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ESP: PubMed Auto Bibliography 28 Apr 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: 2026-04-23
The network structure of cross-feeding impacts microbial community diversity under growth-inhibiting stresses.
Nature communications pii:10.1038/s41467-026-71097-5 [Epub ahead of print].
Perturbations such as dietary shifts and drug treatment can reduce gut microbiome diversity, with negative consequences for host health, yet predicting diversity responses remains challenging because microbial species interact through multiple mechanisms. While nutrient competition and cross-feeding both influence microbiota assembly, environmental stresses such as antibiotics are typically studied experimentally in monoculture, and most theoretical frameworks consider nutrient competition alone. To investigate how these processes jointly shape community structure, we develop a consumer-resource model that incorporates nutrient competition, growth-inhibiting stress, and metabolite cross-feeding with a unified framework spanning varied cross-feeding architectures. For three-species communities, coexistence during narrow-spectrum growth inhibition is maximized by cyclic cross-feeding networks, whereas fully connected cross-feeding networks maximize coexistence during broad-spectrum growth inhibition. However, the benefits of cyclic cross-feeding depend strongly on community size and stress targeting: in communities with more than six species and six resources, cyclic networks can destabilize coexistence. These results are robust to inefficient leakage, dead-end metabolites, and embedding in larger communities, and large communities generalize to random leakage architectures in which connectivity determines the response to stress. Together, this framework shows that cross-feeding network architecture can fundamentally reshape how microbial communities respond to growth-inhibiting stresses.
Additional Links: PMID-42026051
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@article {pmid42026051,
year = {2026},
author = {Newton, DP and Ho, PY and Huang, KC},
title = {The network structure of cross-feeding impacts microbial community diversity under growth-inhibiting stresses.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-71097-5},
pmid = {42026051},
issn = {2041-1723},
support = {RM1 GM135102/GM/NIGMS NIH HHS/United States ; F32 GM143859/GM/NIGMS NIH HHS/United States ; },
abstract = {Perturbations such as dietary shifts and drug treatment can reduce gut microbiome diversity, with negative consequences for host health, yet predicting diversity responses remains challenging because microbial species interact through multiple mechanisms. While nutrient competition and cross-feeding both influence microbiota assembly, environmental stresses such as antibiotics are typically studied experimentally in monoculture, and most theoretical frameworks consider nutrient competition alone. To investigate how these processes jointly shape community structure, we develop a consumer-resource model that incorporates nutrient competition, growth-inhibiting stress, and metabolite cross-feeding with a unified framework spanning varied cross-feeding architectures. For three-species communities, coexistence during narrow-spectrum growth inhibition is maximized by cyclic cross-feeding networks, whereas fully connected cross-feeding networks maximize coexistence during broad-spectrum growth inhibition. However, the benefits of cyclic cross-feeding depend strongly on community size and stress targeting: in communities with more than six species and six resources, cyclic networks can destabilize coexistence. These results are robust to inefficient leakage, dead-end metabolites, and embedding in larger communities, and large communities generalize to random leakage architectures in which connectivity determines the response to stress. Together, this framework shows that cross-feeding network architecture can fundamentally reshape how microbial communities respond to growth-inhibiting stresses.},
}
RevDate: 2026-04-23
Seasonality of composition, genomic potential and activity of coniferous forest soil microbiomes.
Scientific data pii:10.1038/s41597-026-07163-w [Epub ahead of print].
Coniferous forest soils represent a globally important carbon sink, where the microbiome is essential for carbon flux between tree roots, rhizosphere, litter and soil. Soil habitats, such as roots, rhizosphere, bulk soil and litter differ in physicochemical properties and composition of highly specialized microbial communities, whose activity reflects the seasonality of temperature and tree activity of these mid- to high-latitude biomes. Here we present a multi-omic dataset encompassing 160 samples collected from four coniferous forest soil habitats in the Czech Republic and Norway, sampled in early summer, late summer, early winter and late winter that characterize the composition, genomic potential and activity of tree roots and microbiome. For each sample, we provide metabarcoding-based composition of bacterial, fungal and eukaryotic communities, results of shotgun DNA sequencing (metagenomes) and shotgun RNA sequencing (metatranscriptomes) illustrating the functional potential and activity within habitats. This dataset enables analyses of the temporal variation of taxonomic composition, functional potential and transcription across seasons in a temperate and boreal coniferous forest.
Additional Links: PMID-42026082
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@article {pmid42026082,
year = {2026},
author = {Human, ZR and Štursová, M and Odriozola, I and Větrovský, T and Howe, A and Navrátilová, D and López-Mondéjar, R and Žifčáková, L and Brabcová, V and Mundra, S and Thoen, E and Morgado, L and Fiore-Donno, AM and Bonkowski, M and Adamczyk, B and Kohout, P and Lipton, MS and Calhoun, S and LaButti, K and Lipzen, A and Keymanesh, K and Tejomurthula, S and Pennacchio, C and Grigoriev, IV and Martin, F and Kauserud, H and Baldrian, P},
title = {Seasonality of composition, genomic potential and activity of coniferous forest soil microbiomes.},
journal = {Scientific data},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41597-026-07163-w},
pmid = {42026082},
issn = {2052-4463},
support = {240859//Norges Forskningsråd (Research Council of Norway)/ ; },
abstract = {Coniferous forest soils represent a globally important carbon sink, where the microbiome is essential for carbon flux between tree roots, rhizosphere, litter and soil. Soil habitats, such as roots, rhizosphere, bulk soil and litter differ in physicochemical properties and composition of highly specialized microbial communities, whose activity reflects the seasonality of temperature and tree activity of these mid- to high-latitude biomes. Here we present a multi-omic dataset encompassing 160 samples collected from four coniferous forest soil habitats in the Czech Republic and Norway, sampled in early summer, late summer, early winter and late winter that characterize the composition, genomic potential and activity of tree roots and microbiome. For each sample, we provide metabarcoding-based composition of bacterial, fungal and eukaryotic communities, results of shotgun DNA sequencing (metagenomes) and shotgun RNA sequencing (metatranscriptomes) illustrating the functional potential and activity within habitats. This dataset enables analyses of the temporal variation of taxonomic composition, functional potential and transcription across seasons in a temperate and boreal coniferous forest.},
}
RevDate: 2026-04-26
Rumen bacteria, feed utilization, and milk production of Damascus goats fed different levels of azolla meal.
Scientific reports, 16(1):.
UNLABELLED: Azolla could be a promising alternative feed as it is a rich source of nutrients and bioactive compounds that can modulate rumen microbiota and improve animal productivity. This study evaluated the effects of inclusion dietary Azolla (Azolla pinnata) as a partial replacement of concentrate feed mixture (CFM) on rumen bacteria, nutrient digestibility, and milk production in lactating Damascus goats. Thirty-two goats were assigned to four groups (n = 8): a control group (C), A10, A20, and A30 to receive 0, 10%, 20%, and 30% of Azolla as a replacement of CFM, respectively. Microbial diversity increased in Azolla-fed goats, with enrichment of phylum Firmicutes in Azolla-supplemented groups C=13.36%, A10= 31.09%, A20= 25.15%, and A30= 29.85%. Fiber-degrading bacterial genera such as Prevotella, Ruminococcus, and Christensenellaceae R-7 group. .Crude protein digestibility was declined in supplemented groups and was found in order 74.76>69.11>68.24>63.93 %. Total volatile fatty acids (TVFA) and the concentration of acetate, propionate, and butyrate were higher in supplemented groups (p < 0.01). Fat-corrected milk (FCM) was higher in A20 (1139 mL/head) compared to other groups (C=992, A10=1050, A30=888 mL/head and feed efficiency followed the same trend (p < 0.05). Azolla could replace 20% of CFM in goats’ diet, and it is a viable alternative feed resource, particularly under challenges associated with the availability of conventional concentrate mixtures.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-38113-6.
Additional Links: PMID-42026105
PubMed:
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@article {pmid42026105,
year = {2026},
author = {Abd-Elgwad, AFA and Bakr, SA and Sabra, EA and Khorshed, MM and Metwally, HM and Rabee, AE},
title = {Rumen bacteria, feed utilization, and milk production of Damascus goats fed different levels of azolla meal.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42026105},
issn = {2045-2322},
abstract = {UNLABELLED: Azolla could be a promising alternative feed as it is a rich source of nutrients and bioactive compounds that can modulate rumen microbiota and improve animal productivity. This study evaluated the effects of inclusion dietary Azolla (Azolla pinnata) as a partial replacement of concentrate feed mixture (CFM) on rumen bacteria, nutrient digestibility, and milk production in lactating Damascus goats. Thirty-two goats were assigned to four groups (n = 8): a control group (C), A10, A20, and A30 to receive 0, 10%, 20%, and 30% of Azolla as a replacement of CFM, respectively. Microbial diversity increased in Azolla-fed goats, with enrichment of phylum Firmicutes in Azolla-supplemented groups C=13.36%, A10= 31.09%, A20= 25.15%, and A30= 29.85%. Fiber-degrading bacterial genera such as Prevotella, Ruminococcus, and Christensenellaceae R-7 group. .Crude protein digestibility was declined in supplemented groups and was found in order 74.76>69.11>68.24>63.93 %. Total volatile fatty acids (TVFA) and the concentration of acetate, propionate, and butyrate were higher in supplemented groups (p < 0.01). Fat-corrected milk (FCM) was higher in A20 (1139 mL/head) compared to other groups (C=992, A10=1050, A30=888 mL/head and feed efficiency followed the same trend (p < 0.05). Azolla could replace 20% of CFM in goats’ diet, and it is a viable alternative feed resource, particularly under challenges associated with the availability of conventional concentrate mixtures.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-38113-6.},
}
RevDate: 2026-04-23
The long-lived immune system of centenarians.
Nature reviews. Immunology [Epub ahead of print].
Centenarians - individuals aged 100 years or older - constitute a biologically distinct human population that achieves exceptional longevity while frequently retaining functional independence and avoiding major age-related diseases or postponing their onset. Despite their advanced age, many centenarians show relatively preserved immune function and resistance to conditions linked to immunosenescence and chronic low-grade inflammation (inflammageing). These features are especially pronounced in semi-supercentenarians (105-109 years) and supercentenarians (≥110 years), whose immune profiles often resemble those of much younger individuals. In this Review, we explore how centenarians modulate key hallmarks of immune ageing across innate and adaptive immune compartments. We discuss evidence that they limit the pathological effects of inflammageing, potentially through reduced NLRP3 inflammasome activation, enhanced autophagy and a tempered senescence-associated secretory phenotype. Omics studies further reveal transcriptomic, epigenetic and microbial signatures consistent with preserved immune function, including youth-like gene expression patterns in circulating immune cells and beneficial shifts in gut microbiome composition. Together, these findings suggest that centenarians achieve longevity through coordinated adaptations that maintain immune homeostasis and disease resistance and may inform strategies to enhance healthspan in ageing societies.
Additional Links: PMID-42026253
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@article {pmid42026253,
year = {2026},
author = {Plaza-Florido, A and Carrera-Bastos, P and Pérez-Prieto, I and Fiuza-Luces, C and Radom-Aizik, S and Del Pozo Cruz, B and Franceschi, C and López-Soto, A and López-Otín, C and Lucia, A},
title = {The long-lived immune system of centenarians.},
journal = {Nature reviews. Immunology},
volume = {},
number = {},
pages = {},
pmid = {42026253},
issn = {1474-1741},
abstract = {Centenarians - individuals aged 100 years or older - constitute a biologically distinct human population that achieves exceptional longevity while frequently retaining functional independence and avoiding major age-related diseases or postponing their onset. Despite their advanced age, many centenarians show relatively preserved immune function and resistance to conditions linked to immunosenescence and chronic low-grade inflammation (inflammageing). These features are especially pronounced in semi-supercentenarians (105-109 years) and supercentenarians (≥110 years), whose immune profiles often resemble those of much younger individuals. In this Review, we explore how centenarians modulate key hallmarks of immune ageing across innate and adaptive immune compartments. We discuss evidence that they limit the pathological effects of inflammageing, potentially through reduced NLRP3 inflammasome activation, enhanced autophagy and a tempered senescence-associated secretory phenotype. Omics studies further reveal transcriptomic, epigenetic and microbial signatures consistent with preserved immune function, including youth-like gene expression patterns in circulating immune cells and beneficial shifts in gut microbiome composition. Together, these findings suggest that centenarians achieve longevity through coordinated adaptations that maintain immune homeostasis and disease resistance and may inform strategies to enhance healthspan in ageing societies.},
}
RevDate: 2026-04-23
Patterns in Marine Fungal Diversity and Community Structure on Native Versus Invasive Macroalgae at a Local Geographic Scale.
Microbial ecology pii:10.1007/s00248-026-02781-8 [Epub ahead of print].
Additional Links: PMID-42026383
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PubMed:
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@article {pmid42026383,
year = {2026},
author = {Owen, EAM and Griffiths, RI and Golyshin, PN and Chernikova, TN and Kurr, M},
title = {Patterns in Marine Fungal Diversity and Community Structure on Native Versus Invasive Macroalgae at a Local Geographic Scale.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02781-8},
pmid = {42026383},
issn = {1432-184X},
support = {81280//European Regional Development Fund (ERDF)/ ; 81280//European Regional Development Fund (ERDF)/ ; },
}
RevDate: 2026-04-23
Functional remodeling of the gut microbiome and metabolome in primary idiopathic male infertility.
BMC microbiology pii:10.1186/s12866-026-05064-x [Epub ahead of print].
Additional Links: PMID-42026467
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PubMed:
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@article {pmid42026467,
year = {2026},
author = {Luo, C and Yao, H and Xian, Y and Yang, T and Xiao, X and Ying, L and Xu, J and Luo, X and Qiu, D and Liu, Y and Liu, B and Li, F},
title = {Functional remodeling of the gut microbiome and metabolome in primary idiopathic male infertility.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05064-x},
pmid = {42026467},
issn = {1471-2180},
support = {2024NSFSC0647//Sichuan Provincial Science and Technology Support Program/ ; 24SYJS01//Health Commission of Sichuan Province Medical Science and Technology Program/ ; SCU2025J4183//the Fundamental Research Funds for the Central Universities/ ; },
}
RevDate: 2026-04-23
Apple replant disease resistance in different apple rootstocks evaluated using microbiomic and metabolomic analyses.
BMC plant biology pii:10.1186/s12870-026-08844-9 [Epub ahead of print].
Additional Links: PMID-42026475
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PubMed:
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@article {pmid42026475,
year = {2026},
author = {Jia, L and Ren, S and Zhang, J and Ma, J and Yu, Z and Sun, N and Li, B and Zhang, X and Liang, B},
title = {Apple replant disease resistance in different apple rootstocks evaluated using microbiomic and metabolomic analyses.},
journal = {BMC plant biology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12870-026-08844-9},
pmid = {42026475},
issn = {1471-2229},
support = {HBCT2024150205//Hebei Agriculture Research System/ ; 21326308D-02-03//Key Research and Development Project of Hebei Province/ ; C2024204214//Natural Science Foundation of Hebei Province/ ; BJK2022012//Science and Technology Project of Hebei Education Department/ ; },
}
RevDate: 2026-04-24
Application of Gut Microbiota in the Treatment and Efficacy Evaluation of Tic Disorders: A Systematic Review.
Journal of child and adolescent psychopharmacology [Epub ahead of print].
OBJECTIVE: To systematically review existing evidence on the role of gut microbiota in the pathogenesis of tic disorders (TD) and to assess the therapeutic potential of microbiome-targeted interventions such as probiotics and fecal microbiota transplantation in the management of TD.
METHODS: A comprehensive search was conducted in PubMed, Web of Science, EMBASE, and The Cochrane Library (up to May 26, 2025). The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines and was registered in PROSPERO (CRD420251067880).
RESULTS: Eleven studies were included, with four focusing on gut microbiome-based therapies and seven studies with gut microbiota and its metabolites as outcome indicators. At the genus level, children with TD exhibited specific alterations in gut microbiota: increased abundance of Bacteroides, Faecalibacterium, and Ruminococcus, alongside decreased levels of Bifidobacterium and Prevotella. This functional dysbiosis may trigger neuroinflammation via disrupted short-chain fatty acid metabolism and impaired intestinal barrier function, ultimately disturbing the glutamate and γ-aminobutyric acid neurotransmitter balance and leading to dysfunction in the cortico-striato-thalamo-cortical circuit. Meanwhile, probiotics as an intervention have been consistently reported to alleviate tic symptoms, although clinical evidence remains limited.
CONCLUSION: Gut microbiota may contribute to TD pathogenesis via immune modulation and neurotransmitter metabolism. While microbiota-based strategies show promise, heterogeneity and methodological limitations in current studies necessitate further high-quality research to validate mechanisms and support clinical application.
Additional Links: PMID-42026738
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PubMed:
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@article {pmid42026738,
year = {2026},
author = {Cao, B and Zhou, X and Cao, X and Shi, J and Liu, C and Yuan, B},
title = {Application of Gut Microbiota in the Treatment and Efficacy Evaluation of Tic Disorders: A Systematic Review.},
journal = {Journal of child and adolescent psychopharmacology},
volume = {},
number = {},
pages = {10445463261445906},
doi = {10.1177/10445463261445906},
pmid = {42026738},
issn = {1557-8992},
abstract = {OBJECTIVE: To systematically review existing evidence on the role of gut microbiota in the pathogenesis of tic disorders (TD) and to assess the therapeutic potential of microbiome-targeted interventions such as probiotics and fecal microbiota transplantation in the management of TD.
METHODS: A comprehensive search was conducted in PubMed, Web of Science, EMBASE, and The Cochrane Library (up to May 26, 2025). The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines and was registered in PROSPERO (CRD420251067880).
RESULTS: Eleven studies were included, with four focusing on gut microbiome-based therapies and seven studies with gut microbiota and its metabolites as outcome indicators. At the genus level, children with TD exhibited specific alterations in gut microbiota: increased abundance of Bacteroides, Faecalibacterium, and Ruminococcus, alongside decreased levels of Bifidobacterium and Prevotella. This functional dysbiosis may trigger neuroinflammation via disrupted short-chain fatty acid metabolism and impaired intestinal barrier function, ultimately disturbing the glutamate and γ-aminobutyric acid neurotransmitter balance and leading to dysfunction in the cortico-striato-thalamo-cortical circuit. Meanwhile, probiotics as an intervention have been consistently reported to alleviate tic symptoms, although clinical evidence remains limited.
CONCLUSION: Gut microbiota may contribute to TD pathogenesis via immune modulation and neurotransmitter metabolism. While microbiota-based strategies show promise, heterogeneity and methodological limitations in current studies necessitate further high-quality research to validate mechanisms and support clinical application.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Gut microbiome and pregnancy complications: emerging evidence and mechanistic insights.
Gut microbes, 18(1):2661417.
The gut microbiome undergoes significant alterations during pregnancy. Perturbations in these microbial communities are increasingly associated with a range of pregnancy complications, including miscarriage, gestational diabetes mellitus, preeclampsia, preterm birth, and fetal growth restriction, among others. This review synthesizes current evidence on the dynamic changes in the maternal gut microecosystem including bacterial, fungal, and viral communities throughout gestation and examines its relationships with various pregnancy complications. We also summarize the underlying mechanisms driving these interactions, focusing on metabolic regulations involving short-chain fatty acids, bile acids, indoles, sex hormones, intestinal barrier integrity, and the modulation of maternal immune responses essential for fetal tolerance. Additionally, we discuss the lasting impact of the maternal microbiome on offspring health via vertical transmission and developmental programming. This review provides a conceptual framework that integrates mechanistic insights with clinical findings, with the goal of informing future research and supporting the development of microbiome-based interventions to improve maternal and neonatal health outcomes.
Additional Links: PMID-42026776
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@article {pmid42026776,
year = {2026},
author = {Hu, S and Miao, Z and Xiao, C and Fu, Y and Zheng, J and Hu, W and Zheng, JS},
title = {Gut microbiome and pregnancy complications: emerging evidence and mechanistic insights.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2661417},
doi = {10.1080/19490976.2026.2661417},
pmid = {42026776},
issn = {1949-0984},
mesh = {Humans ; Pregnancy ; Female ; *Gastrointestinal Microbiome ; *Pregnancy Complications/microbiology ; Bacteria/classification/genetics/isolation & purification/metabolism ; Animals ; },
abstract = {The gut microbiome undergoes significant alterations during pregnancy. Perturbations in these microbial communities are increasingly associated with a range of pregnancy complications, including miscarriage, gestational diabetes mellitus, preeclampsia, preterm birth, and fetal growth restriction, among others. This review synthesizes current evidence on the dynamic changes in the maternal gut microecosystem including bacterial, fungal, and viral communities throughout gestation and examines its relationships with various pregnancy complications. We also summarize the underlying mechanisms driving these interactions, focusing on metabolic regulations involving short-chain fatty acids, bile acids, indoles, sex hormones, intestinal barrier integrity, and the modulation of maternal immune responses essential for fetal tolerance. Additionally, we discuss the lasting impact of the maternal microbiome on offspring health via vertical transmission and developmental programming. This review provides a conceptual framework that integrates mechanistic insights with clinical findings, with the goal of informing future research and supporting the development of microbiome-based interventions to improve maternal and neonatal health outcomes.},
}
MeSH Terms:
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Humans
Pregnancy
Female
*Gastrointestinal Microbiome
*Pregnancy Complications/microbiology
Bacteria/classification/genetics/isolation & purification/metabolism
Animals
RevDate: 2026-04-24
CmpDate: 2026-04-24
Calorie-restricted oat diet is associated with zonulin and short-chain fatty acid response in metabolic syndrome: a randomized controlled trial.
Gut microbes, 18(1):2662687.
Oats are associated with positive effects on gut health, but human studies are largely lacking. Therefore, we investigated the effects of two different oat diets on gut permeability makers in individuals with metabolic syndrome, each in a randomized, controlled parallel design. Participants either consumed 3 × 100 g oatmeal/d for 2 d or an adapted control diet, or they integrated 1 × 80 g oatmeal/d into their habitual diet for 6 weeks or maintained it unchanged. Serum zonulin decreased upon 2-d calorie-restricted oat diet compared to baseline, while plasma butyric acid increased compared to the control (n = 27). Zonulin reduction correlated inversely with changes in short-chain fatty acids (SCFAs), particularly valeric and butyric acids, which were associated with shifts in microbial composition. During the 6-week isocaloric oat diet, these parameters remained stable (n = 22). Our data suggests that alterations in microbiome and related effects on SCFAs upon a short-term calorie-restricted diet with high-dose oats are contributing factors to changes in gut permeability markers. Thus, an intense oat intake might be a suitable and feasible approach to improve obesity-related intestinal barrier dysfunction in metabolic syndrome.German Clinical Trials Register: 07/28/2020, identifier: DRKS00022169.
