, using a tailored KEGG Orthology (KO) approach complemented by CAZy analysis of carbohydrate-active enzyme transcripts. A clear growth stage effect emerged with higher transcript abundances at flowering. Transcripts for substrate-binding proteins and permeases of ABC transporters (e.g. xylose, trehalose, phospholipids) increased at flowering, while plant polymer-degrading transcripts remained unaffected. Elevated transcripts for chitin synthase, glmS (peptidoglycan precursor), and EPS-related genes (ExoY, algF, cysE) at flowering suggested enhanced microbial activity. Simulated soil erosion impacted only two KO transcripts. CAZy results show the same pattern with GH related to sugars and plant polymers increased at flowering. Despite functional shifts, taxonomic composition stayed stable for most affected transcripts. Our study uncovered metabolic pathways associated with SOC transformation and microbial-derived SOC neosynthesis, offering insights into microbial contributions to SOC formation and persistence.},
}
RevDate: 2026-09-02
CmpDate: 2026-09-02
Arsenic-driven agricultural soil risk exceeds industrial contamination in Punjab, India: a replicated EDXRF and 16S rRNA assessment across three land-use types and three agro-ecological districts.
Environmental geochemistry and health, 48(14):.
Arsenic loading from irrigated agriculture poses a greater composite ecological risk than industrial heavy-metal contamination in Punjab, India, a finding that directly challenges the primacy of metal-load-based soil hazard indices across South Asian agro-industrial regions. Using a formally replicated 3 × 3 factorial design (three land-use types × three agro-ecological districts; N = 36 energy-dispersive X-ray fluorescence (EDXRF) samples; n = 4 field replicates per sampling unit) combined with 16S ribosomal RNA (rRNA) V3-V4 amplicon sequencing at three representative sites, we demonstrate that land-use type is the primary geochemical driver across 15 of 32 quantified elements (partial eta-squared, η[2]p, up to 0.862), with significant land-use × district interaction effects detectable only through factorial design. The agricultural Amritsar sampling unit recorded the highest composite ecological risk (Potential Ecological Risk Index, PERI = 723.54), exceeding the primary industrial hotspot (PERI = 624.17; Pollution Load Index, PLI = 20.11), driven by extreme arsenic enrichment from chronic flood irrigation with arsenic-bearing groundwater (As = 80.8 ± 10.7 mg/kg; Enrichment Factor, EF = 45.19; geo-accumulation index, Igeo, Class 6), a risk pathway invisible to PLI-based ranking. All nine sampling units simultaneously exceeded Central Pollution Control Board (CPCB) guideline values for zinc, lead, arsenic, chromium, nickel, and copper (PLI range 8.46-20.11), confirming region-wide multi-element soil pollution. Descriptive 16S rRNA community profiles revealed a diversity gradient consistent with Pollution-Induced Community Tolerance (PICT) theory (Shannon entropy H': 3.906 → 3.007), with Pseudomonadota enrichment (60.1% → 83.0%), Actinomycetota depletion (20.0% → 3.5%), and eight genera forming a candidate biomonitoring panel. Procrustes alignment (m12 = 0.170) provides exploratory evidence of trace element-microbiome co-structure. Three co-existing contamination pathways are identified, and an integrated EDXRF-16S rRNA framework for land-use-stratified soil health monitoring is proposed for South Asian agro-industrial regions.
Additional Links: PMID-42684477
PubMed:
Citation:
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@article {pmid42684477,
year = {2026},
author = {Chauhan, V and Kumari, K},
title = {Arsenic-driven agricultural soil risk exceeds industrial contamination in Punjab, India: a replicated EDXRF and 16S rRNA assessment across three land-use types and three agro-ecological districts.},
journal = {Environmental geochemistry and health},
volume = {48},
number = {14},
pages = {},
pmid = {42684477},
issn = {1573-2983},
support = {220510324267//University Grants Commission/ ; },
mesh = {India ; *RNA, Ribosomal, 16S/genetics ; *Soil Pollutants/analysis/toxicity ; Environmental Monitoring/methods ; Agriculture ; *Arsenic/analysis/toxicity ; Soil/chemistry ; Soil Microbiology ; Spectrometry, X-Ray Emission ; Risk Assessment ; },
abstract = {Arsenic loading from irrigated agriculture poses a greater composite ecological risk than industrial heavy-metal contamination in Punjab, India, a finding that directly challenges the primacy of metal-load-based soil hazard indices across South Asian agro-industrial regions. Using a formally replicated 3 × 3 factorial design (three land-use types × three agro-ecological districts; N = 36 energy-dispersive X-ray fluorescence (EDXRF) samples; n = 4 field replicates per sampling unit) combined with 16S ribosomal RNA (rRNA) V3-V4 amplicon sequencing at three representative sites, we demonstrate that land-use type is the primary geochemical driver across 15 of 32 quantified elements (partial eta-squared, η[2]p, up to 0.862), with significant land-use × district interaction effects detectable only through factorial design. The agricultural Amritsar sampling unit recorded the highest composite ecological risk (Potential Ecological Risk Index, PERI = 723.54), exceeding the primary industrial hotspot (PERI = 624.17; Pollution Load Index, PLI = 20.11), driven by extreme arsenic enrichment from chronic flood irrigation with arsenic-bearing groundwater (As = 80.8 ± 10.7 mg/kg; Enrichment Factor, EF = 45.19; geo-accumulation index, Igeo, Class 6), a risk pathway invisible to PLI-based ranking. All nine sampling units simultaneously exceeded Central Pollution Control Board (CPCB) guideline values for zinc, lead, arsenic, chromium, nickel, and copper (PLI range 8.46-20.11), confirming region-wide multi-element soil pollution. Descriptive 16S rRNA community profiles revealed a diversity gradient consistent with Pollution-Induced Community Tolerance (PICT) theory (Shannon entropy H': 3.906 → 3.007), with Pseudomonadota enrichment (60.1% → 83.0%), Actinomycetota depletion (20.0% → 3.5%), and eight genera forming a candidate biomonitoring panel. Procrustes alignment (m12 = 0.170) provides exploratory evidence of trace element-microbiome co-structure. Three co-existing contamination pathways are identified, and an integrated EDXRF-16S rRNA framework for land-use-stratified soil health monitoring is proposed for South Asian agro-industrial regions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
India
*RNA, Ribosomal, 16S/genetics
*Soil Pollutants/analysis/toxicity
Environmental Monitoring/methods
Agriculture
*Arsenic/analysis/toxicity
Soil/chemistry
Soil Microbiology
Spectrometry, X-Ray Emission
Risk Assessment
RevDate: 2026-09-02
CmpDate: 2026-09-02
Nutritional Modulation of the Gut Microbiome-Metabolite Axis in Cardiovascular Disease: From Dietary Patterns to Cardiovascular Risk.
Current nutrition reports, 15(1):.
PURPOSE OF REVIEW: Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, and dietary modification represents one of the most important modifiable strategies for its prevention and management. Increasing evidence indicates that the cardiovascular effects of diet extend beyond direct effects of nutrients and are partly mediated by interactions between dietary substrates, the gut microbiota, and host metabolism. This review critically evaluates the role of diet-microbiota interactions in CVD pathogenesis and provides an integrated, metabolite-centered perspective on how major dietary patterns influence gut microbial metabolism and cardiovascular health. Particular attention is given to trimethylamine N-oxide (TMAO), lipopolysaccharides (LPS), short-chain fatty acids (SCFAs), bile acids (BAs), phenylacetylglutamine (PAGln), indolepropionic acid (IPA), and hydrogen sulfide (H2S).
RECENT FINDINGS: Dietary patterns substantially influence microbial composition, substrate availability, intestinal barrier integrity, and the production or transformation of microbiota-associated metabolites. Western-style, animal-based, and high-fat dietary patterns, may promote proteolytic and sulfidogenic fermentation, dysbiosis, impaired intestinal barrier function, and increased production or availability of potentially harmful metabolites. TMAO and PAGln have been associated with atherosclerosis, endothelial dysfunction, platelet activation, thrombosis, and other cardiometabolic outcomes, although their associations with cardiovascular risk may depend on dietary source, renal function, host metabolism, and individual microbial characteristics. LPS provides an important link between intestinal permeability, metabolic endotoxemia, inflammation, and vascular dysfunction. In contrast, fiber-rich and plant-based dietary patterns promote saccharolytic fermentation and SCFA production, support microbial diversity and intestinal barrier integrity, and may reduce endotoxemia and the production of potentially adverse microbial metabolites. Mediterranean dietary patterns, characterized by high consumption of plant foods, whole grains, fiber, olive oil, polyphenols, and fish together with lower intake of red and processed meat and refined sugars, appear to favor a more beneficial microbial and metabolic profile. BAs have more complex and context-dependent effects through microbial transformation and host signaling pathways, particularly FXR and TGR5. Emerging evidence also suggests potentially important cardiovascular roles for IPA and H₂S; however, their dietary regulation and clinical relevance remain less well established. The gut microbiota represents an important metabolic interface linking dietary patterns with cardiovascular physiology and disease. The available evidence suggests that dietary patterns rich in plant foods, fiber, unsaturated fats, polyphenols, and other bioactive components may support beneficial microbial functions and metabolite profiles, whereas Western-style dietary patterns may favor microbial pathways associated with endotoxemia, inflammation, thrombosis, and atherogenesis. However, individual metabolites should not be interpreted in isolation because their cardiovascular effects may vary according to dietary source, microbial phenotype, host metabolism, renal function, and overall dietary context. Emerging evidence supports a biomarker-guided and individualized approach to nutritional modulation of the gut microbiota, including strategies targeting microbial metabolite production. Nevertheless, the clinical efficacy of microbiota-targeted interventions remains to be established. Future longitudinal and randomized interventional studies integrating dietary assessment, microbiome composition, metabolomics, host metabolic characteristics, and cardiovascular outcomes are needed to clarify causality and determine whether personalized nutrition and microbiota-targeted strategies can improve CVD prevention and reduce residual cardiovascular risk.
Additional Links: PMID-42684538
PubMed:
Citation:
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@article {pmid42684538,
year = {2026},
author = {Mohammadzadeh, M and Ünlü Söğüt, M and Fazlzadeh, A and Çelik, MN},
title = {Nutritional Modulation of the Gut Microbiome-Metabolite Axis in Cardiovascular Disease: From Dietary Patterns to Cardiovascular Risk.},
journal = {Current nutrition reports},
volume = {15},
number = {1},
pages = {},
pmid = {42684538},
issn = {2161-3311},
mesh = {Humans ; *Cardiovascular Diseases/microbiology/prevention & control/etiology/metabolism ; *Gastrointestinal Microbiome ; *Diet ; Heart Disease Risk Factors ; Animals ; Intestinal Barrier Function ; Dysbiosis ; Methylamines/metabolism ; Fatty Acids, Volatile/metabolism ; },
abstract = {PURPOSE OF REVIEW: Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, and dietary modification represents one of the most important modifiable strategies for its prevention and management. Increasing evidence indicates that the cardiovascular effects of diet extend beyond direct effects of nutrients and are partly mediated by interactions between dietary substrates, the gut microbiota, and host metabolism. This review critically evaluates the role of diet-microbiota interactions in CVD pathogenesis and provides an integrated, metabolite-centered perspective on how major dietary patterns influence gut microbial metabolism and cardiovascular health. Particular attention is given to trimethylamine N-oxide (TMAO), lipopolysaccharides (LPS), short-chain fatty acids (SCFAs), bile acids (BAs), phenylacetylglutamine (PAGln), indolepropionic acid (IPA), and hydrogen sulfide (H2S).
RECENT FINDINGS: Dietary patterns substantially influence microbial composition, substrate availability, intestinal barrier integrity, and the production or transformation of microbiota-associated metabolites. Western-style, animal-based, and high-fat dietary patterns, may promote proteolytic and sulfidogenic fermentation, dysbiosis, impaired intestinal barrier function, and increased production or availability of potentially harmful metabolites. TMAO and PAGln have been associated with atherosclerosis, endothelial dysfunction, platelet activation, thrombosis, and other cardiometabolic outcomes, although their associations with cardiovascular risk may depend on dietary source, renal function, host metabolism, and individual microbial characteristics. LPS provides an important link between intestinal permeability, metabolic endotoxemia, inflammation, and vascular dysfunction. In contrast, fiber-rich and plant-based dietary patterns promote saccharolytic fermentation and SCFA production, support microbial diversity and intestinal barrier integrity, and may reduce endotoxemia and the production of potentially adverse microbial metabolites. Mediterranean dietary patterns, characterized by high consumption of plant foods, whole grains, fiber, olive oil, polyphenols, and fish together with lower intake of red and processed meat and refined sugars, appear to favor a more beneficial microbial and metabolic profile. BAs have more complex and context-dependent effects through microbial transformation and host signaling pathways, particularly FXR and TGR5. Emerging evidence also suggests potentially important cardiovascular roles for IPA and H₂S; however, their dietary regulation and clinical relevance remain less well established. The gut microbiota represents an important metabolic interface linking dietary patterns with cardiovascular physiology and disease. The available evidence suggests that dietary patterns rich in plant foods, fiber, unsaturated fats, polyphenols, and other bioactive components may support beneficial microbial functions and metabolite profiles, whereas Western-style dietary patterns may favor microbial pathways associated with endotoxemia, inflammation, thrombosis, and atherogenesis. However, individual metabolites should not be interpreted in isolation because their cardiovascular effects may vary according to dietary source, microbial phenotype, host metabolism, renal function, and overall dietary context. Emerging evidence supports a biomarker-guided and individualized approach to nutritional modulation of the gut microbiota, including strategies targeting microbial metabolite production. Nevertheless, the clinical efficacy of microbiota-targeted interventions remains to be established. Future longitudinal and randomized interventional studies integrating dietary assessment, microbiome composition, metabolomics, host metabolic characteristics, and cardiovascular outcomes are needed to clarify causality and determine whether personalized nutrition and microbiota-targeted strategies can improve CVD prevention and reduce residual cardiovascular risk.},
}
MeSH Terms:
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Humans
*Cardiovascular Diseases/microbiology/prevention & control/etiology/metabolism
*Gastrointestinal Microbiome
*Diet
Heart Disease Risk Factors
Animals
Intestinal Barrier Function
Dysbiosis
Methylamines/metabolism
Fatty Acids, Volatile/metabolism
RevDate: 2026-09-02
CmpDate: 2026-09-02
Genetically Proxied Associations Among 473 Gut Microbial Taxa, 1,400 Circulating Metabolites, and Mental and Behavioral Disorders: A Mendelian Randomization Study.
Journal of molecular neuroscience : MN, 76(3):.
Mental and behavioural disorders substantially impair everyday functioning, yet the biological mechanisms through which the gut microbiome may contribute to psychiatric vulnerability remain insufficiently characterized. We jointly analysed genome-wide association study data for 473 gut microbial taxa, approximately 1,400 circulating metabolites, and seven mental and behavioural disorders, including schizophrenia, obsessive-compulsive disorder, post-traumatic stress disorder, attention-deficit/hyperactivity disorder, chronic depression, bulimia nervosa, and hypersomnia. Mendelian randomization was used to estimate genetically proxied associations among these traits, and two-step MR was used to evaluate candidate statistical mediation by circulating metabolites. We identified FDR-supported associations for eight microbial taxa across four disorders: UBA8904, Dorea, and Ruminococcus A sp000432335 with ADHD; Pseudomonas aeruginosa, Bifidobacterium kashiwanohense, and CAG-273 sp003534295 with chronic depression; Syntrophorhabdia with bulimia nervosa; and Aneurinibacillales with hypersomnia. Twelve circulating metabolites were statistically consistent with partial mediation of candidate microbiota-disorder associations. Glycocholate glucuronide (1) accounted for an estimated 5.95% of the Syntrophorhabdia-bulimia nervosa association, whereas 5-dodecenoate (12:1n7) was consistent with mediation of 8.28% of the inverse association between CAG-273 sp003534295 and chronic depression. Target enrichment prioritized lipid metabolism and neuroactive ligand-receptor interaction pathways for further study. The inverse association between genetically predicted 5-dodecenoate and depression was reproduced in an independent depression GWAS. These findings nominate candidate microbiota-metabolite pathways for mechanistic investigation; however, residual horizontal pleiotropy and linkage-disequilibrium-related confounding cannot be excluded, and the results should not be interpreted as definitive causal evidence.
Additional Links: PMID-42684578
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@article {pmid42684578,
year = {2026},
author = {Huang, K and Tang, W},
title = {Genetically Proxied Associations Among 473 Gut Microbial Taxa, 1,400 Circulating Metabolites, and Mental and Behavioral Disorders: A Mendelian Randomization Study.},
journal = {Journal of molecular neuroscience : MN},
volume = {76},
number = {3},
pages = {},
pmid = {42684578},
issn = {1559-1166},
support = {grant No. 2023YJG010//Wei Tang/ ; },
mesh = {Humans ; *Mental Disorders/genetics/microbiology/blood ; *Gastrointestinal Microbiome ; Mendelian Randomization Analysis ; Genome-Wide Association Study ; },
abstract = {Mental and behavioural disorders substantially impair everyday functioning, yet the biological mechanisms through which the gut microbiome may contribute to psychiatric vulnerability remain insufficiently characterized. We jointly analysed genome-wide association study data for 473 gut microbial taxa, approximately 1,400 circulating metabolites, and seven mental and behavioural disorders, including schizophrenia, obsessive-compulsive disorder, post-traumatic stress disorder, attention-deficit/hyperactivity disorder, chronic depression, bulimia nervosa, and hypersomnia. Mendelian randomization was used to estimate genetically proxied associations among these traits, and two-step MR was used to evaluate candidate statistical mediation by circulating metabolites. We identified FDR-supported associations for eight microbial taxa across four disorders: UBA8904, Dorea, and Ruminococcus A sp000432335 with ADHD; Pseudomonas aeruginosa, Bifidobacterium kashiwanohense, and CAG-273 sp003534295 with chronic depression; Syntrophorhabdia with bulimia nervosa; and Aneurinibacillales with hypersomnia. Twelve circulating metabolites were statistically consistent with partial mediation of candidate microbiota-disorder associations. Glycocholate glucuronide (1) accounted for an estimated 5.95% of the Syntrophorhabdia-bulimia nervosa association, whereas 5-dodecenoate (12:1n7) was consistent with mediation of 8.28% of the inverse association between CAG-273 sp003534295 and chronic depression. Target enrichment prioritized lipid metabolism and neuroactive ligand-receptor interaction pathways for further study. The inverse association between genetically predicted 5-dodecenoate and depression was reproduced in an independent depression GWAS. These findings nominate candidate microbiota-metabolite pathways for mechanistic investigation; however, residual horizontal pleiotropy and linkage-disequilibrium-related confounding cannot be excluded, and the results should not be interpreted as definitive causal evidence.},
}
MeSH Terms:
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Humans
*Mental Disorders/genetics/microbiology/blood
*Gastrointestinal Microbiome
Mendelian Randomization Analysis
Genome-Wide Association Study
RevDate: 2026-09-02
Seasonal dynamics of microbial communities and potential human pathogens in Crassostrea hongkongensis and ambient water in southern China.
Applied and environmental microbiology [Epub ahead of print].
UNLABELLED: Oysters are a popular raw seafood worldwide, yet their contamination with human pathogens poses substantial public health risks. However, the seasonal dynamics of host-associated microbiota and the environmental drivers of pathogen accumulation in Crassostrea hongkongensis remain poorly understood. Here, we conducted 16S rRNA amplicon sequencing to profile the gill and intestinal microbiota of C. hongkongensis, sampled quarterly over a 1-year period in Beihai and Zhanjiang, southern China. A pronounced divergence in oyster-associated bacterial communities was observed between the two locations in December. Key bacterial families, such as Lachnospiraceae and Muribaculaceae, showed significant temporal fluctuations in abundance, suggesting their potential role in maintaining bacterial community stability within oysters. These microbial shifts were significantly correlated with environmental parameters such as chlorophyll a and pH. In parallel, we used plate counting to quantify five foodborne pathogens and total viable counts. Vibrios were more frequently detected in oyster tissues than in ambient seawater. Pathogen-associated amplicon sequence variants exhibited a strong response to variations in pH and chlorophyll a, whereas the abundance of culturable Vibrio vulnificus was significantly negatively correlated with temperature and nitrate. The integration of high-throughput sequencing and culture-based methods provides comprehensive insights into the dynamics of pathogenic bacteria within oysters under natural mariculture settings. This study offers valuable ecological insights into the interactions within the oyster-associated microbial ecosystem, contributing to a deeper understanding of its dynamics and implications for public health.
IMPORTANCE: Mariculture of Crassostrea hongkongensis serves as a critical interface between coastal ecology and public health, yet seasonal dynamics of its microbiome and core stabilizing taxa remain poorly understood in subtropical aquaculture. This study identified Acetobacteraceae, Lachnospiraceae, Prevotellaceae, and Muribaculaceae as key families associated with seasonal microbiome stability in C. hongkongensis, highlighting their potential contribution to community resilience. It further revealed that Vibrio species detection was negatively correlated with temperature. These findings advance our understanding of interactions between the oyster microbiome and the environment, and provide a theoretical basis for improving oyster health management and promoting sustainable aquaculture practices.
Additional Links: PMID-42684864
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@article {pmid42684864,
year = {2026},
author = {Liu, X and Wang, X and Zhu, H and Chen, W and Hong, X and Wan, Y and Huang, J and Liu, C},
title = {Seasonal dynamics of microbial communities and potential human pathogens in Crassostrea hongkongensis and ambient water in southern China.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0105626},
doi = {10.1128/aem.01056-26},
pmid = {42684864},
issn = {1098-5336},
abstract = {UNLABELLED: Oysters are a popular raw seafood worldwide, yet their contamination with human pathogens poses substantial public health risks. However, the seasonal dynamics of host-associated microbiota and the environmental drivers of pathogen accumulation in Crassostrea hongkongensis remain poorly understood. Here, we conducted 16S rRNA amplicon sequencing to profile the gill and intestinal microbiota of C. hongkongensis, sampled quarterly over a 1-year period in Beihai and Zhanjiang, southern China. A pronounced divergence in oyster-associated bacterial communities was observed between the two locations in December. Key bacterial families, such as Lachnospiraceae and Muribaculaceae, showed significant temporal fluctuations in abundance, suggesting their potential role in maintaining bacterial community stability within oysters. These microbial shifts were significantly correlated with environmental parameters such as chlorophyll a and pH. In parallel, we used plate counting to quantify five foodborne pathogens and total viable counts. Vibrios were more frequently detected in oyster tissues than in ambient seawater. Pathogen-associated amplicon sequence variants exhibited a strong response to variations in pH and chlorophyll a, whereas the abundance of culturable Vibrio vulnificus was significantly negatively correlated with temperature and nitrate. The integration of high-throughput sequencing and culture-based methods provides comprehensive insights into the dynamics of pathogenic bacteria within oysters under natural mariculture settings. This study offers valuable ecological insights into the interactions within the oyster-associated microbial ecosystem, contributing to a deeper understanding of its dynamics and implications for public health.