Additional Links: PMID-42026801
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PubMed:
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@article {pmid42026801,
year = {2026},
author = {Klümpen, L and Mantri, A and Donkers, A and Seel, W and Stoffel-Wagner, B and Coenen, M and Schmid, M and Weinhold, L and Grein, F and Newels, P and Bedarf, J and Wüllner, U and Stehle, P and Simon, MC},
title = {Calorie-restricted oat diet is associated with zonulin and short-chain fatty acid response in metabolic syndrome: a randomized controlled trial.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2662687},
doi = {10.1080/19490976.2026.2662687},
pmid = {42026801},
issn = {1949-0984},
mesh = {Humans ; *Avena/metabolism ; *Metabolic Syndrome/diet therapy/microbiology/metabolism/blood ; Haptoglobins ; Male ; *Fatty Acids, Volatile/metabolism/blood ; Middle Aged ; Female ; *Protein Precursors/blood ; Gastrointestinal Microbiome ; Adult ; *Cholera Toxin/blood ; *Caloric Restriction ; Permeability ; Bacteria/classification/isolation & purification/genetics/metabolism ; },
abstract = {Oats are associated with positive effects on gut health, but human studies are largely lacking. Therefore, we investigated the effects of two different oat diets on gut permeability makers in individuals with metabolic syndrome, each in a randomized, controlled parallel design. Participants either consumed 3 × 100 g oatmeal/d for 2 d or an adapted control diet, or they integrated 1 × 80 g oatmeal/d into their habitual diet for 6 weeks or maintained it unchanged. Serum zonulin decreased upon 2-d calorie-restricted oat diet compared to baseline, while plasma butyric acid increased compared to the control (n = 27). Zonulin reduction correlated inversely with changes in short-chain fatty acids (SCFAs), particularly valeric and butyric acids, which were associated with shifts in microbial composition. During the 6-week isocaloric oat diet, these parameters remained stable (n = 22). Our data suggests that alterations in microbiome and related effects on SCFAs upon a short-term calorie-restricted diet with high-dose oats are contributing factors to changes in gut permeability markers. Thus, an intense oat intake might be a suitable and feasible approach to improve obesity-related intestinal barrier dysfunction in metabolic syndrome.German Clinical Trials Register: 07/28/2020, identifier: DRKS00022169.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Avena/metabolism
*Metabolic Syndrome/diet therapy/microbiology/metabolism/blood
Haptoglobins
Male
*Fatty Acids, Volatile/metabolism/blood
Middle Aged
Female
*Protein Precursors/blood
Gastrointestinal Microbiome
Adult
*Cholera Toxin/blood
*Caloric Restriction
Permeability
Bacteria/classification/isolation & purification/genetics/metabolism
RevDate: 2026-04-24
CmpDate: 2026-04-24
Gene-level gut microbiome signatures as predictive biomarkers for response to immune checkpoint inhibitors across multiple cancer types.
Gut microbes, 18(1):2662690.
Targeting programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) with immune checkpoint inhibitors (ICIs) has improved survival across multiple cancer types, but the variability in patient response highlights the need for better predictive biomarkers. Existing studies rely on taxonomic abundance derived from reference genome databases, limiting the discovery and functional interpretation of uncharacterized microbes. Here, we integrated metagenomic data from multiple ICI-treated cohorts spanning diverse cancer types and geographic regions and developed a deep learning model, named BioP-VAE, that incorporates biological prior knowledge via protein sequence embeddings and uses gene-level microbial abundance features as input. Gene-level microbial abundance outperformed taxonomy abundance in predicting both ICI response and 12-month progression-free survival (PFS). In patients receiving combination immune checkpoint blockade (CICB), BioP-VAE achieved a mean AUC of 0.89 in intracohort and 0.88 in cross-cohort evaluation. Notably, in the monotherapy-treated intracohorts, BioP-VAE achieved a mean AUC of 0.97. Feature attribution analysis revealed key microbial genes. Additionally, we identified distinct predictive microbial signatures via age-stratified analysis, suggesting that host age may modulate microbiome‒immune interactions. Importantly, this is the first large-scale study to evaluate gene-level microbial abundance features for ICI response prediction across multiple cancer types by deep learning. Our findings demonstrate that incorporating biological prior knowledge into deep learning models can improve the discovery of microbial biomarkers that can be generalized across cancer types and treatment settings, offering a novel strategy for patient stratification in immunotherapy.
Additional Links: PMID-42026803
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@article {pmid42026803,
year = {2026},
author = {Zhang, F and Hu, K and Sun, C and Chen, R and Ni, G and Liu, X and Wei, L and Su, R},
title = {Gene-level gut microbiome signatures as predictive biomarkers for response to immune checkpoint inhibitors across multiple cancer types.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2662690},
doi = {10.1080/19490976.2026.2662690},
pmid = {42026803},
issn = {1949-0984},
mesh = {Humans ; *Immune Checkpoint Inhibitors/therapeutic use ; *Gastrointestinal Microbiome/genetics/drug effects ; *Neoplasms/drug therapy/microbiology ; Deep Learning ; Biomarkers, Tumor/genetics ; *Bacteria/classification/genetics/isolation & purification ; Female ; Male ; Metagenomics ; },
abstract = {Targeting programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) with immune checkpoint inhibitors (ICIs) has improved survival across multiple cancer types, but the variability in patient response highlights the need for better predictive biomarkers. Existing studies rely on taxonomic abundance derived from reference genome databases, limiting the discovery and functional interpretation of uncharacterized microbes. Here, we integrated metagenomic data from multiple ICI-treated cohorts spanning diverse cancer types and geographic regions and developed a deep learning model, named BioP-VAE, that incorporates biological prior knowledge via protein sequence embeddings and uses gene-level microbial abundance features as input. Gene-level microbial abundance outperformed taxonomy abundance in predicting both ICI response and 12-month progression-free survival (PFS). In patients receiving combination immune checkpoint blockade (CICB), BioP-VAE achieved a mean AUC of 0.89 in intracohort and 0.88 in cross-cohort evaluation. Notably, in the monotherapy-treated intracohorts, BioP-VAE achieved a mean AUC of 0.97. Feature attribution analysis revealed key microbial genes. Additionally, we identified distinct predictive microbial signatures via age-stratified analysis, suggesting that host age may modulate microbiome‒immune interactions. Importantly, this is the first large-scale study to evaluate gene-level microbial abundance features for ICI response prediction across multiple cancer types by deep learning. Our findings demonstrate that incorporating biological prior knowledge into deep learning models can improve the discovery of microbial biomarkers that can be generalized across cancer types and treatment settings, offering a novel strategy for patient stratification in immunotherapy.},
}
MeSH Terms:
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Humans
*Immune Checkpoint Inhibitors/therapeutic use
*Gastrointestinal Microbiome/genetics/drug effects
*Neoplasms/drug therapy/microbiology
Deep Learning
Biomarkers, Tumor/genetics
*Bacteria/classification/genetics/isolation & purification
Female
Male
Metagenomics
RevDate: 2026-04-24
Ketogenic diet modulates gut microbiota composition in an experimental model of cerebral palsy.
Nutritional neuroscience [Epub ahead of print].
BACKGROUND: Cerebral palsy (CPa) is a neurodevelopmental disorder often accompanied by gastrointestinal dysfunction and dysbiosis of the gut microbiota (GM). The ketogenic diet (KD) has demonstrated neuroprotective and anti-inflammatory properties in neurological diseases, yet its effects on GM in CPa remain poorly understood.
OBJECTIVE: This study aimed to evaluate the impact of KD on the GM composition in an experimental model of CPa.
METHODS: Male Wistar rats were assigned to four groups (n = 10) according to healthy status and KD intervention: healthy control (C), healthy ketogenic diet (K), cerebral palsy (P), and cerebral palsy with ketogenic diet (PK). CPa was induced by perinatal anoxia and sensorimotor restriction, and, from postnatal day 25-65, animals received a standard or a KD. Body weight, food, and energy intake were monitored. Fecal samples were collected at day 65 for 16S rRNA sequencing and bioinformatics analyses.
RESULTS: The CPa condition was associated with reduced body weight, decreased food intake, and marked alterations in GM composition, characterized by increased abundance of Proteobacteria, Enterobacteriaceae, and Escherichia-Shigella, along with reduced levels of Bifidobacterium and Lactobacillus. KD intervention in animals with CPa was associated with coordinated shifts in GM structure, including reduced representation of taxa linked to inflammatory profiles and increased abundance of short-chain fatty acid-producing bacterial groups, such as members of the Lachnospiraceae and Ruminococcaceae families.
CONCLUSION: Overall, these findings suggest that modulation of GM may contribute to the neuroprotective and anti-inflammatory effects of the KD, highlighting GM as a potential therapeutic target for CPa-associated comorbidities.
Additional Links: PMID-42026999
Publisher:
PubMed:
Citation:
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@article {pmid42026999,
year = {2026},
author = {Dantas Alves, JS and De Oliveira Melo, NC and Toscano, AE and Manhães-De-Castro, R and Fraga Filho, CX and Cruz Neto, JPR and De Brito Alves, JL and Muniz, GS},
title = {Ketogenic diet modulates gut microbiota composition in an experimental model of cerebral palsy.},
journal = {Nutritional neuroscience},
volume = {},
number = {},
pages = {1-11},
doi = {10.1080/1028415X.2026.2656403},
pmid = {42026999},
issn = {1476-8305},
abstract = {BACKGROUND: Cerebral palsy (CPa) is a neurodevelopmental disorder often accompanied by gastrointestinal dysfunction and dysbiosis of the gut microbiota (GM). The ketogenic diet (KD) has demonstrated neuroprotective and anti-inflammatory properties in neurological diseases, yet its effects on GM in CPa remain poorly understood.
OBJECTIVE: This study aimed to evaluate the impact of KD on the GM composition in an experimental model of CPa.
METHODS: Male Wistar rats were assigned to four groups (n = 10) according to healthy status and KD intervention: healthy control (C), healthy ketogenic diet (K), cerebral palsy (P), and cerebral palsy with ketogenic diet (PK). CPa was induced by perinatal anoxia and sensorimotor restriction, and, from postnatal day 25-65, animals received a standard or a KD. Body weight, food, and energy intake were monitored. Fecal samples were collected at day 65 for 16S rRNA sequencing and bioinformatics analyses.
RESULTS: The CPa condition was associated with reduced body weight, decreased food intake, and marked alterations in GM composition, characterized by increased abundance of Proteobacteria, Enterobacteriaceae, and Escherichia-Shigella, along with reduced levels of Bifidobacterium and Lactobacillus. KD intervention in animals with CPa was associated with coordinated shifts in GM structure, including reduced representation of taxa linked to inflammatory profiles and increased abundance of short-chain fatty acid-producing bacterial groups, such as members of the Lachnospiraceae and Ruminococcaceae families.
CONCLUSION: Overall, these findings suggest that modulation of GM may contribute to the neuroprotective and anti-inflammatory effects of the KD, highlighting GM as a potential therapeutic target for CPa-associated comorbidities.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Characterization of the Gut Virome in Patients with Inflammatory Bowel Disease and Non-Alcoholic Fatty Liver Disease.
Journal of inflammation research, 19:581751.
OBJECTIVE: The dysbiosis of the gut microbiota is a well-known correlate in the pathogenesis of inflammatory bowel disease (IBD). However, the microbiome characteristics of patients with IBD who also have non-alcoholic fatty liver disease (NAFLD) are understudied, particularly the potential pathogenic mechanisms of the gut virome.
MATERIALS AND METHODS: In this study, we conducted a comprehensive gut virome correlation study, along with serum metabolomics analysis, by performing virus-like particle (VLP) and metagenomic sequencing on fecal samples from patients with inflammatory bowel disease and non-alcoholic fatty liver disease (IBD-NAFLD) and NAFLD (MASLD) controls without gastrointestinal diseases.
RESULTS: The results showed that changes in the fecal virome were associated with IBD-NAFLD (MASLD), particularly with an increase in the abundance of Caudovirales in IBD-NAFLD (MASLD) patients. Subsequent analysis of the gut virome identified Bacteroides as the top predicted host for the viruses. Additionally, we identified the pathways involved in all differential metabolites through KEGG annotation analysis, with the highest correlation being the galactose metabolism pathway.
CONCLUSION: In conclusion, by using a customized integrated gut virome catalog tailored for IBD, we revealed the fundamental changes in the gut virome of IBD-NAFLD (MASLD) patients. This study is the first to uncover the specificity of the gut virome in IBD-NAFLD (MASLD) patients and predict Bacteroides as a potential host, suggesting a microbial signature primarily influenced by intestinal inflammation.
Additional Links: PMID-42027256
PubMed:
Citation:
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@article {pmid42027256,
year = {2026},
author = {Lu, S and Xia, Y and Sun, Q and Sun, Y and Chen, R and Jin, H and Zhang, J and Liu, W and Huang, J},
title = {Characterization of the Gut Virome in Patients with Inflammatory Bowel Disease and Non-Alcoholic Fatty Liver Disease.},
journal = {Journal of inflammation research},
volume = {19},
number = {},
pages = {581751},
pmid = {42027256},
issn = {1178-7031},
abstract = {OBJECTIVE: The dysbiosis of the gut microbiota is a well-known correlate in the pathogenesis of inflammatory bowel disease (IBD). However, the microbiome characteristics of patients with IBD who also have non-alcoholic fatty liver disease (NAFLD) are understudied, particularly the potential pathogenic mechanisms of the gut virome.
MATERIALS AND METHODS: In this study, we conducted a comprehensive gut virome correlation study, along with serum metabolomics analysis, by performing virus-like particle (VLP) and metagenomic sequencing on fecal samples from patients with inflammatory bowel disease and non-alcoholic fatty liver disease (IBD-NAFLD) and NAFLD (MASLD) controls without gastrointestinal diseases.
RESULTS: The results showed that changes in the fecal virome were associated with IBD-NAFLD (MASLD), particularly with an increase in the abundance of Caudovirales in IBD-NAFLD (MASLD) patients. Subsequent analysis of the gut virome identified Bacteroides as the top predicted host for the viruses. Additionally, we identified the pathways involved in all differential metabolites through KEGG annotation analysis, with the highest correlation being the galactose metabolism pathway.
CONCLUSION: In conclusion, by using a customized integrated gut virome catalog tailored for IBD, we revealed the fundamental changes in the gut virome of IBD-NAFLD (MASLD) patients. This study is the first to uncover the specificity of the gut virome in IBD-NAFLD (MASLD) patients and predict Bacteroides as a potential host, suggesting a microbial signature primarily influenced by intestinal inflammation.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Immune fitness and biomarkers of immune function: Relationships with the oral and gut microbiome composition.
Brain, behavior, & immunity - health, 54:101239.
BACKGROUND: Immune fitness refers to the body's capacity to respond to health challenges, such as infections, by activating an appropriate immune response. The aim of the current study was to investigate the relationship between oral and gut microbiota community structure and immune fitness scores.
METHODS: Stool and saliva samples were collected to assess compositions of both oral and gut microbiota. Immune fitness was assessed with a single-item scale ranging from 0 (very poor) to 10 (excellent). Additionally, saliva samples were analyzed to measure the concentrations (pg/ml) of pro-inflammatory biomarkers interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α). Spearman's correlations were computed between microbiota abundance, immune fitness, and salivary biomarker levels. Bootstrapping was used to adjust for the relatively small sample size in the correlation analysis.
RESULTS: A total of 29 healthy participants (15 males; 14 females) enrolled in the study, with a mean age of 21.1 years old. Analysis of the salivary microbiota revealed significant negative correlations between self-reported immune fitness scores and the relative abundances of putative oral proinflammatory genera Selenomonas (r = -0.610), and Lachnospiraceae uncultured (r = -0.501). In the fecal microbiota, immune fitness scores showed a significant positive correlation with the relative abundance of putative beneficial butyrate-producing genus Lachnoclostridium (r = 0.513), and significant negative correlations with commensal gut bacterial genera Colidextribacter (r = -0.582) and Lachnospiraceae FCS020 group (r = -0.504).
CONCLUSION: Self-reported immune fitness is associated with the oral and gut microbiota community. The findings demonstrate the importance of microbiota in immune function and support the use of self-assessment scales to evaluate immune fitness.
Additional Links: PMID-42027356
PubMed:
Citation:
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@article {pmid42027356,
year = {2026},
author = {Ulijn, GA and Išerić, E and van de Loo, AJAE and Garssen, J and Engen, PA and Naqib, A and Green, SJ and Keshavarzian, A and Verster, JC},
title = {Immune fitness and biomarkers of immune function: Relationships with the oral and gut microbiome composition.},
journal = {Brain, behavior, & immunity - health},
volume = {54},
number = {},
pages = {101239},
pmid = {42027356},
issn = {2666-3546},
abstract = {BACKGROUND: Immune fitness refers to the body's capacity to respond to health challenges, such as infections, by activating an appropriate immune response. The aim of the current study was to investigate the relationship between oral and gut microbiota community structure and immune fitness scores.
METHODS: Stool and saliva samples were collected to assess compositions of both oral and gut microbiota. Immune fitness was assessed with a single-item scale ranging from 0 (very poor) to 10 (excellent). Additionally, saliva samples were analyzed to measure the concentrations (pg/ml) of pro-inflammatory biomarkers interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α). Spearman's correlations were computed between microbiota abundance, immune fitness, and salivary biomarker levels. Bootstrapping was used to adjust for the relatively small sample size in the correlation analysis.
RESULTS: A total of 29 healthy participants (15 males; 14 females) enrolled in the study, with a mean age of 21.1 years old. Analysis of the salivary microbiota revealed significant negative correlations between self-reported immune fitness scores and the relative abundances of putative oral proinflammatory genera Selenomonas (r = -0.610), and Lachnospiraceae uncultured (r = -0.501). In the fecal microbiota, immune fitness scores showed a significant positive correlation with the relative abundance of putative beneficial butyrate-producing genus Lachnoclostridium (r = 0.513), and significant negative correlations with commensal gut bacterial genera Colidextribacter (r = -0.582) and Lachnospiraceae FCS020 group (r = -0.504).
CONCLUSION: Self-reported immune fitness is associated with the oral and gut microbiota community. The findings demonstrate the importance of microbiota in immune function and support the use of self-assessment scales to evaluate immune fitness.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
The eye's coral reef: toward a planetary-health agenda for ocular-microbiome stewardship.
Frontiers in microbiology, 17:1816460.
Coral reefs and the human ocular surface represent ecologically distinct yet structurally comparable microbial ecosystems in which resilience depends on finely regulated host-microbe interactions. In coral reef science, microbial shifts precede visible bleaching and ecosystem collapse, enabling the development of predictive stress indices such as Degree Heating Weeks (DHW). Comparable principles are emerging in host-associated, low-biomass microbiomes, where subtle perturbations may trigger disproportionate functional consequences. Here, we propose a systems-level conceptual framework linking coral reef holobionts and the ocular surface as sentinel ecosystems governed by cumulative stress, threshold dynamics, and microbial instability. We introduce two heuristic constructs-the Cumulative Desiccating Load (CDL) and the Ocular Dysbiosis Sentinel Index (ODSI)-to frame dysbiosis as a trajectory of resilience loss driven by cumulative perturbations. Aging-related conditions such as age-related macular degeneration are discussed as examples of microbial and metabolic senescence within the human holobiont, conceptually paralleling coral reef decline under chronic sublethal stress. By integrating environmental and host-associated microbiome research within a planetary-health perspective, this article advances a resilience-oriented systems framework applicable across biological scales.
Additional Links: PMID-42027463
PubMed:
Citation:
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@article {pmid42027463,
year = {2026},
author = {Drago, L and De La Motte, LR},
title = {The eye's coral reef: toward a planetary-health agenda for ocular-microbiome stewardship.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1816460},
pmid = {42027463},
issn = {1664-302X},
abstract = {Coral reefs and the human ocular surface represent ecologically distinct yet structurally comparable microbial ecosystems in which resilience depends on finely regulated host-microbe interactions. In coral reef science, microbial shifts precede visible bleaching and ecosystem collapse, enabling the development of predictive stress indices such as Degree Heating Weeks (DHW). Comparable principles are emerging in host-associated, low-biomass microbiomes, where subtle perturbations may trigger disproportionate functional consequences. Here, we propose a systems-level conceptual framework linking coral reef holobionts and the ocular surface as sentinel ecosystems governed by cumulative stress, threshold dynamics, and microbial instability. We introduce two heuristic constructs-the Cumulative Desiccating Load (CDL) and the Ocular Dysbiosis Sentinel Index (ODSI)-to frame dysbiosis as a trajectory of resilience loss driven by cumulative perturbations. Aging-related conditions such as age-related macular degeneration are discussed as examples of microbial and metabolic senescence within the human holobiont, conceptually paralleling coral reef decline under chronic sublethal stress. By integrating environmental and host-associated microbiome research within a planetary-health perspective, this article advances a resilience-oriented systems framework applicable across biological scales.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Th17/treg balance in Inflammatory Bowel Disease: the role of microbial, and genetic regulators in disease modulation.
Frontiers in cell and developmental biology, 14:1774790.
Inflammatory Bowel Disease (IBD) is a chronic condition characterized by persistent mucosal inflammation driven by complex interactions among the gut microbiome, host immune genetics, and cellular metabolism. Emerging evidence highlights the central role of the Th17/Treg cell balance in maintaining intestinal immune tolerance, which is tightly regulated by microbe-derived metabolites and host metabolic pathways. In IBD, microbial dysbiosis and altered metabolite profiles disrupt this equilibrium, favoring pro-inflammatory responses. Moreover, genetic variants affecting immune regulation modulate individual susceptibility and disease course. Understanding how microbiome modulation, metabolic reprogramming, and genetic predisposition converge in IBD pathogenesis opens new avenues for precision medicine. This minireview discusses recent advances in this field, emphasizing novel microbiome-targeted strategies, metabolic interventions, and personalized immunomodulatory therapies aimed at restoring Th17/Treg homeostasis. Integrating microbiome, metabolome, and immunogenetic profiling may ultimately guide tailored treatments and improve long-term outcomes in IBD.
Additional Links: PMID-42027582
PubMed:
Citation:
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@article {pmid42027582,
year = {2026},
author = {Giudice, A and Brescia, C and Morano, D and Viglietto, G and Luzza, F and Amato, R and Spagnuolo, R},
title = {Th17/treg balance in Inflammatory Bowel Disease: the role of microbial, and genetic regulators in disease modulation.},
journal = {Frontiers in cell and developmental biology},
volume = {14},
number = {},
pages = {1774790},
pmid = {42027582},
issn = {2296-634X},
abstract = {Inflammatory Bowel Disease (IBD) is a chronic condition characterized by persistent mucosal inflammation driven by complex interactions among the gut microbiome, host immune genetics, and cellular metabolism. Emerging evidence highlights the central role of the Th17/Treg cell balance in maintaining intestinal immune tolerance, which is tightly regulated by microbe-derived metabolites and host metabolic pathways. In IBD, microbial dysbiosis and altered metabolite profiles disrupt this equilibrium, favoring pro-inflammatory responses. Moreover, genetic variants affecting immune regulation modulate individual susceptibility and disease course. Understanding how microbiome modulation, metabolic reprogramming, and genetic predisposition converge in IBD pathogenesis opens new avenues for precision medicine. This minireview discusses recent advances in this field, emphasizing novel microbiome-targeted strategies, metabolic interventions, and personalized immunomodulatory therapies aimed at restoring Th17/Treg homeostasis. Integrating microbiome, metabolome, and immunogenetic profiling may ultimately guide tailored treatments and improve long-term outcomes in IBD.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
The Gut-Brain Axis as a Mediator of Environmental Endocrine Disruptors in Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Mechanistic Synthesis.
Biological psychiatry global open science, 6(3):100717.
The rising global prevalence of attention-deficit/hyperactivity disorder (ADHD) underscores the importance of environmental factors, particularly environmental endocrine-disrupting chemicals (EEDs), whose mechanistic links to ADHD remain unclear. The gut-brain axis, a key modulator of neurodevelopment, is susceptible to EEDs and is altered in ADHD, suggesting a potential mediating pathway. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and PROSPERO registration (CRD420251152480), we systematically searched PubMed, Web of Science, and Embase (January 2014-July 2025) for studies on EEDs, gut microbiota, and ADHD. Data from 127 included studies (observational, experimental, interventional) were narratively synthesized to evaluate the gut-brain axis as a mediator. We found 1) consistent epidemiological associations between prenatal/childhood EED exposure (e.g., phthalates, bisphenol A, pesticides) and increased ADHD risk; 2) a distinct gut microbial signature in ADHD featuring reduced alpha diversity, elevated Firmicutes/Bacteroidetes ratio, depletion of beneficial taxa (Lactobacillus, Bifidobacterium), and impaired short-chain fatty acid (SCFA) production; 3) evidence that EED exposure induces convergent gut dysbiosis; and 4) interventional studies indicating that modulating the microbiota (via probiotics, synbiotics, fecal microbiota transplantation) can ameliorate ADHD-related behaviors. These findings support a novel mechanistic model wherein EEDs disrupt gut microbiota homeostasis, thereby contributing to ADHD pathogenesis via immune-inflammatory, microbial metabolite (e.g., SCFA), and neuroendocrine pathways along the gut-brain axis. This review synthesizes evidence positioning the gut-brain axis as a critical mediator linking EED exposure to ADHD. It proposes a unifying etiological framework and highlights the microbiome as a promising target for preventive and therapeutic strategies. Future longitudinal and intervention studies are needed to establish causality.
Additional Links: PMID-42027687
PubMed:
Citation:
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@article {pmid42027687,
year = {2026},
author = {Wu, H and Yu, M and Huang, S and Peng, Y and Wei, G and Huang, C},
title = {The Gut-Brain Axis as a Mediator of Environmental Endocrine Disruptors in Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Mechanistic Synthesis.},
journal = {Biological psychiatry global open science},
volume = {6},
number = {3},
pages = {100717},
pmid = {42027687},
issn = {2667-1743},
abstract = {The rising global prevalence of attention-deficit/hyperactivity disorder (ADHD) underscores the importance of environmental factors, particularly environmental endocrine-disrupting chemicals (EEDs), whose mechanistic links to ADHD remain unclear. The gut-brain axis, a key modulator of neurodevelopment, is susceptible to EEDs and is altered in ADHD, suggesting a potential mediating pathway. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and PROSPERO registration (CRD420251152480), we systematically searched PubMed, Web of Science, and Embase (January 2014-July 2025) for studies on EEDs, gut microbiota, and ADHD. Data from 127 included studies (observational, experimental, interventional) were narratively synthesized to evaluate the gut-brain axis as a mediator. We found 1) consistent epidemiological associations between prenatal/childhood EED exposure (e.g., phthalates, bisphenol A, pesticides) and increased ADHD risk; 2) a distinct gut microbial signature in ADHD featuring reduced alpha diversity, elevated Firmicutes/Bacteroidetes ratio, depletion of beneficial taxa (Lactobacillus, Bifidobacterium), and impaired short-chain fatty acid (SCFA) production; 3) evidence that EED exposure induces convergent gut dysbiosis; and 4) interventional studies indicating that modulating the microbiota (via probiotics, synbiotics, fecal microbiota transplantation) can ameliorate ADHD-related behaviors. These findings support a novel mechanistic model wherein EEDs disrupt gut microbiota homeostasis, thereby contributing to ADHD pathogenesis via immune-inflammatory, microbial metabolite (e.g., SCFA), and neuroendocrine pathways along the gut-brain axis. This review synthesizes evidence positioning the gut-brain axis as a critical mediator linking EED exposure to ADHD. It proposes a unifying etiological framework and highlights the microbiome as a promising target for preventive and therapeutic strategies. Future longitudinal and intervention studies are needed to establish causality.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Predictors of sensitivity to immune therapies in classic Hodgkin lymphoma.
Blood neoplasia, 3(2):100207.
Immune checkpoint blockade, particularly programmed cell death protein 1 inhibition, has redefined the management of classic Hodgkin lymphoma (cHL), achieving unprecedented efficacy in relapsed/refractory settings. Yet, durable benefit is not universal, because mechanisms of primary and acquired resistance remain incompletely understood. This review integrates current knowledge on predictors of sensitivity to immune therapies in cHL across clinical, biological, and technological dimensions. Established predictors, including disease burden, previous treatment exposure, CD30 intensity, programmed death-ligand 1 (PD-L1)/PD-L2 copy number gains, and loss of major histocompatibility complex expression, offer valuable but incomplete prognostic information. Tumor microenvironmental features such as macrophage polarization, T-cell exhaustion, and immune spatial organization further refine response prediction, whereas circulating biomarkers such as soluble PD-L1, circulating tumor DNA kinetics, and cytokine profiles provide noninvasive insights. Molecular and cellular pathways underlying resistance encompass genetic and epigenetic alterations, immune editing, and adaptive checkpoint upregulation. Emerging predictive frameworks, spanning multiomics and spatial profiling, radiomics, artificial intelligence, and microbiome-host cross talk, promise to enhance precision in patient stratification. Finally, the review outlines key challenges and research priorities for translating these multidimensional biomarkers into clinical trials and practice. A unified predictive framework integrating clinical, molecular, and computational indicators may ultimately enable personalized immunotherapy and overcome resistance in cHL.
Additional Links: PMID-42027746
PubMed:
Citation:
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@article {pmid42027746,
year = {2026},
author = {Alibrahim, MN and Carbone, A and Gloghini, A},
title = {Predictors of sensitivity to immune therapies in classic Hodgkin lymphoma.},
journal = {Blood neoplasia},
volume = {3},
number = {2},
pages = {100207},
pmid = {42027746},
issn = {2950-3280},
abstract = {Immune checkpoint blockade, particularly programmed cell death protein 1 inhibition, has redefined the management of classic Hodgkin lymphoma (cHL), achieving unprecedented efficacy in relapsed/refractory settings. Yet, durable benefit is not universal, because mechanisms of primary and acquired resistance remain incompletely understood. This review integrates current knowledge on predictors of sensitivity to immune therapies in cHL across clinical, biological, and technological dimensions. Established predictors, including disease burden, previous treatment exposure, CD30 intensity, programmed death-ligand 1 (PD-L1)/PD-L2 copy number gains, and loss of major histocompatibility complex expression, offer valuable but incomplete prognostic information. Tumor microenvironmental features such as macrophage polarization, T-cell exhaustion, and immune spatial organization further refine response prediction, whereas circulating biomarkers such as soluble PD-L1, circulating tumor DNA kinetics, and cytokine profiles provide noninvasive insights. Molecular and cellular pathways underlying resistance encompass genetic and epigenetic alterations, immune editing, and adaptive checkpoint upregulation. Emerging predictive frameworks, spanning multiomics and spatial profiling, radiomics, artificial intelligence, and microbiome-host cross talk, promise to enhance precision in patient stratification. Finally, the review outlines key challenges and research priorities for translating these multidimensional biomarkers into clinical trials and practice. A unified predictive framework integrating clinical, molecular, and computational indicators may ultimately enable personalized immunotherapy and overcome resistance in cHL.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
From dysbacteriosis to ecological remodeling: A new breakthrough in microbial treatment of inflammatory bowel disease.
iScience, 29(5):115483.
Inflammatory bowel disease (IBD) is a group of chronic and recurrent inflammatory conditions of the gastrointestinal tract, arising from complex interactions among genetic susceptibility, environmental factors, immune dysregulation, and alterations in the gut microbiota. Increasing evidence suggests that gut microbiota dysbiosis is closely associated with IBD pathogenesis and disease progression, providing a promising target for microbiome-oriented therapeutic strategies. However, due to the multi-factorial and dynamic nature of microbial alterations in IBD, single-intervention approaches often show limited efficacy and durability. On this basis, this review highlights emerging strategies based on engineered microbial ecosystems, which aim to systematically modulate microbial composition and function, reinforce intestinal barrier integrity, and regulate host immune responses. While these approaches hold significant potential, their therapeutic value should be interpreted in the context of current preclinical and early clinical evidence, and further validation is required to determine their long-term efficacy and safety in patients with IBD.
Additional Links: PMID-42028017
PubMed:
Citation:
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@article {pmid42028017,
year = {2026},
author = {Xie, J and Deng, S and Zhang, X and Zhang, L and Jia, X},
title = {From dysbacteriosis to ecological remodeling: A new breakthrough in microbial treatment of inflammatory bowel disease.},
journal = {iScience},
volume = {29},
number = {5},
pages = {115483},
pmid = {42028017},
issn = {2589-0042},
abstract = {Inflammatory bowel disease (IBD) is a group of chronic and recurrent inflammatory conditions of the gastrointestinal tract, arising from complex interactions among genetic susceptibility, environmental factors, immune dysregulation, and alterations in the gut microbiota. Increasing evidence suggests that gut microbiota dysbiosis is closely associated with IBD pathogenesis and disease progression, providing a promising target for microbiome-oriented therapeutic strategies. However, due to the multi-factorial and dynamic nature of microbial alterations in IBD, single-intervention approaches often show limited efficacy and durability. On this basis, this review highlights emerging strategies based on engineered microbial ecosystems, which aim to systematically modulate microbial composition and function, reinforce intestinal barrier integrity, and regulate host immune responses. While these approaches hold significant potential, their therapeutic value should be interpreted in the context of current preclinical and early clinical evidence, and further validation is required to determine their long-term efficacy and safety in patients with IBD.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Postbiotics and phage synergy in precision oral microbiome engineering: systems biology strategies targeting Streptococcus mutans in dental caries.
Frontiers in molecular biosciences, 13:1766853.
Dental caries continues to represent a major global public health concern and arises from complex ecological shifts within oral biofilms. The dominance of Streptococcus mutans, in combination with broader microbial imbalance and interactions involving the oral virome, plays a central role in disease progression. Although established preventive measures such as fluoride therapy and mechanical plaque control reduce enamel demineralization and microbial load, they do not comprehensively address dysbiosis, virulence regulation, or host-microbial signaling dynamics. Postbiotics are non-viable microbial products or metabolic derivatives with biological activity, are gaining attention as targeted modulators of the oral ecosystem. These agents include organic acids, exopolysaccharides, bacteriocins, and structural components derived from inactivated probiotic cells. Through diverse mechanisms, postbiotics can reduce acidogenic potential, weaken extracellular matrix integrity within biofilms, disrupt bacterial communication systems, and modulate mucosal immune pathways. Such effects may limit colonization efficiency and pathogenic behavior of S. mutans while preserving commensal balance. Emerging strategies propose combining postbiotics with bacteriophage-based approaches, immunomodulatory platforms, and innovative delivery systems such as nanoformulations and bioadhesive matrices to improve site-specific efficacy. Advances in multi-omics technologies, systems biology modeling, and artificial intelligence-driven diagnostics further support the development of personalized interventions tailored to individual microbial signatures. In addition, postbiotic-mediated modulation of viral-bacterial interactions and horizontal gene exchange may contribute to restoring ecological stability and reducing antimicrobial resistance dissemination. This review integrates current knowledge on postbiotic-driven regulation of the oral microbiome and virome and examines their potential role in precision-oriented caries management. Addressing translational challenges, including formulation stability, safety evaluation, regulatory pathways, and comprehensive virome profiling, will be critical for future clinical application.
Additional Links: PMID-42028131
PubMed:
Citation:
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@article {pmid42028131,
year = {2026},
author = {Radhamanalan, G},
title = {Postbiotics and phage synergy in precision oral microbiome engineering: systems biology strategies targeting Streptococcus mutans in dental caries.},
journal = {Frontiers in molecular biosciences},
volume = {13},
number = {},
pages = {1766853},
pmid = {42028131},
issn = {2296-889X},
abstract = {Dental caries continues to represent a major global public health concern and arises from complex ecological shifts within oral biofilms. The dominance of Streptococcus mutans, in combination with broader microbial imbalance and interactions involving the oral virome, plays a central role in disease progression. Although established preventive measures such as fluoride therapy and mechanical plaque control reduce enamel demineralization and microbial load, they do not comprehensively address dysbiosis, virulence regulation, or host-microbial signaling dynamics. Postbiotics are non-viable microbial products or metabolic derivatives with biological activity, are gaining attention as targeted modulators of the oral ecosystem. These agents include organic acids, exopolysaccharides, bacteriocins, and structural components derived from inactivated probiotic cells. Through diverse mechanisms, postbiotics can reduce acidogenic potential, weaken extracellular matrix integrity within biofilms, disrupt bacterial communication systems, and modulate mucosal immune pathways. Such effects may limit colonization efficiency and pathogenic behavior of S. mutans while preserving commensal balance. Emerging strategies propose combining postbiotics with bacteriophage-based approaches, immunomodulatory platforms, and innovative delivery systems such as nanoformulations and bioadhesive matrices to improve site-specific efficacy. Advances in multi-omics technologies, systems biology modeling, and artificial intelligence-driven diagnostics further support the development of personalized interventions tailored to individual microbial signatures. In addition, postbiotic-mediated modulation of viral-bacterial interactions and horizontal gene exchange may contribute to restoring ecological stability and reducing antimicrobial resistance dissemination. This review integrates current knowledge on postbiotic-driven regulation of the oral microbiome and virome and examines their potential role in precision-oriented caries management. Addressing translational challenges, including formulation stability, safety evaluation, regulatory pathways, and comprehensive virome profiling, will be critical for future clinical application.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Characteristics of CD4[+]T-cell reduction and pulmonary infections in critically ill immunocompromised patients.
Journal of intensive medicine, 6(2):157-165.
BACKGROUND: The CD4[+]T-cell count is a key indicator for evaluating immunosuppression. Infections significantly influence the survival and prognosis of critically ill patients. This study aims to systematically evaluate the association between reduced CD4[+] T-cell counts and lung infections in immunosuppressed ICU patients, offering clinical evidence to guide the management of lung infections in this population.
METHODS: This retrospective, single-center study included 40 immunocompromised patients admitted to the ICU from January 1, 2021, to June 30, 2023. All participants underwent metagenomic next-generation sequencing. Patients with suspected lung infections based on their CD4[+]T-cell counts were divided into mild (350/µL
RESULTS: Amang these forty immunosuppressed patients, 8 were assigned to the mild group, 16 to the moderate group, and 16 to the severe group. Streptococcus pneumoniae was almost all distributed in moderate patients (75.0%), while severe patients had a higher proportion of fungi detected (25.7%). Respiratory microbiome analysis identified Acinetobacter baumannii, Human alphaherpesvirus 1, and Klebsiella pneumoniae as the most abundant species. Although no significant difference in the alpha diversity index was found among the groups, index values were lower in the severe group than in the moderate group. Beta diversity analysis showed that the microbial community structure did not significantly differ among the three groups. A total of 27 microbial markers were obtained, with multiple streptococcal species showing enrichment in moderate group and Candida tropicalis in severe group. By day 28, four patients (50.0%) in the mild group had died compared with six (37.5%) in the moderate group and nine (56.3%) in the severe group. There were no significant difference in the duration of ICU or hospital stays.
CONCLUSIONS: This study on ICU-admitted immunocompromised patients identified the prevalent pathogens and microbiome features associated with pulmonary infections, as well as their relationship with CD4[+]T-cell depletion. These findings are valuable for optimizing clinical diagnosis and treatment strategies and may contribute to improving patient outcomes.
Additional Links: PMID-42028145
PubMed:
Citation:
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@article {pmid42028145,
year = {2026},
author = {Chen, Y and Zhang, L and Wang, T and Pan, X and Chen, D and Liu, J},
title = {Characteristics of CD4[+]T-cell reduction and pulmonary infections in critically ill immunocompromised patients.},
journal = {Journal of intensive medicine},
volume = {6},
number = {2},
pages = {157-165},
pmid = {42028145},
issn = {2667-100X},
abstract = {BACKGROUND: The CD4[+]T-cell count is a key indicator for evaluating immunosuppression. Infections significantly influence the survival and prognosis of critically ill patients. This study aims to systematically evaluate the association between reduced CD4[+] T-cell counts and lung infections in immunosuppressed ICU patients, offering clinical evidence to guide the management of lung infections in this population.
METHODS: This retrospective, single-center study included 40 immunocompromised patients admitted to the ICU from January 1, 2021, to June 30, 2023. All participants underwent metagenomic next-generation sequencing. Patients with suspected lung infections based on their CD4[+]T-cell counts were divided into mild (350/µL
RESULTS: Amang these forty immunosuppressed patients, 8 were assigned to the mild group, 16 to the moderate group, and 16 to the severe group. Streptococcus pneumoniae was almost all distributed in moderate patients (75.0%), while severe patients had a higher proportion of fungi detected (25.7%). Respiratory microbiome analysis identified Acinetobacter baumannii, Human alphaherpesvirus 1, and Klebsiella pneumoniae as the most abundant species. Although no significant difference in the alpha diversity index was found among the groups, index values were lower in the severe group than in the moderate group. Beta diversity analysis showed that the microbial community structure did not significantly differ among the three groups. A total of 27 microbial markers were obtained, with multiple streptococcal species showing enrichment in moderate group and Candida tropicalis in severe group. By day 28, four patients (50.0%) in the mild group had died compared with six (37.5%) in the moderate group and nine (56.3%) in the severe group. There were no significant difference in the duration of ICU or hospital stays.
CONCLUSIONS: This study on ICU-admitted immunocompromised patients identified the prevalent pathogens and microbiome features associated with pulmonary infections, as well as their relationship with CD4[+]T-cell depletion. These findings are valuable for optimizing clinical diagnosis and treatment strategies and may contribute to improving patient outcomes.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Mode of birth and risk of inflammatory bowel disease in offspring: an updated systematic review and meta-analysis.
Frontiers in reproductive health, 8:1776110.
BACKGROUND: Cesarean section (CS) rates continue rising worldwide, raising concerns about long-term offspring health consequences, including inflammatory bowel disease (IBD). This systematic review and meta-analysis evaluate the association between CS and risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC).
METHODS: PubMed, Scopus, CENTRAL, and Web of Science were searched through June 2025. Eligible studies included observational cohorts and case-control studies reporting CS vs. vaginal delivery (VD) and IBD outcomes. Data extraction and risk of bias assessment were performed independently. Pooled relative risks (RRs), hazard ratios (HRs), and odds ratios (ORs) were calculated using fixed or random-effects models. Subgroup analyses and publication bias assessment were conducted.
RESULTS: Twenty-two studies comprising over 13 million births were included. Unadjusted analyses showed no association between CS and IBD (RR: 0.98, 95% CI: 0.88-1.08), CD (RR: 0.99, 95% CI: 0.88-1.12), however, an inverse association was observed for UC (RR: 0.82, 95% CI: 0.72-0.95). Regional variation was observed, with CS associated with reduced IBD risk in Denmark, Switzerland, and Norway, but increased risk in Germany and Australia. Adjusted analyses consistently demonstrated no association: IBD (HR: 1.14, 95% CI: 0.99-1.30; OR: 0.91, 95% CI: 0.65-1.25), CD (HR: 1.07, 95% CI: 0.90-1.28; OR: 1.11, 95% CI: 0.98-1.26), and UC (HR: 0.96, 95% CI: 0.87-1.05; OR: 1.05, 95% CI: 0.86-1.27). No publication bias was detected.
CONCLUSION: Across over 13 million births, delivery mode was not associated with IBD, CD, or UC risk. Despite biologically plausible mechanisms linking CS to altered microbiome patterns, epidemiological evidence does not support CS as an independent IBD risk factor. These findings provide reassurance for clinical counseling regarding CS and long-term IBD risk.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420251237413, PROSPERO CRD420251237413.
Additional Links: PMID-42028273
PubMed:
Citation:
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@article {pmid42028273,
year = {2026},
author = {Taha, H and Al-Shalalfeh, M and Khalil, A and Khasawneh, Y and Abu Ata, A and AbuEin, H and Issa, A and Alhawamdeh, T and BaniMustafa, M and Al-Sabbagh, MQ and Jönsson, L},
title = {Mode of birth and risk of inflammatory bowel disease in offspring: an updated systematic review and meta-analysis.},
journal = {Frontiers in reproductive health},
volume = {8},
number = {},
pages = {1776110},
pmid = {42028273},
issn = {2673-3153},
abstract = {BACKGROUND: Cesarean section (CS) rates continue rising worldwide, raising concerns about long-term offspring health consequences, including inflammatory bowel disease (IBD). This systematic review and meta-analysis evaluate the association between CS and risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC).
METHODS: PubMed, Scopus, CENTRAL, and Web of Science were searched through June 2025. Eligible studies included observational cohorts and case-control studies reporting CS vs. vaginal delivery (VD) and IBD outcomes. Data extraction and risk of bias assessment were performed independently. Pooled relative risks (RRs), hazard ratios (HRs), and odds ratios (ORs) were calculated using fixed or random-effects models. Subgroup analyses and publication bias assessment were conducted.
RESULTS: Twenty-two studies comprising over 13 million births were included. Unadjusted analyses showed no association between CS and IBD (RR: 0.98, 95% CI: 0.88-1.08), CD (RR: 0.99, 95% CI: 0.88-1.12), however, an inverse association was observed for UC (RR: 0.82, 95% CI: 0.72-0.95). Regional variation was observed, with CS associated with reduced IBD risk in Denmark, Switzerland, and Norway, but increased risk in Germany and Australia. Adjusted analyses consistently demonstrated no association: IBD (HR: 1.14, 95% CI: 0.99-1.30; OR: 0.91, 95% CI: 0.65-1.25), CD (HR: 1.07, 95% CI: 0.90-1.28; OR: 1.11, 95% CI: 0.98-1.26), and UC (HR: 0.96, 95% CI: 0.87-1.05; OR: 1.05, 95% CI: 0.86-1.27). No publication bias was detected.
CONCLUSION: Across over 13 million births, delivery mode was not associated with IBD, CD, or UC risk. Despite biologically plausible mechanisms linking CS to altered microbiome patterns, epidemiological evidence does not support CS as an independent IBD risk factor. These findings provide reassurance for clinical counseling regarding CS and long-term IBD risk.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420251237413, PROSPERO CRD420251237413.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Investigating microbiota and biochemical changes in vaginal fluid toward point-of-care microbial monitoring using surface-enhanced Raman spectroscopy.
Biophotonics discovery, 2(4):042102.
SIGNIFICANCE: Vaginal health is maintained by the vaginal microbiome, and dysbiosis of this community can have lifelong negative consequences for women. Current clinical techniques for detecting bacteria in the vagina rely on subjective visual and microscopic analysis or untimely microbial culturing. Surface-enhanced Raman spectroscopy (SERS), a biochemical fingerprinting technique, shows potential for filling this gap as it can identify bacterial species and strains.
AIM: In this study, SERS was used to investigate biochemical changes in vaginal fluid when common vaginal bacteria were present and absent. Subsequently, the performance of a portable Raman spectrometer to detect these biochemical changes was evaluated.
APPROACH: Vaginal fluid was collected from participants attending routine gynecology exams, and SERS spectra were collected using a Raman microscope and a portable spectrometer. Partial least squares, peak intensity, and peak ratio analysis were used to investigate biochemical differences. Quantitative polymerase chain reaction was performed for characterization of Lactobacillus iners, Lactobacillus crispatus, Gardnerella vaginalis, and Streptococcus agalactiae content.
RESULTS: Gardnerella vaginalis presence was characterized by a significant increase in protein and lipid-related features and a decrease in organic acid peaks. The presence of Lactobacillus iners was represented by increased organic acid peaks and a reduction of protein, amino acid, and polysaccharide-related features. Similar trends with little loss of significance were observed when comparing the performance of a Raman microscope and a portable spectrometer.