IMPORTANCE: Mariculture of Crassostrea hongkongensis serves as a critical interface between coastal ecology and public health, yet seasonal dynamics of its microbiome and core stabilizing taxa remain poorly understood in subtropical aquaculture. This study identified Acetobacteraceae, Lachnospiraceae, Prevotellaceae, and Muribaculaceae as key families associated with seasonal microbiome stability in C. hongkongensis, highlighting their potential contribution to community resilience. It further revealed that Vibrio species detection was negatively correlated with temperature. These findings advance our understanding of interactions between the oyster microbiome and the environment, and provide a theoretical basis for improving oyster health management and promoting sustainable aquaculture practices.},
}
RevDate: 2026-09-02
Mother-infant sharing of gut and vaginal microbes at the species and strain level.
Cell reports, 45(9):117920 pii:S2211-1247(26)00998-8 [Epub ahead of print].
Mother-to-offspring microbial transmission is a foundational process for seeding the infant gut microbiome, yet the relative contributions of maternal body sites and the influence of birth delivery mode remain incompletely understood. We use shotgun metagenomic sequencing in 68 mother-infant dyads to investigate species- and strain-level sharing of the maternal gut and vaginal microbiomes with the infant gut during the first year of life. At 2-4 months of age, infants share an average of 35% of species with their mother's microbiomes, with markedly greater sharing from the maternal gut than the vagina. Vaginally delivered infants exhibit higher levels of sharing than those born by cesarean section (C-section). Strain-level analyses reveal persistent mother-infant transmission across multiple Bacteroides and Bifidobacterium species genome bins, with strain-sharing frequencies varying by species and birth mode. C-section reduces the extent of mother-infant species- and strain-level sharing.
Additional Links: PMID-42684889
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@article {pmid42684889,
year = {2026},
author = {Mueller, NT and Xiao, S and Liu, T and Debelius, J and Kress, AM and Zhao, N and Moore, B and McKee, KS and Jacobson, LP and Comstock, SS and , },
title = {Mother-infant sharing of gut and vaginal microbes at the species and strain level.},
journal = {Cell reports},
volume = {45},
number = {9},
pages = {117920},
doi = {10.1016/j.celrep.2026.117920},
pmid = {42684889},
issn = {2211-1247},
abstract = {Mother-to-offspring microbial transmission is a foundational process for seeding the infant gut microbiome, yet the relative contributions of maternal body sites and the influence of birth delivery mode remain incompletely understood. We use shotgun metagenomic sequencing in 68 mother-infant dyads to investigate species- and strain-level sharing of the maternal gut and vaginal microbiomes with the infant gut during the first year of life. At 2-4 months of age, infants share an average of 35% of species with their mother's microbiomes, with markedly greater sharing from the maternal gut than the vagina. Vaginally delivered infants exhibit higher levels of sharing than those born by cesarean section (C-section). Strain-level analyses reveal persistent mother-infant transmission across multiple Bacteroides and Bifidobacterium species genome bins, with strain-sharing frequencies varying by species and birth mode. C-section reduces the extent of mother-infant species- and strain-level sharing.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-31
Species-specific structuring of gut bacterial and fungal communities in honey bees Apis cerana and Apis mellifera.
Antonie van Leeuwenhoek, 119(9):.
Honey bee gut microbiome studies have primarily emphasized bacteria, leaving fungal communities comparatively overlooked despite their ecological and functional importance. Whole-genome shotgun metagenomics of Apis cerana and Apis mellifera revealed fungal assemblages dominated by Ascomycota, with Basidiomycota and Microsporidia in minor proportions, alongside gut bacterial communities composed mainly of Pseudomonadota, Bacillota, and Actinomycetota. The bacterial diversity was markedly higher in A. mellifera (Shannon = 5.90; Simpson = 0.98) than in A. cerana (Shannon = 4.01; Simpson = 0.94; p > 0.05), while fungal diversity remained comparable between species (p > 0.05). Beta-diversity analyses revealed strong host-specific clustering for both bacterial (PERMANOVA R[2] = 0.7989, p > 0.05) and fungal communities (R[2] = 0.7218, p > 0.05), indicating distinct microbial organization driven by host species. Bacterial-fungal co-occurrence patterns exhibited host-specific structuring, suggesting differential inter-kingdom community organization between A. cerana and A. mellifera. Linear Discriminant Analysis Effect Size (LEfSe) identified 93 discriminatory fungal taxa (45 enriched in A. cerana, 48 in A. mellifera), highlighting yeast-dominated signatures in A. mellifera and Basidiomycota-affiliated enrichments in A. cerana. KEGG and CAZy profiling revealed host- and kingdom-specific functional differences, with bacterial communities of A. mellifera showing distinct representation of carbohydrate metabolism and nutrient-cycling functions, while fungal communities exhibited a comparatively narrower functional repertoire. Together, these findings provide a high-resolution view of honey bee bacterial and fungal microbiomes, highlighting strong host-driven divergence in taxonomy, function, and cross-kingdom interactions.
Additional Links: PMID-42671657
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@article {pmid42671657,
year = {2026},
author = {Nazrin, MRR and Gouda, MNR and Kumaranag, KM and Suroshe, SS and Subramanian, S},
title = {Species-specific structuring of gut bacterial and fungal communities in honey bees Apis cerana and Apis mellifera.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {9},
pages = {},
pmid = {42671657},
issn = {1572-9699},
mesh = {Animals ; Bees/microbiology ; *Bacteria/classification/genetics/isolation & purification ; *Fungi/classification/genetics/isolation & purification ; *Gastrointestinal Microbiome ; Species Specificity ; Metagenomics ; Phylogeny ; Biodiversity ; *Mycobiome ; },
abstract = {Honey bee gut microbiome studies have primarily emphasized bacteria, leaving fungal communities comparatively overlooked despite their ecological and functional importance. Whole-genome shotgun metagenomics of Apis cerana and Apis mellifera revealed fungal assemblages dominated by Ascomycota, with Basidiomycota and Microsporidia in minor proportions, alongside gut bacterial communities composed mainly of Pseudomonadota, Bacillota, and Actinomycetota. The bacterial diversity was markedly higher in A. mellifera (Shannon = 5.90; Simpson = 0.98) than in A. cerana (Shannon = 4.01; Simpson = 0.94; p > 0.05), while fungal diversity remained comparable between species (p > 0.05). Beta-diversity analyses revealed strong host-specific clustering for both bacterial (PERMANOVA R[2] = 0.7989, p > 0.05) and fungal communities (R[2] = 0.7218, p > 0.05), indicating distinct microbial organization driven by host species. Bacterial-fungal co-occurrence patterns exhibited host-specific structuring, suggesting differential inter-kingdom community organization between A. cerana and A. mellifera. Linear Discriminant Analysis Effect Size (LEfSe) identified 93 discriminatory fungal taxa (45 enriched in A. cerana, 48 in A. mellifera), highlighting yeast-dominated signatures in A. mellifera and Basidiomycota-affiliated enrichments in A. cerana. KEGG and CAZy profiling revealed host- and kingdom-specific functional differences, with bacterial communities of A. mellifera showing distinct representation of carbohydrate metabolism and nutrient-cycling functions, while fungal communities exhibited a comparatively narrower functional repertoire. Together, these findings provide a high-resolution view of honey bee bacterial and fungal microbiomes, highlighting strong host-driven divergence in taxonomy, function, and cross-kingdom interactions.},
}
MeSH Terms:
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Animals
Bees/microbiology
*Bacteria/classification/genetics/isolation & purification
*Fungi/classification/genetics/isolation & purification
*Gastrointestinal Microbiome
Species Specificity
Metagenomics
Phylogeny
Biodiversity
*Mycobiome
RevDate: 2026-08-31
CmpDate: 2026-08-31
The COVID-19 pandemic influenced the temporal dynamics of antimicrobial resistance markers and bacterial community across urban wastewater treatment plants.
Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology], 57(1):.
Urban wastewater systems represent important interfaces between human activity and the environmental occurrence of antimicrobial resistance (AMR) markers. We assessed the temporal dynamics of intI1, ermB, and the 16 S rRNA gene by quantitative PCR across three wastewater systems (EPC, CJC, and JW) in Fortaleza, Brazil, from November 2021 to November 2023. Bacterial communities were additionally characterized by 16 S rRNA gene metabarcoding in 18 samples collected in December 2021 and January 2022. A synchronized decline in 16 S rRNA gene and intI1 concentrations beginning in late 2022 was observed across all three wastewater systems, suggesting a shift toward lower microbial abundance. The ermB gene showed higher and more variable concentrations during part of the pandemic period, followed by convergence toward lower levels; however, the absence of antimicrobial-consumption data precluded attribution of this pattern to changes in macrolide selective pressure. Normalized antimicrobial resistance marker abundances were comparatively stable at EPC and JW but more variable at CJC. EPC exhibited the highest ASV richness, whereas CJC and JW showed greater diversity according to Shannon and inverse Simpson indices. Beta-diversity analyses identified wastewater system as the principal factor associated with bacterial community structure, while the effect of sampling period was smaller and metric-dependent. Neither ermB nor intI1 was individually associated with community composition, although intI1 showed a limited effect after adjustment for wastewater system in one model. Physicochemical parameters were not significantly associated with normalized marker abundances in the exploratory paired analysis. Arcobacter, Acinetobacter, and other potentially relevant genera were detected, but no direct associations between these taxa and the monitored AMR markers could be established. These findings highlight the value of integrating longitudinal qPCR, microbiome profiling, and environmental characterization to improve the interpretation of targeted AMR markers in One Health wastewater surveillance.
Additional Links: PMID-42671719
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@article {pmid42671719,
year = {2026},
author = {Filho, CGB and Oliveira, FAS and Rodrigues, VLM and Hissa, DC and Barros, MVH and de Farias, AA and Dantas, GT and Dos Santos, AB and Ximenes, JCM and Melo, VMM},
title = {The COVID-19 pandemic influenced the temporal dynamics of antimicrobial resistance markers and bacterial community across urban wastewater treatment plants.},
journal = {Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]},
volume = {57},
number = {1},
pages = {},
pmid = {42671719},
issn = {1678-4405},
mesh = {*Wastewater/microbiology ; Brazil/epidemiology ; *Bacteria/genetics/drug effects/classification/isolation & purification ; RNA, Ribosomal, 16S/genetics ; *COVID-19/epidemiology ; *Drug Resistance, Bacterial/genetics ; Humans ; Anti-Bacterial Agents/pharmacology ; SARS-CoV-2 ; *Microbiota ; },
abstract = {Urban wastewater systems represent important interfaces between human activity and the environmental occurrence of antimicrobial resistance (AMR) markers. We assessed the temporal dynamics of intI1, ermB, and the 16 S rRNA gene by quantitative PCR across three wastewater systems (EPC, CJC, and JW) in Fortaleza, Brazil, from November 2021 to November 2023. Bacterial communities were additionally characterized by 16 S rRNA gene metabarcoding in 18 samples collected in December 2021 and January 2022. A synchronized decline in 16 S rRNA gene and intI1 concentrations beginning in late 2022 was observed across all three wastewater systems, suggesting a shift toward lower microbial abundance. The ermB gene showed higher and more variable concentrations during part of the pandemic period, followed by convergence toward lower levels; however, the absence of antimicrobial-consumption data precluded attribution of this pattern to changes in macrolide selective pressure. Normalized antimicrobial resistance marker abundances were comparatively stable at EPC and JW but more variable at CJC. EPC exhibited the highest ASV richness, whereas CJC and JW showed greater diversity according to Shannon and inverse Simpson indices. Beta-diversity analyses identified wastewater system as the principal factor associated with bacterial community structure, while the effect of sampling period was smaller and metric-dependent. Neither ermB nor intI1 was individually associated with community composition, although intI1 showed a limited effect after adjustment for wastewater system in one model. Physicochemical parameters were not significantly associated with normalized marker abundances in the exploratory paired analysis. Arcobacter, Acinetobacter, and other potentially relevant genera were detected, but no direct associations between these taxa and the monitored AMR markers could be established. These findings highlight the value of integrating longitudinal qPCR, microbiome profiling, and environmental characterization to improve the interpretation of targeted AMR markers in One Health wastewater surveillance.},
}
MeSH Terms:
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*Wastewater/microbiology
Brazil/epidemiology
*Bacteria/genetics/drug effects/classification/isolation & purification
RNA, Ribosomal, 16S/genetics
*COVID-19/epidemiology
*Drug Resistance, Bacterial/genetics
Humans
Anti-Bacterial Agents/pharmacology
SARS-CoV-2
*Microbiota
RevDate: 2026-08-31
CmpDate: 2026-08-31
Dietary Sulfur Compounds and Halitosis: Bridging Food Science, Microbial Metabolism, and Oral Health: A Comprehensive Review.
Molecular nutrition & food research, 70(17):e70526.
Intraoral halitosis is predominantly caused by anaerobic microbes within the tongue biofilm that break down sulfur-containing amino acids, especially cysteine and methionine, to volatile sulfur compounds (VSCs). In addition to microbial activity, there is growing evidence to suggest that dietary factors are able to influence VSC formation by affecting substrate availability, redox equilibrium, and oral ecological stability and that some of these effects are due to extraoral metabolic activity. This review integrates food chemistry, microbial ecology, and oral health to explain how dietary exposures can interact with the oral microbiome to trigger and maintain halitosis. We synthesize current evidence on tongue biofilm ecology, key microbial taxa and metabolic pathways, and the modifying roles of salivary flow, periodontal inflammation, and common beverages and condiments. Diagnostic approaches are discussed with a mechanistic viewpoint, which has focused on combined organoleptic, gas specific analysis, tongue biofilm imaging, and selective provocation testing. Comprehensively, halitosis is presented as a diet modifiable, ecology-driven disease, the diagnostics of which should be guided by phenotype, and the intervention based on microbiomes and tailored care plans should be sustainable so that evidence-based functional foods and personalized care plans can be developed.
Additional Links: PMID-42672061
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@article {pmid42672061,
year = {2026},
author = {Acheampong, R and Otu-Ayeboafo, JO},
title = {Dietary Sulfur Compounds and Halitosis: Bridging Food Science, Microbial Metabolism, and Oral Health: A Comprehensive Review.},
journal = {Molecular nutrition & food research},
volume = {70},
number = {17},
pages = {e70526},
pmid = {42672061},
issn = {1613-4133},
mesh = {*Halitosis/microbiology/etiology ; Humans ; *Oral Health ; *Sulfur Compounds/metabolism/adverse effects ; Microbiota ; Biofilms ; *Diet ; Tongue/microbiology ; },
abstract = {Intraoral halitosis is predominantly caused by anaerobic microbes within the tongue biofilm that break down sulfur-containing amino acids, especially cysteine and methionine, to volatile sulfur compounds (VSCs). In addition to microbial activity, there is growing evidence to suggest that dietary factors are able to influence VSC formation by affecting substrate availability, redox equilibrium, and oral ecological stability and that some of these effects are due to extraoral metabolic activity. This review integrates food chemistry, microbial ecology, and oral health to explain how dietary exposures can interact with the oral microbiome to trigger and maintain halitosis. We synthesize current evidence on tongue biofilm ecology, key microbial taxa and metabolic pathways, and the modifying roles of salivary flow, periodontal inflammation, and common beverages and condiments. Diagnostic approaches are discussed with a mechanistic viewpoint, which has focused on combined organoleptic, gas specific analysis, tongue biofilm imaging, and selective provocation testing. Comprehensively, halitosis is presented as a diet modifiable, ecology-driven disease, the diagnostics of which should be guided by phenotype, and the intervention based on microbiomes and tailored care plans should be sustainable so that evidence-based functional foods and personalized care plans can be developed.},
}
MeSH Terms:
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*Halitosis/microbiology/etiology
Humans
*Oral Health
*Sulfur Compounds/metabolism/adverse effects
Microbiota
Biofilms
*Diet
Tongue/microbiology
RevDate: 2026-08-31
CmpDate: 2026-08-31
Root-associated bacterial and fungal communities of the endangered páramo bromeliad Puya goudotiana.
PloS one, 21(8):e0357104.
Páramo, a tropical high-altitude ecosystem, is threatened by climate change and land-use change. This ecosystem hosts unique biodiversity like the endangered bromeliad Puya goudotiana. While root-associated microbiomes are essential for plant survival and stress tolerance, the microbial communities associated with this species remain uncharacterized. Oxford Nanopore amplicon sequencing was used on root endosphere and bulk soil samples of P. goudotiana, targeting the 16S rRNA gene to evaluate bacterial communities, and the 18S rRNA gene as an exploratory marker for fungal communities. We assessed the taxonomic composition, diversity, functional profiles and co-occurrence networks. Microbial communities were highly differentiated by sample type, with roots exhibiting lower alpha diversity than bulk soil. The root microbiome showed higher prevalence of acidophilic taxa such as Granulicella and Acidipila and symbionts like Bradyrhizobium, whereas bulk soils were dominated by typical páramo taxa, including Candidatus Solibacter, Candidatus Koribacter and Bryobacter. Both bulk soil and roots were characterized by a high abundance of saprotrophic fungi (e.g., Psilocybe) and potential pathogens such as Fusarium, Botrytis and Puccinia. Functional predictions indicated higher prevalence of chemoheterotrophic functions in the roots, while nitrogen and sulfur cycling functions were enriched in bulk soil. Notably, and contrary to prior expectations, co-occurrence networks were more complex in the root endosphere than in bulk soil, suggesting that rhizosphere filtering promotes structured microbial assemblages despite reducing overall diversity. These findings provide a first microbial baseline for P. goudotiana and open new perspectives for understanding plant-microbe interactions and enhancing páramo vegetation resilience under climate change.
Additional Links: PMID-42672062
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Citation:
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@article {pmid42672062,
year = {2026},
author = {RodrÃguez-Lugo, N and Patiño, LH and Cáceres, TM and Vega, L and Hantson, S and RamÃrez, JD and Sanchez, A},
title = {Root-associated bacterial and fungal communities of the endangered páramo bromeliad Puya goudotiana.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0357104},
pmid = {42672062},
issn = {1932-6203},
mesh = {*Plant Roots/microbiology ; *Bromeliaceae/microbiology ; *Bacteria/genetics/classification/isolation & purification ; Soil Microbiology ; *Fungi/genetics/classification/isolation & purification ; RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; Endangered Species ; Biodiversity ; Phylogeny ; RNA, Ribosomal, 18S/genetics ; },
abstract = {Páramo, a tropical high-altitude ecosystem, is threatened by climate change and land-use change. This ecosystem hosts unique biodiversity like the endangered bromeliad Puya goudotiana. While root-associated microbiomes are essential for plant survival and stress tolerance, the microbial communities associated with this species remain uncharacterized. Oxford Nanopore amplicon sequencing was used on root endosphere and bulk soil samples of P. goudotiana, targeting the 16S rRNA gene to evaluate bacterial communities, and the 18S rRNA gene as an exploratory marker for fungal communities. We assessed the taxonomic composition, diversity, functional profiles and co-occurrence networks. Microbial communities were highly differentiated by sample type, with roots exhibiting lower alpha diversity than bulk soil. The root microbiome showed higher prevalence of acidophilic taxa such as Granulicella and Acidipila and symbionts like Bradyrhizobium, whereas bulk soils were dominated by typical páramo taxa, including Candidatus Solibacter, Candidatus Koribacter and Bryobacter. Both bulk soil and roots were characterized by a high abundance of saprotrophic fungi (e.g., Psilocybe) and potential pathogens such as Fusarium, Botrytis and Puccinia. Functional predictions indicated higher prevalence of chemoheterotrophic functions in the roots, while nitrogen and sulfur cycling functions were enriched in bulk soil. Notably, and contrary to prior expectations, co-occurrence networks were more complex in the root endosphere than in bulk soil, suggesting that rhizosphere filtering promotes structured microbial assemblages despite reducing overall diversity. These findings provide a first microbial baseline for P. goudotiana and open new perspectives for understanding plant-microbe interactions and enhancing páramo vegetation resilience under climate change.},
}
MeSH Terms:
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hide MeSH Terms
*Plant Roots/microbiology
*Bromeliaceae/microbiology
*Bacteria/genetics/classification/isolation & purification
Soil Microbiology
*Fungi/genetics/classification/isolation & purification
RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
Endangered Species
Biodiversity
Phylogeny
RNA, Ribosomal, 18S/genetics
RevDate: 2026-08-31
CmpDate: 2026-08-31
Kelp forest collapse alters the reef microbiome and associated metabolome.
Proceedings of the National Academy of Sciences of the United States of America, 123(36):e2525548123.
In many temperate regions experiencing rapid ocean warming, kelp forests are being replaced by low-lying turf algae. Yet, whether this change in biogenic habitat alters reef-level microbial structure and function, including carbon and nutrient cycling, remains largely unknown. Here, we integrated shotgun metagenomics and nontargeted metabolomics to reveal that kelp forest loss alters the composition of the reef microbial community and its associated biochemical machinery, resulting in distinct metabolomes and microbially driven elemental use/transformations on kelp- vs. turf-dominated reefs. Our results therefore suggest that microbes play a key role in shaping kelp forest ecosystem functioning. Further, they demonstrate that human-induced ocean warming has cascading effects on microbially mediated chemistry, with implications for coastal carbon storage and nutrient regeneration.
Additional Links: PMID-42673455
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@article {pmid42673455,
year = {2026},
author = {Farrell, SP and D'Angelo, T and Yiu, DS and Kelminal Pakkir Shah, A and Stincone, P and Countway, PD and Petras, D and Brady, DC and Rasher, DB},
title = {Kelp forest collapse alters the reef microbiome and associated metabolome.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {36},
pages = {e2525548123},
doi = {10.1073/pnas.2525548123},
pmid = {42673455},
issn = {1091-6490},
support = {OIA-1489227//NSF (NSF)/ ; NA//Louise H. & David S. Ingalls Foundation/ ; 2124-390838134//Deutsche Forschungsgemeinschaft (DFG)/ ; NA//Essex Avenue Foundation/ ; NA//PADI Foundation (The PADI Foundation)/ ; },
mesh = {*Microbiota/physiology ; *Kelp/microbiology ; *Metabolome ; *Coral Reefs ; Ecosystem ; Climate Change ; },
abstract = {In many temperate regions experiencing rapid ocean warming, kelp forests are being replaced by low-lying turf algae. Yet, whether this change in biogenic habitat alters reef-level microbial structure and function, including carbon and nutrient cycling, remains largely unknown. Here, we integrated shotgun metagenomics and nontargeted metabolomics to reveal that kelp forest loss alters the composition of the reef microbial community and its associated biochemical machinery, resulting in distinct metabolomes and microbially driven elemental use/transformations on kelp- vs. turf-dominated reefs. Our results therefore suggest that microbes play a key role in shaping kelp forest ecosystem functioning. Further, they demonstrate that human-induced ocean warming has cascading effects on microbially mediated chemistry, with implications for coastal carbon storage and nutrient regeneration.},
}
MeSH Terms:
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*Microbiota/physiology
*Kelp/microbiology
*Metabolome
*Coral Reefs
Ecosystem
Climate Change
RevDate: 2026-08-31
Effects of different biochar application rates on CH4 emissions and Microbial Carbon Pump (MCP) mediated carbon sequestration in paddy fields: a quantitative modeling approach.