CONCLUSION: We highlight the feasibility of SERS for detecting differences in bacterial species presence in vaginal fluid and showcase the potential for clinical translation.
Additional Links: PMID-42028293
PubMed:
Citation:
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@article {pmid42028293,
year = {2025},
author = {Rourke-Funderburg, AS and Francisco, VA and Nelson, DJ and Goncalves, KL and Haselton, FR and Elsamadicy, E and Locke, AK},
title = {Investigating microbiota and biochemical changes in vaginal fluid toward point-of-care microbial monitoring using surface-enhanced Raman spectroscopy.},
journal = {Biophotonics discovery},
volume = {2},
number = {4},
pages = {042102},
pmid = {42028293},
issn = {3005-4745},
abstract = {SIGNIFICANCE: Vaginal health is maintained by the vaginal microbiome, and dysbiosis of this community can have lifelong negative consequences for women. Current clinical techniques for detecting bacteria in the vagina rely on subjective visual and microscopic analysis or untimely microbial culturing. Surface-enhanced Raman spectroscopy (SERS), a biochemical fingerprinting technique, shows potential for filling this gap as it can identify bacterial species and strains.
AIM: In this study, SERS was used to investigate biochemical changes in vaginal fluid when common vaginal bacteria were present and absent. Subsequently, the performance of a portable Raman spectrometer to detect these biochemical changes was evaluated.
APPROACH: Vaginal fluid was collected from participants attending routine gynecology exams, and SERS spectra were collected using a Raman microscope and a portable spectrometer. Partial least squares, peak intensity, and peak ratio analysis were used to investigate biochemical differences. Quantitative polymerase chain reaction was performed for characterization of Lactobacillus iners, Lactobacillus crispatus, Gardnerella vaginalis, and Streptococcus agalactiae content.
RESULTS: Gardnerella vaginalis presence was characterized by a significant increase in protein and lipid-related features and a decrease in organic acid peaks. The presence of Lactobacillus iners was represented by increased organic acid peaks and a reduction of protein, amino acid, and polysaccharide-related features. Similar trends with little loss of significance were observed when comparing the performance of a Raman microscope and a portable spectrometer.
CONCLUSION: We highlight the feasibility of SERS for detecting differences in bacterial species presence in vaginal fluid and showcase the potential for clinical translation.},
}
RevDate: 2026-04-26
CmpDate: 2026-04-24
Emerging Therapeutic Strategies in Oral Cancer: Epigenetic, Mitochondrial and Immunotherapy Approaches.
Journal of cellular and molecular medicine, 30(8):e71107.
Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer and poses treatment challenges owing to genetic, epigenetic and environmental factors. Conventional treatments, including surgery, chemotherapy and radiation therapy, often have limitations in terms of efficacy and tolerability. Advances in epigenetic therapies such as DNA methyltransferase and histone deacetylase inhibitors offer promising avenues for reversing abnormal gene expression in OSCC. Mitochondria-targeted therapies leverage metabolic disruption and reactive oxygen species modulation to induce apoptosis. Immunotherapy, particularly with immune checkpoint inhibitors and cancer vaccines, enhances the immune response against cancer cells. This review explores the interplay between the tumour microenvironment and oral microbiome in OSCC progression and treatment response. Additionally, RNA interference therapy and nanoparticle-based drug delivery systems enable targeted therapeutic strategies, reduce off-target effects and improve efficacy. Although these approaches show potential, challenges in clinical translation remain. The integration of precision medicine with innovative drug delivery systems can significantly improve patient outcomes in oral cancer management.
Additional Links: PMID-42028862
PubMed:
Citation:
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@article {pmid42028862,
year = {2026},
author = {Shanmugam, G and Singh, CD and Thiruvengadam, R and Thiruvengadam, M and Morozov, V and Kolesnikov, R and Alkaladi, A and Saleh, R and Shariati, MA},
title = {Emerging Therapeutic Strategies in Oral Cancer: Epigenetic, Mitochondrial and Immunotherapy Approaches.},
journal = {Journal of cellular and molecular medicine},
volume = {30},
number = {8},
pages = {e71107},
pmid = {42028862},
issn = {1582-4934},
mesh = {Humans ; *Mouth Neoplasms/therapy/genetics/immunology/pathology ; *Epigenesis, Genetic/drug effects ; *Mitochondria/drug effects/metabolism/genetics ; *Immunotherapy/methods ; Tumor Microenvironment/drug effects ; Animals ; },
abstract = {Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer and poses treatment challenges owing to genetic, epigenetic and environmental factors. Conventional treatments, including surgery, chemotherapy and radiation therapy, often have limitations in terms of efficacy and tolerability. Advances in epigenetic therapies such as DNA methyltransferase and histone deacetylase inhibitors offer promising avenues for reversing abnormal gene expression in OSCC. Mitochondria-targeted therapies leverage metabolic disruption and reactive oxygen species modulation to induce apoptosis. Immunotherapy, particularly with immune checkpoint inhibitors and cancer vaccines, enhances the immune response against cancer cells. This review explores the interplay between the tumour microenvironment and oral microbiome in OSCC progression and treatment response. Additionally, RNA interference therapy and nanoparticle-based drug delivery systems enable targeted therapeutic strategies, reduce off-target effects and improve efficacy. Although these approaches show potential, challenges in clinical translation remain. The integration of precision medicine with innovative drug delivery systems can significantly improve patient outcomes in oral cancer management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mouth Neoplasms/therapy/genetics/immunology/pathology
*Epigenesis, Genetic/drug effects
*Mitochondria/drug effects/metabolism/genetics
*Immunotherapy/methods
Tumor Microenvironment/drug effects
Animals
RevDate: 2026-04-24
Decoding Microbial Reductive Dechlorination of 209 Polychlorinated Biphenyl Congeners through Experiment-Aided Quantum Chemistry and Machine Learning.
Environmental science & technology [Epub ahead of print].
Polychlorinated biphenyls (PCBs) persist globally as legacy pollutants with a complex structural diversity that complicates the understanding of their microbial conversion processes and remediation. In this study, high-throughput enzymatic assays, quantum chemical calculations, and machine learning were integrated to elucidate the reductive dechlorination pathways and reactivity of all 209 PCB congeners. By coupling Hirshfeld charge analysis with empirically derived steric effects, 98.3% accuracy was achieved in predicting dechlorination pathways across diverse Dehalococcoides isolates and enrichment cultures containing distinct organohalide-respiring bacteria. Furthermore, XGBoost models incorporating electronic, steric, and physicochemical descriptors were developed to quantify the dechlorination reactivity of PCBs, revealing that the steric effect-corrected Hirshfeld charge and PCB solubility primarily control microbial reductive dechlorination potential. The model successfully captured the observed trends in the dechlorination reactivity of PCBs across multiple dechlorinating cultures and predicted that 11 of the 12 dioxin-like PCB congeners were susceptible to microbial reductive dechlorination, highlighting intrinsic microbial detoxification potential under anaerobic conditions. This integrative framework unveils the first full picture of microbial dechlorination pathways and reactivity for the entire PCB family, providing mechanistic insight into how molecular properties dictate halogen removal. The findings advance the predictive understanding of organohalide respiration and offer a roadmap for designing microbiome-based bioremediation strategies for persistent halogenated pollutants like PCBs.
Additional Links: PMID-42028897
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PubMed:
Citation:
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@article {pmid42028897,
year = {2026},
author = {Wang, S and He, H and Zhang, S and Tian, L and Lu, Q and Mai, B and Adrian, L and Dolfing, J and Xu, G},
title = {Decoding Microbial Reductive Dechlorination of 209 Polychlorinated Biphenyl Congeners through Experiment-Aided Quantum Chemistry and Machine Learning.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.5c16226},
pmid = {42028897},
issn = {1520-5851},
abstract = {Polychlorinated biphenyls (PCBs) persist globally as legacy pollutants with a complex structural diversity that complicates the understanding of their microbial conversion processes and remediation. In this study, high-throughput enzymatic assays, quantum chemical calculations, and machine learning were integrated to elucidate the reductive dechlorination pathways and reactivity of all 209 PCB congeners. By coupling Hirshfeld charge analysis with empirically derived steric effects, 98.3% accuracy was achieved in predicting dechlorination pathways across diverse Dehalococcoides isolates and enrichment cultures containing distinct organohalide-respiring bacteria. Furthermore, XGBoost models incorporating electronic, steric, and physicochemical descriptors were developed to quantify the dechlorination reactivity of PCBs, revealing that the steric effect-corrected Hirshfeld charge and PCB solubility primarily control microbial reductive dechlorination potential. The model successfully captured the observed trends in the dechlorination reactivity of PCBs across multiple dechlorinating cultures and predicted that 11 of the 12 dioxin-like PCB congeners were susceptible to microbial reductive dechlorination, highlighting intrinsic microbial detoxification potential under anaerobic conditions. This integrative framework unveils the first full picture of microbial dechlorination pathways and reactivity for the entire PCB family, providing mechanistic insight into how molecular properties dictate halogen removal. The findings advance the predictive understanding of organohalide respiration and offer a roadmap for designing microbiome-based bioremediation strategies for persistent halogenated pollutants like PCBs.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
[Cutaneous pre- and probiotics: Modulating the axillary microbiome to control body odors].
Medecine sciences : M/S, 42(4):398-401.
Additional Links: PMID-42028948
Publisher:
PubMed:
Citation:
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@article {pmid42028948,
year = {2026},
author = {Joncour, G and Saghbini, S},
title = {[Cutaneous pre- and probiotics: Modulating the axillary microbiome to control body odors].},
journal = {Medecine sciences : M/S},
volume = {42},
number = {4},
pages = {398-401},
doi = {10.1051/medsci/2026062},
pmid = {42028948},
issn = {1958-5381},
mesh = {*Probiotics/administration & dosage/therapeutic use ; Humans ; *Microbiota/drug effects/physiology ; *Axilla/microbiology ; *Odorants/prevention & control/analysis ; *Skin/microbiology ; *Prebiotics/administration & dosage ; Administration, Cutaneous ; },
}
MeSH Terms:
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*Probiotics/administration & dosage/therapeutic use
Humans
*Microbiota/drug effects/physiology
*Axilla/microbiology
*Odorants/prevention & control/analysis
*Skin/microbiology
*Prebiotics/administration & dosage
Administration, Cutaneous
RevDate: 2026-04-24
Bacillus aerius synergizes with coal gangue to enhance Medicago sativa growth via soil microbiome and gene regulation.
Applied and environmental microbiology [Epub ahead of print].
UNLABELLED: The extensive accumulation of coal gangue poses significant environmental threats through water contamination, soil degradation, and atmospheric pollution, necessitating the urgent development of ecological utilization strategies. This study elucidates the mechanistic basis by which the thermophilic bacterium Bacillus aerius (B. aerius) enhances plant growth in coal gangue-amended sandy soils. Through integrated analysis of nutrient dynamics, phytohormonal activities, soil enzymatic profiles, and metagenomic functional profiling, we demonstrate significant synergy between coal gangue and B. aerius. When applied together in sandy soils, the germination rate, plant height, root length, and fresh biomass of Medicago sativa (alfalfa) increased by 1.18-2.06 times. The levels of soil nitrogen, phosphorus, and potassium also significantly increased, resulting in notable improvements in soil fertility. The bacterial treatment enhanced the activities of indole-3-acetic acid, 1-aminocyclopropane-1-carboxylate (ACC) deaminase, and various soil enzyme activities while also optimizing the microbial community structure and increasing the abundance of beneficial bacteria, including Bacillus. Metagenomic analysis revealed the upregulation of growth-promoting genes such as acdS, nifK, and phnG, which collectively drive plant growth through multiple pathways, including enhanced soil nutrient availability, hormone regulation, soil enzyme activities, and nutrient cycling. Collectively, this work deciphers molecular-scale bacteria-gangue synergism, providing a theoretical foundation for sustainable coal gangue utilization and ecological restoration of degraded soils.
IMPORTANCE: The accumulation of coal gangue poses significant environmental challenges, necessitating the development of eco-friendly utilization strategies. This study demonstrates that the thermophilic bacterium Bacillus aerius acts synergistically with coal gangue to promote alfalfa growth in sandy soils while improving soil fertility. The combined treatment enhanced plant morphological traits, soil nutrient availability, beneficial microbial communities, and associated biological activities, with these effects supported by molecular evidence. As the first study to verify this growth-promoting mechanism, our findings address a critical knowledge gap and provide a theoretical foundation for the sustainable utilization of coal gangue in the ecological restoration of degraded soils.
Additional Links: PMID-42028995
Publisher:
PubMed:
Citation:
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@article {pmid42028995,
year = {2026},
author = {Liu, M and Du, M and Xi, Z and Tastambek, KT and Bao, Y and Song, X and Zhou, A and Wang, Y},
title = {Bacillus aerius synergizes with coal gangue to enhance Medicago sativa growth via soil microbiome and gene regulation.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0026826},
doi = {10.1128/aem.00268-26},
pmid = {42028995},
issn = {1098-5336},
abstract = {UNLABELLED: The extensive accumulation of coal gangue poses significant environmental threats through water contamination, soil degradation, and atmospheric pollution, necessitating the urgent development of ecological utilization strategies. This study elucidates the mechanistic basis by which the thermophilic bacterium Bacillus aerius (B. aerius) enhances plant growth in coal gangue-amended sandy soils. Through integrated analysis of nutrient dynamics, phytohormonal activities, soil enzymatic profiles, and metagenomic functional profiling, we demonstrate significant synergy between coal gangue and B. aerius. When applied together in sandy soils, the germination rate, plant height, root length, and fresh biomass of Medicago sativa (alfalfa) increased by 1.18-2.06 times. The levels of soil nitrogen, phosphorus, and potassium also significantly increased, resulting in notable improvements in soil fertility. The bacterial treatment enhanced the activities of indole-3-acetic acid, 1-aminocyclopropane-1-carboxylate (ACC) deaminase, and various soil enzyme activities while also optimizing the microbial community structure and increasing the abundance of beneficial bacteria, including Bacillus. Metagenomic analysis revealed the upregulation of growth-promoting genes such as acdS, nifK, and phnG, which collectively drive plant growth through multiple pathways, including enhanced soil nutrient availability, hormone regulation, soil enzyme activities, and nutrient cycling. Collectively, this work deciphers molecular-scale bacteria-gangue synergism, providing a theoretical foundation for sustainable coal gangue utilization and ecological restoration of degraded soils.
IMPORTANCE: The accumulation of coal gangue poses significant environmental challenges, necessitating the development of eco-friendly utilization strategies. This study demonstrates that the thermophilic bacterium Bacillus aerius acts synergistically with coal gangue to promote alfalfa growth in sandy soils while improving soil fertility. The combined treatment enhanced plant morphological traits, soil nutrient availability, beneficial microbial communities, and associated biological activities, with these effects supported by molecular evidence. As the first study to verify this growth-promoting mechanism, our findings address a critical knowledge gap and provide a theoretical foundation for the sustainable utilization of coal gangue in the ecological restoration of degraded soils.},
}
RevDate: 2026-04-24
Applying microbial ecology frameworks to microbial therapies for wildlife.
mSystems [Epub ahead of print].
Microbial ecology is increasingly incorporated into human and animal medicine via the study and purposeful manipulation of host-associated microbiomes. Microbial therapies-treatments with the aim of beneficially modulating microbiomes-are a burgeoning area of research and industry. These microbial therapies include prebiotic dietary items, live probiotics, and whole microbiota transplants (e.g., fecal microbiota transplants). Although microbial therapies for humans and domestic animals are now widely produced for commercial use and application, evidence supporting the efficacy of commercial microbial therapies is mixed. We suggest that microbial therapies are most effective when paired with concepts from ecology and rigorous empirical research. This is particularly relevant for the development and use of microbial therapies in wildlife animal species, in which we see large-scale variation in microbial communities across hosts of varying ecologies. Identifying and developing microbial therapies that can simultaneously be accessible and effective in a variety of hosts poses a novel challenge for microbial ecologists, animal scientists, and human and animal medical professionals. In addition to pre- and probiotics, we suggest that whole microbiota transplants provide a method of microbial supplementation that may better align with species-specific microbial ecology. Moving forward, emerging methods used in human medicine such as machine learning, network analysis, and microbiome engineering using high-throughput culturomics will likely be key to identifying and applying functionally relevant (e.g., disease suppressive) microbial taxa for wildlife therapies.
Additional Links: PMID-42029022
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PubMed:
Citation:
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@article {pmid42029022,
year = {2026},
author = {Bornbusch, SL and Muletz-Wolz, CR},
title = {Applying microbial ecology frameworks to microbial therapies for wildlife.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0059825},
doi = {10.1128/msystems.00598-25},
pmid = {42029022},
issn = {2379-5077},
abstract = {Microbial ecology is increasingly incorporated into human and animal medicine via the study and purposeful manipulation of host-associated microbiomes. Microbial therapies-treatments with the aim of beneficially modulating microbiomes-are a burgeoning area of research and industry. These microbial therapies include prebiotic dietary items, live probiotics, and whole microbiota transplants (e.g., fecal microbiota transplants). Although microbial therapies for humans and domestic animals are now widely produced for commercial use and application, evidence supporting the efficacy of commercial microbial therapies is mixed. We suggest that microbial therapies are most effective when paired with concepts from ecology and rigorous empirical research. This is particularly relevant for the development and use of microbial therapies in wildlife animal species, in which we see large-scale variation in microbial communities across hosts of varying ecologies. Identifying and developing microbial therapies that can simultaneously be accessible and effective in a variety of hosts poses a novel challenge for microbial ecologists, animal scientists, and human and animal medical professionals. In addition to pre- and probiotics, we suggest that whole microbiota transplants provide a method of microbial supplementation that may better align with species-specific microbial ecology. Moving forward, emerging methods used in human medicine such as machine learning, network analysis, and microbiome engineering using high-throughput culturomics will likely be key to identifying and applying functionally relevant (e.g., disease suppressive) microbial taxa for wildlife therapies.},
}
RevDate: 2026-04-24
The Paradoxical Toxicity of Microplastics under Predation Risk: The Driving Role of Gut Microbiota-Mediated Tolerance.
Environmental science & technology [Epub ahead of print].
Accurate predictions of the ecological risks of microplastics require understanding of their interplay with natural stressors. Here, we revealed that predation risk fundamentally altered the microplastics ecotoxicity on the keystone species Daphnia magna. The microplastics alone were toxic (e.g., reduced growth rate, body size, spine length, and delayed maturity) and became more toxic under predation risk. For instance, the maturation delay at high MP concentrations increased 6.67-fold. Paradoxically, microplastics also enhanced inducible defenses, with fish cues offsetting microplastics that induced reductions in spine length and somatic growth. Contrasting Daphnia genotypes revealed that the fish-adapted clone exhibited superior tolerance to combined exposure to stressors, maintaining robust growth and defensive integrity, unlike the fish-naïve clone. The gut microbiome was identified as a key mechanistic driver. The fish-adapted clone maintained a more stable microbial community structure with functions enriched in carbohydrate metabolism and immune defense. A reciprocal transplantation experiment provided causal evidence: transplanting the adapted microbiota into the predator-naïve clone reduced mortality by 39% and increased intrinsic growth by 22% under combined stress. These findings highlight that microplastics risk assessment may be flawed if they ignore the eco-evolutionary context of natural stressors.
Additional Links: PMID-42029232
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PubMed:
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@article {pmid42029232,
year = {2026},
author = {Li, J and Zhang, C and Zhang, H and Xu, W and Protopopov, M and Chang, M and Stoks, R},
title = {The Paradoxical Toxicity of Microplastics under Predation Risk: The Driving Role of Gut Microbiota-Mediated Tolerance.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.6c01355},
pmid = {42029232},
issn = {1520-5851},
abstract = {Accurate predictions of the ecological risks of microplastics require understanding of their interplay with natural stressors. Here, we revealed that predation risk fundamentally altered the microplastics ecotoxicity on the keystone species Daphnia magna. The microplastics alone were toxic (e.g., reduced growth rate, body size, spine length, and delayed maturity) and became more toxic under predation risk. For instance, the maturation delay at high MP concentrations increased 6.67-fold. Paradoxically, microplastics also enhanced inducible defenses, with fish cues offsetting microplastics that induced reductions in spine length and somatic growth. Contrasting Daphnia genotypes revealed that the fish-adapted clone exhibited superior tolerance to combined exposure to stressors, maintaining robust growth and defensive integrity, unlike the fish-naïve clone. The gut microbiome was identified as a key mechanistic driver. The fish-adapted clone maintained a more stable microbial community structure with functions enriched in carbohydrate metabolism and immune defense. A reciprocal transplantation experiment provided causal evidence: transplanting the adapted microbiota into the predator-naïve clone reduced mortality by 39% and increased intrinsic growth by 22% under combined stress. These findings highlight that microplastics risk assessment may be flawed if they ignore the eco-evolutionary context of natural stressors.},
}
RevDate: 2026-04-24
A urinary three-metabolite signature enables non-invasive identification of high-risk ovarian cancer patients.
Clinical cancer research : an official journal of the American Association for Cancer Research pii:784360 [Epub ahead of print].
BACKGROUND: Reliable prognostic tools in ovarian cancer are urgently needed to guide risk-adapted treatment decisions, yet the clinical utility of urinary metabolites for non-invasive risk stratification remains largely undefined. Here, we define a clinically relevant urinary metabolite signature that enables non-invasive prognostic risk stratification in ovarian cancer.
METHODS: Using targeted ¹H NMR spectroscopy, we profiled 149 metabolites involved in energy metabolism, oxidative stress, mitochondrial function, nitrogen metabolism, amino acid degradation, gut microbiome activity and inflammation in pre-operative urine from 199 consecutive patients with newly diagnosed ovarian cancer treated in routine clinical practice between 2013 and 2022.
RESULTS: Unsupervised clustering revealed biologically heterogeneous subgroups but lacked prognostic resolution and alignment with overt clinical phenotypes. However, single-metabolite analysis identified a condensed three-metabolite prognostic signature comprising glycine, alanine and citrate. A final parsimonious model integrating this metabolite-signature with clinical covariates outperformed established risk factors alone (FIGO-stage, surgical outcome), accurately predicted 60-month overall survival (AUC = 0.839) and stratified risk. Patients in the highest-risk quartile (Q4) had markedly shorter progression-free survival (Δmedian ≈ 56 months; HR = 2.63, 95% CI: 1.54-4.52, p < 0.001) and overall survival (Δmedian ≈ 86 months; HR = 2.49, 95% CI: 1.39-4.46, p = 0.009) compared to the lowest-risk group (Q1).
CONCLUSION: We define a urinary three-metabolite signature that enables non-invasive identification of high-risk ovarian cancer patients beyond established clinical factors and may support molecular stratification and risk-adapted clinical decisions, thereby supporting the clinical scalability of urine as a matrix for metabolic risk profiling in ovarian cancer.
Additional Links: PMID-42029478
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PubMed:
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@article {pmid42029478,
year = {2026},
author = {Funk, AM and Brieske, M and Schwarz, FM and Link, T and Jonas, S and Wimberger, P and Freitag, L and Klimova, A and Chavakis, T and Mirtschink, P and Kuhlmann, JD},
title = {A urinary three-metabolite signature enables non-invasive identification of high-risk ovarian cancer patients.},
journal = {Clinical cancer research : an official journal of the American Association for Cancer Research},
volume = {},
number = {},
pages = {},
doi = {10.1158/1078-0432.CCR-25-4260},
pmid = {42029478},
issn = {1557-3265},
abstract = {BACKGROUND: Reliable prognostic tools in ovarian cancer are urgently needed to guide risk-adapted treatment decisions, yet the clinical utility of urinary metabolites for non-invasive risk stratification remains largely undefined. Here, we define a clinically relevant urinary metabolite signature that enables non-invasive prognostic risk stratification in ovarian cancer.