Journal of environmental management, 416:130772 pii:S0301-4797(26)02232-2 [Epub ahead of print].
Biochar amendment is a proven strategy for mitigating methane (CH4) emissions and enhancing soil carbon sequestration in rice paddies. However, the depth-dependent dynamics of microbial carbon pump (MCP)-driven recalcitrant organic carbon (ROC) formation and the underlying microbial mechanisms remain poorly characterized, particularly in the purple paddy soils of the central Sichuan Basin, China. To address this gap, we developed a novel quantitative MCP-driven ROC model and conducted a field experiment with four biochar treatments (CK, C2, C4, and C6 t ha[-1]) to investigate CH4 emissions, methane-cycling microbial community, and soil carbon fractions across a 0-80 cm profile. Biochar amendment significantly reduced CH4 emissions by 57.88-84.51% (peaking at 6 t ha[-1]) and increased methanogen and methanotroph diversity by 1.30-1.66 times. Although the concentrations of soil organic carbon (SOC), dissolved organic carbon (DOC), microbial biomass carbon (MBC), and absolute ROC decreased significantly with depth, the ROC/SOC ratio consistently increased. Crucially, our quantitative model revealed that biochar stimulated both the in vivo turnover and ex vivo modification pathways of the MCP by supplying essential labile substrates, explaining up to 92% of the variance in deep-soil carbon fractions. In conclusion, this study demonstrates that biochar serves as an effective dual-action strategy: mitigating CH4 emissions via microbiome regulation while enhancing long-term carbon sequestration through intensified MCP-driven ROC formation across the entire soil profile.
Additional Links: PMID-42673821
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PubMed:
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@article {pmid42673821,
year = {2026},
author = {Li, Y and Chen, H and Chen, J and Jiang, W and Liu, X and Liang, J and Zhang, K and Jiang, B and Luo, H and Xie, W and An, X and Chen, W and Yang, Z and Zhang, X},
title = {Effects of different biochar application rates on CH4 emissions and Microbial Carbon Pump (MCP) mediated carbon sequestration in paddy fields: a quantitative modeling approach.},
journal = {Journal of environmental management},
volume = {416},
number = {},
pages = {130772},
doi = {10.1016/j.jenvman.2026.130772},
pmid = {42673821},
issn = {1095-8630},
abstract = {Biochar amendment is a proven strategy for mitigating methane (CH4) emissions and enhancing soil carbon sequestration in rice paddies. However, the depth-dependent dynamics of microbial carbon pump (MCP)-driven recalcitrant organic carbon (ROC) formation and the underlying microbial mechanisms remain poorly characterized, particularly in the purple paddy soils of the central Sichuan Basin, China. To address this gap, we developed a novel quantitative MCP-driven ROC model and conducted a field experiment with four biochar treatments (CK, C2, C4, and C6 t ha[-1]) to investigate CH4 emissions, methane-cycling microbial community, and soil carbon fractions across a 0-80 cm profile. Biochar amendment significantly reduced CH4 emissions by 57.88-84.51% (peaking at 6 t ha[-1]) and increased methanogen and methanotroph diversity by 1.30-1.66 times. Although the concentrations of soil organic carbon (SOC), dissolved organic carbon (DOC), microbial biomass carbon (MBC), and absolute ROC decreased significantly with depth, the ROC/SOC ratio consistently increased. Crucially, our quantitative model revealed that biochar stimulated both the in vivo turnover and ex vivo modification pathways of the MCP by supplying essential labile substrates, explaining up to 92% of the variance in deep-soil carbon fractions. In conclusion, this study demonstrates that biochar serves as an effective dual-action strategy: mitigating CH4 emissions via microbiome regulation while enhancing long-term carbon sequestration through intensified MCP-driven ROC formation across the entire soil profile.},
}
RevDate: 2026-08-31
Association Between Ultra-Processed Foods and Clinical Relapse in Crohn's Disease: A Systematic Review and Meta-Analysis.
Journal of the Academy of Nutrition and Dietetics pii:S2212-2672(26)00553-8 [Epub ahead of print].
BACKGROUND: Higher consumption of ultra-processed foods (UPFs) has been linked to an increased risk of developing Crohn's Disease (CD) and is hypothesized to worsen activity of CD through mechanisms such as gut microbiome alterations and increased intestinal permeability.
OBJECTIVE: To assess the association between dietary intake of UPFs and clinical relapse in patients with CD.
METHODS: A comprehensive search of MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials from database inception to March 18, 2025. At the time of the search, records in the Cochrane Central Register of Controlled Trials were available through February 28, 2025. The study included prospective cohort studies and randomized controlled trials enrolling adults with CD in clinical remission, comparing higher versus lower UPF intake or no UPF, with a minimum follow-up of 6 months. Studies not meeting these criteria, including retrospective designs and non-English publications, were excluded. The primary outcome was clinical relapse within one year. Study quality was assessed using the Newcastle-Ottawa Scale, and overall certainty of evidence was evaluated using the GRADE framework. Pooled odd ratios (ORs) and 95% confidence intervals (CIs) were calculated using DerSimonian-Laird random-effects meta-analysis based on estimates and standard errors. Heterogeneity was assessed using the I[2] statistic. The publication bias was planned to assess using funnel plots and statistical tests if sufficient studies were available.
RESULTS: 1945 studies were identified through the search. After removing duplicates, and abstract screening, 13 studies were selected for full-text review and 3 prospective cohort studies involving 276 patients with CD were included in the analysis. Pooled analysis demonstrated a significant association between UPF intake and relapse in patients with CD. Patients with higher versus lower UPF intake had increased odds for clinical relapse (OR 2.27, 95% CI 1.01-5.13, p = 0.048; I[2] = 20.95%), although the certainty of the evidence was rated as very low according to the GRADE framework.
CONCLUSION: This study suggests that higher UPF intake is associated with increased odds of clinical relapse in patients with Crohn's disease in remission. However, the certainty of evidence is very low, and additional well-designed prospective studies and randomized trials are required before firm dietary recommendations can be made.
Additional Links: PMID-42674185
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PubMed:
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@article {pmid42674185,
year = {2026},
author = {Samnani, S and Tran, HR and Vagianos, K and Bernstein, CN and Marshall, JK and Narula, N},
title = {Association Between Ultra-Processed Foods and Clinical Relapse in Crohn's Disease: A Systematic Review and Meta-Analysis.},
journal = {Journal of the Academy of Nutrition and Dietetics},
volume = {},
number = {},
pages = {156838},
doi = {10.1016/j.jand.2026.156838},
pmid = {42674185},
issn = {2212-2672},
abstract = {BACKGROUND: Higher consumption of ultra-processed foods (UPFs) has been linked to an increased risk of developing Crohn's Disease (CD) and is hypothesized to worsen activity of CD through mechanisms such as gut microbiome alterations and increased intestinal permeability.
OBJECTIVE: To assess the association between dietary intake of UPFs and clinical relapse in patients with CD.
METHODS: A comprehensive search of MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials from database inception to March 18, 2025. At the time of the search, records in the Cochrane Central Register of Controlled Trials were available through February 28, 2025. The study included prospective cohort studies and randomized controlled trials enrolling adults with CD in clinical remission, comparing higher versus lower UPF intake or no UPF, with a minimum follow-up of 6 months. Studies not meeting these criteria, including retrospective designs and non-English publications, were excluded. The primary outcome was clinical relapse within one year. Study quality was assessed using the Newcastle-Ottawa Scale, and overall certainty of evidence was evaluated using the GRADE framework. Pooled odd ratios (ORs) and 95% confidence intervals (CIs) were calculated using DerSimonian-Laird random-effects meta-analysis based on estimates and standard errors. Heterogeneity was assessed using the I[2] statistic. The publication bias was planned to assess using funnel plots and statistical tests if sufficient studies were available.
RESULTS: 1945 studies were identified through the search. After removing duplicates, and abstract screening, 13 studies were selected for full-text review and 3 prospective cohort studies involving 276 patients with CD were included in the analysis. Pooled analysis demonstrated a significant association between UPF intake and relapse in patients with CD. Patients with higher versus lower UPF intake had increased odds for clinical relapse (OR 2.27, 95% CI 1.01-5.13, p = 0.048; I[2] = 20.95%), although the certainty of the evidence was rated as very low according to the GRADE framework.
CONCLUSION: This study suggests that higher UPF intake is associated with increased odds of clinical relapse in patients with Crohn's disease in remission. However, the certainty of evidence is very low, and additional well-designed prospective studies and randomized trials are required before firm dietary recommendations can be made.},
}
RevDate: 2026-08-31
Nano-bio interfaces as regulators of bacterial electron metabolism: from extracellular electron transfer to community-scale electron networks.
Biotechnology advances pii:S0734-9750(26)00235-1 [Epub ahead of print].
Nanomaterial-bacterium interactions are commonly interpreted through antibacterial mechanisms such as reactive oxygen species generation, photothermal effects, membrane disruption and ion toxicity. However, under nonlethal or sublethal conditions, nano-bio interfaces can also regulate bacterial electron metabolism by reshaping extracellular electron dissipation, interfacial charge transfer, charge-transfer resistance (Rct), redox buffering and biofilm-associated electron networks. Here, we propose a functional framework that views bacterial metabolism as an integrated process of electron generation, interfacial transfer and electron dissipation. Within this framework, nanomaterials are classified by their positions in bacterial electron-flow networks as electron sinks, electron relays or electron buffers. We further distinguish beneficial coupling from electron hijacking by determining whether enhanced interfacial electron transfer is coupled to NADH/NAD[+] balance, ATP production, membrane-potential maintenance and productive carbon-flux redistribution, or instead leads to futile electron loss, oxidative damage and energetic collapse. Extending this view from single cells to extracellular polymeric substances (EPS), electroactive biofilms and direct interspecies electron transfer (DIET), we discuss how nano-bio interfaces re-gate microbial electron flow at the community scale. This Review shifts the focus from how nanomaterials kill bacteria to how they reprogram microbial redox boundaries, providing a conceptual basis for antibacterial interface design, biofilm control, microbial sensing, biomanufacturing and microbiome engineering.
Additional Links: PMID-42674192
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PubMed:
Citation:
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@article {pmid42674192,
year = {2026},
author = {Ge, CA and Huang, EC and Zhang, Y},
title = {Nano-bio interfaces as regulators of bacterial electron metabolism: from extracellular electron transfer to community-scale electron networks.},
journal = {Biotechnology advances},
volume = {},
number = {},
pages = {109029},
doi = {10.1016/j.biotechadv.2026.109029},
pmid = {42674192},
issn = {1873-1899},
abstract = {Nanomaterial-bacterium interactions are commonly interpreted through antibacterial mechanisms such as reactive oxygen species generation, photothermal effects, membrane disruption and ion toxicity. However, under nonlethal or sublethal conditions, nano-bio interfaces can also regulate bacterial electron metabolism by reshaping extracellular electron dissipation, interfacial charge transfer, charge-transfer resistance (Rct), redox buffering and biofilm-associated electron networks. Here, we propose a functional framework that views bacterial metabolism as an integrated process of electron generation, interfacial transfer and electron dissipation. Within this framework, nanomaterials are classified by their positions in bacterial electron-flow networks as electron sinks, electron relays or electron buffers. We further distinguish beneficial coupling from electron hijacking by determining whether enhanced interfacial electron transfer is coupled to NADH/NAD[+] balance, ATP production, membrane-potential maintenance and productive carbon-flux redistribution, or instead leads to futile electron loss, oxidative damage and energetic collapse. Extending this view from single cells to extracellular polymeric substances (EPS), electroactive biofilms and direct interspecies electron transfer (DIET), we discuss how nano-bio interfaces re-gate microbial electron flow at the community scale. This Review shifts the focus from how nanomaterials kill bacteria to how they reprogram microbial redox boundaries, providing a conceptual basis for antibacterial interface design, biofilm control, microbial sensing, biomanufacturing and microbiome engineering.},
}
RevDate: 2026-08-31
A Call for Pan-European Prevention of Chronic Inflammatory Diseases and Allergies.
Additional Links: PMID-42674272
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PubMed:
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@article {pmid42674272,
year = {2026},
author = {Maaren, MSV and van Wijk, RG and Diamant, Z},
title = {A Call for Pan-European Prevention of Chronic Inflammatory Diseases and Allergies.},
journal = {Respiratory medicine},
volume = {},
number = {},
pages = {109136},
doi = {10.1016/j.rmed.2026.109136},
pmid = {42674272},
issn = {1532-3064},
}
RevDate: 2026-08-31
The airway microbiome in asthma.
Chest pii:S0012-3692(26)06527-X [Epub ahead of print].
TOPIC IMPORTANCE: Asthma is a heterogenous airways disease characterized by variable airflow limitation, airway inflammation and bronchial hyperresponsiveness. There is evidence to suggest that the airway microbiome plays an important role in asthma pathophysiology. Most microbiome studies have investigated the bacterial constituents of the microbiome and further studies are needed to investigate the role of the airway virome and mycobiome in asthma.
REVIEW FINDINGS: Airway microbiome dysbiosis is associated with asthma development, disease severity and inflammatory endotypes. However, it remains unclear whether dysbiosis drives inflammation or is a result of inflammation. Haemophilus and Moraxella alongside rhinovirus and respiratory syncytial virus have been shown to be associated with the development of asthma in children. In established asthma, airway microbiome dysbiosis is associated with severity and risk of exacerbation. Distinct airway microbiome profiles are observed for the different inflammatory endotypes. Asthmatic patients with eosinophilic inflammation have higher microbial diversity similar to healthy individuals while neutrophilic inflammation is associated with reduced microbial diversity, higher bacterial load and a pathogen-dominated microbiome profile suggesting an important role for dysbiosis in asthma that is currently refractory to anti-T2 biologic therapy.
SUMMARY: To understand the role of the microbiome in asthma, microbiome data must be integrated with other 'omic approaches' such as proteomics. Recent studies have used a multi-omic approach to investigate the microbiome and host interaction as well as identifying asthma endotypes and potential therapeutic targets. Antibiotics, probiotics, monoclonal antibodies, and diet could theoretically be used to therapeutically target the airway and gut microbiome in asthma.
Additional Links: PMID-42674280
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PubMed:
Citation:
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@article {pmid42674280,
year = {2026},
author = {Richardson, H and Pollock, J and Chan, R and Chalmers, JD},
title = {The airway microbiome in asthma.},
journal = {Chest},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chest.2026.08.032},
pmid = {42674280},
issn = {1931-3543},
abstract = {TOPIC IMPORTANCE: Asthma is a heterogenous airways disease characterized by variable airflow limitation, airway inflammation and bronchial hyperresponsiveness. There is evidence to suggest that the airway microbiome plays an important role in asthma pathophysiology. Most microbiome studies have investigated the bacterial constituents of the microbiome and further studies are needed to investigate the role of the airway virome and mycobiome in asthma.
REVIEW FINDINGS: Airway microbiome dysbiosis is associated with asthma development, disease severity and inflammatory endotypes. However, it remains unclear whether dysbiosis drives inflammation or is a result of inflammation. Haemophilus and Moraxella alongside rhinovirus and respiratory syncytial virus have been shown to be associated with the development of asthma in children. In established asthma, airway microbiome dysbiosis is associated with severity and risk of exacerbation. Distinct airway microbiome profiles are observed for the different inflammatory endotypes. Asthmatic patients with eosinophilic inflammation have higher microbial diversity similar to healthy individuals while neutrophilic inflammation is associated with reduced microbial diversity, higher bacterial load and a pathogen-dominated microbiome profile suggesting an important role for dysbiosis in asthma that is currently refractory to anti-T2 biologic therapy.
SUMMARY: To understand the role of the microbiome in asthma, microbiome data must be integrated with other 'omic approaches' such as proteomics. Recent studies have used a multi-omic approach to investigate the microbiome and host interaction as well as identifying asthma endotypes and potential therapeutic targets. Antibiotics, probiotics, monoclonal antibodies, and diet could theoretically be used to therapeutically target the airway and gut microbiome in asthma.},
}
RevDate: 2026-08-31
Simultaneous GC-MS Determination of Unsubstituted, Hydroxy-, Amino-, and Hydroxy-amino Short-Chain Fatty Acids Together with Amino Acids in Biological and Food Samples Following Derivatization.
Analytical biochemistry pii:S0003-2697(26)00197-1 [Epub ahead of print].
The simultaneous determination of short-chain fatty acids (SCFAs) and amino acids is of increasing interest, as these metabolite classes are important indicators of host metabolism and gut microbiota activity. They also serve as biomarkers for disease diagnosis and indicators of food composition. In this study, a gas chromatography-mass spectrometry method was developed for the simultaneous determination of both substituted (hydroxy-, amino- and hydroxy-amino-) and unsubstituted SCFAs, alongside amino acids, following derivatization and liquid-liquid extraction. Isobutyl chloroformate was employed as the derivatization reagent. The proposed method demonstrated excellent linearity, with coefficients of determination (R[2]) ranging from 0.9840 to 0.9992. Method limits of detection ranged from 0.011 to 7.2 μg/mL, while method limits of quantification ranged from 0.033 to 8.0 μg/mL. Intra-day precision (%RSD) ranged from 1.0% to 6.5% for biological samples and from 1.1% to 4.5% for eggs. Inter-day precision (%RSD) ranged from 1.0% to 5.6% for biological samples and from 2.0% to 6.7% for eggs. Matrix effects ranged from 98% to 108% for biological samples and from 96% to 113% for egg, while recoveries ranged from 90% to 111% and from 95% to 108%, respectively. To the best of our knowledge, this is the first GC-MS method enabling the simultaneous determination of substituted and unsubstituted SCFAs together with amino acids in a single analytical procedure. The proposed approach provides a reliable and versatile platform for metabolomics, microbiome research, clinical investigations, and food analysis, and can readily be extended to a broader range of target metabolites.
Additional Links: PMID-42674308
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@article {pmid42674308,
year = {2026},
author = {Katsari, KM and Stalikas, CD},
title = {Simultaneous GC-MS Determination of Unsubstituted, Hydroxy-, Amino-, and Hydroxy-amino Short-Chain Fatty Acids Together with Amino Acids in Biological and Food Samples Following Derivatization.},
journal = {Analytical biochemistry},
volume = {},
number = {},
pages = {116241},
doi = {10.1016/j.ab.2026.116241},
pmid = {42674308},
issn = {1096-0309},
abstract = {The simultaneous determination of short-chain fatty acids (SCFAs) and amino acids is of increasing interest, as these metabolite classes are important indicators of host metabolism and gut microbiota activity. They also serve as biomarkers for disease diagnosis and indicators of food composition. In this study, a gas chromatography-mass spectrometry method was developed for the simultaneous determination of both substituted (hydroxy-, amino- and hydroxy-amino-) and unsubstituted SCFAs, alongside amino acids, following derivatization and liquid-liquid extraction. Isobutyl chloroformate was employed as the derivatization reagent. The proposed method demonstrated excellent linearity, with coefficients of determination (R[2]) ranging from 0.9840 to 0.9992. Method limits of detection ranged from 0.011 to 7.2 μg/mL, while method limits of quantification ranged from 0.033 to 8.0 μg/mL. Intra-day precision (%RSD) ranged from 1.0% to 6.5% for biological samples and from 1.1% to 4.5% for eggs. Inter-day precision (%RSD) ranged from 1.0% to 5.6% for biological samples and from 2.0% to 6.7% for eggs. Matrix effects ranged from 98% to 108% for biological samples and from 96% to 113% for egg, while recoveries ranged from 90% to 111% and from 95% to 108%, respectively. To the best of our knowledge, this is the first GC-MS method enabling the simultaneous determination of substituted and unsubstituted SCFAs together with amino acids in a single analytical procedure. The proposed approach provides a reliable and versatile platform for metabolomics, microbiome research, clinical investigations, and food analysis, and can readily be extended to a broader range of target metabolites.},
}
RevDate: 2026-08-31
Effect of sucrose-free brazzein-sweetened ice cream on continuously monitored glycemic response in patients with metabolic dysfunction-associated steatotic liver disease: a randomized controlled double-blind crossover trial.
Clinical nutrition ESPEN pii:S2405-4577(26)02163-7 [Epub ahead of print].
BACKGROUND & AIMS: Reducing sugar intake is one of the key targets for improving metabolic health in metabolic dysfunction-associated steatotic liver disease (MASLD), and natural sugar substitutes remain insufficiently studied. Brazzein, a natural sweet protein 500-2000 times sweeter than sucrose, may allow replacement of sucrose while preserving sweetness, but clinical data are lacking. We aimed to evaluate postprandial glycemic responses to brazzein-sweetened ice cream, with and without inulin, compared with sucrose-sweetened ice cream in adults with MASLD, using continuous glucose monitoring (CGM).
METHODS: In this double-blind, randomized, 3-period crossover trial, 101 adults with MASLD (mean age: 54.6 y; 76% female; 44% with type 2 diabetes) consumed 100 g of ice cream sweetened with sucrose (14 g), brazzein (0.014%), or brazzein plus inulin (0.014% + 4 g) on separate days. Factory-calibrated CGM sensors were used. Principal analytic outcomes were glucose over 150 min and incremental area under the curve (iAUC). Linear mixed-effects models estimated treatment effects with adjustment for baseline glucose, period, sequence, and diabetes status. Complementary analyses evaluated whether between-formulation differences were explained by total carbohydrate content alone.
RESULTS: Compared with sucrose-sweetened, both brazzein-containing formulations produced smaller postprandial glucose excursions from 30 to 135 min (treatment × time interaction, P < 0.001). Model-adjusted iAUC was 66.3 mmol/L × min (95% CI: 54.5, 78.0) for sucrose, 31.7 (19.9, 43.6) for brazzein, and 34.3 (22.5, 46.1) for brazzein plus inulin formulations. Relative to sucrose-sweetened, iAUC was 52% lower with brazzein and 48% lower with brazzein plus inulin formulations (both P < 0.001), whereas brazzein and brazzein plus inulin formulations did not differ significantly. Complementary analyses showed that the between-formulation differences were not explained by total carbohydrate content alone. Exploratory analyses showed that formulation-related glucose trajectories differed according to diabetes status (P < 0.001). Within-stratum analyses showed lower iAUC for both brazzein-sweetened products relative to the sucrose control in participants with and without diabetes. No period, sequence, or carryover effects were observed.
CONCLUSIONS: In adults with MASLD, the tested sucrose-free brazzein-containing ice cream formulations produced substantially smaller acute CGM-derived postprandial glucose excursions and lower iAUC over 150 min than sucrose-sweetened ice cream. The similar responses observed with brazzein alone and brazzein plus inulin suggest that adding 4 g inulin did not abolish the acute glycemic advantage of the brazzein-containing formulation. Longer-term studies are needed to determine whether repeated substitution of sucrose-containing desserts with brazzein-sweetened alternatives translates into sustained metabolic, hepatic, microbiome, or behavioral benefits.
TRIAL REGISTRATION: ClinicalTrials.gov NCT06724913.
Additional Links: PMID-42674358
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PubMed:
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@article {pmid42674358,
year = {2026},
author = {Isakov, VA and Pilipenko, VI and Goncharov, AA and Sasunova, A},
title = {Effect of sucrose-free brazzein-sweetened ice cream on continuously monitored glycemic response in patients with metabolic dysfunction-associated steatotic liver disease: a randomized controlled double-blind crossover trial.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105066},
doi = {10.1016/j.clnesp.2026.105066},
pmid = {42674358},
issn = {2405-4577},
abstract = {BACKGROUND & AIMS: Reducing sugar intake is one of the key targets for improving metabolic health in metabolic dysfunction-associated steatotic liver disease (MASLD), and natural sugar substitutes remain insufficiently studied. Brazzein, a natural sweet protein 500-2000 times sweeter than sucrose, may allow replacement of sucrose while preserving sweetness, but clinical data are lacking. We aimed to evaluate postprandial glycemic responses to brazzein-sweetened ice cream, with and without inulin, compared with sucrose-sweetened ice cream in adults with MASLD, using continuous glucose monitoring (CGM).
METHODS: In this double-blind, randomized, 3-period crossover trial, 101 adults with MASLD (mean age: 54.6 y; 76% female; 44% with type 2 diabetes) consumed 100 g of ice cream sweetened with sucrose (14 g), brazzein (0.014%), or brazzein plus inulin (0.014% + 4 g) on separate days. Factory-calibrated CGM sensors were used. Principal analytic outcomes were glucose over 150 min and incremental area under the curve (iAUC). Linear mixed-effects models estimated treatment effects with adjustment for baseline glucose, period, sequence, and diabetes status. Complementary analyses evaluated whether between-formulation differences were explained by total carbohydrate content alone.
RESULTS: Compared with sucrose-sweetened, both brazzein-containing formulations produced smaller postprandial glucose excursions from 30 to 135 min (treatment × time interaction, P < 0.001). Model-adjusted iAUC was 66.3 mmol/L × min (95% CI: 54.5, 78.0) for sucrose, 31.7 (19.9, 43.6) for brazzein, and 34.3 (22.5, 46.1) for brazzein plus inulin formulations. Relative to sucrose-sweetened, iAUC was 52% lower with brazzein and 48% lower with brazzein plus inulin formulations (both P < 0.001), whereas brazzein and brazzein plus inulin formulations did not differ significantly. Complementary analyses showed that the between-formulation differences were not explained by total carbohydrate content alone. Exploratory analyses showed that formulation-related glucose trajectories differed according to diabetes status (P < 0.001). Within-stratum analyses showed lower iAUC for both brazzein-sweetened products relative to the sucrose control in participants with and without diabetes. No period, sequence, or carryover effects were observed.
CONCLUSIONS: In adults with MASLD, the tested sucrose-free brazzein-containing ice cream formulations produced substantially smaller acute CGM-derived postprandial glucose excursions and lower iAUC over 150 min than sucrose-sweetened ice cream. The similar responses observed with brazzein alone and brazzein plus inulin suggest that adding 4 g inulin did not abolish the acute glycemic advantage of the brazzein-containing formulation. Longer-term studies are needed to determine whether repeated substitution of sucrose-containing desserts with brazzein-sweetened alternatives translates into sustained metabolic, hepatic, microbiome, or behavioral benefits.
TRIAL REGISTRATION: ClinicalTrials.gov NCT06724913.},
}
RevDate: 2026-08-31
Saccharin Revisited: Chemistry, Metabolism, Toxicology and Human Health Risk Assessment in the Era of Evidence-Based Food Safety.
Journal of applied toxicology : JAT [Epub ahead of print].
Saccharin is one of the oldest and most extensively used nonnutritive sweeteners, valued for its intense sweetness, chemical stability and negligible caloric contribution. Since its discovery in 1879, it has been widely incorporated into foods, beverages, pharmaceuticals and personal care products, while its safety has remained the subject of considerable scientific and regulatory debate. Early experimental studies linking saccharin to bladder tumour formation in rodents raised concerns regarding its carcinogenic potential; however, subsequent mechanistic investigations, epidemiological evidence and comprehensive risk assessments have demonstrated that these findings are species-specific and not directly applicable to humans. This review provides a comprehensive and critical synthesis of current knowledge on saccharin, encompassing its chemical characteristics, physicochemical properties, industrial and pharmaceutical applications, absorption, metabolism, excretion and toxicological profile. Particular emphasis is placed on evaluating evidence related to carcinogenicity, genotoxicity, metabolic effects, oxidative stress, gut microbiota interactions and other emerging health concerns through the integration of experimental, clinical and population-based studies. In addition, the review examines the scientific basis of international regulatory decisions, discusses the challenges of translating animal toxicology findings into human health risk assessment and identifies persistent knowledge gaps requiring further investigation. Current evidence consistently supports the safety of saccharin when consumed within established acceptable daily intake limits established by international regulatory agencies. Nevertheless, well-designed long-term human studies and mechanistic investigations remain necessary to better define its potential effects on metabolic health, the gut microbiome and susceptible populations. By integrating historical evidence with contemporary advances in toxicology and regulatory science, this review provides an updated framework for understanding the safety, biological effects and public health implications of saccharin consumption.
Additional Links: PMID-42674673
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@article {pmid42674673,
year = {2026},
author = {Qadir, AM and Ahmed, AMA and Zorab, MM and Omer, RA},
title = {Saccharin Revisited: Chemistry, Metabolism, Toxicology and Human Health Risk Assessment in the Era of Evidence-Based Food Safety.},
journal = {Journal of applied toxicology : JAT},
volume = {},
number = {},
pages = {},
doi = {10.1002/jat.70423},
pmid = {42674673},
issn = {1099-1263},
abstract = {Saccharin is one of the oldest and most extensively used nonnutritive sweeteners, valued for its intense sweetness, chemical stability and negligible caloric contribution. Since its discovery in 1879, it has been widely incorporated into foods, beverages, pharmaceuticals and personal care products, while its safety has remained the subject of considerable scientific and regulatory debate. Early experimental studies linking saccharin to bladder tumour formation in rodents raised concerns regarding its carcinogenic potential; however, subsequent mechanistic investigations, epidemiological evidence and comprehensive risk assessments have demonstrated that these findings are species-specific and not directly applicable to humans. This review provides a comprehensive and critical synthesis of current knowledge on saccharin, encompassing its chemical characteristics, physicochemical properties, industrial and pharmaceutical applications, absorption, metabolism, excretion and toxicological profile. Particular emphasis is placed on evaluating evidence related to carcinogenicity, genotoxicity, metabolic effects, oxidative stress, gut microbiota interactions and other emerging health concerns through the integration of experimental, clinical and population-based studies. In addition, the review examines the scientific basis of international regulatory decisions, discusses the challenges of translating animal toxicology findings into human health risk assessment and identifies persistent knowledge gaps requiring further investigation. Current evidence consistently supports the safety of saccharin when consumed within established acceptable daily intake limits established by international regulatory agencies. Nevertheless, well-designed long-term human studies and mechanistic investigations remain necessary to better define its potential effects on metabolic health, the gut microbiome and susceptible populations. By integrating historical evidence with contemporary advances in toxicology and regulatory science, this review provides an updated framework for understanding the safety, biological effects and public health implications of saccharin consumption.},
}
RevDate: 2026-08-31
CmpDate: 2026-08-31
Intratumoral Mycobacterium abscessus promotes cytidine deaminase mutagenesis in non-small cell lung cancer.
Signal transduction and targeted therapy, 11(1):.
The intratumoral microbiota is increasingly recognized as an active component of the tumor microenvironment, yet whether it directly drives tumor mutagenesis remains unclear. Here, integrated multi-omics analysis of human non-small cell lung cancer (NSCLC) identifies Mycobacterium abscessus as a microbial determinant of APOBEC3A-associated mutagenesis. Mechanistically, the bacterial effector nucleoside diphosphate kinase (NDK) directly targets the host transcription factor IRF3 and installs a non-canonical 1-phosphohistidine modification at H263, thereby amplifying type I interferon signaling and sustaining APOBEC3A expression. This inter-kingdom phosphotransfer event links intratumoral microbial colonization to an endogenous mutational process that promotes genomic diversification. Genetic inactivation of NDK, or pharmacologic elimination using an engineered NDK-PROTAC, suppresses APOBEC3A activation and attenuates microbe driven mutagenesis. Together, these findings establish a direct microbial effector mechanism that promotes APOBEC3A-associated mutagenesis and provide a therapeutic framework to intercept microbiome driven mutagenesis in NSCLC.
Additional Links: PMID-42675040
PubMed:
Citation:
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@article {pmid42675040,
year = {2026},
author = {Li, X and Li, MT and Ou, KP and Gao, PQ and Xiao, AH and Yang, J and Li, JN and Deng, WY and Bie, MJ and Huang, AL and Shi, XF and Long, QX},
title = {Intratumoral Mycobacterium abscessus promotes cytidine deaminase mutagenesis in non-small cell lung cancer.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {42675040},
issn = {2059-3635},
mesh = {Humans ; *Carcinoma, Non-Small-Cell Lung/genetics/microbiology/pathology ; *Cytidine Deaminase/genetics ; *Lung Neoplasms/genetics/microbiology/pathology ; *Mutagenesis/genetics ; *Mycobacterium abscessus/genetics/pathogenicity ; },
abstract = {The intratumoral microbiota is increasingly recognized as an active component of the tumor microenvironment, yet whether it directly drives tumor mutagenesis remains unclear. Here, integrated multi-omics analysis of human non-small cell lung cancer (NSCLC) identifies Mycobacterium abscessus as a microbial determinant of APOBEC3A-associated mutagenesis. Mechanistically, the bacterial effector nucleoside diphosphate kinase (NDK) directly targets the host transcription factor IRF3 and installs a non-canonical 1-phosphohistidine modification at H263, thereby amplifying type I interferon signaling and sustaining APOBEC3A expression. This inter-kingdom phosphotransfer event links intratumoral microbial colonization to an endogenous mutational process that promotes genomic diversification. Genetic inactivation of NDK, or pharmacologic elimination using an engineered NDK-PROTAC, suppresses APOBEC3A activation and attenuates microbe driven mutagenesis. Together, these findings establish a direct microbial effector mechanism that promotes APOBEC3A-associated mutagenesis and provide a therapeutic framework to intercept microbiome driven mutagenesis in NSCLC.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Carcinoma, Non-Small-Cell Lung/genetics/microbiology/pathology
*Cytidine Deaminase/genetics
*Lung Neoplasms/genetics/microbiology/pathology
*Mutagenesis/genetics
*Mycobacterium abscessus/genetics/pathogenicity
RevDate: 2026-08-31
CmpDate: 2026-09-01
Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.
Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 34(2):.
BACKGROUND: Trehalose is a promising therapeutic candidate for Alzheimer's disease (AD) that is known to induce autophagy and facilitate misfolded proteins clearance such as amyloid-β and hyperphosphorylated tau. Despite there is emerging evidence that trehalose has a wider range of molecular mechanisms and thus has a greater neuroprotective profile.
OBJECTIVE: To summarize the emerging molecular mechanisms underlying the neuroprotective effects of trehalose beyond classical autophagy and discuss its therapeutic potential in AD.
METHODS: Published evidence from preclinical studies including in-vitro and in-vivo models, along with hypothetical and emerging findings from early clinical investigations was reviewed to evaluate the molecular mechanisms, therapeutic effects, and translational challenges associated with trehalose in AD.
RESULTS: In addition to classical autophagy signalling, recent studies have demonstrated that autophagy can also regulate the stability of neuronal membrane microdomains, prevent lipid bilayers disruption by amyloid proteins, and regulate stress granules dynamics that affect the function of RNA-binding proteins. Other discoveries indicate that interactions with nutrient-sensing pathways and glucose transporter systems that simulate metabolic stress, which may activate protective mechanisms separate from the inhibition of mTOR. Trehalose could also involve in lysosomal-autophagosome fusion and modulate the microglia and astrocytes activation, suggesting an important immunometabolic function. Trehalose often connects to the gut-brain axis and show their effect in gut microbiota composition, microbial metabolite signalling and gut barrier function. These effects can influence systemic inflammation, availability of short-chain fatty acids, bile acid profiles and vagus-mediated gut-to-brain communication, all of which can influence neuroinflammation networks in AD.
CONCLUSION: Although promising results have been reported, primarily from preclinical studies, with early human investigations now beginning to emerge, opportunities remain to address, such as poor oral bioavailability, penetration into the brain and long-term safety in elderly patients. Mechanistic dissection in multi-omics approaches, microbiome-stratified models and early-phase clinical testing are the areas that need to be targeted in future research. A broader understanding of the mechanisms of action of trehalose provides a good chance to reimagine its therapeutic implications and develop novel approaches to AD.
Additional Links: PMID-42675343
PubMed:
Citation:
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@article {pmid42675343,
year = {2026},
author = {Gunasekaran, SK and K, HKC and Gobinath, M and Roychowdhury, P and N, MS},
title = {Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.},
journal = {Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences},
volume = {34},
number = {2},
pages = {},
pmid = {42675343},
issn = {2008-2231},
mesh = {Humans ; *Trehalose/pharmacology/therapeutic use ; *Alzheimer Disease/drug therapy/metabolism ; Animals ; *Brain/metabolism/drug effects ; Signal Transduction/drug effects ; *Autophagy/drug effects ; *Neuroprotective Agents/pharmacology/therapeutic use ; Gastrointestinal Microbiome/drug effects ; },
abstract = {BACKGROUND: Trehalose is a promising therapeutic candidate for Alzheimer's disease (AD) that is known to induce autophagy and facilitate misfolded proteins clearance such as amyloid-β and hyperphosphorylated tau. Despite there is emerging evidence that trehalose has a wider range of molecular mechanisms and thus has a greater neuroprotective profile.
OBJECTIVE: To summarize the emerging molecular mechanisms underlying the neuroprotective effects of trehalose beyond classical autophagy and discuss its therapeutic potential in AD.
METHODS: Published evidence from preclinical studies including in-vitro and in-vivo models, along with hypothetical and emerging findings from early clinical investigations was reviewed to evaluate the molecular mechanisms, therapeutic effects, and translational challenges associated with trehalose in AD.
RESULTS: In addition to classical autophagy signalling, recent studies have demonstrated that autophagy can also regulate the stability of neuronal membrane microdomains, prevent lipid bilayers disruption by amyloid proteins, and regulate stress granules dynamics that affect the function of RNA-binding proteins. Other discoveries indicate that interactions with nutrient-sensing pathways and glucose transporter systems that simulate metabolic stress, which may activate protective mechanisms separate from the inhibition of mTOR. Trehalose could also involve in lysosomal-autophagosome fusion and modulate the microglia and astrocytes activation, suggesting an important immunometabolic function. Trehalose often connects to the gut-brain axis and show their effect in gut microbiota composition, microbial metabolite signalling and gut barrier function. These effects can influence systemic inflammation, availability of short-chain fatty acids, bile acid profiles and vagus-mediated gut-to-brain communication, all of which can influence neuroinflammation networks in AD.
CONCLUSION: Although promising results have been reported, primarily from preclinical studies, with early human investigations now beginning to emerge, opportunities remain to address, such as poor oral bioavailability, penetration into the brain and long-term safety in elderly patients. Mechanistic dissection in multi-omics approaches, microbiome-stratified models and early-phase clinical testing are the areas that need to be targeted in future research. A broader understanding of the mechanisms of action of trehalose provides a good chance to reimagine its therapeutic implications and develop novel approaches to AD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Trehalose/pharmacology/therapeutic use
*Alzheimer Disease/drug therapy/metabolism
Animals
*Brain/metabolism/drug effects
Signal Transduction/drug effects
*Autophagy/drug effects
*Neuroprotective Agents/pharmacology/therapeutic use
Gastrointestinal Microbiome/drug effects
RevDate: 2026-09-01
CmpDate: 2026-09-01
Rumen DNA virome plasticity and viral metabolic potential are associated with seasonal adaptation in grazing yak and cattle on the Qinghai-Tibet Plateau.
Journal of animal science and biotechnology, 17(1):.
BACKGROUND: As a diverse and abundant component of the rumen ecosystem, viruses interact with other microorganisms and are thought to influence microbial metabolism and host productivity. However, how the rumen virome responds to seasonal fluctuations in extreme environments remains poorly understood. Here, metagenomic analyses were used to investigate temporal dynamics of viral diversity, functional potential, and virus-host associations in the rumen virome of yak and cattle on the Qinghai-Tibet Plateau across warm and cold seasons.
RESULTS: Rumen viral communities exhibited pronounced seasonal variation in both yaks and cattle, with higher alpha diversity observed during the cold season than in the warm season. Across seasons, the yak rumen virome showed greater alpha diversity and community stability than that of cattle. In total, 27,353 temperate and 31,976 virulent viral operational taxonomic units (vOTUs) were identified, predominantly belonging to the class Caudoviricetes. These viruses were linked to microbial hosts spanning 24 bacterial and 8 archaeal phyla, with Bacteroidota and Bacillota representing the dominant lineages. Virus-host associations were more numerous in the cold season and showed distinct host-specific patterns between yaks and cattle. Cold-season virome exhibited reduced diversity of anti-defense genes and enrichment of auxiliary metabolic genes (AMGs) associated with fatty acid metabolism and hemicellulose degradation. Notably, greater divergence between yaks and cattle was observed during the cold season: the yak rumen virome was enriched in pathways related to amino acid, lipid, and energy metabolism, as well as cellulose-degrading CAZyme families, whereas the cattle rumen virome showed enrichment in general carbohydrate metabolism and replication and repair processes.
CONCLUSION: Seasonal plasticity of rumen DNA virome and pronounced interspecific divergence between yaks and cattle provide insight into their distinct microbial processes in the harsh environment of the Qinghai-Tibet Plateau. These findings suggest that the rumen DNA virome exhibits complex ecological and functional responses to seasonal variation and may be associated with host-microbiome interactions and nutrient utilization under environmental stress. This study highlights the ecological relevance of rumen viral genomes in understanding virus-microbiome interactions, microbial adaptation, and nutrient utilization in high-altitude ruminants.
Additional Links: PMID-42675508
PubMed:
Citation:
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@article {pmid42675508,
year = {2026},
author = {Guo, W and Yu, Y and Wang, W and Yu, J and Zhou, M and Long, R},
title = {Rumen DNA virome plasticity and viral metabolic potential are associated with seasonal adaptation in grazing yak and cattle on the Qinghai-Tibet Plateau.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42675508},
issn = {1674-9782},
support = {32402705//National Natural Science Foundation of China/ ; XZ202502ZY0058//Science and Technology Projects of Xizang Autonomous Region, China/ ; },
abstract = {BACKGROUND: As a diverse and abundant component of the rumen ecosystem, viruses interact with other microorganisms and are thought to influence microbial metabolism and host productivity. However, how the rumen virome responds to seasonal fluctuations in extreme environments remains poorly understood. Here, metagenomic analyses were used to investigate temporal dynamics of viral diversity, functional potential, and virus-host associations in the rumen virome of yak and cattle on the Qinghai-Tibet Plateau across warm and cold seasons.
RESULTS: Rumen viral communities exhibited pronounced seasonal variation in both yaks and cattle, with higher alpha diversity observed during the cold season than in the warm season. Across seasons, the yak rumen virome showed greater alpha diversity and community stability than that of cattle. In total, 27,353 temperate and 31,976 virulent viral operational taxonomic units (vOTUs) were identified, predominantly belonging to the class Caudoviricetes. These viruses were linked to microbial hosts spanning 24 bacterial and 8 archaeal phyla, with Bacteroidota and Bacillota representing the dominant lineages. Virus-host associations were more numerous in the cold season and showed distinct host-specific patterns between yaks and cattle. Cold-season virome exhibited reduced diversity of anti-defense genes and enrichment of auxiliary metabolic genes (AMGs) associated with fatty acid metabolism and hemicellulose degradation. Notably, greater divergence between yaks and cattle was observed during the cold season: the yak rumen virome was enriched in pathways related to amino acid, lipid, and energy metabolism, as well as cellulose-degrading CAZyme families, whereas the cattle rumen virome showed enrichment in general carbohydrate metabolism and replication and repair processes.
CONCLUSION: Seasonal plasticity of rumen DNA virome and pronounced interspecific divergence between yaks and cattle provide insight into their distinct microbial processes in the harsh environment of the Qinghai-Tibet Plateau. These findings suggest that the rumen DNA virome exhibits complex ecological and functional responses to seasonal variation and may be associated with host-microbiome interactions and nutrient utilization under environmental stress. This study highlights the ecological relevance of rumen viral genomes in understanding virus-microbiome interactions, microbial adaptation, and nutrient utilization in high-altitude ruminants.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Causal relationships between oral-gut microbiome and bone neoplasm-related phenotypes: Insights from bidirectional Mendelian randomization.
Medicine, 105(35):e50422.
The human oral and gut microbiota are the 4 largest microbial communities in the body and play crucial roles in maintaining homeostasis and influencing disease. Observational studies have suggested links between these microbiota and bone neoplasm-related phenotypes, but establishing causality has been challenging due to confounding factors and reverse causality. We conducted a bidirectional, 2-sample Mendelian randomization (MR) study to investigate evidence consistent with a potential causal association between the saliva and gut microbiota and various bone neoplasm-related phenotypes. Genetic instruments for saliva and gut microbiota were sourced from large genome-wide association studies. Inverse variance weighted was the primary MR method, supplemented by 4 other MR techniques. Sensitivity analyses, including MR-Egger regression, were performed to assess pleiotropy and heterogeneity. In the forward MR analysis, Veillonella parvula from the saliva microbiota was associated with a decreased risk of bone and connective tissue neoplasms (β: -0.236, 95% CI: [-0.275, -0.197], P = 8.20E-33). MR analyses identified genetically predicted associations between several microbial taxa and bone neoplasm-related phenotypes. Reverse MR analyses showed that genetic liability to bone neoplasm-related phenotypes was associated with variation in the composition of the oral (e.g., Order Bacteroidales, Rothia mucilaginosa) and gut microbiota (e.g., Class Methanobacteria, Genus Eubacterium oxidoreducens group). Sensitivity analyses confirmed the robustness of these findings, as no statistical evidence of substantial heterogeneity or directional horizontal pleiotropy was detected. This study provides genetic evidence supporting a bidirectional causal relationship between specific saliva and gut microbiota and bone neoplasm-related phenotypes. Our findings identify several microbial taxa as potential candidates for future biomarker development and therapeutic investigation in bone neoplasm-related phenotypes. However, these genetically informed associations require further mechanistic, experimental, and prospective clinical validation before clinical application.