METHODS: Using targeted ¹H NMR spectroscopy, we profiled 149 metabolites involved in energy metabolism, oxidative stress, mitochondrial function, nitrogen metabolism, amino acid degradation, gut microbiome activity and inflammation in pre-operative urine from 199 consecutive patients with newly diagnosed ovarian cancer treated in routine clinical practice between 2013 and 2022.
RESULTS: Unsupervised clustering revealed biologically heterogeneous subgroups but lacked prognostic resolution and alignment with overt clinical phenotypes. However, single-metabolite analysis identified a condensed three-metabolite prognostic signature comprising glycine, alanine and citrate. A final parsimonious model integrating this metabolite-signature with clinical covariates outperformed established risk factors alone (FIGO-stage, surgical outcome), accurately predicted 60-month overall survival (AUC = 0.839) and stratified risk. Patients in the highest-risk quartile (Q4) had markedly shorter progression-free survival (Δmedian ≈ 56 months; HR = 2.63, 95% CI: 1.54-4.52, p < 0.001) and overall survival (Δmedian ≈ 86 months; HR = 2.49, 95% CI: 1.39-4.46, p = 0.009) compared to the lowest-risk group (Q1).
CONCLUSION: We define a urinary three-metabolite signature that enables non-invasive identification of high-risk ovarian cancer patients beyond established clinical factors and may support molecular stratification and risk-adapted clinical decisions, thereby supporting the clinical scalability of urine as a matrix for metabolic risk profiling in ovarian cancer.},
}
RevDate: 2026-04-26
CmpDate: 2026-04-24
HBV and the Microbiome-PubMed Database Literature Review.
Infectious disease reports, 18(3):.
OBJECTIVE: Hepatitis B virus (HBV) is a globally distributed infectious disease affecting the liver. This literature review aims to summarize all available relevant information on the PubMed database about HBV's connection to the microbiome and to consider possible treatment adjuncts.
MATERIALS AND METHODS: Database used: PubMed. Keywords used: "HBV", "Hepatitis B", "microbiome". In the PubMed database, 179 research publications were identified using these keywords; 69 studies were excluded as they were irrelevant or retracted. Of the remaining, 110 were analyzed in this literature review, and four additional literature sources were used to supply background information and context. Information was summarized. The analysed studies in total included 14,814 participants (excluding animal studies), of whom 8564 were HBV-infected individuals.
RESULTS: Results characterizing abundance or decrease in specific bacterial, viral, and fungal species are heterogeneous; multiple studies support that the HBV patient oral and fecal microbiome is different from that in healthy controls (HCs) and varies throughout disease progression. The HBV seems to transform the microbiome negatively, leading to dysbiosis and decreased microbial diversity in most studies. Evidence links HBV microbiome changes with influence on HbeAg seroconversion, HBV-DNA load, metabolic pathways, liver cirrhosis, and hepatocellular carcinoma. The research proposes that members of microbiota could potentially promote or protect against liver injury in HBV. Four studies proposed that the plasma virome in HBV patients was primarily composed of members of the Anelloviridae. One study researched a parasite (Entamoeba gingivalis) in HBV patients. Two studies analyzed HBV patients' fungal profiles.
CONCLUSIONS: Microbiota research, although promising, at the present moment is heterogeneous. HBV patients' microbiota is distinguishable from HCs, and multiple studies have tried to identify the HBV characteristic microbiome; however, more precise information is needed to draw conclusions. Fecal microbiota transplantation and probiotics have the potential to be therapy adjuncts for HBV patients, but more research is needed.
Additional Links: PMID-42029644
PubMed:
Citation:
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@article {pmid42029644,
year = {2026},
author = {Prince, AM and Zeltiņa, I and Reinis, A and Valciņa, O and Krūmiņa, A},
title = {HBV and the Microbiome-PubMed Database Literature Review.},
journal = {Infectious disease reports},
volume = {18},
number = {3},
pages = {},
pmid = {42029644},
issn = {2036-7430},
abstract = {OBJECTIVE: Hepatitis B virus (HBV) is a globally distributed infectious disease affecting the liver. This literature review aims to summarize all available relevant information on the PubMed database about HBV's connection to the microbiome and to consider possible treatment adjuncts.
MATERIALS AND METHODS: Database used: PubMed. Keywords used: "HBV", "Hepatitis B", "microbiome". In the PubMed database, 179 research publications were identified using these keywords; 69 studies were excluded as they were irrelevant or retracted. Of the remaining, 110 were analyzed in this literature review, and four additional literature sources were used to supply background information and context. Information was summarized. The analysed studies in total included 14,814 participants (excluding animal studies), of whom 8564 were HBV-infected individuals.
RESULTS: Results characterizing abundance or decrease in specific bacterial, viral, and fungal species are heterogeneous; multiple studies support that the HBV patient oral and fecal microbiome is different from that in healthy controls (HCs) and varies throughout disease progression. The HBV seems to transform the microbiome negatively, leading to dysbiosis and decreased microbial diversity in most studies. Evidence links HBV microbiome changes with influence on HbeAg seroconversion, HBV-DNA load, metabolic pathways, liver cirrhosis, and hepatocellular carcinoma. The research proposes that members of microbiota could potentially promote or protect against liver injury in HBV. Four studies proposed that the plasma virome in HBV patients was primarily composed of members of the Anelloviridae. One study researched a parasite (Entamoeba gingivalis) in HBV patients. Two studies analyzed HBV patients' fungal profiles.
CONCLUSIONS: Microbiota research, although promising, at the present moment is heterogeneous. HBV patients' microbiota is distinguishable from HCs, and multiple studies have tried to identify the HBV characteristic microbiome; however, more precise information is needed to draw conclusions. Fecal microbiota transplantation and probiotics have the potential to be therapy adjuncts for HBV patients, but more research is needed.},
}
RevDate: 2026-04-24
Genomic and Functional Diversity of Pseudoalteromonas Associated with the Tropical Bivalve Anadara Tuberculosa.
Microbial ecology pii:10.1007/s00248-026-02753-y [Epub ahead of print].
Additional Links: PMID-42029730
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PubMed:
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@article {pmid42029730,
year = {2026},
author = {Restrepo-Benavides, M and Jiménez, P and Figueras, MJ and Restrepo, S and Zambrano, MM and Pujol, I and Guevara-Suarez, M and Fernández-Bravo, A},
title = {Genomic and Functional Diversity of Pseudoalteromonas Associated with the Tropical Bivalve Anadara Tuberculosa.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02753-y},
pmid = {42029730},
issn = {1432-184X},
}
RevDate: 2026-04-27
CmpDate: 2026-04-24
Bacterial diversity in ferruginous duricrust (canga) and the physicochemical variables affecting their prevalence, distribution and predicted metabolic pathways.
Antonie van Leeuwenhoek, 119(5):.
The ferruginous duricrust (canga) in the Iron Quadrangle (IQ), Minas Gerais, Brazil, occurs within the Campo Rupestre and presents remarkable levels of endemism and species richness. Despite the recognized importance of microorganisms for the maintenance of this ecosystem, current molecular-based studies reveal that both the taxonomic composition and the ecological functions of the canga microbiome are undiscovered. In this study, eighteen samples of canga were collected from the Serra da Piedade State Natural Monument, and their taxonomic diversity was investigated using 16S rRNA metabarcoding. Additionally, the influence of physicochemical variables on microbial diversity and community structure was estimated using statistical tools. Most of the 856,667 reads clustered into ASVs corresponded to Bacteria (99.7%), and the most abundant of the 184 identified genera were Conexibacter, Acidothermus and Bryobacter. Microbial diversity was explained by a combination of physicochemical variables, such as organic matter (OM), iron (Fe), aluminum (Al) and pH, whereas microbial community structure was influenced by the concentrations of Fe, Al and the cation exchange capacity (CEC). Functional prediction analysis based on the main genera identified in the samples indicated that the denitrification pathway may play an important role in the ecosystem. The investigation of the genera and their metabolic pathways based on the literature revealed that they are unexplored and emphasized the biodiversity hotspot yet to be explored in ferruginous duricrust. Therefore, our results reinforce the importance of further studies in this environment, both for future biotechnological applications and for appropriate management and preservation actions.
Additional Links: PMID-42029786
PubMed:
Citation:
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@article {pmid42029786,
year = {2026},
author = {Jotta, VFM and Silva, CA and García, GJY and Marques, AR and Dos Santos Freitas, A and Góes-Neto, A and Badotti, F},
title = {Bacterial diversity in ferruginous duricrust (canga) and the physicochemical variables affecting their prevalence, distribution and predicted metabolic pathways.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {5},
pages = {},
pmid = {42029786},
issn = {1572-9699},
mesh = {*Bacteria/classification/genetics/metabolism/isolation & purification ; RNA, Ribosomal, 16S/genetics ; Brazil ; *Biodiversity ; *Metabolic Networks and Pathways ; Phylogeny ; *Microbiota ; *Soil Microbiology ; Iron/analysis ; DNA, Bacterial/genetics ; },
abstract = {The ferruginous duricrust (canga) in the Iron Quadrangle (IQ), Minas Gerais, Brazil, occurs within the Campo Rupestre and presents remarkable levels of endemism and species richness. Despite the recognized importance of microorganisms for the maintenance of this ecosystem, current molecular-based studies reveal that both the taxonomic composition and the ecological functions of the canga microbiome are undiscovered. In this study, eighteen samples of canga were collected from the Serra da Piedade State Natural Monument, and their taxonomic diversity was investigated using 16S rRNA metabarcoding. Additionally, the influence of physicochemical variables on microbial diversity and community structure was estimated using statistical tools. Most of the 856,667 reads clustered into ASVs corresponded to Bacteria (99.7%), and the most abundant of the 184 identified genera were Conexibacter, Acidothermus and Bryobacter. Microbial diversity was explained by a combination of physicochemical variables, such as organic matter (OM), iron (Fe), aluminum (Al) and pH, whereas microbial community structure was influenced by the concentrations of Fe, Al and the cation exchange capacity (CEC). Functional prediction analysis based on the main genera identified in the samples indicated that the denitrification pathway may play an important role in the ecosystem. The investigation of the genera and their metabolic pathways based on the literature revealed that they are unexplored and emphasized the biodiversity hotspot yet to be explored in ferruginous duricrust. Therefore, our results reinforce the importance of further studies in this environment, both for future biotechnological applications and for appropriate management and preservation actions.},
}
MeSH Terms:
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*Bacteria/classification/genetics/metabolism/isolation & purification
RNA, Ribosomal, 16S/genetics
Brazil
*Biodiversity
*Metabolic Networks and Pathways
Phylogeny
*Microbiota
*Soil Microbiology
Iron/analysis
DNA, Bacterial/genetics
RevDate: 2026-04-27
CmpDate: 2026-04-24
Gut microbiome alterations among Ghanaian children with asymptomatic malaria infections.
PloS one, 21(4):e0348120.
The human gut microbiome, consisting of bacteria, archaea, fungi, and viruses, influences various physiological processes of the body. The gut microbiome composition is shaped by factors such as diet, geography, and antibiotic use. Malaria has been a global health challenge over the years, especially in low- and middle-income countries. This study investigated how asymptomatic malaria infection altered gut microbial communities in Ghanaian children, offering insights for novel malaria control strategies. Standard aseptic phlebotomy procedures were employed to collect venous blood samples for Plasmodium species detection. The gut microbial community was profiled by sequencing the 16S rRNA V4 region, and sequence data were processed using the DADA2 pipeline in R. Asymptomatic malaria infections were predominantly mixed with P. falciparum and P. malariae. Microbiome analysis revealed that Firmicutes and Bacteroidetes comprised nearly 70% of the total microbial population. Asymptomatic individuals showed a decrease in Firmicutes abundance from 52.5% to 44.0% and an increase in Bacteroidetes from 34.7% to 45.6%. There was also a slight increase in the abundance of Proteobacteria from 3.0% to 4.8%. At the genus level, Prevotella_9 was the most abundant and exhibited the highest variability in the infected groups. The Alloprevotella and Streptococcus genera increased in both infected groups, but Escherichia-Shigella was significantly elevated in only those with mixed infections. Faecalibacterium significantly declined in asymptomatic malaria-infected individuals compared to healthy controls, with variability further reduced in mixed infections. Beta-diversity analysis indicated a significant effect of malaria status on microbial composition (PERMANOVA, p < 0.05), explaining approximately 19.1% of the total variation captured by a 2D Principal Component Analysis (PCA) projection. These findings suggest a potential link between malaria infection and gut microbiota alterations and highlight microbial shifts associated with disease status.
Additional Links: PMID-42030348
PubMed:
Citation:
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@article {pmid42030348,
year = {2026},
author = {Larbi, AA and Etsey, M and Brew, O and Koduah, B and Mawuenyega, RE and Amewu, EKA and Essilfie, NK and Wireko, S and Kwarteng, A and Gyan, BA},
title = {Gut microbiome alterations among Ghanaian children with asymptomatic malaria infections.},
journal = {PloS one},
volume = {21},
number = {4},
pages = {e0348120},
pmid = {42030348},
issn = {1932-6203},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; Ghana/epidemiology ; *Malaria/microbiology/epidemiology/parasitology ; Child, Preschool ; Male ; Female ; Child ; RNA, Ribosomal, 16S/genetics ; Asymptomatic Infections ; Bacteria/genetics/classification ; Infant ; },
abstract = {The human gut microbiome, consisting of bacteria, archaea, fungi, and viruses, influences various physiological processes of the body. The gut microbiome composition is shaped by factors such as diet, geography, and antibiotic use. Malaria has been a global health challenge over the years, especially in low- and middle-income countries. This study investigated how asymptomatic malaria infection altered gut microbial communities in Ghanaian children, offering insights for novel malaria control strategies. Standard aseptic phlebotomy procedures were employed to collect venous blood samples for Plasmodium species detection. The gut microbial community was profiled by sequencing the 16S rRNA V4 region, and sequence data were processed using the DADA2 pipeline in R. Asymptomatic malaria infections were predominantly mixed with P. falciparum and P. malariae. Microbiome analysis revealed that Firmicutes and Bacteroidetes comprised nearly 70% of the total microbial population. Asymptomatic individuals showed a decrease in Firmicutes abundance from 52.5% to 44.0% and an increase in Bacteroidetes from 34.7% to 45.6%. There was also a slight increase in the abundance of Proteobacteria from 3.0% to 4.8%. At the genus level, Prevotella_9 was the most abundant and exhibited the highest variability in the infected groups. The Alloprevotella and Streptococcus genera increased in both infected groups, but Escherichia-Shigella was significantly elevated in only those with mixed infections. Faecalibacterium significantly declined in asymptomatic malaria-infected individuals compared to healthy controls, with variability further reduced in mixed infections. Beta-diversity analysis indicated a significant effect of malaria status on microbial composition (PERMANOVA, p < 0.05), explaining approximately 19.1% of the total variation captured by a 2D Principal Component Analysis (PCA) projection. These findings suggest a potential link between malaria infection and gut microbiota alterations and highlight microbial shifts associated with disease status.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/genetics
Ghana/epidemiology
*Malaria/microbiology/epidemiology/parasitology
Child, Preschool
Male
Female
Child
RNA, Ribosomal, 16S/genetics
Asymptomatic Infections
Bacteria/genetics/classification
Infant
RevDate: 2026-04-24
Gut microbiota modulation of regulatory DNA elements revealed by massively parallel functional characterization.
Molecular cell pii:S1097-2765(26)00232-7 [Epub ahead of print].
Cis-regulatory elements (CREs) are central to dynamic gene regulation in hepatocytes, yet most functional annotations derive from in vitro models that poorly capture physiological regulation. We systematically profiled 109,386 human liver-derived CREs using massively parallel reporter assays in hepatocytes under matched in vitro and in vivo conditions. In vivo-active functional CREs (fCREs) were enriched for H3K27ac and chromatin accessibility and were regulated by diverse transcription factors in the human liver. We further demonstrate that gut microbiota-derived signals modulate fCRE activity and target gene expression in vivo, in part via the KEAP1/NFE2L2 antioxidant pathway. Specific microbial metabolites directly altered the activity of selected fCREs, and genetic variation within fCREs modified their responsiveness to microbial signals. Together, these findings reveal microbiota-dependent regulation of hepatic CREs and highlight condition-specific gene regulatory mechanisms in vivo.
Additional Links: PMID-42030942
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PubMed:
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@article {pmid42030942,
year = {2026},
author = {Zaratiana, C and M, Y and Lee, YA and Ong, ABL and Liu, TZY and Low, SMC and Chang, SMS and Tan, S and Mustafa, DNA and Ganesh, A and Chang, X and Koh, XQ and Tay, SH and Lee, WJJ and Yuan, JM and Khor, CC and Koh, WP and Dorajoo, R and Li, YE and Kasahara, K and Wuestefeld, T and Chen, PB},
title = {Gut microbiota modulation of regulatory DNA elements revealed by massively parallel functional characterization.},
journal = {Molecular cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.molcel.2026.03.036},
pmid = {42030942},
issn = {1097-4164},
abstract = {Cis-regulatory elements (CREs) are central to dynamic gene regulation in hepatocytes, yet most functional annotations derive from in vitro models that poorly capture physiological regulation. We systematically profiled 109,386 human liver-derived CREs using massively parallel reporter assays in hepatocytes under matched in vitro and in vivo conditions. In vivo-active functional CREs (fCREs) were enriched for H3K27ac and chromatin accessibility and were regulated by diverse transcription factors in the human liver. We further demonstrate that gut microbiota-derived signals modulate fCRE activity and target gene expression in vivo, in part via the KEAP1/NFE2L2 antioxidant pathway. Specific microbial metabolites directly altered the activity of selected fCREs, and genetic variation within fCREs modified their responsiveness to microbial signals. Together, these findings reveal microbiota-dependent regulation of hepatic CREs and highlight condition-specific gene regulatory mechanisms in vivo.},
}
RevDate: 2026-04-24
Neutrophil-Derived Reactive Oxygen Species and Bystander Tissue Damage in Inflammatory Bowel Disease.
Free radical biology & medicine pii:S0891-5849(26)00446-6 [Epub ahead of print].
Neutrophils (PMNs) are indispensable effectors of innate immunity whose oxidative and proteolytic capabilities permit rapid microbial containment at mucosal surfaces. Nowhere is this more functionally consequential than in the gastrointestinal tract, where PMN recruitment to the intestinal mucosa serves as both a critical antimicrobial safeguard and a primary driver of epithelial injury in inflammatory bowel diseases (IBD). Upon activation, PMNs deploy an intricate oxidative network centered on the phagocyte NADPH oxidase complex-derived superoxide and hydrogen peroxide in conjunction with the halogenating and nitrating chemistries catalyzed by myeloperoxidase (MPO). These pathways generate a rich repertoire of oxidants-including hypochlorous acid (HOCl), hypobromous acid, reactive nitrogen species, and secondary radical products-that interact with proteins, lipids, nucleic acids, and extracellular matrix components with distinct reaction kinetics and spatial preferences. Importantly, the magnitude, composition, and distribution of these oxidants shape tissue outcomes ranging from transient signaling alterations to epithelial barrier dysfunction and mutational injury contributing to dysplasia. Recent advances in redox proteomics, spatial transcriptomics, intravital imaging, and single-cell analyses have expanded our understanding of how PMN oxidative radical pathways operate within specific mucosal microenvironments and how their outputs intersect with epithelial repair pathways, the microbiome, innate immune crosstalk, and disease chronicity. These studies reveal that PMNs do not function as a uniform oxidative manner; rather, distinct subsets specialize in oxidative burst, extracellular trap formation, metabolic adaptation, or reparative functions. Together, these data emphasize that oxidative injury in IBD is not an unavoidable byproduct of inflammation but rather a dynamic, context-dependent process that with significant potential as a therapeutic target. In this review, we synthesize current knowledge of PMN oxidative radical biology with a focus on the gastrointestinal mucosa. We examine the architecture of PMN reactive oxygen species (ROS) systems, delineate mechanisms of oxidative tissue injury, integrate translational and microbiome implications, and evaluate therapeutic strategies aimed at reducing bystander damage while preserving essential host defense. Through this framework, we highlight future directions that may enable the development of selective redox-modulating therapies capable of restoring mucosal integrity without compromising antimicrobial function.
Additional Links: PMID-42031118
Publisher:
PubMed:
Citation:
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@article {pmid42031118,
year = {2026},
author = {Kim, JY and Colgan, SP and Cartwright, IM},
title = {Neutrophil-Derived Reactive Oxygen Species and Bystander Tissue Damage in Inflammatory Bowel Disease.},
journal = {Free radical biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.freeradbiomed.2026.04.146},
pmid = {42031118},
issn = {1873-4596},
abstract = {Neutrophils (PMNs) are indispensable effectors of innate immunity whose oxidative and proteolytic capabilities permit rapid microbial containment at mucosal surfaces. Nowhere is this more functionally consequential than in the gastrointestinal tract, where PMN recruitment to the intestinal mucosa serves as both a critical antimicrobial safeguard and a primary driver of epithelial injury in inflammatory bowel diseases (IBD). Upon activation, PMNs deploy an intricate oxidative network centered on the phagocyte NADPH oxidase complex-derived superoxide and hydrogen peroxide in conjunction with the halogenating and nitrating chemistries catalyzed by myeloperoxidase (MPO). These pathways generate a rich repertoire of oxidants-including hypochlorous acid (HOCl), hypobromous acid, reactive nitrogen species, and secondary radical products-that interact with proteins, lipids, nucleic acids, and extracellular matrix components with distinct reaction kinetics and spatial preferences. Importantly, the magnitude, composition, and distribution of these oxidants shape tissue outcomes ranging from transient signaling alterations to epithelial barrier dysfunction and mutational injury contributing to dysplasia. Recent advances in redox proteomics, spatial transcriptomics, intravital imaging, and single-cell analyses have expanded our understanding of how PMN oxidative radical pathways operate within specific mucosal microenvironments and how their outputs intersect with epithelial repair pathways, the microbiome, innate immune crosstalk, and disease chronicity. These studies reveal that PMNs do not function as a uniform oxidative manner; rather, distinct subsets specialize in oxidative burst, extracellular trap formation, metabolic adaptation, or reparative functions. Together, these data emphasize that oxidative injury in IBD is not an unavoidable byproduct of inflammation but rather a dynamic, context-dependent process that with significant potential as a therapeutic target. In this review, we synthesize current knowledge of PMN oxidative radical biology with a focus on the gastrointestinal mucosa. We examine the architecture of PMN reactive oxygen species (ROS) systems, delineate mechanisms of oxidative tissue injury, integrate translational and microbiome implications, and evaluate therapeutic strategies aimed at reducing bystander damage while preserving essential host defense. Through this framework, we highlight future directions that may enable the development of selective redox-modulating therapies capable of restoring mucosal integrity without compromising antimicrobial function.},
}
RevDate: 2026-04-24
Shared pathogenic mechanisms between systemic lupus erythematosus and autoimmune hepatitis: A unified view of autoimmune convergence.
Biochimica et biophysica acta. Molecular basis of disease pii:S0925-4439(26)00137-7 [Epub ahead of print].