Additional Links: PMID-42675685
Publisher:
PubMed:
Citation:
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@article {pmid42675685,
year = {2026},
author = {Zou, Q and Sun, F and Xu, W and Peng, D and Jiang, Z and Liao, H},
title = {Causal relationships between oral-gut microbiome and bone neoplasm-related phenotypes: Insights from bidirectional Mendelian randomization.},
journal = {Medicine},
volume = {105},
number = {35},
pages = {e50422},
doi = {10.1097/MD.0000000000050422},
pmid = {42675685},
issn = {1536-5964},
mesh = {Humans ; *Mendelian Randomization Analysis ; Phenotype ; *Gastrointestinal Microbiome/genetics ; *Saliva/microbiology ; *Bone Neoplasms/genetics/microbiology ; Genome-Wide Association Study ; *Mouth/microbiology ; Microbiota ; },
abstract = {The human oral and gut microbiota are the 4 largest microbial communities in the body and play crucial roles in maintaining homeostasis and influencing disease. Observational studies have suggested links between these microbiota and bone neoplasm-related phenotypes, but establishing causality has been challenging due to confounding factors and reverse causality. We conducted a bidirectional, 2-sample Mendelian randomization (MR) study to investigate evidence consistent with a potential causal association between the saliva and gut microbiota and various bone neoplasm-related phenotypes. Genetic instruments for saliva and gut microbiota were sourced from large genome-wide association studies. Inverse variance weighted was the primary MR method, supplemented by 4 other MR techniques. Sensitivity analyses, including MR-Egger regression, were performed to assess pleiotropy and heterogeneity. In the forward MR analysis, Veillonella parvula from the saliva microbiota was associated with a decreased risk of bone and connective tissue neoplasms (β: -0.236, 95% CI: [-0.275, -0.197], P = 8.20E-33). MR analyses identified genetically predicted associations between several microbial taxa and bone neoplasm-related phenotypes. Reverse MR analyses showed that genetic liability to bone neoplasm-related phenotypes was associated with variation in the composition of the oral (e.g., Order Bacteroidales, Rothia mucilaginosa) and gut microbiota (e.g., Class Methanobacteria, Genus Eubacterium oxidoreducens group). Sensitivity analyses confirmed the robustness of these findings, as no statistical evidence of substantial heterogeneity or directional horizontal pleiotropy was detected. This study provides genetic evidence supporting a bidirectional causal relationship between specific saliva and gut microbiota and bone neoplasm-related phenotypes. Our findings identify several microbial taxa as potential candidates for future biomarker development and therapeutic investigation in bone neoplasm-related phenotypes. However, these genetically informed associations require further mechanistic, experimental, and prospective clinical validation before clinical application.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mendelian Randomization Analysis
Phenotype
*Gastrointestinal Microbiome/genetics
*Saliva/microbiology
*Bone Neoplasms/genetics/microbiology
Genome-Wide Association Study
*Mouth/microbiology
Microbiota
RevDate: 2026-09-01
CmpDate: 2026-09-01
Characterization of gut microbiota in Vietnamese children under 5 years of age with acute and persistent diarrhea: A cross-sectional study.
Medicine, 105(35):e50433.
Gut microbiota alterations have been increasingly associated with diarrheal diseases, a leading cause of morbidity and mortality in children under 5 years of age. However, explorations examining microbiota profiles across different diarrhea durations remain limited. Our study investigated microbiota alterations in Vietnamese children with diarrhea. We recruited 97 children under 5 years of age and divided them into 3 groups: healthy children (HC; n = 48), children with acute diarrhea (AD; n = 32), and children with persistent diarrhea (PD; n = 17). We collected and analyzed stool samples using 16S rRNA gene sequencing targeting the V3 to V4 region. Taxonomic classification was performed. Alpha diversity and beta diversity metrics were estimated. LEfSe analysis identified differentially abundant bacterial taxa across groups. Gut microbiota composition and diversity differed significantly among HC, AD, and PD. Alpha diversity tended to decline from HC to AD and was lowest in PD, with significant reductions observed for the Shannon index and Faith PD. Compared with HC, AD showed enrichment of Actinobacteriota and potentially pathogenic genera, including Streptococcus and Escherichia-Shigella, together with depletion of beneficial commensal taxa. PD exhibited more pronounced dysbiosis, including expansion of Proteobacteria, depletion of Bacteroidota-associated commensals, and a significantly reduced Bacteroidota-to-Firmicutes ratio. Children with AD and PD exhibited distinct gut microbiota alterations, with more pronounced microbial dysbiosis observed in PD. These findings improve our understanding of gut microbiota alterations associated with pediatric diarrhea and support future longitudinal studies incorporating comprehensive pathogen identification to clarify temporal relationships, evaluate microbiome-based biomarkers, and explore microbiota-targeted interventions.
Additional Links: PMID-42675693
Publisher:
PubMed:
Citation:
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@article {pmid42675693,
year = {2026},
author = {Chung, NH and Nguyen, TA and Pham, VH and Nguyen, LT and Phan, NT and Vo, CQ and Nhu, NT},
title = {Characterization of gut microbiota in Vietnamese children under 5 years of age with acute and persistent diarrhea: A cross-sectional study.},
journal = {Medicine},
volume = {105},
number = {35},
pages = {e50433},
doi = {10.1097/MD.0000000000050433},
pmid = {42675693},
issn = {1536-5964},
mesh = {Humans ; Vietnam/epidemiology ; *Diarrhea/microbiology/epidemiology ; Child, Preschool ; *Gastrointestinal Microbiome/genetics ; Female ; Infant ; Male ; Cross-Sectional Studies ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Dysbiosis/microbiology ; Acute Disease ; Bacteria/classification/genetics ; },
abstract = {Gut microbiota alterations have been increasingly associated with diarrheal diseases, a leading cause of morbidity and mortality in children under 5 years of age. However, explorations examining microbiota profiles across different diarrhea durations remain limited. Our study investigated microbiota alterations in Vietnamese children with diarrhea. We recruited 97 children under 5 years of age and divided them into 3 groups: healthy children (HC; n = 48), children with acute diarrhea (AD; n = 32), and children with persistent diarrhea (PD; n = 17). We collected and analyzed stool samples using 16S rRNA gene sequencing targeting the V3 to V4 region. Taxonomic classification was performed. Alpha diversity and beta diversity metrics were estimated. LEfSe analysis identified differentially abundant bacterial taxa across groups. Gut microbiota composition and diversity differed significantly among HC, AD, and PD. Alpha diversity tended to decline from HC to AD and was lowest in PD, with significant reductions observed for the Shannon index and Faith PD. Compared with HC, AD showed enrichment of Actinobacteriota and potentially pathogenic genera, including Streptococcus and Escherichia-Shigella, together with depletion of beneficial commensal taxa. PD exhibited more pronounced dysbiosis, including expansion of Proteobacteria, depletion of Bacteroidota-associated commensals, and a significantly reduced Bacteroidota-to-Firmicutes ratio. Children with AD and PD exhibited distinct gut microbiota alterations, with more pronounced microbial dysbiosis observed in PD. These findings improve our understanding of gut microbiota alterations associated with pediatric diarrhea and support future longitudinal studies incorporating comprehensive pathogen identification to clarify temporal relationships, evaluate microbiome-based biomarkers, and explore microbiota-targeted interventions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Vietnam/epidemiology
*Diarrhea/microbiology/epidemiology
Child, Preschool
*Gastrointestinal Microbiome/genetics
Female
Infant
Male
Cross-Sectional Studies
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Dysbiosis/microbiology
Acute Disease
Bacteria/classification/genetics
RevDate: 2026-09-01
CmpDate: 2026-09-01
Healthy subjects gut microbiome modulation by Bacillus coagulans BCP92: A randomized, double-blind, placebo-controlled clinical trial.
Medicine, 105(35):e50435.
BACKGROUND: Probiotics are recognized for their ability to restore balance in the gut microbiome during dysbiosis. However, their effects on the gut microbiota of healthy individuals have rarely been investigated. This study aimed to evaluate the safety and efficacy of Bacillus coagulans (Heyndrickxia coagulans) BCP92 and its influence on microbiota composition in healthy subjects.
METHODS: In the present investigation, healthy participants (n = 48) were allocated into 2 groups and administered either Bacillus coagulans BCP92 capsules (1 billion CFU/capsule) or a placebo containing maltodextrin for 42 days. Microbiome composition and short-chain fatty acid analyses were subsequently conducted.
RESULTS: Analysis of metagenomes showed no major alterations in gut microbiome composition among participants who received B. coagulans BCP92 supplementation. However, subtle beneficial changes were observed in the treatment group, suggesting that probiotic administration may increase advantageous phyla, classes, orders, families, and some genera, while decreasing potentially harmful groups. A slight increase in short-chain fatty acids (SCFA) was also observed in the fecal samples.
CONCLUSIONS: This study implies that extended supplementation with the probiotic B. coagulans BCP92 may lead to substantial improvements in gut microbiome composition and SCFA levels.
Additional Links: PMID-42675742
Publisher:
PubMed:
Citation:
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@article {pmid42675742,
year = {2026},
author = {Shaikh, SS and Malek, F},
title = {Healthy subjects gut microbiome modulation by Bacillus coagulans BCP92: A randomized, double-blind, placebo-controlled clinical trial.},
journal = {Medicine},
volume = {105},
number = {35},
pages = {e50435},
doi = {10.1097/MD.0000000000050435},
pmid = {42675742},
issn = {1536-5964},
mesh = {Humans ; *Probiotics/administration & dosage ; *Bacillus coagulans/physiology ; Double-Blind Method ; *Gastrointestinal Microbiome/drug effects ; Feces/microbiology/chemistry ; Male ; Adult ; Fatty Acids, Volatile/analysis/metabolism ; Female ; Healthy Volunteers ; Young Adult ; Metagenome ; },
abstract = {BACKGROUND: Probiotics are recognized for their ability to restore balance in the gut microbiome during dysbiosis. However, their effects on the gut microbiota of healthy individuals have rarely been investigated. This study aimed to evaluate the safety and efficacy of Bacillus coagulans (Heyndrickxia coagulans) BCP92 and its influence on microbiota composition in healthy subjects.
METHODS: In the present investigation, healthy participants (n = 48) were allocated into 2 groups and administered either Bacillus coagulans BCP92 capsules (1 billion CFU/capsule) or a placebo containing maltodextrin for 42 days. Microbiome composition and short-chain fatty acid analyses were subsequently conducted.
RESULTS: Analysis of metagenomes showed no major alterations in gut microbiome composition among participants who received B. coagulans BCP92 supplementation. However, subtle beneficial changes were observed in the treatment group, suggesting that probiotic administration may increase advantageous phyla, classes, orders, families, and some genera, while decreasing potentially harmful groups. A slight increase in short-chain fatty acids (SCFA) was also observed in the fecal samples.
CONCLUSIONS: This study implies that extended supplementation with the probiotic B. coagulans BCP92 may lead to substantial improvements in gut microbiome composition and SCFA levels.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/administration & dosage
*Bacillus coagulans/physiology
Double-Blind Method
*Gastrointestinal Microbiome/drug effects
Feces/microbiology/chemistry
Male
Adult
Fatty Acids, Volatile/analysis/metabolism
Female
Healthy Volunteers
Young Adult
Metagenome
RevDate: 2026-09-01
Gut microbiome reorganization as a signal of physiological acclimation in escaped hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀).
Journal of fish biology [Epub ahead of print].
The introduction of aquaculture-derived hybrid fishes into natural marine ecosystems raises critical questions regarding their physiological capacity to acclimate to novel environments. The hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀), a widely farmed teleost in southern China, has increasingly been reported in coastal habitats following escape events. However, the gut microbiome-associated mechanisms underlying its acclimation to natural conditions remain poorly understood. Here, we compared the gut microbiomes of cultured and wild-caught individuals collected from two coastal regions using 16S rRNA gene sequencing integrated with functional prediction and microbial co-occurrence network analysis. Following their transition to natural habitats, escapees retained some dominant aquaculture-associated genera (Halomonas, Cetobacterium, Photobacterium and Vibrio) and clustered closely with local cultured counterparts rather than rearing condition. Beneath this partial taxonomic stability, however, the significant difference in intestinal microbiome between wild-caught and cultured individuals was manifested in predicted functional pathways and microbial interaction networks, characterized by shifts in immune-related processes, energy metabolism and keystone taxa. These findings indicate that hybrid groupers respond to environmental transition through functional and association-level plasticity rather than simple replacement of the gut microbial community. We propose that this dynamic microbiome rewiring may reflect microbiome-level adjustments associated with environmental transition, offering a microbial perspective on the acclimation of aquaculture-derived fishes to heterogeneous marine environments.
Additional Links: PMID-42675797
Publisher:
PubMed:
Citation:
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@article {pmid42675797,
year = {2026},
author = {Song, W and Du, X and Zhang, X and Zhao, J and Ding, S},
title = {Gut microbiome reorganization as a signal of physiological acclimation in escaped hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀).},
journal = {Journal of fish biology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jfb.70631},
pmid = {42675797},
issn = {1095-8649},
support = {2022YFC2601303//National Key Research and Development Program of China/ ; 3502Z20226031//Xiamen Science and Technology Program of China/ ; },
abstract = {The introduction of aquaculture-derived hybrid fishes into natural marine ecosystems raises critical questions regarding their physiological capacity to acclimate to novel environments. The hybrid grouper (Epinephelus lanceolatus ♂ × E. fuscoguttatus ♀), a widely farmed teleost in southern China, has increasingly been reported in coastal habitats following escape events. However, the gut microbiome-associated mechanisms underlying its acclimation to natural conditions remain poorly understood. Here, we compared the gut microbiomes of cultured and wild-caught individuals collected from two coastal regions using 16S rRNA gene sequencing integrated with functional prediction and microbial co-occurrence network analysis. Following their transition to natural habitats, escapees retained some dominant aquaculture-associated genera (Halomonas, Cetobacterium, Photobacterium and Vibrio) and clustered closely with local cultured counterparts rather than rearing condition. Beneath this partial taxonomic stability, however, the significant difference in intestinal microbiome between wild-caught and cultured individuals was manifested in predicted functional pathways and microbial interaction networks, characterized by shifts in immune-related processes, energy metabolism and keystone taxa. These findings indicate that hybrid groupers respond to environmental transition through functional and association-level plasticity rather than simple replacement of the gut microbial community. We propose that this dynamic microbiome rewiring may reflect microbiome-level adjustments associated with environmental transition, offering a microbial perspective on the acclimation of aquaculture-derived fishes to heterogeneous marine environments.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
The Oral Microbiome: A Silent Contributor to Systemic Health and Disease National Institutes of Health 2024 Workshop.
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 35(9):1490-1494.
Previously considered primarily only in the context of dental diseases, the oral microbiome is now recognized as a contributor to a variety of systemic diseases, including cancer and cardiovascular diseases. This commentary explores the evolving view of the oral cavity as a gateway to the body's broader physiologic networks, implicating oral microbiome dysbiosis in a spectrum of chronic conditions. Drawing on current evidence, we propose a re-envisioned healthcare model that integrates oral and systemic health and outline research gaps and clinical priorities to harness the oral microbiome for preventive and therapeutic gains, emphasizing cancer-relevant biomarkers and intervention opportunities.
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@article {pmid42676127,
year = {2026},
author = {Riscuta, G and Wali, A and Mongodin, EF and Verma, M and Cardone, M and Kim, HS and McNealy, T and Mohammed, A},
title = {The Oral Microbiome: A Silent Contributor to Systemic Health and Disease National Institutes of Health 2024 Workshop.},
journal = {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
volume = {35},
number = {9},
pages = {1490-1494},
doi = {10.1158/1055-9965.EPI-25-1553},
pmid = {42676127},
issn = {1538-7755},
mesh = {Humans ; *Microbiota ; *Mouth/microbiology ; United States ; *Cardiovascular Diseases/microbiology ; *Neoplasms/microbiology/prevention & control ; National Institutes of Health (U.S.) ; *Dysbiosis ; },
abstract = {Previously considered primarily only in the context of dental diseases, the oral microbiome is now recognized as a contributor to a variety of systemic diseases, including cancer and cardiovascular diseases. This commentary explores the evolving view of the oral cavity as a gateway to the body's broader physiologic networks, implicating oral microbiome dysbiosis in a spectrum of chronic conditions. Drawing on current evidence, we propose a re-envisioned healthcare model that integrates oral and systemic health and outline research gaps and clinical priorities to harness the oral microbiome for preventive and therapeutic gains, emphasizing cancer-relevant biomarkers and intervention opportunities.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
*Mouth/microbiology
United States
*Cardiovascular Diseases/microbiology
*Neoplasms/microbiology/prevention & control
National Institutes of Health (U.S.)
*Dysbiosis
RevDate: 2026-09-01
CmpDate: 2026-09-01
An Interpretable Machine Learning Approach to Ecologically Characterize Soil Carbon and Structure From Multi-Kingdom Microbiome, Texture and Climate.
Molecular ecology, 35(17):e70535.
Soil physical structure is a critical determinant of agricultural landscape resilience, yet standard pedotransfer functions estimate soil hydraulic and structural properties using static abiotic variables, often overlooking the biological mechanisms that actively organize soil structure. This study evaluates the predictive power of multi-kingdom microbiome data (prokaryotes, fungi and microeukaryotes) for three key soil functions: soil organic carbon (SOC) stock, mean weight diameter (MWD) and macroporosity. Using a dataset of 2251 agricultural soil samples from Quebec, Canada, we benchmarked four machine learning algorithms (HGBR, RFR, XGBoost, SVR) and four data aggregation strategies. The integration of microbiome data with texture and climate variables achieved high peak predictive accuracy (R 2 range: 0.70-0.82). Methodologically, high-resolution compositional approaches (ASV-level centered log-ratio) and kingdom-balanced absolute abundances consistently outperformed taxonomic or functional aggregations. The loss of predictive power at the family level indicates that traits governing soil physical modification are phylogenetically shallow and strain-specific. Interpretability analysis using Shapley Additive Explanations (SHAP) revealed a clear functional hierarchy in soil assembly. Specific prokaryotic and fungal features drove biochemical stabilization and physical scaffolding via the microbial carbon pump and structural enmeshment dynamics. In contrast, the architectural openness of macroporosity was fundamentally constrained by abiotic physical limits (e.g., texture). Within this physical framework, specific microbial taxa, including anaerobic bacteria and microeukaryotic amoebae, functioned not as active engineers, but as high-sensitivity bio-indicators of the resulting aeration and hydrological connectivity. These results define soil physical organization as a biologically mediated hierarchy rather than a passive geological byproduct. Consequently, we propose shifting from static pedotransfer functions to a dynamic biotransfer framework that leverages multi-kingdom omic signatures to monitor soil physical resilience and crop adaptation potential.
Additional Links: PMID-42676225
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@article {pmid42676225,
year = {2026},
author = {Jeanne, T and Prunier, J and Hogue, R and Droit, A},
title = {An Interpretable Machine Learning Approach to Ecologically Characterize Soil Carbon and Structure From Multi-Kingdom Microbiome, Texture and Climate.},
journal = {Molecular ecology},
volume = {35},
number = {17},
pages = {e70535},
doi = {10.1111/mec.70535},
pmid = {42676225},
issn = {1365-294X},
support = {//Ministère de l'Agriculture, des Pêcheries et de l'Alimentation/ ; //Natural Sciences and Engineering Research Council of Canada/ ; },
mesh = {*Soil Microbiology ; *Carbon/analysis ; *Machine Learning ; *Soil/chemistry ; *Microbiota/genetics ; *Climate ; Quebec ; Fungi/classification ; },
abstract = {Soil physical structure is a critical determinant of agricultural landscape resilience, yet standard pedotransfer functions estimate soil hydraulic and structural properties using static abiotic variables, often overlooking the biological mechanisms that actively organize soil structure. This study evaluates the predictive power of multi-kingdom microbiome data (prokaryotes, fungi and microeukaryotes) for three key soil functions: soil organic carbon (SOC) stock, mean weight diameter (MWD) and macroporosity. Using a dataset of 2251 agricultural soil samples from Quebec, Canada, we benchmarked four machine learning algorithms (HGBR, RFR, XGBoost, SVR) and four data aggregation strategies. The integration of microbiome data with texture and climate variables achieved high peak predictive accuracy (R 2 range: 0.70-0.82). Methodologically, high-resolution compositional approaches (ASV-level centered log-ratio) and kingdom-balanced absolute abundances consistently outperformed taxonomic or functional aggregations. The loss of predictive power at the family level indicates that traits governing soil physical modification are phylogenetically shallow and strain-specific. Interpretability analysis using Shapley Additive Explanations (SHAP) revealed a clear functional hierarchy in soil assembly. Specific prokaryotic and fungal features drove biochemical stabilization and physical scaffolding via the microbial carbon pump and structural enmeshment dynamics. In contrast, the architectural openness of macroporosity was fundamentally constrained by abiotic physical limits (e.g., texture). Within this physical framework, specific microbial taxa, including anaerobic bacteria and microeukaryotic amoebae, functioned not as active engineers, but as high-sensitivity bio-indicators of the resulting aeration and hydrological connectivity. These results define soil physical organization as a biologically mediated hierarchy rather than a passive geological byproduct. Consequently, we propose shifting from static pedotransfer functions to a dynamic biotransfer framework that leverages multi-kingdom omic signatures to monitor soil physical resilience and crop adaptation potential.},
}
MeSH Terms:
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*Soil Microbiology
*Carbon/analysis
*Machine Learning
*Soil/chemistry
*Microbiota/genetics
*Climate
Quebec
Fungi/classification
RevDate: 2026-09-01
CmpDate: 2026-09-01
Predictors of impaired growth during the first year of life: findings from a longitudinal cohort study in Pakistan.
Frontiers in nutrition, 13:1912329.
BACKGROUND: This study aimed to prospectively identify sociodemographic, maternal and child-related predictors of linear growth (height-for-age-z-score, HAZ) and underweight status (weight-for-age- z-score, WAZ) at 12 months among infants from the CHAMP longitudinal cohort in Pakistan.
METHODS: We analysed data from the Child Health and Microbiome Development Study (CHAMP), a prospective cohort of 70 mother-infant dyads (72 infants, including one set of triplets) recruited within 0-28 days postpartum from rural District Swat, Pakistan, and followed at 3, 6 and 12 months, using sociodemographic, anthropometric, dietary intake and morbidity data. Weight-for-age (WAZ) and height-for-age (HAZ) z-scores were computed against the 2006 WHO Child Growth Standards. A time-staged multivariable linear regression models were fitted separately for four domains (sociodemographic, maternal, infant morbidity and infant feeding) with WAZ and HAZ at 12 months as primary outcomes. All models were adjusted for infant sex and maternal education.
RESULTS: Anthropometric assessment showed a sharp decline in WAZ between recruitment and 3-months with partial recovery thereafter, whereas HAZ improved initially but declined again at 6 and 12 months. Among all measured predictors, maternal education emerged as the most consistent upstream correlate of growth, showing positive associations with both WAZ and HAZ across sociodemographic, maternal, morbidity and feeding models. In addition, feeding practice at 6 months provided an overall statistical significance (WAZ: R [2] = 0.159, p = 0.030; HAZ: R [2] = 0.157, p = 0.032) with respect to growth. Within this model, exclusive breastfeeding for less than 6 months was associated with lower HAZ (B = -0.613, 95% CI: -1.166 to -0.060, p = 0.030), while egg and/or flesh food consumption showed a positive but borderline association with WAZ (B = 0.550, 95% CI: -0.106 to 1.205, p = 0.099).
CONCLUSION: Maternal education and infant feeding practices (specifically, not maintaining exclusive breastfeeding to 6 months and the consumption of animal-sourced foods at 6 months) were associated with infant growth during the first year of life. The exclusive breastfeeding association was attenuated after adjustment for baseline height-for-age and should be regarded as suggestive. These findings are hypothesis-generating and require confirmation in adequately powered studies.
Additional Links: PMID-42676361
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Citation:
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@article {pmid42676361,
year = {2026},
author = {Saidal, A and Ghani, M and Melhem, AL and Khattak, MI and Ullah, Q and Hajira, B and Shaheen, S and Tariq, K and Al Nabhani, Z and Andrews, SC and Alfheeaid, HA and Shahzad, M},
title = {Predictors of impaired growth during the first year of life: findings from a longitudinal cohort study in Pakistan.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1912329},
pmid = {42676361},
issn = {2296-861X},
abstract = {BACKGROUND: This study aimed to prospectively identify sociodemographic, maternal and child-related predictors of linear growth (height-for-age-z-score, HAZ) and underweight status (weight-for-age- z-score, WAZ) at 12 months among infants from the CHAMP longitudinal cohort in Pakistan.
METHODS: We analysed data from the Child Health and Microbiome Development Study (CHAMP), a prospective cohort of 70 mother-infant dyads (72 infants, including one set of triplets) recruited within 0-28 days postpartum from rural District Swat, Pakistan, and followed at 3, 6 and 12 months, using sociodemographic, anthropometric, dietary intake and morbidity data. Weight-for-age (WAZ) and height-for-age (HAZ) z-scores were computed against the 2006 WHO Child Growth Standards. A time-staged multivariable linear regression models were fitted separately for four domains (sociodemographic, maternal, infant morbidity and infant feeding) with WAZ and HAZ at 12 months as primary outcomes. All models were adjusted for infant sex and maternal education.
RESULTS: Anthropometric assessment showed a sharp decline in WAZ between recruitment and 3-months with partial recovery thereafter, whereas HAZ improved initially but declined again at 6 and 12 months. Among all measured predictors, maternal education emerged as the most consistent upstream correlate of growth, showing positive associations with both WAZ and HAZ across sociodemographic, maternal, morbidity and feeding models. In addition, feeding practice at 6 months provided an overall statistical significance (WAZ: R [2] = 0.159, p = 0.030; HAZ: R [2] = 0.157, p = 0.032) with respect to growth. Within this model, exclusive breastfeeding for less than 6 months was associated with lower HAZ (B = -0.613, 95% CI: -1.166 to -0.060, p = 0.030), while egg and/or flesh food consumption showed a positive but borderline association with WAZ (B = 0.550, 95% CI: -0.106 to 1.205, p = 0.099).
CONCLUSION: Maternal education and infant feeding practices (specifically, not maintaining exclusive breastfeeding to 6 months and the consumption of animal-sourced foods at 6 months) were associated with infant growth during the first year of life. The exclusive breastfeeding association was attenuated after adjustment for baseline height-for-age and should be regarded as suggestive. These findings are hypothesis-generating and require confirmation in adequately powered studies.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Spatiotemporal and tissue-specific dynamics of bacterial communities in adult female Ixodes ricinus during a four-year period.
Frontiers in cellular and infection microbiology, 16:1880365.
INTRODUCTION: The hard tick Ixodes ricinus serves as vector for life-threatening tick-borne diseases (TBDs) such as Lyme borreliosis, relapsing fever, and tick-borne encephalitis. Due to the ticks` ability to adjust to climate changes, their habitat is expanding quickly across Europe, and the incidences of TBD´s are increasing. Therefore, to better understand and control TBDs it is essential to expand the knowledge about the ticks´ microbiome, particularly the spatiotemporal and tissue-specific dynamics of I. ricinus bacterial community. This study was designed to investigate the differences in the detected bacterial communities according to the locations, where ticks had been collected, according to ticks´ tissue types and to seasonal impacts.
MATERIALS AND METHODS: A total of 723 adult female I. ricinus were collected from two locations in Bavaria over a four-year period. A defined number of individual ticks were dissected; DNA was extracted from tissue samples or complete ticks, and subsequently 16S rRNA-gene amplicon sequencing was performed.
RESULTS AND DISCUSSION: No clear impact of the seasons was detected across the complete four-year period. However, a yearly seasonal pattern was observed in spring (Sp) compared to autumn (Au). Particularly, Sp22, Sp23 and Sp24 showed no difference in effective richness. These results are consistent with previous studies. While the species richness changed between different locations, the effective richness did not. Specific tissue samples of the ticks recovered by dissection (salivary glands, midgut, exoskeleton) carried significant, distinct bacterial communities. The genus Candidatus Midichloria was most abundant and was detected in all tissue types. Borrelia spp. were not detected in any of the collected samples, besides in the mock communities, possibly due to limitations in 16S rRNA gene analysis.
Additional Links: PMID-42676372
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@article {pmid42676372,
year = {2026},
author = {Heuser, SL and Zenner, C and Wiesinger, A and Gänzle, M and Hiereth, S and Girl, P and Neuhaus, K and Straubinger, RK},
title = {Spatiotemporal and tissue-specific dynamics of bacterial communities in adult female Ixodes ricinus during a four-year period.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1880365},
pmid = {42676372},
issn = {2235-2988},
mesh = {Animals ; *Ixodes/microbiology ; Female ; RNA, Ribosomal, 16S/genetics ; Seasons ; *Bacteria/classification/genetics/isolation & purification ; DNA, Bacterial/genetics ; *Microbiota ; Sequence Analysis, DNA ; Spatio-Temporal Analysis ; Germany ; DNA, Ribosomal/genetics/chemistry ; },
abstract = {INTRODUCTION: The hard tick Ixodes ricinus serves as vector for life-threatening tick-borne diseases (TBDs) such as Lyme borreliosis, relapsing fever, and tick-borne encephalitis. Due to the ticks` ability to adjust to climate changes, their habitat is expanding quickly across Europe, and the incidences of TBD´s are increasing. Therefore, to better understand and control TBDs it is essential to expand the knowledge about the ticks´ microbiome, particularly the spatiotemporal and tissue-specific dynamics of I. ricinus bacterial community. This study was designed to investigate the differences in the detected bacterial communities according to the locations, where ticks had been collected, according to ticks´ tissue types and to seasonal impacts.
MATERIALS AND METHODS: A total of 723 adult female I. ricinus were collected from two locations in Bavaria over a four-year period. A defined number of individual ticks were dissected; DNA was extracted from tissue samples or complete ticks, and subsequently 16S rRNA-gene amplicon sequencing was performed.
RESULTS AND DISCUSSION: No clear impact of the seasons was detected across the complete four-year period. However, a yearly seasonal pattern was observed in spring (Sp) compared to autumn (Au). Particularly, Sp22, Sp23 and Sp24 showed no difference in effective richness. These results are consistent with previous studies. While the species richness changed between different locations, the effective richness did not. Specific tissue samples of the ticks recovered by dissection (salivary glands, midgut, exoskeleton) carried significant, distinct bacterial communities. The genus Candidatus Midichloria was most abundant and was detected in all tissue types. Borrelia spp. were not detected in any of the collected samples, besides in the mock communities, possibly due to limitations in 16S rRNA gene analysis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Ixodes/microbiology
Female
RNA, Ribosomal, 16S/genetics
Seasons
*Bacteria/classification/genetics/isolation & purification
DNA, Bacterial/genetics
*Microbiota
Sequence Analysis, DNA
Spatio-Temporal Analysis
Germany
DNA, Ribosomal/genetics/chemistry
RevDate: 2026-09-01
CmpDate: 2026-09-01
rCCLasso: a robust framework for microbial correlation network analysis reveals age-related microbial dynamics.
Frontiers in cellular and infection microbiology, 16:1828471.
INTRODUCTION: The human gut microbiome continues to evolve beyond early adulthood, yet most microbiome aging studies focus on changes in individual taxa or overall diversity, leaving microbial interaction dynamics largely unexplored. Correlation-based microbial networks offer an interpretable framework for studying such interactions but are challenging to estimate from compositional microbiome data. Although compositionality-aware methods such as CCLasso provide principled multivariate inference, we identify a previously overlooked limitation: sensitivity to random seeds, which leads to unstable correlation estimates and irreproducible significance assessments.
METHODS: To address this issue, we propose Robust CCLasso (rCCLasso), a statistically rigorous framework that stabilizes microbial correlation estimation by integrating CCLasso outputs across multiple runs. rCCLasso aggregates sparse correlation estimates using median-based integration with positive-definite projection and combines run-specific inference through the Cauchy combination test with an additional stability criterion to control type-I error. The method is naturally parallelizable and computationally scalable.
RESULTS: Simulation studies demonstrate that rCCLasso improves inferential stability, type-I error control, and power relative to the original CCLasso. Applying rCCLasso to data from over 4,000 healthy adults in the American Gut Project (ages 18--101), we uncover age-related microbial network dynamics, characterized by marked fluctuations from early to mid-adulthood, followed by a relatively stable phase and a substantial decline in network strength in the elderly group.
DISCUSSION: Together, these results establish rCCLasso as a robust and interpretable framework for studying microbial networks in aging research.
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@article {pmid42676412,
year = {2026},
author = {Xie, T and Zhou, J and Wang, Y},
title = {rCCLasso: a robust framework for microbial correlation network analysis reveals age-related microbial dynamics.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1828471},
pmid = {42676412},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Aging ; *Microbial Interactions ; Computer Simulation ; *Computational Biology/methods ; },
abstract = {INTRODUCTION: The human gut microbiome continues to evolve beyond early adulthood, yet most microbiome aging studies focus on changes in individual taxa or overall diversity, leaving microbial interaction dynamics largely unexplored. Correlation-based microbial networks offer an interpretable framework for studying such interactions but are challenging to estimate from compositional microbiome data. Although compositionality-aware methods such as CCLasso provide principled multivariate inference, we identify a previously overlooked limitation: sensitivity to random seeds, which leads to unstable correlation estimates and irreproducible significance assessments.
METHODS: To address this issue, we propose Robust CCLasso (rCCLasso), a statistically rigorous framework that stabilizes microbial correlation estimation by integrating CCLasso outputs across multiple runs. rCCLasso aggregates sparse correlation estimates using median-based integration with positive-definite projection and combines run-specific inference through the Cauchy combination test with an additional stability criterion to control type-I error. The method is naturally parallelizable and computationally scalable.
RESULTS: Simulation studies demonstrate that rCCLasso improves inferential stability, type-I error control, and power relative to the original CCLasso. Applying rCCLasso to data from over 4,000 healthy adults in the American Gut Project (ages 18--101), we uncover age-related microbial network dynamics, characterized by marked fluctuations from early to mid-adulthood, followed by a relatively stable phase and a substantial decline in network strength in the elderly group.
DISCUSSION: Together, these results establish rCCLasso as a robust and interpretable framework for studying microbial networks in aging research.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
*Aging
*Microbial Interactions
Computer Simulation
*Computational Biology/methods
RevDate: 2026-09-01
CmpDate: 2026-09-01
Light governed plant-microbe interactions: the role of light in biotic stress resilience.
Physiology and molecular biology of plants : an international journal of functional plant biology, 32(9):1939-1953.
The global agricultural system is continuously facing many threats that arise from phytopathogens, which pose a serious challenge to food security worldwide. Synthetic biology approaches and advances in biotechnology have developed various methods to control these diseases, they are not yet fully effective in protecting plants from all phytopathogens. In this context, nature offers an alternative solution through plant associated microbiome. These beneficial microorganisms play a crucial role in mediating plant survival under biotic stress by influencing host immunity and metabolic responses. A better understanding of plant-microbe interactions at both genetic and metabolite levels is important. These interactions are controlled by complex regulatory networks and studying them will help us use their full potential. Consequently, research is expanding into how environmental factors, specifically light, influence plant physiology, immunity and secondary metabolism. Recent studies have suggested that light not only shapes plant immunity but also modulates the accumulation and behaviour of associated microbial community, therefore influencing the outcome of biotic stress interactions. This review focuses on the role of light as a regulatory signal in plant-microbe interactions under biotic stress. It explains how light controls secondary metabolite production and plant defence mechanisms. It also highlights how light responsive pathways can be used to develop disease-resistant and climate smart crops. The integration of photobiology with microbiome research may open new approaches for sustainable and resilient agricultural systems. This approach can help address the challenges posed by emerging phytopathogen.
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@article {pmid42676416,
year = {2026},
author = {Sharma, E and Shrivastava, V and Aeron, R and Sharma, P and Baliyan, S and Pandey, S},
title = {Light governed plant-microbe interactions: the role of light in biotic stress resilience.},
journal = {Physiology and molecular biology of plants : an international journal of functional plant biology},
volume = {32},
number = {9},
pages = {1939-1953},
pmid = {42676416},
issn = {0971-5894},
abstract = {The global agricultural system is continuously facing many threats that arise from phytopathogens, which pose a serious challenge to food security worldwide. Synthetic biology approaches and advances in biotechnology have developed various methods to control these diseases, they are not yet fully effective in protecting plants from all phytopathogens. In this context, nature offers an alternative solution through plant associated microbiome. These beneficial microorganisms play a crucial role in mediating plant survival under biotic stress by influencing host immunity and metabolic responses. A better understanding of plant-microbe interactions at both genetic and metabolite levels is important. These interactions are controlled by complex regulatory networks and studying them will help us use their full potential. Consequently, research is expanding into how environmental factors, specifically light, influence plant physiology, immunity and secondary metabolism. Recent studies have suggested that light not only shapes plant immunity but also modulates the accumulation and behaviour of associated microbial community, therefore influencing the outcome of biotic stress interactions. This review focuses on the role of light as a regulatory signal in plant-microbe interactions under biotic stress. It explains how light controls secondary metabolite production and plant defence mechanisms. It also highlights how light responsive pathways can be used to develop disease-resistant and climate smart crops. The integration of photobiology with microbiome research may open new approaches for sustainable and resilient agricultural systems. This approach can help address the challenges posed by emerging phytopathogen.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
From Mouth to Mind: Unraveling the Oral Microbiome's Role in Orofacial Pain and Neurodegeneration.
Journal of clinical practice and research, 48(4):356-367.
The human oral cavity hosts a diverse and dynamic microbiome comprising more than 700 microbial species, which plays a crucial role in maintaining oral and systemic health. Oral dysbiosis, defined as disruption of this microbial balance, has been increasingly implicated not only in periodontal disease but also in the pathogenesis of orofacial pain and neurodegenerative diseases. Key pathogens, such as Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum, have been proposed to release virulence factors, including lipopolysaccharides and gingipains, which may activate immune pathways and nociceptors, thereby driving peripheral sensitization and neuroinflammation. These organisms have also been suggested to breach mucosal and vascular barriers, enter the systemic circulation, and, in some cases, access the central nervous system. Evidence has linked oral pathogens to Alzheimer's disease, Parkinson's disease, autism spectrum disorder, and multiple sclerosis. Notably, P. gingivalis and its gingipains have been identified in postmortem brain tissue from patients with Alzheimer's disease, with proposed roles in neuroinflammation and amyloid plaque formation. Salivary microbial alterations in burning mouth syndrome and temporomandibular disorders further highlight the influence of the oral microbiome on neuropathic pain. Therefore, the oral-gut-brain axis represents a novel and promising area of investigation, offering potential diagnostic biomarkers and targeted microbial therapies for the management of chronic orofacial pain and neurological disorders.
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@article {pmid42676548,
year = {2026},
author = {Moses, S and Phulambrikar, T and Dosi, T},
title = {From Mouth to Mind: Unraveling the Oral Microbiome's Role in Orofacial Pain and Neurodegeneration.},
journal = {Journal of clinical practice and research},
volume = {48},
number = {4},
pages = {356-367},
pmid = {42676548},
issn = {2980-2156},
abstract = {The human oral cavity hosts a diverse and dynamic microbiome comprising more than 700 microbial species, which plays a crucial role in maintaining oral and systemic health. Oral dysbiosis, defined as disruption of this microbial balance, has been increasingly implicated not only in periodontal disease but also in the pathogenesis of orofacial pain and neurodegenerative diseases. Key pathogens, such as Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum, have been proposed to release virulence factors, including lipopolysaccharides and gingipains, which may activate immune pathways and nociceptors, thereby driving peripheral sensitization and neuroinflammation. These organisms have also been suggested to breach mucosal and vascular barriers, enter the systemic circulation, and, in some cases, access the central nervous system. Evidence has linked oral pathogens to Alzheimer's disease, Parkinson's disease, autism spectrum disorder, and multiple sclerosis. Notably, P. gingivalis and its gingipains have been identified in postmortem brain tissue from patients with Alzheimer's disease, with proposed roles in neuroinflammation and amyloid plaque formation. Salivary microbial alterations in burning mouth syndrome and temporomandibular disorders further highlight the influence of the oral microbiome on neuropathic pain. Therefore, the oral-gut-brain axis represents a novel and promising area of investigation, offering potential diagnostic biomarkers and targeted microbial therapies for the management of chronic orofacial pain and neurological disorders.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Disrupted terminal bilirubin catabolism links Lachnospiraceae depletion to inflammatory bowel disease.
Frontiers in microbiology, 17:1871609.
BACKGROUND: The gut microbiome mediates the reductive catabolism of bilirubin into urobilinoids, yet the bacteria and enzymes responsible for the later steps of this pathway remain largely unknown.
METHODS: Here, we combine untargeted UPLC/HRMS metabolomics with shotgun metagenomic sequencing of fecal samples from 119 participants, including patients with Crohn's disease, ulcerative colitis, and healthy controls, to map disruptions in the bilirubin catabolic pathway in inflammatory bowel disease (IBD).
RESULTS: We show that stercobilinogen and stercobilin, the terminal metabolites of this pathway, are depleted (p < 0.01) in IBD patients irrespective of disease subtype, while upstream intermediates, D-urobilinogen, remain unchanged. This metabolic bottleneck coincides with a marked reduction in members of the Lachnospiraceae family, specifically Blautia sp. SG-772 and three uncharacterized species, which show strong positive correlations with stercobilinogen and stercobilin levels.
DISCUSSION: These findings implicate Lachnospiraceae as key mediators of the yet unknown enzymatic conversion of I-urobilinogen to stercobilinogen, extending the family's known metabolic repertoire beyond short-chain fatty acid production. Given that bilirubin and its reduced metabolite stercobilinogen possess antioxidant properties, their depletion may contribute to the oxidative burden in the IBD gut. Conversely, the concurrent elevation of D-urobilin, which lacks these protective properties and has been linked to metabolic dysfunction in other contexts, may further exacerbate inflammation. Our results identify fecal bilirubin metabolites as candidate biomarkers of microbial dysbiosis in IBD and nominate specific Lachnospiraceae taxa for functional characterization of the missing stercobilinogen reductase.
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@article {pmid42676636,
year = {2026},
author = {Sabti, O and Lialin-Tzadikov, K and Ivanova, V and Dori-Bachash, M and Uzi-Gavrilov, S and Tik, Z and Mashiach, R and Zorea, A and Mizrahi, I and Segal, A and Moyal-Attias, K and Elinav, E and Meijler, MM},
title = {Disrupted terminal bilirubin catabolism links Lachnospiraceae depletion to inflammatory bowel disease.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1871609},
pmid = {42676636},
issn = {1664-302X},
abstract = {BACKGROUND: The gut microbiome mediates the reductive catabolism of bilirubin into urobilinoids, yet the bacteria and enzymes responsible for the later steps of this pathway remain largely unknown.
METHODS: Here, we combine untargeted UPLC/HRMS metabolomics with shotgun metagenomic sequencing of fecal samples from 119 participants, including patients with Crohn's disease, ulcerative colitis, and healthy controls, to map disruptions in the bilirubin catabolic pathway in inflammatory bowel disease (IBD).
RESULTS: We show that stercobilinogen and stercobilin, the terminal metabolites of this pathway, are depleted (p < 0.01) in IBD patients irrespective of disease subtype, while upstream intermediates, D-urobilinogen, remain unchanged. This metabolic bottleneck coincides with a marked reduction in members of the Lachnospiraceae family, specifically Blautia sp. SG-772 and three uncharacterized species, which show strong positive correlations with stercobilinogen and stercobilin levels.
DISCUSSION: These findings implicate Lachnospiraceae as key mediators of the yet unknown enzymatic conversion of I-urobilinogen to stercobilinogen, extending the family's known metabolic repertoire beyond short-chain fatty acid production. Given that bilirubin and its reduced metabolite stercobilinogen possess antioxidant properties, their depletion may contribute to the oxidative burden in the IBD gut. Conversely, the concurrent elevation of D-urobilin, which lacks these protective properties and has been linked to metabolic dysfunction in other contexts, may further exacerbate inflammation. Our results identify fecal bilirubin metabolites as candidate biomarkers of microbial dysbiosis in IBD and nominate specific Lachnospiraceae taxa for functional characterization of the missing stercobilinogen reductase.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Salivary gland microbiome of Anopheles gambiae: a mini-review of acquisition, composition, and functional significance.
Frontiers in insect science, 6:1911294.