BACKGROUND: Systemic lupus erythematosus (SLE) and autoimmune hepatitis (AIH) are clinically distinct autoimmune disorders characterized by multisystem involvement and liver-restricted inflammation, respectively; nevertheless, they exhibit considerable overlap in their underlying immunopathogenic features.
AIM: To provide a systematic synthesis of recent advances in genetics, immunology, and microbiome science, and to delineate the convergent pathogenic mechanisms that underpin both SLE and AIH.
METHODS: A comprehensive literature review was conducted using PubMed and other databases up to 2025, focusing on shared genetic, cellular, and microbial determinants in SLE and AIH. Core topics included genetic susceptibility loci, breakdown of immune tolerance, T-cell dysregulation, innate immune activation, and alterations in gut microbiota composition and function.
RESULTS: SLE and AIH share several genetic risk variants, including HLA-DRB1*03:01, PTPN22, STAT4, and TNFAIP3. Both diseases are characterized by defective central and peripheral immune tolerance, imbalances in Th17/Treg and Tfh/Tfr compartments, and aberrant B-cell activation. Innate immune pathways-encompassing Toll-like receptor and NLRP3 inflammasome signaling as well as complement dysregulation-further amplify inflammation. Moreover, gut dysbiosis and perturbations in microbial metabolites, such as short-chain fatty acids, bile acids, and tryptophan derivatives, function as key mediators linking intestinal homeostasis to both systemic and hepatic autoimmunity.
CONCLUSION: SLE and AIH represent overlapping entities along a unified autoimmune spectrum, driven by shared genetic susceptibility, convergent immune dysregulation, and microbial influences. This review advances an integrated immunological framework that bridges systemic and organ-specific autoimmunity, underscores the pivotal role of innate immunity and gut-liver crosstalk, and provides a mechanistic rationale for cross-disease therapeutic strategies targeting these common pathways.
Additional Links: PMID-42031176
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PubMed:
Citation:
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@article {pmid42031176,
year = {2026},
author = {Yechen, W and Wang, F and Xiao, L and Chen, Y and Li, L},
title = {Shared pathogenic mechanisms between systemic lupus erythematosus and autoimmune hepatitis: A unified view of autoimmune convergence.},
journal = {Biochimica et biophysica acta. Molecular basis of disease},
volume = {},
number = {},
pages = {168274},
doi = {10.1016/j.bbadis.2026.168274},
pmid = {42031176},
issn = {1879-260X},
abstract = {BACKGROUND: Systemic lupus erythematosus (SLE) and autoimmune hepatitis (AIH) are clinically distinct autoimmune disorders characterized by multisystem involvement and liver-restricted inflammation, respectively; nevertheless, they exhibit considerable overlap in their underlying immunopathogenic features.
AIM: To provide a systematic synthesis of recent advances in genetics, immunology, and microbiome science, and to delineate the convergent pathogenic mechanisms that underpin both SLE and AIH.
METHODS: A comprehensive literature review was conducted using PubMed and other databases up to 2025, focusing on shared genetic, cellular, and microbial determinants in SLE and AIH. Core topics included genetic susceptibility loci, breakdown of immune tolerance, T-cell dysregulation, innate immune activation, and alterations in gut microbiota composition and function.
RESULTS: SLE and AIH share several genetic risk variants, including HLA-DRB1*03:01, PTPN22, STAT4, and TNFAIP3. Both diseases are characterized by defective central and peripheral immune tolerance, imbalances in Th17/Treg and Tfh/Tfr compartments, and aberrant B-cell activation. Innate immune pathways-encompassing Toll-like receptor and NLRP3 inflammasome signaling as well as complement dysregulation-further amplify inflammation. Moreover, gut dysbiosis and perturbations in microbial metabolites, such as short-chain fatty acids, bile acids, and tryptophan derivatives, function as key mediators linking intestinal homeostasis to both systemic and hepatic autoimmunity.
CONCLUSION: SLE and AIH represent overlapping entities along a unified autoimmune spectrum, driven by shared genetic susceptibility, convergent immune dysregulation, and microbial influences. This review advances an integrated immunological framework that bridges systemic and organ-specific autoimmunity, underscores the pivotal role of innate immunity and gut-liver crosstalk, and provides a mechanistic rationale for cross-disease therapeutic strategies targeting these common pathways.},
}
RevDate: 2026-04-24
Arsenic oxidation by root endophytes mediates arsenic speciation within rice (Oryza sativa).
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(26)00564-6 [Epub ahead of print].
Arsenic (As) uptake through rice consumption is a major exposure pathway that severely threatens the health of over 140 million people. Since flooded cultivation makes rice specifically vulnerable to As contamination, dry rice cultivation has been proposed to reduce As accumulation. While microorganisms play important roles in As biogeochemical cycles, the impact of the root-associated microbiome, especially endophytes, on As uptake and metabolism in rice growing under different water regimes remains elusive. In this study, different water regimes significantly altered As speciation in the rhizosphere but less impacted those in roots, in which As(V) dominated. While the endosphere community was significantly altered, microbial As transformation potentials were less impacted by different water treatments. Within rice roots, As(III) oxidase gene (aioA) abundance was consistently higher than that of the genes for As reduction (As(V) respiratory reductase arrA and As(V) detoxification reductase arsC) under both treatments, indicating that As(III) oxidation might be the major As transformation pathway in planta. Activity measurements of the endosphere microbial community demonstrated that As(III) oxidation was significantly faster compared to reduction processes. The major endosphere microbial communities harboring aioA genes were affiliated with Rhodocyclaceae, Xanthobacteraceae, and Burkholderiaceae under dry conditions, while members of Rhodocyclaceae dominated under flooded conditions. These results suggest that dominant microbial As(III) oxidation in rice roots may contribute to maintaining a higher As(V) proportion in planta and potentially reduce As translocation to edible grains.
Additional Links: PMID-42031199
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@article {pmid42031199,
year = {2026},
author = {Wang, Z and Song, B and Sun, X and Huang, D and Häggblom, MM and Yu, Z and Kong, T and He, B and He, B and Zhang, H and Sun, W},
title = {Arsenic oxidation by root endophytes mediates arsenic speciation within rice (Oryza sativa).},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128194},
doi = {10.1016/j.envpol.2026.128194},
pmid = {42031199},
issn = {1873-6424},
abstract = {Arsenic (As) uptake through rice consumption is a major exposure pathway that severely threatens the health of over 140 million people. Since flooded cultivation makes rice specifically vulnerable to As contamination, dry rice cultivation has been proposed to reduce As accumulation. While microorganisms play important roles in As biogeochemical cycles, the impact of the root-associated microbiome, especially endophytes, on As uptake and metabolism in rice growing under different water regimes remains elusive. In this study, different water regimes significantly altered As speciation in the rhizosphere but less impacted those in roots, in which As(V) dominated. While the endosphere community was significantly altered, microbial As transformation potentials were less impacted by different water treatments. Within rice roots, As(III) oxidase gene (aioA) abundance was consistently higher than that of the genes for As reduction (As(V) respiratory reductase arrA and As(V) detoxification reductase arsC) under both treatments, indicating that As(III) oxidation might be the major As transformation pathway in planta. Activity measurements of the endosphere microbial community demonstrated that As(III) oxidation was significantly faster compared to reduction processes. The major endosphere microbial communities harboring aioA genes were affiliated with Rhodocyclaceae, Xanthobacteraceae, and Burkholderiaceae under dry conditions, while members of Rhodocyclaceae dominated under flooded conditions. These results suggest that dominant microbial As(III) oxidation in rice roots may contribute to maintaining a higher As(V) proportion in planta and potentially reduce As translocation to edible grains.},
}
RevDate: 2026-04-24
The skin microbiome and affective symptoms: neuroimmune, neuroendocrine, and sensory pathways linking inflammatory dermatoses to mood and anxiety burden.
Frontiers in neuroendocrinology pii:S0091-3022(26)00021-X [Epub ahead of print].
The skin functions as a neuro-immuno-endocrine organ with an extensive microbial interface capable of bidirectional signaling with the central nervous system. While the gut-brain axis is well established, the skin-microbiota-brain (SMB) axis remains underexplored, particularly with respect to affective symptom dimensions (depression, anxiety, stress) that commonly co-occur with chronic inflammatory dermatoses. This review synthesizes evidence across clinical, translational, and experimental studies and organizes it by strength (associational findings, mechanistic plausibility, and limited interventional signals). We outline a systems-level model in which cutaneous microbial dysbiosis is associated with brain-relevant pathways via immune, neuropeptide, and metabolic routes. Candidate mediators include cytokines (IL-6, IL-17, TNF-α), neuropeptides (e.g., substance P, CGRP), and microbial-derived metabolites (e.g., SCFA-like compounds and tryptophan catabolites). These signals are hypothesized to influence neuroimmune tone and neurovascular signaling based largely on broader systemic inflammation and stress biology; direct causal evidence specifically attributing affective outcomes to skin microbiome perturbations in humans remains limited. In parallel, top-down neuroendocrine signaling via hypothalamic-pituitary-adrenal (HPA) axis activation, cortisol-related signaling, and sympathetic outflow can alter skin barrier function, antimicrobial peptide expression, and microbial ecology, potentially contributing to symptom-maintaining loops (e.g., itch-sleep disruption-stress). Importantly, we consider counterarguments (psychosocial burden, reverse causality, treatment effects, and the localized nature of lesions) and identify research priorities required to test causality (longitudinal sampling, mechanistic biomarker panels, and preregistered interventional studies with affective endpoints and mediation analyses). By integrating dermatological, microbiological, and neuroimmunological evidence within a symptom-centered framework, the SMB axis is positioned as a biologically plausible but still evolving model that may help explain affective symptom burden in subsets of patients with inflammatory skin disease and guide mechanism-informed translational research.
Additional Links: PMID-42031220
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PubMed:
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@article {pmid42031220,
year = {2026},
author = {Coccurello, R},
title = {The skin microbiome and affective symptoms: neuroimmune, neuroendocrine, and sensory pathways linking inflammatory dermatoses to mood and anxiety burden.},
journal = {Frontiers in neuroendocrinology},
volume = {},
number = {},
pages = {101251},
doi = {10.1016/j.yfrne.2026.101251},
pmid = {42031220},
issn = {1095-6808},
abstract = {The skin functions as a neuro-immuno-endocrine organ with an extensive microbial interface capable of bidirectional signaling with the central nervous system. While the gut-brain axis is well established, the skin-microbiota-brain (SMB) axis remains underexplored, particularly with respect to affective symptom dimensions (depression, anxiety, stress) that commonly co-occur with chronic inflammatory dermatoses. This review synthesizes evidence across clinical, translational, and experimental studies and organizes it by strength (associational findings, mechanistic plausibility, and limited interventional signals). We outline a systems-level model in which cutaneous microbial dysbiosis is associated with brain-relevant pathways via immune, neuropeptide, and metabolic routes. Candidate mediators include cytokines (IL-6, IL-17, TNF-α), neuropeptides (e.g., substance P, CGRP), and microbial-derived metabolites (e.g., SCFA-like compounds and tryptophan catabolites). These signals are hypothesized to influence neuroimmune tone and neurovascular signaling based largely on broader systemic inflammation and stress biology; direct causal evidence specifically attributing affective outcomes to skin microbiome perturbations in humans remains limited. In parallel, top-down neuroendocrine signaling via hypothalamic-pituitary-adrenal (HPA) axis activation, cortisol-related signaling, and sympathetic outflow can alter skin barrier function, antimicrobial peptide expression, and microbial ecology, potentially contributing to symptom-maintaining loops (e.g., itch-sleep disruption-stress). Importantly, we consider counterarguments (psychosocial burden, reverse causality, treatment effects, and the localized nature of lesions) and identify research priorities required to test causality (longitudinal sampling, mechanistic biomarker panels, and preregistered interventional studies with affective endpoints and mediation analyses). By integrating dermatological, microbiological, and neuroimmunological evidence within a symptom-centered framework, the SMB axis is positioned as a biologically plausible but still evolving model that may help explain affective symptom burden in subsets of patients with inflammatory skin disease and guide mechanism-informed translational research.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Fundamentals of Neurogastroenterology: Basic Science.
Gastroenterology, 170(6):1099-1113.
This review highlights major advances in neurogastroenterology since Rome IV, offering a condensed summary of a comprehensive document to appear in the forthcoming Rome V book. Prepared by an international team of experts, it emphasizes pivotal studies that have deepened understanding of the physiological and pathophysiological mechanisms underlying disorders of gut-brain interaction (DGBI). These disorders are inherently complex and multifactorial, shaped by interactions among neuronal, epithelial, immune, smooth muscle, interstitial, and microbial populations. The review outlines cutting-edge technologies advancing the field and explores key themes, including brain-gut interactions, neurobiology, and neuroplasticity of the enteric nervous system, neuroimmune function, microbiome influences, and abnormalities of the gut-brain axis in DGBI. Risk factors for DGBI are considered, with serotonergic signaling presented as a conceptual framework for linking symptomatology and pathophysiology. Finally, we discuss how these scientific advances can translate into novel therapeutic strategies to improve patient care.
Additional Links: PMID-42031436
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@article {pmid42031436,
year = {2026},
author = {Greenwood-Van Meerveld, B and Mawe, GM and Beyder, A and Brierley, SM and Clarke, G and Gulbransen, BD and Margolis, KG},
title = {Fundamentals of Neurogastroenterology: Basic Science.},
journal = {Gastroenterology},
volume = {170},
number = {6},
pages = {1099-1113},
doi = {10.1053/j.gastro.2026.01.040},
pmid = {42031436},
issn = {1528-0012},
mesh = {Humans ; *Enteric Nervous System/physiopathology ; *Gastrointestinal Diseases/physiopathology/therapy/microbiology ; *Gastroenterology/trends ; Gastrointestinal Microbiome ; *Brain-Gut Axis/physiology ; Animals ; *Gastrointestinal Tract/innervation/physiopathology ; Neuronal Plasticity ; Neuroimmunomodulation ; *Brain/physiopathology ; Risk Factors ; },
abstract = {This review highlights major advances in neurogastroenterology since Rome IV, offering a condensed summary of a comprehensive document to appear in the forthcoming Rome V book. Prepared by an international team of experts, it emphasizes pivotal studies that have deepened understanding of the physiological and pathophysiological mechanisms underlying disorders of gut-brain interaction (DGBI). These disorders are inherently complex and multifactorial, shaped by interactions among neuronal, epithelial, immune, smooth muscle, interstitial, and microbial populations. The review outlines cutting-edge technologies advancing the field and explores key themes, including brain-gut interactions, neurobiology, and neuroplasticity of the enteric nervous system, neuroimmune function, microbiome influences, and abnormalities of the gut-brain axis in DGBI. Risk factors for DGBI are considered, with serotonergic signaling presented as a conceptual framework for linking symptomatology and pathophysiology. Finally, we discuss how these scientific advances can translate into novel therapeutic strategies to improve patient care.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Enteric Nervous System/physiopathology
*Gastrointestinal Diseases/physiopathology/therapy/microbiology
*Gastroenterology/trends
Gastrointestinal Microbiome
*Brain-Gut Axis/physiology
Animals
*Gastrointestinal Tract/innervation/physiopathology
Neuronal Plasticity
Neuroimmunomodulation
*Brain/physiopathology
Risk Factors
RevDate: 2026-04-24
CmpDate: 2026-04-24
Sociocultural Aspects of the Pathophysiology, Clinical Presentation, and Management of Disorders of Gut-Brain Interaction.
Gastroenterology, 170(6):1190-1204.
Sociocultural determinants such as cultural norms, diet, and environmental factors, along with their effects on the gastrointestinal microbiome, can modify the risk to develop disorders of gut-brain interaction (DGBI). These factors also shape symptom perception and health care-seeking behaviors, and how society and health care providers respond to patients with DGBI. This document summarizes the knowledge about the role of sociocultural factors in the manifestation of DGBI and the management of these patients. Symptom expression and societal response to DGBI varies across different cultural settings, influencing individual patient outcomes and the overall societal burden of disease. Patients with DGBI are often stigmatized, leading to a bias toward conditions with visible abnormalities and underfunded services for DGBI. Recognizing the role of sociocultural factors for DGBI outcomes presents an opportunity to refine pathophysiologic concepts and improve patient outcomes. This calls for greater awareness and equitable resource allocation for DGBI research and treatment.
Additional Links: PMID-42031439
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@article {pmid42031439,
year = {2026},
author = {Wong, RK and Fang, X and Ghoshal, UC and Kashyap, PC and Mulak, A and Lee, YY and Sperber, AD and Holtmann, G},
title = {Sociocultural Aspects of the Pathophysiology, Clinical Presentation, and Management of Disorders of Gut-Brain Interaction.},
journal = {Gastroenterology},
volume = {170},
number = {6},
pages = {1190-1204},
doi = {10.1053/j.gastro.2026.02.006},
pmid = {42031439},
issn = {1528-0012},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Brain-Gut Axis/physiology ; *Gastrointestinal Diseases/physiopathology/therapy/psychology ; Risk Factors ; *Brain/physiopathology ; Social Stigma ; Diet ; },
abstract = {Sociocultural determinants such as cultural norms, diet, and environmental factors, along with their effects on the gastrointestinal microbiome, can modify the risk to develop disorders of gut-brain interaction (DGBI). These factors also shape symptom perception and health care-seeking behaviors, and how society and health care providers respond to patients with DGBI. This document summarizes the knowledge about the role of sociocultural factors in the manifestation of DGBI and the management of these patients. Symptom expression and societal response to DGBI varies across different cultural settings, influencing individual patient outcomes and the overall societal burden of disease. Patients with DGBI are often stigmatized, leading to a bias toward conditions with visible abnormalities and underfunded services for DGBI. Recognizing the role of sociocultural factors for DGBI outcomes presents an opportunity to refine pathophysiologic concepts and improve patient outcomes. This calls for greater awareness and equitable resource allocation for DGBI research and treatment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
*Brain-Gut Axis/physiology
*Gastrointestinal Diseases/physiopathology/therapy/psychology
Risk Factors
*Brain/physiopathology
Social Stigma
Diet
RevDate: 2026-04-24
A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis.
Annals of the rheumatic diseases pii:S0003-4967(26)00146-9 [Epub ahead of print].
OBJECTIVES: The gut microbiome plays a crucial role in regulating systemic immunity and has been implicated in several chronic inflammatory diseases. Intestinal expansions of Ruminococcus gnavus (RG), a dominant gut commensal, correlate with disease flares in lupus nephritis (LN), but the underlying mechanism remains unknown.
METHODS: In a Pilot cohort of patients with biopsy-proven LN, subsetted by gut microbiota community, immune status was characterised using bulk-blood RNA sequencing libraries, serum levels of representative host proteins, and levels of immunoglobulin (Ig)G antibodies to the novel lipoglycan (LG) produced by pathogenic RG strains. A Validation LN cohort was evaluated for blood transcriptomic profiles and levels of anti-LG antibodies. In murine models, mechanistic hypotheses were tested after RG gut colonisation or after intraperitoneal injection with an LG preparation, with outcomes determined by transcriptomic analyses, platelet functional readouts, and tissue histology.
RESULTS: In a Pilot cohort of patients with LN, RG gut expansions were associated with high-level platelet, neutrophil, and monocyte activation. Serum levels of platelet factor 4 and release of neutrophil extracellular traps (NETs) were significantly higher in patients with high serum IgG antibody against the novel RG-specific LG, a marker of in vivo immune exposure. An LN Validation cohort confirmed these correlates and showed that anti-LG antibodies serve as a surrogate for thromboinflammatory profile in this LN-associated endotype. In mice, gut colonisation with LG-producing RG strains or a single LG injection caused megakaryocytosis and platelet activation; RG colonisation with LG-producing strains induced tubulointerstitial injury with NETosis. In vivo responses to LG toxin were Toll-like receptor 2-dependent.
CONCLUSIONS: Gut expansions of the RG pathobiont may contribute to autoimmune pathogenesis through the LG toxin and cause LN flares through thromboinflammatory mechanisms in this previously unrecognised LN endotype.
Additional Links: PMID-42031645
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PubMed:
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@article {pmid42031645,
year = {2027},
author = {Amarnani, A and Rivera, CF and Cornwell, M and Weinstein, T and Azad, Z and Gottesman, SRS and Loomis, C and Lee, A and Ullah, N and Prasad, J and Yi, M and Cooney, L and Barnes, BJ and Gisch, N and Ruggles, KV and Ramkhelawon, B and Silverman, GJ},
title = {A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis.},
journal = {Annals of the rheumatic diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ard.2026.03.002},
pmid = {42031645},
issn = {1468-2060},
abstract = {OBJECTIVES: The gut microbiome plays a crucial role in regulating systemic immunity and has been implicated in several chronic inflammatory diseases. Intestinal expansions of Ruminococcus gnavus (RG), a dominant gut commensal, correlate with disease flares in lupus nephritis (LN), but the underlying mechanism remains unknown.
METHODS: In a Pilot cohort of patients with biopsy-proven LN, subsetted by gut microbiota community, immune status was characterised using bulk-blood RNA sequencing libraries, serum levels of representative host proteins, and levels of immunoglobulin (Ig)G antibodies to the novel lipoglycan (LG) produced by pathogenic RG strains. A Validation LN cohort was evaluated for blood transcriptomic profiles and levels of anti-LG antibodies. In murine models, mechanistic hypotheses were tested after RG gut colonisation or after intraperitoneal injection with an LG preparation, with outcomes determined by transcriptomic analyses, platelet functional readouts, and tissue histology.
RESULTS: In a Pilot cohort of patients with LN, RG gut expansions were associated with high-level platelet, neutrophil, and monocyte activation. Serum levels of platelet factor 4 and release of neutrophil extracellular traps (NETs) were significantly higher in patients with high serum IgG antibody against the novel RG-specific LG, a marker of in vivo immune exposure. An LN Validation cohort confirmed these correlates and showed that anti-LG antibodies serve as a surrogate for thromboinflammatory profile in this LN-associated endotype. In mice, gut colonisation with LG-producing RG strains or a single LG injection caused megakaryocytosis and platelet activation; RG colonisation with LG-producing strains induced tubulointerstitial injury with NETosis. In vivo responses to LG toxin were Toll-like receptor 2-dependent.
CONCLUSIONS: Gut expansions of the RG pathobiont may contribute to autoimmune pathogenesis through the LG toxin and cause LN flares through thromboinflammatory mechanisms in this previously unrecognised LN endotype.},
}
RevDate: 2026-04-27
Gut virome-microbiome interactions across hosts and environments.
NPJ biofilms and microbiomes, 12(1):.
The Gut microbiome-virome dynamics and interactions Collection highlights gut viruses, mainly bacteriophages, as determinants of microbial community structure and host-relevant functions across human, animal, and environmental systems. The Collection welcomes studies that quantify virus-microbe interactions, evidence-based linking viruses to microbial hosts, characterise infection dynamics, and connect them to ecological or clinical outcomes. It prioritises methodological rigour and translational relevance in diagnostics, surveillance, and phage-based interventions.
Additional Links: PMID-42031776
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@article {pmid42031776,
year = {2026},
author = {Samson, R and Hassard, F and Dharne, M},
title = {Gut virome-microbiome interactions across hosts and environments.},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {42031776},
issn = {2055-5008},
abstract = {The Gut microbiome-virome dynamics and interactions Collection highlights gut viruses, mainly bacteriophages, as determinants of microbial community structure and host-relevant functions across human, animal, and environmental systems. The Collection welcomes studies that quantify virus-microbe interactions, evidence-based linking viruses to microbial hosts, characterise infection dynamics, and connect them to ecological or clinical outcomes. It prioritises methodological rigour and translational relevance in diagnostics, surveillance, and phage-based interventions.},
}
RevDate: 2026-04-24
Gut microbiome-metabolome profiling reveals divergent growth performance in the spotted knifejaw (Oplegnathus punctatus).