The salivary gland (SG) is the final barrier for Plasmodium transmission to humans but remains comparatively understudied relative to the midgut microbiome. This review synthesizes current knowledge on SG microbiome acquisition routes, composition, and functional significance. Acquisition may occur via larval filter feeding, vertical (egg smearing), transstadial, or horizontal transmission during blood feeding, though their relative contributions are unknown. Compositional studies show Gram-negative genera Serratia, Elizabethkingia, Acinetobacter, Pseudomonas, and Asaia predominate; Plasmodium infection correlates with increased Serratia and decreased Elizabethkingia abundance. While immune-related genes (e.g., cecropins, defensin, GNBP, SRPN6) expressed in the SG may be modulated by resident bacteria, direct evidence of their effect on sporozoite invasion remains lacking. Gram-negative bacteria trigger Toll, Imd, and JAK-STAT pathways, but emerging evidence suggests the SG may mount a distinct, locally independent immune response compared to the systemic pathway. Paratransgenesis using Asaia shows promise, yet SG-targeted effector delivery remains untested. Ecological pressures common in West Africa, including agricultural pesticides, insecticide resistance, and larval water contamination, may influence mosquito-associated bacteria, but no studies explicitly link these to the SG microbiome. Significant knowledge gaps persist, notably the absence of field studies in high-burden regions like Nigeria and the lack of experimental manipulation to establish causality. Addressing these priorities is critical to determine whether the SG microbiome can be exploited as a transmission-blocking target.
Additional Links: PMID-42676645
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Citation:
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@article {pmid42676645,
year = {2026},
author = {Olafusi, CO and Afolabi, IS and Ogunlana, OO},
title = {Salivary gland microbiome of Anopheles gambiae: a mini-review of acquisition, composition, and functional significance.},
journal = {Frontiers in insect science},
volume = {6},
number = {},
pages = {1911294},
pmid = {42676645},
issn = {2673-8600},
abstract = {The salivary gland (SG) is the final barrier for Plasmodium transmission to humans but remains comparatively understudied relative to the midgut microbiome. This review synthesizes current knowledge on SG microbiome acquisition routes, composition, and functional significance. Acquisition may occur via larval filter feeding, vertical (egg smearing), transstadial, or horizontal transmission during blood feeding, though their relative contributions are unknown. Compositional studies show Gram-negative genera Serratia, Elizabethkingia, Acinetobacter, Pseudomonas, and Asaia predominate; Plasmodium infection correlates with increased Serratia and decreased Elizabethkingia abundance. While immune-related genes (e.g., cecropins, defensin, GNBP, SRPN6) expressed in the SG may be modulated by resident bacteria, direct evidence of their effect on sporozoite invasion remains lacking. Gram-negative bacteria trigger Toll, Imd, and JAK-STAT pathways, but emerging evidence suggests the SG may mount a distinct, locally independent immune response compared to the systemic pathway. Paratransgenesis using Asaia shows promise, yet SG-targeted effector delivery remains untested. Ecological pressures common in West Africa, including agricultural pesticides, insecticide resistance, and larval water contamination, may influence mosquito-associated bacteria, but no studies explicitly link these to the SG microbiome. Significant knowledge gaps persist, notably the absence of field studies in high-burden regions like Nigeria and the lack of experimental manipulation to establish causality. Addressing these priorities is critical to determine whether the SG microbiome can be exploited as a transmission-blocking target.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Drug-resistant bacterial infections in end-stage liver disease: immune imbalance and intervention advances.
Frontiers in immunology, 17:1888293.
Patients with end-stage liver disease (ESLD) face a markedly elevated risk of infections caused by multidrug-resistant (MDR) and extensively drug-resistant (XDR) bacteria. This vulnerability worsens prognosis and severely limits therapeutic options. The underlying mechanisms extend beyond hepatic synthetic and detoxification failure to encompass a complex and multifaceted state of immune dysfunction. In this review, we synthesize current evidence on how ESLD-associated immune defects drive susceptibility to drug-resistant infections. We examine key abnormalities across multiple interconnected domains: depletion and dysfunction of Kupffer cells, complement deficiency, T-cell exhaustion with regulatory T-cell expansion, disruption of the gut-liver axis, immunometabolic reprogramming driven by hyperammonemia and lactate accumulation, and upregulation of immune checkpoint molecules such as PD-1/PD-L1. These pathways collectively promote colonization, persistence, and therapeutic refractoriness of MDR pathogens. We also evaluate emerging therapeutic strategies targeting these immune defects, including checkpoint inhibitors, cytokine and cellular therapies, microbiome modulation, and metabolic interventions, while acknowledging the challenges that limit their clinical translation. By proposing an integrated framework that links distinct immune defects to MDR infection pathogenesis, we aim to guide the development of biomarker-driven, personalized immunomodulatory approaches that complement antimicrobial therapy and ultimately improve outcomes in this high-risk population.
Additional Links: PMID-42676711
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@article {pmid42676711,
year = {2026},
author = {Liu, J and Wu, J and Zheng, X},
title = {Drug-resistant bacterial infections in end-stage liver disease: immune imbalance and intervention advances.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1888293},
pmid = {42676711},
issn = {1664-3224},
mesh = {Humans ; *Bacterial Infections/immunology/drug therapy/microbiology ; Animals ; *End Stage Liver Disease/immunology/complications/microbiology ; *Drug Resistance, Multiple, Bacterial/immunology ; Host-Directed Therapy ; T-Cell Exhaustion ; },
abstract = {Patients with end-stage liver disease (ESLD) face a markedly elevated risk of infections caused by multidrug-resistant (MDR) and extensively drug-resistant (XDR) bacteria. This vulnerability worsens prognosis and severely limits therapeutic options. The underlying mechanisms extend beyond hepatic synthetic and detoxification failure to encompass a complex and multifaceted state of immune dysfunction. In this review, we synthesize current evidence on how ESLD-associated immune defects drive susceptibility to drug-resistant infections. We examine key abnormalities across multiple interconnected domains: depletion and dysfunction of Kupffer cells, complement deficiency, T-cell exhaustion with regulatory T-cell expansion, disruption of the gut-liver axis, immunometabolic reprogramming driven by hyperammonemia and lactate accumulation, and upregulation of immune checkpoint molecules such as PD-1/PD-L1. These pathways collectively promote colonization, persistence, and therapeutic refractoriness of MDR pathogens. We also evaluate emerging therapeutic strategies targeting these immune defects, including checkpoint inhibitors, cytokine and cellular therapies, microbiome modulation, and metabolic interventions, while acknowledging the challenges that limit their clinical translation. By proposing an integrated framework that links distinct immune defects to MDR infection pathogenesis, we aim to guide the development of biomarker-driven, personalized immunomodulatory approaches that complement antimicrobial therapy and ultimately improve outcomes in this high-risk population.},
}
MeSH Terms:
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Humans
*Bacterial Infections/immunology/drug therapy/microbiology
Animals
*End Stage Liver Disease/immunology/complications/microbiology
*Drug Resistance, Multiple, Bacterial/immunology
Host-Directed Therapy
T-Cell Exhaustion
RevDate: 2026-09-01
CmpDate: 2026-09-01
Correlation between oral microbiome characteristics and clinical phenotypes in patients with GERD and its changes after anti-reflux surgery.
Frontiers in microbiology, 17:1878947.
BACKGROUND: Gastroesophageal reflux disease is defined by the reflux of gastroduodenal material into the esophagus, leading to troublesome symptoms and complications. Although the gastrointestinal microbiome has been increasingly implicated in gastroesophageal reflux disease pathogenesis, existing research has largely centered on esophageal and intestinal microbiota. The alterations and clinical relevance of the oral microbiome in gastroesophageal reflux disease remain underexplored. Therefore, this study was designed to: (1) systematically compare the oral microbiome structure between gastroesophageal reflux disease patients and healthy controls, and to examine the correlations between differentially abundant microbial taxa and key clinical phenotypes; (2) longitudinally assess the dynamic changes in the oral microbiome after anti-reflux surgery.
METHODS: We conducted a study integrating a case-control design with a longitudinal self-controlled component. Initially, 40 patients and 20 healthy volunteers were enrolled. Following exclusions based on diagnostic confirmation, 36 gastroesophageal reflux disease patients comprised the preoperative group (Group Pre), and 17 age-, gender-, and BMI-matched healthy volunteers served as controls (Group HC). Non-stimulated whole saliva samples were collected from all participants. A subgroup of 18 patients from Group Pre subsequently underwent laparoscopic fundoplication. Their saliva samples collected 3 months postoperatively constituted the postoperative group (Group Post) for longitudinal comparison. The V3-V4 hypervariable regions of the bacterial 16S rRNA gene were amplified and sequenced using high-throughput sequencing. Sequencing data were processed and analyzed with bioinformatics pipelines to evaluate α- and β-diversity. Differential microbial features across groups were identified using Linear Discriminant Analysis Effect Size. Correlations between microbial relative abundance and clinical parameters were assessed via Spearman's rank correlation. Changes in the microbiome following surgery were evaluated using paired non-parametric statistical tests.
RESULTS: (1) Cross-sectional comparisons: no significant differences were observed in α-diversity indices (ACE, Chao1, Shannon, and Simpson; all P > 0.05) of the oral microbiome between GERD patients (Group Pre) and healthy controls (Group HC). In contrast, β-diversity analysis indicated a significant overall structural disparity between the groups (PERMANOVA, R [2] = 0.044, P = 0.003). Linear Discriminant Analysis Effect Size (LEfSe) identified discriminant taxa distinguishing the two groups, with genera like Alloprevotella and Veillonella being enriched in Group Pre, and Streptococcus enriched in Group HC. Furthermore, Spearman correlation analyses identified significant associations between specific genera and clinical parameters: the relative abundance of Veillonella showed a positive correlation with the gastroesophageal reflux disease questionaire score (r = 0.347, P = 0.038), and that of Alloprevotella correlated positively with the severity of esophagitis as graded by the Los Angeles classification (r = 0.335, P = 0.046).(2) Longitudinal analysis revealed that bacterial genera such as Veillonella, which were associated with phenotypes in cross-sectional studies, did not show significant changes in the oral microbiota between the Pre- and Post- groups. The most characteristic alteration was that the relative abundance of the pro-inflammatory genus Fusobacteriumwas succeeded by Selenomonas, a genus with potential metabolic benefits.
CONCLUSION: Our study demonstrates that gastroesophageal reflux disease is characterized by a specific oral dysbiosis, with the abundance of particular bacterial taxa correlating with clinical disease severity. Although laparoscopic anti-reflux surgery did not drastically alter the global oral microbiome architecture, it induced a targeted ecological shift. This shift was marked by the suppression of pro-inflammatory taxa, an increase in potentially beneficial commensals, and a trend toward restored α-diversity. These findings suggest that laparoscopic anti-reflux surgery may facilitate a shift of the oral microbiome toward a healthier ecological state following restoration of the anti-reflux barrier function. This observation provides a new microbiological perspective for understanding the broader physiological impact of anti-reflux surgery.
Additional Links: PMID-42676736
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Citation:
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@article {pmid42676736,
year = {2026},
author = {Wang, Z and Liu, Y and Han, Z and Wang, FK},
title = {Correlation between oral microbiome characteristics and clinical phenotypes in patients with GERD and its changes after anti-reflux surgery.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1878947},
pmid = {42676736},
issn = {1664-302X},
abstract = {BACKGROUND: Gastroesophageal reflux disease is defined by the reflux of gastroduodenal material into the esophagus, leading to troublesome symptoms and complications. Although the gastrointestinal microbiome has been increasingly implicated in gastroesophageal reflux disease pathogenesis, existing research has largely centered on esophageal and intestinal microbiota. The alterations and clinical relevance of the oral microbiome in gastroesophageal reflux disease remain underexplored. Therefore, this study was designed to: (1) systematically compare the oral microbiome structure between gastroesophageal reflux disease patients and healthy controls, and to examine the correlations between differentially abundant microbial taxa and key clinical phenotypes; (2) longitudinally assess the dynamic changes in the oral microbiome after anti-reflux surgery.
METHODS: We conducted a study integrating a case-control design with a longitudinal self-controlled component. Initially, 40 patients and 20 healthy volunteers were enrolled. Following exclusions based on diagnostic confirmation, 36 gastroesophageal reflux disease patients comprised the preoperative group (Group Pre), and 17 age-, gender-, and BMI-matched healthy volunteers served as controls (Group HC). Non-stimulated whole saliva samples were collected from all participants. A subgroup of 18 patients from Group Pre subsequently underwent laparoscopic fundoplication. Their saliva samples collected 3 months postoperatively constituted the postoperative group (Group Post) for longitudinal comparison. The V3-V4 hypervariable regions of the bacterial 16S rRNA gene were amplified and sequenced using high-throughput sequencing. Sequencing data were processed and analyzed with bioinformatics pipelines to evaluate α- and β-diversity. Differential microbial features across groups were identified using Linear Discriminant Analysis Effect Size. Correlations between microbial relative abundance and clinical parameters were assessed via Spearman's rank correlation. Changes in the microbiome following surgery were evaluated using paired non-parametric statistical tests.
RESULTS: (1) Cross-sectional comparisons: no significant differences were observed in α-diversity indices (ACE, Chao1, Shannon, and Simpson; all P > 0.05) of the oral microbiome between GERD patients (Group Pre) and healthy controls (Group HC). In contrast, β-diversity analysis indicated a significant overall structural disparity between the groups (PERMANOVA, R [2] = 0.044, P = 0.003). Linear Discriminant Analysis Effect Size (LEfSe) identified discriminant taxa distinguishing the two groups, with genera like Alloprevotella and Veillonella being enriched in Group Pre, and Streptococcus enriched in Group HC. Furthermore, Spearman correlation analyses identified significant associations between specific genera and clinical parameters: the relative abundance of Veillonella showed a positive correlation with the gastroesophageal reflux disease questionaire score (r = 0.347, P = 0.038), and that of Alloprevotella correlated positively with the severity of esophagitis as graded by the Los Angeles classification (r = 0.335, P = 0.046).(2) Longitudinal analysis revealed that bacterial genera such as Veillonella, which were associated with phenotypes in cross-sectional studies, did not show significant changes in the oral microbiota between the Pre- and Post- groups. The most characteristic alteration was that the relative abundance of the pro-inflammatory genus Fusobacteriumwas succeeded by Selenomonas, a genus with potential metabolic benefits.
CONCLUSION: Our study demonstrates that gastroesophageal reflux disease is characterized by a specific oral dysbiosis, with the abundance of particular bacterial taxa correlating with clinical disease severity. Although laparoscopic anti-reflux surgery did not drastically alter the global oral microbiome architecture, it induced a targeted ecological shift. This shift was marked by the suppression of pro-inflammatory taxa, an increase in potentially beneficial commensals, and a trend toward restored α-diversity. These findings suggest that laparoscopic anti-reflux surgery may facilitate a shift of the oral microbiome toward a healthier ecological state following restoration of the anti-reflux barrier function. This observation provides a new microbiological perspective for understanding the broader physiological impact of anti-reflux surgery.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Astragalus polysaccharide alleviates neuropathology and cognitive deficits by modulating gut microbiota and neuroinflammation in an Alzheimer's disease model.
Frontiers in pharmacology, 17:1830927.
BACKGROUND: Emerging evidence indicates that the neuroprotective effects of Astragalus polysaccharides (APS), an extract compound and bioactive constituent derived from traditional Chinese herbs, may be relevant to an effective prescription for delaying progression of Alzheimer's disease (AD), yet the underlying mechanisms remain to be fully elucidated. This study aimed to investigate the therapeutic efficacy of APS in alleviating cognitive impairment and neuropathology in 5×FAD transgenic mice, with a specific focus on the regulatory role of the gut-brain axis.
METHODS: Male 5×FAD mice were orally administered APS (200 mg/kg/day) for 60 days. General observations were conducted to assess the in vivo tolerance of APS. Cognitive function was evaluated using the Morris water maze (MWM). Neuropathological assessments included immunofluorescence and Western blotting for amyloid-β (Aβ) deposition, synaptic proteins, and neuroinflammatory markers. Gut microbiota composition and metabolic profiles were analyzed via 16S rRNA gene sequencing and targeted metabolomics. Furthermore, fecal microbiota transplantation (FMT) was performed to verify the causal contribution of gut microbiota to the observed therapeutic effects.
RESULTS: APS administration was well-tolerated throughout the study period, with no overt toxic effects observed. Moreover, APS administration significantly ameliorated spatial learning and memory deficits in 5×FAD mice. Mechanistically, APS treatment reduced Aβ plaque burden, restored synaptic protein expression (PSD-95 and Syntaxin), and attenuated microglia-mediated neuroinflammation by suppressing pro-inflammatory cytokines (IL-6, TNF-α) and upregulating TREM2. Microbiome analysis revealed that APS reshaped gut microbial diversity and composition, enriching beneficial taxa such as Lactobacillus. Metabolomics indicated a partial restoration of amino acid metabolism. Notably, FMT from APS-treated donors successfully reproduced the cognitive improvements and anti-inflammatory effects in recipient mice.
CONCLUSION: These findings demonstrate that APS alleviates cognitive deficits and AD-like pathology, partially through remodeling gut microbiota and modulating the gut-brain axis. APS represents a promising natural compound-based therapeutic candidate for managing cognitive decline associated with Alzheimer's disease.
Additional Links: PMID-42676794
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Citation:
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@article {pmid42676794,
year = {2026},
author = {Cui, X and Wei, Z and Wang, Q and Du, S and Lin, Z and Chen, Z and Zhang, J and Li, C and Tang, L and Dai, X and He, W},
title = {Astragalus polysaccharide alleviates neuropathology and cognitive deficits by modulating gut microbiota and neuroinflammation in an Alzheimer's disease model.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1830927},
pmid = {42676794},
issn = {1663-9812},
abstract = {BACKGROUND: Emerging evidence indicates that the neuroprotective effects of Astragalus polysaccharides (APS), an extract compound and bioactive constituent derived from traditional Chinese herbs, may be relevant to an effective prescription for delaying progression of Alzheimer's disease (AD), yet the underlying mechanisms remain to be fully elucidated. This study aimed to investigate the therapeutic efficacy of APS in alleviating cognitive impairment and neuropathology in 5×FAD transgenic mice, with a specific focus on the regulatory role of the gut-brain axis.
METHODS: Male 5×FAD mice were orally administered APS (200 mg/kg/day) for 60 days. General observations were conducted to assess the in vivo tolerance of APS. Cognitive function was evaluated using the Morris water maze (MWM). Neuropathological assessments included immunofluorescence and Western blotting for amyloid-β (Aβ) deposition, synaptic proteins, and neuroinflammatory markers. Gut microbiota composition and metabolic profiles were analyzed via 16S rRNA gene sequencing and targeted metabolomics. Furthermore, fecal microbiota transplantation (FMT) was performed to verify the causal contribution of gut microbiota to the observed therapeutic effects.
RESULTS: APS administration was well-tolerated throughout the study period, with no overt toxic effects observed. Moreover, APS administration significantly ameliorated spatial learning and memory deficits in 5×FAD mice. Mechanistically, APS treatment reduced Aβ plaque burden, restored synaptic protein expression (PSD-95 and Syntaxin), and attenuated microglia-mediated neuroinflammation by suppressing pro-inflammatory cytokines (IL-6, TNF-α) and upregulating TREM2. Microbiome analysis revealed that APS reshaped gut microbial diversity and composition, enriching beneficial taxa such as Lactobacillus. Metabolomics indicated a partial restoration of amino acid metabolism. Notably, FMT from APS-treated donors successfully reproduced the cognitive improvements and anti-inflammatory effects in recipient mice.
CONCLUSION: These findings demonstrate that APS alleviates cognitive deficits and AD-like pathology, partially through remodeling gut microbiota and modulating the gut-brain axis. APS represents a promising natural compound-based therapeutic candidate for managing cognitive decline associated with Alzheimer's disease.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Characterization of oral microbiome alterations in thalassemia patients using 16S rRNA gene sequencing.
Frontiers in microbiology, 17:1853312.
BACKGROUND: This study investigates the composition of the oral microbiota in thalassemia patients and compares it with healthy individuals from Saudi Arabia. Thalassemia is an inherited blood disorder characterized by reduced or absent production of globin chains, resulting in hypochromic microcytic anemia and multiple complications, such as iron overload resulting from frequent blood transfusions.
METHODS: Using 16S rRNA gene sequencing, 28 saliva samples (14 thalassemia patients and 14 healthy controls) were analyzed to assess changes in the richness and diversity of the oral microbiota.
RESULTS: Taxonomic analysis demonstrated nominal differences between the two groups, with notable variations in the abundance of several bacterial species. All taxa showing differential abundance belonged to two phyla-Firmicutes and Bacteroidota; including taxa such as Prevotella intermedia, Eubacterium sulci, and Porphyromonas gingivalis. Although several taxa showed nominal differences based on raw p-values, none remained statistically significant after Benjamini-Hochberg false discovery rate (FDR) correction. Thalassemia patients exhibited a nominal reduction in the relative abundance of bacteria such as Prevotella.
CONCLUSION: Overall, this study suggests possible alterations in the oral microbiome associated with thalassemia; however, these findings require validation in larger cohorts with comprehensive clinical and oral health data.
Additional Links: PMID-42676816
PubMed:
Citation:
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@article {pmid42676816,
year = {2026},
author = {Alghamdi, MA and Almalki, SA and Bahieldin, A and Radhwi, O and Rather, IA},
title = {Characterization of oral microbiome alterations in thalassemia patients using 16S rRNA gene sequencing.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1853312},
pmid = {42676816},
issn = {1664-302X},
abstract = {BACKGROUND: This study investigates the composition of the oral microbiota in thalassemia patients and compares it with healthy individuals from Saudi Arabia. Thalassemia is an inherited blood disorder characterized by reduced or absent production of globin chains, resulting in hypochromic microcytic anemia and multiple complications, such as iron overload resulting from frequent blood transfusions.
METHODS: Using 16S rRNA gene sequencing, 28 saliva samples (14 thalassemia patients and 14 healthy controls) were analyzed to assess changes in the richness and diversity of the oral microbiota.
RESULTS: Taxonomic analysis demonstrated nominal differences between the two groups, with notable variations in the abundance of several bacterial species. All taxa showing differential abundance belonged to two phyla-Firmicutes and Bacteroidota; including taxa such as Prevotella intermedia, Eubacterium sulci, and Porphyromonas gingivalis. Although several taxa showed nominal differences based on raw p-values, none remained statistically significant after Benjamini-Hochberg false discovery rate (FDR) correction. Thalassemia patients exhibited a nominal reduction in the relative abundance of bacteria such as Prevotella.
CONCLUSION: Overall, this study suggests possible alterations in the oral microbiome associated with thalassemia; however, these findings require validation in larger cohorts with comprehensive clinical and oral health data.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Mechanistic evidence and assumptions in mycotoxin-gut interaction.
Frontiers in fungal biology, 7:1855881.
Mycotoxins are increasingly recognised as ecological mediators that act through a bidirectional gut-microbiota axis. Microbial metabolism governs toxin fate by driving detoxification, bioactivation, sequestration and deconjugation, whereas mycotoxin exposure reshapes microbial communities, disrupts epithelial barrier function and amplifies immune signalling. Across aflatoxin B1, ochratoxin A, fumonisin B1, deoxynivalenol and T-2 toxin, the microbiome emerges as both a determinant and a target of toxicity, with strain-level functional diversity influencing susceptibility, detoxification capacity and host outcome. A further consequence of chronic exposure may be selection for pathobionts and antibiotic-resistant populations, raising the possibility that mycotoxins contribute to microbiome instability beyond direct toxic effects. Despite these advances, most evidence remains correlative or model-specific, and causal validation in vivo is still limited. Integrating microbiology, metabolomics, epithelial biology and ecological theory is essential to understand these interactions and to better guide microbiome-informed strategies for mycotoxin exposure mitigation.
Additional Links: PMID-42676822
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@article {pmid42676822,
year = {2026},
author = {Garcia-Cela, E and Marcon Gasperini, A},
title = {Mechanistic evidence and assumptions in mycotoxin-gut interaction.},
journal = {Frontiers in fungal biology},
volume = {7},
number = {},
pages = {1855881},
pmid = {42676822},
issn = {2673-6128},
abstract = {Mycotoxins are increasingly recognised as ecological mediators that act through a bidirectional gut-microbiota axis. Microbial metabolism governs toxin fate by driving detoxification, bioactivation, sequestration and deconjugation, whereas mycotoxin exposure reshapes microbial communities, disrupts epithelial barrier function and amplifies immune signalling. Across aflatoxin B1, ochratoxin A, fumonisin B1, deoxynivalenol and T-2 toxin, the microbiome emerges as both a determinant and a target of toxicity, with strain-level functional diversity influencing susceptibility, detoxification capacity and host outcome. A further consequence of chronic exposure may be selection for pathobionts and antibiotic-resistant populations, raising the possibility that mycotoxins contribute to microbiome instability beyond direct toxic effects. Despite these advances, most evidence remains correlative or model-specific, and causal validation in vivo is still limited. Integrating microbiology, metabolomics, epithelial biology and ecological theory is essential to understand these interactions and to better guide microbiome-informed strategies for mycotoxin exposure mitigation.},
}
RevDate: 2026-09-01
Soil-derived, gut-dominant generalist bacteria shape the fitness of folivorous larvae.
Whether Lepidoptera harbor a conserved core gut microbiome has long remained contentious. Through large-scale microbiome profiling of folivorous larvae, their host plants, and associated soils across three climatically distinct regions of China, we identify two soil-derived generalist bacteria, Ralstonia insidiosa and Delftia sp., that colonize 97.92% of larval species examined, attaining mean relative abundances exceeding 47%, with the soil microbial reservoir as their principal source. Strikingly, these two taxa exhibit strong mutual exclusion within the larval gut yet govern host development through diametrically opposed metabolic strategies: R. insidiosa promotes larval weight gain, whereas Delftia sp. suppresses growth. This functional bifurcation, in which two widespread generalists exert opposite phenotypic effects, represents a previously undescribed phenomenon in insect-microbe symbiosis. Our findings provide broad evidence that soil microbial reservoirs can shape aboveground herbivore fitness via horizontally acquired bacteria, offering mechanistic insights for microbiome-based ecological management.
Additional Links: PMID-42676834
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@article {pmid42676834,
year = {2026},
author = {Zheng, YX and Wang, Y and Zhang, XM and Jin, Q and Zhang, Y and Wang, GF and Shao, YQ and Li, J and Sun, C and Kong, WD and Yang, CQ and Zhang, AB},
title = {Soil-derived, gut-dominant generalist bacteria shape the fitness of folivorous larvae.},
journal = {iMeta},
volume = {},
number = {},
pages = {e70169},
pmid = {42676834},
issn = {2770-596X},
abstract = {Whether Lepidoptera harbor a conserved core gut microbiome has long remained contentious. Through large-scale microbiome profiling of folivorous larvae, their host plants, and associated soils across three climatically distinct regions of China, we identify two soil-derived generalist bacteria, Ralstonia insidiosa and Delftia sp., that colonize 97.92% of larval species examined, attaining mean relative abundances exceeding 47%, with the soil microbial reservoir as their principal source. Strikingly, these two taxa exhibit strong mutual exclusion within the larval gut yet govern host development through diametrically opposed metabolic strategies: R. insidiosa promotes larval weight gain, whereas Delftia sp. suppresses growth. This functional bifurcation, in which two widespread generalists exert opposite phenotypic effects, represents a previously undescribed phenomenon in insect-microbe symbiosis. Our findings provide broad evidence that soil microbial reservoirs can shape aboveground herbivore fitness via horizontally acquired bacteria, offering mechanistic insights for microbiome-based ecological management.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Lung microbiome features associated with ICU delirium in mechanically ventilated patients: a secondary cohort analysis.
Brain, behavior, & immunity - health, 56:101335.
BACKGROUND: Delirium in mechanically ventilated intensive care unit (ICU) patients is linked to inflammatory dysregulation, but whether the pulmonary microbiome contributes to delirium risk remains unclear.
METHODS: We performed a secondary analysis of 132 mechanically ventilated adults from the MicroNAV cohort. Baseline bronchoalveolar lavage (BAL) samples collected within 12 h of intubation were profiled by 16S rRNA gene sequencing; total bacterial burden was quantified by droplet digital PCR (ddPCR; n = 125), and BAL cytokines were measured using a multiplex assay (n = 70). Concordant genus-level signals identified by four differential-abundance methods were aggregated into ecological scores and tested using logistic regression adjusted for age and Glasgow Coma Scale at intubation. Absolute abundance was estimated by multiplying relative abundance by ddPCR-derived bacterial burden.
RESULTS: Delirium was recorded in 45 patients (34.1%). Total bacterial DNA concentration was lower in patients with delirium (median 7419 vs 98,326 copies/μL, P = 0.001). A putative short-chain fatty acid (SCFA)-producing commensal score (Phocaeicola, Selenomonas, and Fretibacterium) was inversely associated with delirium in compositional analysis (OR 0.83, 95% CI 0.75-0.92, P < 0.001) and after ddPCR-anchored absolute quantification (OR 0.84, 95% CI 0.75-0.94, P = 0.002). This depletion extended to oral-core commensals (absolute OR 0.80, P < 0.001) and a pre-specified oral anaerobe score (absolute OR 0.82, P = 0.002). Opportunistic colonizers were enriched compositionally but not in absolute abundance (OR 1.10, P = 0.187). Commensal scores were positively associated with BAL IL-1β and TNF-α, whereas opportunistic-colonizer scores showed inverse associations.
CONCLUSIONS: Early pulmonary depletion of oral-derived commensals, particularly putative SCFA producers, was associated with ICU delirium. Prospective studies with standardized delirium assessment and functional metabolite measurements are needed.
Additional Links: PMID-42676966
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@article {pmid42676966,
year = {2026},
author = {Xiao, S and Lin, F and Li, Y and Zhuang, Q},
title = {Lung microbiome features associated with ICU delirium in mechanically ventilated patients: a secondary cohort analysis.},
journal = {Brain, behavior, & immunity - health},
volume = {56},
number = {},
pages = {101335},
pmid = {42676966},
issn = {2666-3546},
abstract = {BACKGROUND: Delirium in mechanically ventilated intensive care unit (ICU) patients is linked to inflammatory dysregulation, but whether the pulmonary microbiome contributes to delirium risk remains unclear.
METHODS: We performed a secondary analysis of 132 mechanically ventilated adults from the MicroNAV cohort. Baseline bronchoalveolar lavage (BAL) samples collected within 12 h of intubation were profiled by 16S rRNA gene sequencing; total bacterial burden was quantified by droplet digital PCR (ddPCR; n = 125), and BAL cytokines were measured using a multiplex assay (n = 70). Concordant genus-level signals identified by four differential-abundance methods were aggregated into ecological scores and tested using logistic regression adjusted for age and Glasgow Coma Scale at intubation. Absolute abundance was estimated by multiplying relative abundance by ddPCR-derived bacterial burden.
RESULTS: Delirium was recorded in 45 patients (34.1%). Total bacterial DNA concentration was lower in patients with delirium (median 7419 vs 98,326 copies/μL, P = 0.001). A putative short-chain fatty acid (SCFA)-producing commensal score (Phocaeicola, Selenomonas, and Fretibacterium) was inversely associated with delirium in compositional analysis (OR 0.83, 95% CI 0.75-0.92, P < 0.001) and after ddPCR-anchored absolute quantification (OR 0.84, 95% CI 0.75-0.94, P = 0.002). This depletion extended to oral-core commensals (absolute OR 0.80, P < 0.001) and a pre-specified oral anaerobe score (absolute OR 0.82, P = 0.002). Opportunistic colonizers were enriched compositionally but not in absolute abundance (OR 1.10, P = 0.187). Commensal scores were positively associated with BAL IL-1β and TNF-α, whereas opportunistic-colonizer scores showed inverse associations.
CONCLUSIONS: Early pulmonary depletion of oral-derived commensals, particularly putative SCFA producers, was associated with ICU delirium. Prospective studies with standardized delirium assessment and functional metabolite measurements are needed.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Endoscopic Prevalence of Barrett's Esophagus in a Predominantly African American and Hispanic Population.
Cureus, 18(8):e113784.
Background and aim Barrett's esophagus (BE) is a well-known premalignant disorder. Investigators have shown that the prevalence of histologically confirmed BE varies among ethnic groups in the US. However, these studies were not performed at institutions that predominantly serve US minority populations. The aim of this study was to assess the prevalence of histologically confirmed BE at an institution that serves a predominantly African American (AA) and Hispanic American patient population. Methods The Harlem Hospital endoscopy and pathology databases were searched to identify all patients who underwent esophagogastroduodenoscopy (EGD) with biopsy and had histologically confirmed BE. Histological confirmation of BE was determined by the presence of intestinal metaplasia and Alcian blue-stained goblet cells in biopsies obtained from salmon-colored esophageal mucosa. Demographic data collected included age, sex, race/ethnicity, BMI, history of gastroesophageal reflux disease, endoscopic BE length, presence of hiatal hernia, esophagitis, or esophageal ulcer, presence or absence of dysplasia, proton pump inhibitor use, active Helicobacter pylori infection, and smoking and alcohol use. Results A total of 3,012 patients underwent EGD during the study period. Esophageal biopsy was performed on salmon-colored esophageal mucosa suspicious for BE in 18 individuals. BE was histologically confirmed in eight patients: five AAs, two Hispanics, and one non-Hispanic White (nHW). The overall prevalence of BE was 0.2%, with a lower prevalence observed among AA patients (0.3%) and Hispanic patients (0.1%) than among nHW patients (3.3%, p < 0.05). Four patients had dysplasia (three with low-grade dysplasia and one with high-grade dysplasia; three AA and one Hispanic). Conclusions The prevalence of BE in our predominantly minority population was lower than that observed among nHW patients, consistent with previous literature. Investigations at the microbiome and genetic levels are needed to explain the observed disparity in BE prevalence among ethnic groups.
Additional Links: PMID-42677001
PubMed:
Citation:
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hide bibtex listing
@article {pmid42677001,
year = {2026},
author = {Akpoigbe, K and Culpepper-Morgan, J and Barnes, A and Kwentoh, I and Vega, KJ},
title = {Endoscopic Prevalence of Barrett's Esophagus in a Predominantly African American and Hispanic Population.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e113784},
pmid = {42677001},
issn = {2168-8184},
abstract = {Background and aim Barrett's esophagus (BE) is a well-known premalignant disorder. Investigators have shown that the prevalence of histologically confirmed BE varies among ethnic groups in the US. However, these studies were not performed at institutions that predominantly serve US minority populations. The aim of this study was to assess the prevalence of histologically confirmed BE at an institution that serves a predominantly African American (AA) and Hispanic American patient population. Methods The Harlem Hospital endoscopy and pathology databases were searched to identify all patients who underwent esophagogastroduodenoscopy (EGD) with biopsy and had histologically confirmed BE. Histological confirmation of BE was determined by the presence of intestinal metaplasia and Alcian blue-stained goblet cells in biopsies obtained from salmon-colored esophageal mucosa. Demographic data collected included age, sex, race/ethnicity, BMI, history of gastroesophageal reflux disease, endoscopic BE length, presence of hiatal hernia, esophagitis, or esophageal ulcer, presence or absence of dysplasia, proton pump inhibitor use, active Helicobacter pylori infection, and smoking and alcohol use. Results A total of 3,012 patients underwent EGD during the study period. Esophageal biopsy was performed on salmon-colored esophageal mucosa suspicious for BE in 18 individuals. BE was histologically confirmed in eight patients: five AAs, two Hispanics, and one non-Hispanic White (nHW). The overall prevalence of BE was 0.2%, with a lower prevalence observed among AA patients (0.3%) and Hispanic patients (0.1%) than among nHW patients (3.3%, p < 0.05). Four patients had dysplasia (three with low-grade dysplasia and one with high-grade dysplasia; three AA and one Hispanic). Conclusions The prevalence of BE in our predominantly minority population was lower than that observed among nHW patients, consistent with previous literature. Investigations at the microbiome and genetic levels are needed to explain the observed disparity in BE prevalence among ethnic groups.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Ecosystem retrogression enhances cross-domain microbial stability and increases the genetic potential for nutrient cycling.
mLife, 5(4):486-506.
Ecosystem retrogression drives nutrient depletion, reduced productivity, and profound reorganization of soil microbial communities. Using amplicon sequencing and genome-resolved metagenomics, we examined how cross-domain microbial networks and functional gene potential respond to long-term phosphorus and nitrogen limitation along the well-characterized Ecological Staircase chronosequence in Mendocino, California, USA. Microbial diversity and abundance declined sharply with terrace age for prokaryotes, predatory protists, and bacteriophages, whereas fungi and phototrophic protists increased in nutrient-depleted, acidic soils. These compositional shifts were accompanied by major changes in reconstructed microbial networks: relative modularity increased alongside robustness, indicating adaptive reorganization that may sustain ecosystem function under resource scarcity. Fungi emerged as central stabilizers in these restructured networks, carrying enriched genetic potential to degrade plant polymers and mobilize phosphorus and nitrogen. Despite a decline in overall phage diversity, the relative abundance of phages encoding phosphorus-mobilizing auxiliary metabolic genes increased, suggesting that viral contributions to host phosphorus metabolism may be enhanced under nutrient limitation. Together, these results demonstrate that ecosystem retrogression drives cross-domain microbial reorganization toward fewer but more interconnected lineages, characterized by greater integration of functional genetic potential. This reorganization enhances the potential for functional resilience under extreme nutrient limitation, revealing how microbial networks adapt to maintain the capacity for nutrient cycling and stability as soils age and fertility declines.
Additional Links: PMID-42677031
PubMed:
Citation:
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hide bibtex listing
@article {pmid42677031,
year = {2026},
author = {Ceja-Navarro, JA and Patel, D and Genco, G and Byer, A and Ning, D and Wan, KH and Celniker, SE and Zhou, J and Dijkstra, P and Hungate, BA and Pett-Ridge, J and Brodie, EL},
title = {Ecosystem retrogression enhances cross-domain microbial stability and increases the genetic potential for nutrient cycling.},
journal = {mLife},
volume = {5},
number = {4},
pages = {486-506},
pmid = {42677031},
issn = {2770-100X},
abstract = {Ecosystem retrogression drives nutrient depletion, reduced productivity, and profound reorganization of soil microbial communities. Using amplicon sequencing and genome-resolved metagenomics, we examined how cross-domain microbial networks and functional gene potential respond to long-term phosphorus and nitrogen limitation along the well-characterized Ecological Staircase chronosequence in Mendocino, California, USA. Microbial diversity and abundance declined sharply with terrace age for prokaryotes, predatory protists, and bacteriophages, whereas fungi and phototrophic protists increased in nutrient-depleted, acidic soils. These compositional shifts were accompanied by major changes in reconstructed microbial networks: relative modularity increased alongside robustness, indicating adaptive reorganization that may sustain ecosystem function under resource scarcity. Fungi emerged as central stabilizers in these restructured networks, carrying enriched genetic potential to degrade plant polymers and mobilize phosphorus and nitrogen. Despite a decline in overall phage diversity, the relative abundance of phages encoding phosphorus-mobilizing auxiliary metabolic genes increased, suggesting that viral contributions to host phosphorus metabolism may be enhanced under nutrient limitation. Together, these results demonstrate that ecosystem retrogression drives cross-domain microbial reorganization toward fewer but more interconnected lineages, characterized by greater integration of functional genetic potential. This reorganization enhances the potential for functional resilience under extreme nutrient limitation, revealing how microbial networks adapt to maintain the capacity for nutrient cycling and stability as soils age and fertility declines.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Biological and Habitual Factors That Influence Sleep and Circadian Rhythm: A Narrative Review.
Cureus, 18(8):e113792.
Sleep loss and circadian misalignment can adversely affect health. As such, a comprehensive understanding of what factors influence sleep loss and circadian misalignment benefits medical and scientific progress. While the interaction between light exposure and circadian entrainment and their relationship to circadian alignment is long-established, other factors that influence central or peripheral clocks (bodily oscillators) also contribute to circadian alignment and the potential for sleep loss. In this review, we will highlight the core factors that influence vulnerability or resilience to sleep loss and circadian misalignment, including biologic factors, such as gene haplotype, chronotype, and the gut microbiome. Furthermore, we will consider how habitual and largely modifiable variables, such as timing of meals and physical activity, can be manipulated to affect circadian and sleep cycles. Gaps in current scientific research on the effects of circadian misalignment and sleep loss will also be identified. This review will thus help inform future research and enhance the understanding of how healthy sleep and balanced circadian rhythm can improve quality of life.
Additional Links: PMID-42677033
PubMed:
Citation:
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hide bibtex listing
@article {pmid42677033,
year = {2026},
author = {Harmon, VJ and Davis, CJ},
title = {Biological and Habitual Factors That Influence Sleep and Circadian Rhythm: A Narrative Review.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e113792},
pmid = {42677033},
issn = {2168-8184},
abstract = {Sleep loss and circadian misalignment can adversely affect health. As such, a comprehensive understanding of what factors influence sleep loss and circadian misalignment benefits medical and scientific progress. While the interaction between light exposure and circadian entrainment and their relationship to circadian alignment is long-established, other factors that influence central or peripheral clocks (bodily oscillators) also contribute to circadian alignment and the potential for sleep loss. In this review, we will highlight the core factors that influence vulnerability or resilience to sleep loss and circadian misalignment, including biologic factors, such as gene haplotype, chronotype, and the gut microbiome. Furthermore, we will consider how habitual and largely modifiable variables, such as timing of meals and physical activity, can be manipulated to affect circadian and sleep cycles. Gaps in current scientific research on the effects of circadian misalignment and sleep loss will also be identified. This review will thus help inform future research and enhance the understanding of how healthy sleep and balanced circadian rhythm can improve quality of life.},
}
RevDate: 2026-09-01
CmpDate: 2026-09-01
Gut microbiota-targeted bioactive peptides as emerging axis in nutritional therapeutics: trends, challenges, and prospects.
Frontiers in nutrition, 13:1905173.
The gut microbiota is a dynamic, complex microbial ecosystem that is fundamental to human health and influences metabolism, immunity, and susceptibility to disease. There is growing evidence that bioactive peptides (BAPs) are important regulators of gut microbiota composition and function. BAPs are short protein fragments liberated through enzymatic hydrolysis or microbial fermentation in vitro and during the digestion of food proteins in vivo. The biological activities of these BAPs, beyond their antioxidant, antihypertensive, and antimicrobial effects, include maintaining gut balance and supporting overall well-being. The relationship between BAPs and gut microbiota is two-way: peptides selectively promote beneficial microbes, and the microbiota enzymatically convert peptides into bioactive metabolites such as short-chain fatty acids and altered bile acids, or further hydrolyze them into shorter BAPs. This interaction between gut microbiota and BAPs has been shown to confer significant therapeutic benefits from combined nutritional interventions in the management of chronic diseases, including obesity, diabetes, inflammatory bowel diseases, and neurological diseases. This review examines the current state of gut microbiota-targeted BAPs, including their sources, properties, and mechanisms. It underscores their contribution to microbial diversity and metabolic activity, which support immune balance and the functioning of the gut-brain axis. In addition, it addresses novel ways to increase the activity of BAPs with respect to stability and delivery. Challenges such as peptide bioavailability, microbiome diversity, and a lack of clinical evidence are also critically discussed. Future perspectives focus on leveraging omics technologies and personalized nutrition to unlock the potential of BAPs for therapeutic and functional food applications. The review indicates the promising potential of BAPs as microbiota-based, innovative, and useful agents in nutritional therapy.
Additional Links: PMID-42677167
PubMed:
Citation:
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hide bibtex listing
@article {pmid42677167,
year = {2026},
author = {Singh, BP and Bose, P and Je, JY},
title = {Gut microbiota-targeted bioactive peptides as emerging axis in nutritional therapeutics: trends, challenges, and prospects.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1905173},
pmid = {42677167},
issn = {2296-861X},
abstract = {The gut microbiota is a dynamic, complex microbial ecosystem that is fundamental to human health and influences metabolism, immunity, and susceptibility to disease. There is growing evidence that bioactive peptides (BAPs) are important regulators of gut microbiota composition and function. BAPs are short protein fragments liberated through enzymatic hydrolysis or microbial fermentation in vitro and during the digestion of food proteins in vivo. The biological activities of these BAPs, beyond their antioxidant, antihypertensive, and antimicrobial effects, include maintaining gut balance and supporting overall well-being. The relationship between BAPs and gut microbiota is two-way: peptides selectively promote beneficial microbes, and the microbiota enzymatically convert peptides into bioactive metabolites such as short-chain fatty acids and altered bile acids, or further hydrolyze them into shorter BAPs. This interaction between gut microbiota and BAPs has been shown to confer significant therapeutic benefits from combined nutritional interventions in the management of chronic diseases, including obesity, diabetes, inflammatory bowel diseases, and neurological diseases. This review examines the current state of gut microbiota-targeted BAPs, including their sources, properties, and mechanisms. It underscores their contribution to microbial diversity and metabolic activity, which support immune balance and the functioning of the gut-brain axis. In addition, it addresses novel ways to increase the activity of BAPs with respect to stability and delivery. Challenges such as peptide bioavailability, microbiome diversity, and a lack of clinical evidence are also critically discussed. Future perspectives focus on leveraging omics technologies and personalized nutrition to unlock the potential of BAPs for therapeutic and functional food applications. The review indicates the promising potential of BAPs as microbiota-based, innovative, and useful agents in nutritional therapy.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
ESP Usage
Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
ESP Content
When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
ESP Help
Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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Fossils of miniature humans (hobbits) discovered in Indonesia
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Dinosaur tail, complete with feathers, found preserved in amber.
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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.