Scientific reports pii:10.1038/s41598-026-50031-1 [Epub ahead of print].
Additional Links: PMID-42032033
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PubMed:
Citation:
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@article {pmid42032033,
year = {2026},
author = {Ma, C and Chen, C and Shang, X and Wang, Y and Liu, H and Yu, Y and Wang, Q and Wang, X and Jia, L and Liang, S},
title = {Gut microbiome-metabolome profiling reveals divergent growth performance in the spotted knifejaw (Oplegnathus punctatus).},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-50031-1},
pmid = {42032033},
issn = {2045-2322},
support = {24ZYCGSN00150//Tianjin Science and Technology Plan Project/ ; CARS-47-Z01//Tianjin Comprehensive Experimental Station of the National Marine Fish Industry Technology System/ ; },
}
RevDate: 2026-04-24
Fecal virome transplantation alleviates weaning stress-induced behavioral alterations and intestinal health by reshaping the gut microbiome.
Scientific reports pii:10.1038/s41598-026-49647-0 [Epub ahead of print].
Additional Links: PMID-42032216
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PubMed:
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@article {pmid42032216,
year = {2026},
author = {Choi, Y and Ryu, S and Kang, A and Lee, W and Park, J and Kang, MG and Jang, KB and Kwon, Y and Kwak, MJ and Jeong, KC and Song, M and Kim, Y},
title = {Fecal virome transplantation alleviates weaning stress-induced behavioral alterations and intestinal health by reshaping the gut microbiome.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-49647-0},
pmid = {42032216},
issn = {2045-2322},
support = {RS-2025-16068814//National Research Foundation of Korea/ ; },
}
RevDate: 2026-04-24
Cayman enables large-scale analysis of gut microbiome carbohydrate-active enzyme repertoires.
Nature microbiology [Epub ahead of print].
Carbohydrate-active enzymes (CAZymes) are crucial for digesting glycans, but tools for CAZyme profiling and interpretation of substrate preferences in microbiome data are lacking. Here we develop a CAZyme profiler called Cayman (Carbohydrate Active Enzymes Profiling of Metagenomes) and a hierarchical substrate annotation scheme for use with genomic or shotgun metagenomic datasets. Using these tools, we systematically surveyed CAZymes in human gut microorganisms (n = 107,683 genomes) and identified several putative mucin-foraging bacteria, including Hungatella and Eisenbergiella species, which were confirmed experimentally. We compared CAZymes in gut metagenomes (n = 3,960) from high-income settings versus low- and middle-income settings and found that low- and middle-income setting metagenomes are enriched in fibre-degrading CAZymes, while CAZyme richness is generally higher in high-income setting metagenomes. Additional analysis (n = 1,998) indicated that metagenomes of individuals with colorectal cancer are depleted in fibre-targeting and enriched in glycosaminoglycan-targeting CAZymes. Finally, we inferred CAZyme substrates from genomic co-localization of CAZyme domains. Cayman is broadly applicable and freely available from https://github.com/zellerlab/cayman .
Additional Links: PMID-42032279
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Citation:
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@article {pmid42032279,
year = {2026},
author = {Ducarmon, QR and Karcher, N and Giri, S and Tytgat, HLP and Delannoy-Bruno, O and Pekel, S and Springer, F and Wörz, P and Schudoma, C and Typas, A and Zeller, G},
title = {Cayman enables large-scale analysis of gut microbiome carbohydrate-active enzyme repertoires.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42032279},
issn = {2058-5276},
support = {LUMC Fellowship//Leids Universitair Medisch Centrum (Leiden University Medical Center)/ ; 395357507//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 01KD2102A//Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research)/ ; ALTF 1030-2022//European Molecular Biology Organization (EMBO)/ ; },
abstract = {Carbohydrate-active enzymes (CAZymes) are crucial for digesting glycans, but tools for CAZyme profiling and interpretation of substrate preferences in microbiome data are lacking. Here we develop a CAZyme profiler called Cayman (Carbohydrate Active Enzymes Profiling of Metagenomes) and a hierarchical substrate annotation scheme for use with genomic or shotgun metagenomic datasets. Using these tools, we systematically surveyed CAZymes in human gut microorganisms (n = 107,683 genomes) and identified several putative mucin-foraging bacteria, including Hungatella and Eisenbergiella species, which were confirmed experimentally. We compared CAZymes in gut metagenomes (n = 3,960) from high-income settings versus low- and middle-income settings and found that low- and middle-income setting metagenomes are enriched in fibre-degrading CAZymes, while CAZyme richness is generally higher in high-income setting metagenomes. Additional analysis (n = 1,998) indicated that metagenomes of individuals with colorectal cancer are depleted in fibre-targeting and enriched in glycosaminoglycan-targeting CAZymes. Finally, we inferred CAZyme substrates from genomic co-localization of CAZyme domains. Cayman is broadly applicable and freely available from https://github.com/zellerlab/cayman .},
}
RevDate: 2026-04-27
Representing dental caries and dysbiosis within the oral microbiome in the Oral Health and Disease Ontology.
Journal of biomedical semantics, 17(1):.
BACKGROUND: Dental caries is an oral health condition in which cariogenic bacteria demineralize and decay teeth. It arises due to interaction between the host, environment, and oral microbiome. Current terminologies and ontologies, however, do not accurately represent the important role that the microbiome has in the formation of carious lesions. Rather, they focus on the anatomical features of carious lesions and often obfuscate the distinctions between dental caries as a disease affecting a tooth, as lesions that are produced because of the disease, and as lesions produced as a result of dysbiosis in the oral microbiome. To capture the current state of evidence and provide flexibility for evolving literature on host-environment-microbiome interactions, there is a need to revise and expand the ontological framework for dental caries.
RESULTS: Several established terminologies and ontologies were reviewed for terms used to represent dental caries and the oral microbiome. We found that they either did not represent or misrepresented the current scientific understanding of caries and its relation to the microbial dysbiosis. As a result of these deficiencies, we added terms and relations to the Oral Health and Disease Ontology (OHD) that more accurately represent how oral microbial dysbiosis influences the development of dental caries.
CONCLUSIONS: The Oral Health and Disease Ontology is an advance over existing ontologies for representing the impact of oral microbial dysbiosis on dental caries. It provides a semantic framework that better serves the needs of cariology researchers and can more easily incorporate new oral microbiome findings.
Additional Links: PMID-42032627
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Citation:
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@article {pmid42032627,
year = {2026},
author = {Duncan, WD and Sabharwal, A and Diehl, AD and Dutta, N and Diller, M and Joachimiak, MP and Chandrasekharan, GM},
title = {Representing dental caries and dysbiosis within the oral microbiome in the Oral Health and Disease Ontology.},
journal = {Journal of biomedical semantics},
volume = {17},
number = {1},
pages = {},
pmid = {42032627},
issn = {2041-1480},
abstract = {BACKGROUND: Dental caries is an oral health condition in which cariogenic bacteria demineralize and decay teeth. It arises due to interaction between the host, environment, and oral microbiome. Current terminologies and ontologies, however, do not accurately represent the important role that the microbiome has in the formation of carious lesions. Rather, they focus on the anatomical features of carious lesions and often obfuscate the distinctions between dental caries as a disease affecting a tooth, as lesions that are produced because of the disease, and as lesions produced as a result of dysbiosis in the oral microbiome. To capture the current state of evidence and provide flexibility for evolving literature on host-environment-microbiome interactions, there is a need to revise and expand the ontological framework for dental caries.
RESULTS: Several established terminologies and ontologies were reviewed for terms used to represent dental caries and the oral microbiome. We found that they either did not represent or misrepresented the current scientific understanding of caries and its relation to the microbial dysbiosis. As a result of these deficiencies, we added terms and relations to the Oral Health and Disease Ontology (OHD) that more accurately represent how oral microbial dysbiosis influences the development of dental caries.
CONCLUSIONS: The Oral Health and Disease Ontology is an advance over existing ontologies for representing the impact of oral microbial dysbiosis on dental caries. It provides a semantic framework that better serves the needs of cariology researchers and can more easily incorporate new oral microbiome findings.},
}
RevDate: 2026-04-25
Rhizosphere microbiome influences fruit quality in citrus.
The New phytologist [Epub ahead of print].
Fruit quality is shaped by both crop genetics and cultivation environments, with soil conditions driving rhizosphere microbiome assembly. While rhizosphere microbes are known to enhance nutrient utilization and plant metabolism, their direct contribution to fruit quality regulation remains poorly understood. In this study, we demonstrate that the Satsuma mandarin (Citrus unshiu Marc.) and Navel orange (Citrus sinensis L. Osbeck) rhizosphere microbiome influence fruit sugar concentration, a key determinant of fruit quality. The rhizosphere core microbiota and soil mineral nutrients were positively correlated with fruit quality indices. Fruit quality-correlated bacterial operational taxonomic units (OTUs) explained an average of 32.6% of the observed variation in quality parameters. Inoculation with three bacterial strains (affiliated with Burkholderia, Pseudomonas, Rhizobium) and two bacterial consortia significantly increased fruit sugar concentrations. Metagenomic analysis linked sugar-associated microbes to iron (Fe) utilization, revealing genomic enrichment of siderophore biosynthesis gene clusters. Consistently, the selected bacterial strains exhibited siderophore secretion capabilities, increased leaf Fe content by 23.3-47.8% in citrus rootstock. Further field application of chelated-Fe fertilizer also increased fruit sugar concentration. Collectively, our results revealed an influence of the rhizosphere microbiome on fruit quality that is related to Fe acquisition optimization and subsequent sugar accumulation in citrus.
Additional Links: PMID-42032888
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PubMed:
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@article {pmid42032888,
year = {2026},
author = {Wu, S and Wang, Y and Li, H and Fang, X and Guo, J and Luo, X and Li, M and Song, F and Tan, Q and Deng, X and Xiao, S and Liu, H and Hu, C and Pan, Z},
title = {Rhizosphere microbiome influences fruit quality in citrus.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71159},
pmid = {42032888},
issn = {1469-8137},
support = {2023YFD2300603//The National Key Research and Development Program of China/ ; 2017YFD0202001//The National Key Research and Development Program of China/ ; 2019YFD1000103//The National Key Research and Development Program of China/ ; },
abstract = {Fruit quality is shaped by both crop genetics and cultivation environments, with soil conditions driving rhizosphere microbiome assembly. While rhizosphere microbes are known to enhance nutrient utilization and plant metabolism, their direct contribution to fruit quality regulation remains poorly understood. In this study, we demonstrate that the Satsuma mandarin (Citrus unshiu Marc.) and Navel orange (Citrus sinensis L. Osbeck) rhizosphere microbiome influence fruit sugar concentration, a key determinant of fruit quality. The rhizosphere core microbiota and soil mineral nutrients were positively correlated with fruit quality indices. Fruit quality-correlated bacterial operational taxonomic units (OTUs) explained an average of 32.6% of the observed variation in quality parameters. Inoculation with three bacterial strains (affiliated with Burkholderia, Pseudomonas, Rhizobium) and two bacterial consortia significantly increased fruit sugar concentrations. Metagenomic analysis linked sugar-associated microbes to iron (Fe) utilization, revealing genomic enrichment of siderophore biosynthesis gene clusters. Consistently, the selected bacterial strains exhibited siderophore secretion capabilities, increased leaf Fe content by 23.3-47.8% in citrus rootstock. Further field application of chelated-Fe fertilizer also increased fruit sugar concentration. Collectively, our results revealed an influence of the rhizosphere microbiome on fruit quality that is related to Fe acquisition optimization and subsequent sugar accumulation in citrus.},
}
RevDate: 2026-04-25
Gut Microbiome and Psychoneurological Symptoms Among Patients With Colorectal Cancer and Their Caregivers: A Pilot Study.
Biological research for nursing [Epub ahead of print].
Purpose: Survivorship in colorectal cancer (CRC) is often accompanied by co-occurring psychoneurological symptoms (PNS, e.g., fatigue, depression, pain), which negatively affect quality of life. Caregivers of individuals with CRC also experience PNS due to caregiving burdens, amplifying distress across the dyad. PNS may be influenced by the activity of the gut microbes. The purpose of this pilot study was to examine gut microbiome diversity and composition, and their association with PNS in CRC patients and their caregivers. Methods: Baseline data from a technology-based dyadic intervention were included in this analysis. Eleven patients and eight caregivers provided stool samples and completed PROMIS measures of PNS at baseline. Gut microbiome profiles were assessed using 16S rRNA gene sequencing. Alpha and beta diversity metrics and differential abundance analyses were used to characterize the gut microbiome and examine its associations with PNS. Results: Patients exhibited significantly lower microbial alpha diversity than caregivers in the full sample (p = 0.033). Dyadic comparisons identified 92 differentially abundant taxa, with patients showing depletion of short-chain fatty acid-producing taxa and enrichment of opportunistic taxa. Microbiome-symptom models revealed significant interactions by group (patient vs. caregiver) and taxa-level effects, with patients showing stronger positive associations between microbial alterations and higher PNS severity. Conclusions: CRC patients actively on chemotherapy demonstrated reduced diversity and depletion of beneficial taxa that may contribute to heightened PNS. Caregivers, despite healthier profiles, reported substantial symptom burden that were linked to gut microbiome features, highlighting dyadic interdependence and the potential for microbiome-targeted, dyadic interventions in survivorship care.
Additional Links: PMID-42032897
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PubMed:
Citation:
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@article {pmid42032897,
year = {2026},
author = {Lin, Y and Barandouzi, ZA and Houser, MC and Xiao, C and Alese, OB and Mathebula, S and Bai, J and Gbolahan, O and Bruner, DW},
title = {Gut Microbiome and Psychoneurological Symptoms Among Patients With Colorectal Cancer and Their Caregivers: A Pilot Study.},
journal = {Biological research for nursing},
volume = {},
number = {},
pages = {10998004261447509},
doi = {10.1177/10998004261447509},
pmid = {42032897},
issn = {1552-4175},
abstract = {Purpose: Survivorship in colorectal cancer (CRC) is often accompanied by co-occurring psychoneurological symptoms (PNS, e.g., fatigue, depression, pain), which negatively affect quality of life. Caregivers of individuals with CRC also experience PNS due to caregiving burdens, amplifying distress across the dyad. PNS may be influenced by the activity of the gut microbes. The purpose of this pilot study was to examine gut microbiome diversity and composition, and their association with PNS in CRC patients and their caregivers. Methods: Baseline data from a technology-based dyadic intervention were included in this analysis. Eleven patients and eight caregivers provided stool samples and completed PROMIS measures of PNS at baseline. Gut microbiome profiles were assessed using 16S rRNA gene sequencing. Alpha and beta diversity metrics and differential abundance analyses were used to characterize the gut microbiome and examine its associations with PNS. Results: Patients exhibited significantly lower microbial alpha diversity than caregivers in the full sample (p = 0.033). Dyadic comparisons identified 92 differentially abundant taxa, with patients showing depletion of short-chain fatty acid-producing taxa and enrichment of opportunistic taxa. Microbiome-symptom models revealed significant interactions by group (patient vs. caregiver) and taxa-level effects, with patients showing stronger positive associations between microbial alterations and higher PNS severity. Conclusions: CRC patients actively on chemotherapy demonstrated reduced diversity and depletion of beneficial taxa that may contribute to heightened PNS. Caregivers, despite healthier profiles, reported substantial symptom burden that were linked to gut microbiome features, highlighting dyadic interdependence and the potential for microbiome-targeted, dyadic interventions in survivorship care.},
}
RevDate: 2026-04-25
The lizard microbiome: patterns, drivers, and functional implications.
FEMS microbiology letters pii:8662450 [Epub ahead of print].
The lizard microbiome is a dynamic community that plays a crucial role in the health and survival of these animals. As global change poses significant threats to lizard populations around the world, understanding the interactions between lizards and their microbial communities is increasingly important. Here, we synthesize a rapidly growing body of research on the composition, diversity, transmission, and functional roles of lizard microbiomes. We discuss the implications of microbiome variation for lizard physiology, as well as the potential for microbiomes to inform conservation strategies for threatened species. Finally, we highlight priorities for future research, which include the need to quantify microbiome diversity and function across additional taxa, as lizards remain underrepresented in the microbiome literature. We also stress the importance of experimental and field research that can reveal the adaptive significance of lizard microbiomes in the face of environmental change. Our synthesis highlights the contributions of lizard microbiome science to the fields of ecology, evolution, and conservation biology and demonstrates how the microbial communities that live in and on lizards enhance our understanding of their biodiversity and inform efforts to protect vulnerable populations.
Additional Links: PMID-42033327
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PubMed:
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@article {pmid42033327,
year = {2026},
author = {Williams, CE and Tacoaman, YFL and Fontaine, SS and Logan, ML},
title = {The lizard microbiome: patterns, drivers, and functional implications.},
journal = {FEMS microbiology letters},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsle/fnag049},
pmid = {42033327},
issn = {1574-6968},
abstract = {The lizard microbiome is a dynamic community that plays a crucial role in the health and survival of these animals. As global change poses significant threats to lizard populations around the world, understanding the interactions between lizards and their microbial communities is increasingly important. Here, we synthesize a rapidly growing body of research on the composition, diversity, transmission, and functional roles of lizard microbiomes. We discuss the implications of microbiome variation for lizard physiology, as well as the potential for microbiomes to inform conservation strategies for threatened species. Finally, we highlight priorities for future research, which include the need to quantify microbiome diversity and function across additional taxa, as lizards remain underrepresented in the microbiome literature. We also stress the importance of experimental and field research that can reveal the adaptive significance of lizard microbiomes in the face of environmental change. Our synthesis highlights the contributions of lizard microbiome science to the fields of ecology, evolution, and conservation biology and demonstrates how the microbial communities that live in and on lizards enhance our understanding of their biodiversity and inform efforts to protect vulnerable populations.},
}
RevDate: 2026-04-25
Comparative analysis of microbial diversity and pathogenic potential in marine litter reveals timber as a key reservoir in sandy beaches ecosystems.
Journal of hazardous materials, 511:141937 pii:S0304-3894(26)00915-5 [Epub ahead of print].
Many materials create new habitats for microbial colonization and the persistence of potentially pathogenic bacteria. Despite this, comparative studies addressing the microbial diversity and pathogenic potential across different types of marine litter remain scarce. This study investigated microbial communities associated with plastics, aluminum, and timber collected from the strandline of two types of beaches. Amplicon sequencing of the 16S rRNA gene revealed that bacterial community structure and diversity varied primarily according to substrate type rather than beach environment. Nevertheless, all types of marine litter evaluated hosted rich and diverse bacterial communities, with several taxa recognized as potential pathogens of both marine organisms and humans. Timber supported the richest, most diverse, and most specific microbiome, including a high number of taxa known to contain potential pathogens. Among these, Flavobacterium, Mycobacterium, Pseudoalteromonas, Acinetobacter, and Staphylococcus were particularly notable, as they are recognized pathogens of both marine organisms and humans, representing potential ecological and sanitary risks. These findings highlight that marine litter on sandy beaches functions as a selective substrate influencing biofilm formation, microbial dispersal, and the persistence of pathogens in coastal ecosystems. Timber, in particular, emerges as an underrecognized reservoir for microbial diversity and resistance genes, warranting greater attention in marine pollution and public health monitoring.
Additional Links: PMID-42033818
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PubMed:
Citation:
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@article {pmid42033818,
year = {2026},
author = {Póvoa, AA and Amorim Magalhães, E and Dos Santos, KP and Canellas, AL and Soares-Gomes, A and Dos Santos, HF},
title = {Comparative analysis of microbial diversity and pathogenic potential in marine litter reveals timber as a key reservoir in sandy beaches ecosystems.},
journal = {Journal of hazardous materials},
volume = {511},
number = {},
pages = {141937},
doi = {10.1016/j.jhazmat.2026.141937},
pmid = {42033818},
issn = {1873-3336},
abstract = {Many materials create new habitats for microbial colonization and the persistence of potentially pathogenic bacteria. Despite this, comparative studies addressing the microbial diversity and pathogenic potential across different types of marine litter remain scarce. This study investigated microbial communities associated with plastics, aluminum, and timber collected from the strandline of two types of beaches. Amplicon sequencing of the 16S rRNA gene revealed that bacterial community structure and diversity varied primarily according to substrate type rather than beach environment. Nevertheless, all types of marine litter evaluated hosted rich and diverse bacterial communities, with several taxa recognized as potential pathogens of both marine organisms and humans. Timber supported the richest, most diverse, and most specific microbiome, including a high number of taxa known to contain potential pathogens. Among these, Flavobacterium, Mycobacterium, Pseudoalteromonas, Acinetobacter, and Staphylococcus were particularly notable, as they are recognized pathogens of both marine organisms and humans, representing potential ecological and sanitary risks. These findings highlight that marine litter on sandy beaches functions as a selective substrate influencing biofilm formation, microbial dispersal, and the persistence of pathogens in coastal ecosystems. Timber, in particular, emerges as an underrecognized reservoir for microbial diversity and resistance genes, warranting greater attention in marine pollution and public health monitoring.},
}
RevDate: 2026-04-25
Xenobiotic dynamics in mangroves and peatlands: Microbial mechanisms for nature-based mitigation.
Journal of hazardous materials, 511:142149 pii:S0304-3894(26)01127-1 [Epub ahead of print].
Peatlands and mangroves provide substantial ecosystem services, but are increasingly threatened by xenobiotic contamination, posing escalating ecological risks. Here, we present the first integrative synthesis of the xenobiotic dynamics in these systems, mapping contaminant distributions and identifying emerging research priorities. Over time, research has shifted from oil spills and heavy metal pollution towards persistent organic pollutants, microplastics and climate risks. Peatlands remain substantially understudied compared to mangroves, especially for emerging contaminant classes. Xenobiotics disrupt the environment-biota linkages in these systems by impairing microbiome functionality; yet, subsets of microbial communities persist through adaptation and sharing of genomic traits. These traits enable xenobiotic sequestration, degradation or utilization. We compile a wetland-associated catalogue of microbial mechanisms and cross-environment analogues to guide bioprospecting and nature-based xenobiotic transformations. We recommend coupling wetland restoration with systematic microbiome exploration, positioning wetlands as in-situ buffers and ex-situ reservoirs for scalable, nature-based solutions for xenobiotic mitigation.
Additional Links: PMID-42033825
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PubMed:
Citation:
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@article {pmid42033825,
year = {2026},
author = {Mukhopadhyay, S and Ooi, QE and Mukherjee, A and Bhattacharya, R and Sarkar, P and Tan, ZD and Phang, B and Chey, SL and Lupascu, M and Bandla, A and Swarup, S},
title = {Xenobiotic dynamics in mangroves and peatlands: Microbial mechanisms for nature-based mitigation.},
journal = {Journal of hazardous materials},
volume = {511},
number = {},
pages = {142149},
doi = {10.1016/j.jhazmat.2026.142149},
pmid = {42033825},
issn = {1873-3336},
abstract = {Peatlands and mangroves provide substantial ecosystem services, but are increasingly threatened by xenobiotic contamination, posing escalating ecological risks. Here, we present the first integrative synthesis of the xenobiotic dynamics in these systems, mapping contaminant distributions and identifying emerging research priorities. Over time, research has shifted from oil spills and heavy metal pollution towards persistent organic pollutants, microplastics and climate risks. Peatlands remain substantially understudied compared to mangroves, especially for emerging contaminant classes. Xenobiotics disrupt the environment-biota linkages in these systems by impairing microbiome functionality; yet, subsets of microbial communities persist through adaptation and sharing of genomic traits. These traits enable xenobiotic sequestration, degradation or utilization. We compile a wetland-associated catalogue of microbial mechanisms and cross-environment analogues to guide bioprospecting and nature-based xenobiotic transformations. We recommend coupling wetland restoration with systematic microbiome exploration, positioning wetlands as in-situ buffers and ex-situ reservoirs for scalable, nature-based solutions for xenobiotic mitigation.},
}
RevDate: 2026-04-25
Polyphenols and physical activity stimulate gut microbiota mediated Nrf2 signaling to combat neurodegeneration.
Pathology, research and practice, 283:156478 pii:S0344-0338(26)00131-7 [Epub ahead of print].
Polyphenols and regular physical activity are increasingly recognized as complementary lifestyle interventions that influence the gut-brain axis and contribute to neuroprotection. Emerging evidence highlights the central role of the gut microbiota in mediating these effects by transforming dietary and host-derived substrates into bioactive metabolites. These metabolites can activate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, a key regulator of cellular antioxidant defenses, mitochondrial function, and anti-inflammatory responses processes that are critically impaired in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This review synthesizes current mechanistic insights into how polyphenol-derived metabolites and exercise-induced alterations in gut microbial composition converge to modulate Nrf2 signaling. We discuss the roles of key microbiota-derived metabolites, including short-chain fatty acids, urolithins, and indole derivatives, in regulating oxidative stress, neuroinflammation, and synaptic function. Furthermore, we examine evidence from preclinical models supporting the synergistic effects of dietary polyphenols and physical activity on gut microbiota-mediated neuroprotection. Finally, we address translational challenges and highlight the potential of integrating dietary and exercise-based strategies to harness microbiota-dependent Nrf2 activation. This integrative framework provides a basis for developing personalized, microbiome-informed interventions aimed at delaying or mitigating neurodegeneration.
Additional Links: PMID-42033865
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PubMed:
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@article {pmid42033865,
year = {2026},
author = {Wang, F},
title = {Polyphenols and physical activity stimulate gut microbiota mediated Nrf2 signaling to combat neurodegeneration.},
journal = {Pathology, research and practice},
volume = {283},
number = {},
pages = {156478},
doi = {10.1016/j.prp.2026.156478},
pmid = {42033865},
issn = {1618-0631},
abstract = {Polyphenols and regular physical activity are increasingly recognized as complementary lifestyle interventions that influence the gut-brain axis and contribute to neuroprotection. Emerging evidence highlights the central role of the gut microbiota in mediating these effects by transforming dietary and host-derived substrates into bioactive metabolites. These metabolites can activate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, a key regulator of cellular antioxidant defenses, mitochondrial function, and anti-inflammatory responses processes that are critically impaired in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This review synthesizes current mechanistic insights into how polyphenol-derived metabolites and exercise-induced alterations in gut microbial composition converge to modulate Nrf2 signaling. We discuss the roles of key microbiota-derived metabolites, including short-chain fatty acids, urolithins, and indole derivatives, in regulating oxidative stress, neuroinflammation, and synaptic function. Furthermore, we examine evidence from preclinical models supporting the synergistic effects of dietary polyphenols and physical activity on gut microbiota-mediated neuroprotection. Finally, we address translational challenges and highlight the potential of integrating dietary and exercise-based strategies to harness microbiota-dependent Nrf2 activation. This integrative framework provides a basis for developing personalized, microbiome-informed interventions aimed at delaying or mitigating neurodegeneration.},
}
RevDate: 2026-04-25
Oxygen vacancy-rich nanosystems eradicate stubborn periodontal biofilms by synergistic EPS degradation, metabolic activation and microbiome restoration.
Biomaterials, 333:124234 pii:S0142-9612(26)00258-9 [Epub ahead of print].
Periodontitis-associated biofilms pose a severe public health threat due to a dual defense mechanism. This involves a protective physical matrix barrier and biological interference from persistent bacteria and microbial dysbiosis. Current strategies often fail to penetrate deeply, eradicate dormant persisters and resolve microbial dysbiosis, leading to biofilm resistance and disease recurrence. In this study, we develop a multifunctional nanoplatform combining photothermal, photodynamic therapy and peroxidase-like catalysis to execute a sequential strategy. This system integrates molybdenum oxide nanodots rich in oxygen vacancy (MoO3-x) with the photosensitizer indocyanine green (ICG). It exhibits improved optical and enzymatic performance due to the introduced oxygen vacancies. Upon irradiation, the system produces localized hyperthermia and ROS storms to destabilize the biofilm matrix and promote ultrasmall nanodots penetration. The thermal and oxidative stress increase membrane permeability and reactivate metabolism of dormant persisters. Metagenomic analyses confirms that MoO3-x/ICG-treated biofilms show decreased abundance of key persistence-related genes and great enrichment in metabolic pathways. Additionally, the platform exhibits therapeutic effects and a successful shift towards a healthier oral microbiota in periodontitis model. Overall, MoO3-x/ICG demonstrates excellent biofilm eradication and successfully prevents biofilm regrowth or secondary infection. This work targets the entire biofilm lifecycle and presents a nanoplatform for long-term management of periodontal infections.
Additional Links: PMID-42033990
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PubMed:
Citation:
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@article {pmid42033990,
year = {2026},
author = {Wu, Q and You, J and Li, D and Tang, S and Wu, S and Wang, Q and Teng, W},
title = {Oxygen vacancy-rich nanosystems eradicate stubborn periodontal biofilms by synergistic EPS degradation, metabolic activation and microbiome restoration.},
journal = {Biomaterials},
volume = {333},
number = {},
pages = {124234},
doi = {10.1016/j.biomaterials.2026.124234},
pmid = {42033990},
issn = {1878-5905},
abstract = {Periodontitis-associated biofilms pose a severe public health threat due to a dual defense mechanism. This involves a protective physical matrix barrier and biological interference from persistent bacteria and microbial dysbiosis. Current strategies often fail to penetrate deeply, eradicate dormant persisters and resolve microbial dysbiosis, leading to biofilm resistance and disease recurrence. In this study, we develop a multifunctional nanoplatform combining photothermal, photodynamic therapy and peroxidase-like catalysis to execute a sequential strategy. This system integrates molybdenum oxide nanodots rich in oxygen vacancy (MoO3-x) with the photosensitizer indocyanine green (ICG). It exhibits improved optical and enzymatic performance due to the introduced oxygen vacancies. Upon irradiation, the system produces localized hyperthermia and ROS storms to destabilize the biofilm matrix and promote ultrasmall nanodots penetration. The thermal and oxidative stress increase membrane permeability and reactivate metabolism of dormant persisters. Metagenomic analyses confirms that MoO3-x/ICG-treated biofilms show decreased abundance of key persistence-related genes and great enrichment in metabolic pathways. Additionally, the platform exhibits therapeutic effects and a successful shift towards a healthier oral microbiota in periodontitis model. Overall, MoO3-x/ICG demonstrates excellent biofilm eradication and successfully prevents biofilm regrowth or secondary infection. This work targets the entire biofilm lifecycle and presents a nanoplatform for long-term management of periodontal infections.},
}
RevDate: 2026-04-25
Engineered commensals for metabolic modulation of the gut-liver-brain axis.
Cell pii:S0092-8674(26)00384-3 [Epub ahead of print].
The gut-liver-brain axis is central to metabolic and neurological homeostasis and is mediated by host- and microbiota-derived metabolites. Disruptions in this axis contribute to complex disorders, underscoring the need for targeted, multi-metabolite interventions. Here, we engineered commensal Lactobacillus plantarum WCFS1 strains to specifically modulate metabolites dysregulated in hepatic encephalopathy (HE), a disorder driven by hyperammonemia and amino acid imbalance. One strain couples ammonia assimilation with branched-chain amino acid (BCAA) biosynthesis, whereas the other enhances L-glutamine utilization to suppress ammonia generation. In two preclinical HE models, these strains reduced systemic ammonia by up to 10-fold, restored BCAA and L-glutamine balance, and improved anxiety-like and cognitive behaviors. Notably, they outperformed rifaximin, a clinically used HE therapy, while preserving gut microbiota diversity. These findings establish engineered commensals as a modular, responsive platform for multi-metabolite modulation of host-microbiota metabolism, offering a programmable strategy to restore metabolic homeostasis in disorders of the gut-liver-brain axis.
Additional Links: PMID-42034052
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PubMed:
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@article {pmid42034052,
year = {2026},
author = {Aggarwal, N and Shen, H and Lee, LT and Zhou, L and Zhu, MT and Koh, XQ and Ng, AXY and Li, M and Jumat, NHB and Cheah, WY and Li, S and Saini, M and Lee, JWJ and Foo, JL and Wun, KS and Hwang, IY and Ho, CL and Lee, YS and Dan, YY and Chang, MW},
title = {Engineered commensals for metabolic modulation of the gut-liver-brain axis.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2026.03.048},
pmid = {42034052},
issn = {1097-4172},
abstract = {The gut-liver-brain axis is central to metabolic and neurological homeostasis and is mediated by host- and microbiota-derived metabolites. Disruptions in this axis contribute to complex disorders, underscoring the need for targeted, multi-metabolite interventions. Here, we engineered commensal Lactobacillus plantarum WCFS1 strains to specifically modulate metabolites dysregulated in hepatic encephalopathy (HE), a disorder driven by hyperammonemia and amino acid imbalance. One strain couples ammonia assimilation with branched-chain amino acid (BCAA) biosynthesis, whereas the other enhances L-glutamine utilization to suppress ammonia generation. In two preclinical HE models, these strains reduced systemic ammonia by up to 10-fold, restored BCAA and L-glutamine balance, and improved anxiety-like and cognitive behaviors. Notably, they outperformed rifaximin, a clinically used HE therapy, while preserving gut microbiota diversity. These findings establish engineered commensals as a modular, responsive platform for multi-metabolite modulation of host-microbiota metabolism, offering a programmable strategy to restore metabolic homeostasis in disorders of the gut-liver-brain axis.},
}
RevDate: 2026-04-25
Eating for Inflammatory Bowel Disease: Assessing the Effect of Dietary Carbohydrates on Gut Microbiota and Implications for Disease Management.
The Journal of nutrition pii:S0022-3166(26)00200-2 [Epub ahead of print].
Targeting the gut microbiome through diet remains a priority in the treatment and management of inflammatory bowel diseases (IBD) for patients and clinicians alike. However, expert consensus is lacking, and cross-sectional studies indicate that patients with IBD often adopt low-fiber, high-sugar, and high-protein diets in an effort to control gastrointestinal symptoms and inflammation with negative implications for gut microbial functions and gastrointestinal inflammation. Although dietary carbohydrates are key modulators of gut microbial composition and function, substantial disagreement persists regarding how carbohydrate digestibility and structural properties influence IBD outcomes. This narrative review summarizes current knowledge on the role of dietary carbohydrates in IBD risk and progression and critically evaluates recent dietary interventions in which the gut microbiota was included among outcomes to elaborate a potential role of dietary carbohydrates in the clinical management of IBD. We conclude by outlining research priorities needed to affirm a role for dietary carbohydrate modification in the clinical management of IBD and to support the development of practical, evidence-based dietary guidance.
Additional Links: PMID-42034241
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PubMed:
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@article {pmid42034241,
year = {2026},
author = {Juritsch, AF and Deehan, EC and Armet, AM and Mannon, PJ and Ramer-Tait, AE},
title = {Eating for Inflammatory Bowel Disease: Assessing the Effect of Dietary Carbohydrates on Gut Microbiota and Implications for Disease Management.},
journal = {The Journal of nutrition},
volume = {},
number = {},
pages = {101551},
doi = {10.1016/j.tjnut.2026.101551},
pmid = {42034241},
issn = {1541-6100},
abstract = {Targeting the gut microbiome through diet remains a priority in the treatment and management of inflammatory bowel diseases (IBD) for patients and clinicians alike. However, expert consensus is lacking, and cross-sectional studies indicate that patients with IBD often adopt low-fiber, high-sugar, and high-protein diets in an effort to control gastrointestinal symptoms and inflammation with negative implications for gut microbial functions and gastrointestinal inflammation. Although dietary carbohydrates are key modulators of gut microbial composition and function, substantial disagreement persists regarding how carbohydrate digestibility and structural properties influence IBD outcomes. This narrative review summarizes current knowledge on the role of dietary carbohydrates in IBD risk and progression and critically evaluates recent dietary interventions in which the gut microbiota was included among outcomes to elaborate a potential role of dietary carbohydrates in the clinical management of IBD. We conclude by outlining research priorities needed to affirm a role for dietary carbohydrate modification in the clinical management of IBD and to support the development of practical, evidence-based dietary guidance.},
}
RevDate: 2026-04-25
CmpDate: 2026-04-25
Trichoderma asperellum 152-42 confers resistance to Fusarium root rot in alfalfa through JA-mediated induced systemic resistance and reshaping of the rhizosphere microbiome.
Pesticide biochemistry and physiology, 220:107087.
Fusarium root rot, caused by Fusarium spp., threatens alfalfa production, and Trichoderma species are emerging as potential biocontrol agents against this soilborne pathogen. However, the mechanisms by which Trichoderma strains trigger plant systemic resistance and remodel the rhizosphere microbiome to suppress pathogen infection remain unclear. Here, we screened five Trichoderma strains through in vitro antagonism, siderophore production, and growth-promoting assays to identify the optimal strain. Integrating pot experiments, physiological and biochemical analyses, transcriptome sequencing, and microbiome amplicon sequencing, we elucidated its mode of action and validated its effects in field trials. Our results demonstrate that Trichoderma asperellum 152-42 exhibited the strongest comprehensive performance, achieving 72% pathogen inhibition in dual culture assays. In pot experiments, pretreatment with this strain reduced the disease index by 25%. Mechanistically, the strain activated the jasmonic acid (JA) signaling pathway, enhanced defense enzyme activities and defense gene expression, and induced coordinated upregulation of genes involved in sucrose metabolism and MAPK signaling. Rhizosphere microbiome analysis revealed that the strain selectively enriched beneficial taxa, including plant growth-promoting bacteria and arbuscular mycorrhizal fungi, suppressed pathogenic Fusarium, and enhanced both bacterial community stability and fungal network complexity. Field trials confirmed that this strain increased crude protein content by 26% and hay yield by 10-13%. Our study reveals the integrated mechanism by which T. asperellum 152-42 controls Fusarium root rot through "direct antagonism-JA/ET immune priming-metabolic reprogramming-microecological regulation," providing both a valuable strain resource and a theoretical foundation for sustainable alfalfa production.
Additional Links: PMID-42034408
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PubMed:
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@article {pmid42034408,
year = {2026},
author = {Liu, M and Suo, X and Mai, X and Smagghe, G and Yin, S and Wang, Z and Gai, Y and Niu, Q},
title = {Trichoderma asperellum 152-42 confers resistance to Fusarium root rot in alfalfa through JA-mediated induced systemic resistance and reshaping of the rhizosphere microbiome.},
journal = {Pesticide biochemistry and physiology},
volume = {220},
number = {},
pages = {107087},
doi = {10.1016/j.pestbp.2026.107087},
pmid = {42034408},
issn = {1095-9939},
mesh = {*Medicago sativa/microbiology ; *Fusarium/physiology ; Rhizosphere ; *Oxylipins/metabolism/pharmacology ; *Cyclopentanes/metabolism/pharmacology ; *Plant Diseases/microbiology/prevention & control ; Plant Roots/microbiology ; *Microbiota ; Disease Resistance ; *Hypocreales ; *Trichoderma/physiology ; Soil Microbiology ; Plant Systemic Acquired Resistance ; },
abstract = {Fusarium root rot, caused by Fusarium spp., threatens alfalfa production, and Trichoderma species are emerging as potential biocontrol agents against this soilborne pathogen. However, the mechanisms by which Trichoderma strains trigger plant systemic resistance and remodel the rhizosphere microbiome to suppress pathogen infection remain unclear. Here, we screened five Trichoderma strains through in vitro antagonism, siderophore production, and growth-promoting assays to identify the optimal strain. Integrating pot experiments, physiological and biochemical analyses, transcriptome sequencing, and microbiome amplicon sequencing, we elucidated its mode of action and validated its effects in field trials. Our results demonstrate that Trichoderma asperellum 152-42 exhibited the strongest comprehensive performance, achieving 72% pathogen inhibition in dual culture assays. In pot experiments, pretreatment with this strain reduced the disease index by 25%. Mechanistically, the strain activated the jasmonic acid (JA) signaling pathway, enhanced defense enzyme activities and defense gene expression, and induced coordinated upregulation of genes involved in sucrose metabolism and MAPK signaling. Rhizosphere microbiome analysis revealed that the strain selectively enriched beneficial taxa, including plant growth-promoting bacteria and arbuscular mycorrhizal fungi, suppressed pathogenic Fusarium, and enhanced both bacterial community stability and fungal network complexity. Field trials confirmed that this strain increased crude protein content by 26% and hay yield by 10-13%. Our study reveals the integrated mechanism by which T. asperellum 152-42 controls Fusarium root rot through "direct antagonism-JA/ET immune priming-metabolic reprogramming-microecological regulation," providing both a valuable strain resource and a theoretical foundation for sustainable alfalfa production.},
}
MeSH Terms:
show MeSH Terms
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*Medicago sativa/microbiology
*Fusarium/physiology
Rhizosphere
*Oxylipins/metabolism/pharmacology
*Cyclopentanes/metabolism/pharmacology
*Plant Diseases/microbiology/prevention & control
Plant Roots/microbiology
*Microbiota
Disease Resistance
*Hypocreales
*Trichoderma/physiology
Soil Microbiology
Plant Systemic Acquired Resistance
RevDate: 2026-04-25
CmpDate: 2026-04-25
Nano-bioprotectant dsRsGH1@ε-PL@CMCS enhances RNAi efficacy against Rhizoctonia solani via dual mechanisms: Interacting with the vesicle transport protein SEC22 and modulating the tobacco phyllosphere microbiota.
Pesticide biochemistry and physiology, 220:107104.
Nanocarrier-mediated delivery of double-stranded RNA (dsRNA) is a promising strategy for plant disease control. Our previous study has shown that the self-assembled ε-poly-l-lysine/carboxymethyl chitosan (ε-PL@CMCS) nanocarrier significantly improves the efficiency of RNA interference (RNAi) against Rhizoctonia solani AG3 TB. However, the molecular mechanisms underlying this enhancement and the potential ecological impacts on phyllosphere microbial communities remain unclear. In this study, we confirmed that dsRsGH1@ε-PL@CMCS had no adverse effects on the growth and development of plants. Transcriptome analysis revealed that DEGs were significantly enriched in 'SNARE interactions in vesicular transport' pathway. Among them, dsRsGH1@ε-PL@CMCS specifically upregulate the vesicle transport protein SEC22 in Nicotiana tabacum. Surface plasmon resonance (SPR) assay demonstrated that the dsRsGH1@ε-PL@CMCS binds to SEC22 protein with 7.6-fold higher affinity than that of the naked dsRsGH1. Silencing SEC22 in the dsRsGH1@ε-PL@CMCS treatment reduced the silencing efficiency of RsGH1 from 53.3% to 39%, confirming its essential role. Concurrently, high-throughput sequencing revealed that SIGS treatments did not disrupt bacterial community structure but increased fungal diversity and suppressed the pathogen, while enriching beneficial fungi such as Tulasnella. Our findings elucidate a molecular link between nano-bioprotectant dsRsGH1@ε-PL@CMCS-enhanced RNAi and host vesicle transport, while confirming the biocompatible and microbiome-modulating potential. This provides a dual perspective for developing efficient and sustainable RNAi-based strategies for protecting plants.
Additional Links: PMID-42034417
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@article {pmid42034417,
year = {2026},
author = {Ding, X and Cao, K and Li, Y and Li, X and Zhong, Q and Chen, Y and An, M and Liu, H and Zhou, R and Wu, Y},
title = {Nano-bioprotectant dsRsGH1@ε-PL@CMCS enhances RNAi efficacy against Rhizoctonia solani via dual mechanisms: Interacting with the vesicle transport protein SEC22 and modulating the tobacco phyllosphere microbiota.},
journal = {Pesticide biochemistry and physiology},
volume = {220},
number = {},
pages = {107104},
doi = {10.1016/j.pestbp.2026.107104},
pmid = {42034417},
issn = {1095-9939},
mesh = {*Nicotiana/microbiology/drug effects/genetics ; *Rhizoctonia/drug effects/genetics ; *Chitosan/analogs & derivatives/chemistry/pharmacology ; *RNA Interference ; *Microbiota/drug effects ; *RNA, Double-Stranded/pharmacology ; Plant Diseases/microbiology/prevention & control ; Plant Proteins/genetics/metabolism ; },
abstract = {Nanocarrier-mediated delivery of double-stranded RNA (dsRNA) is a promising strategy for plant disease control. Our previous study has shown that the self-assembled ε-poly-l-lysine/carboxymethyl chitosan (ε-PL@CMCS) nanocarrier significantly improves the efficiency of RNA interference (RNAi) against Rhizoctonia solani AG3 TB. However, the molecular mechanisms underlying this enhancement and the potential ecological impacts on phyllosphere microbial communities remain unclear. In this study, we confirmed that dsRsGH1@ε-PL@CMCS had no adverse effects on the growth and development of plants. Transcriptome analysis revealed that DEGs were significantly enriched in 'SNARE interactions in vesicular transport' pathway. Among them, dsRsGH1@ε-PL@CMCS specifically upregulate the vesicle transport protein SEC22 in Nicotiana tabacum. Surface plasmon resonance (SPR) assay demonstrated that the dsRsGH1@ε-PL@CMCS binds to SEC22 protein with 7.6-fold higher affinity than that of the naked dsRsGH1. Silencing SEC22 in the dsRsGH1@ε-PL@CMCS treatment reduced the silencing efficiency of RsGH1 from 53.3% to 39%, confirming its essential role. Concurrently, high-throughput sequencing revealed that SIGS treatments did not disrupt bacterial community structure but increased fungal diversity and suppressed the pathogen, while enriching beneficial fungi such as Tulasnella. Our findings elucidate a molecular link between nano-bioprotectant dsRsGH1@ε-PL@CMCS-enhanced RNAi and host vesicle transport, while confirming the biocompatible and microbiome-modulating potential. This provides a dual perspective for developing efficient and sustainable RNAi-based strategies for protecting plants.},
}
MeSH Terms:
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*Nicotiana/microbiology/drug effects/genetics
*Rhizoctonia/drug effects/genetics
*Chitosan/analogs & derivatives/chemistry/pharmacology
*RNA Interference
*Microbiota/drug effects
*RNA, Double-Stranded/pharmacology
Plant Diseases/microbiology/prevention & control
Plant Proteins/genetics/metabolism
RevDate: 2026-04-25
CmpDate: 2026-04-25
Antibiotic resistance gene profiles in the gut microbiomes of Apis cerana, Apis mellifera, and Bombus terrestris.
Pesticide biochemistry and physiology, 220:107059.
The gut microbiota of honeybees has been increasingly recognized as a reservoir of antibiotic resistance genes (ARGs). However, comprehensive comparisons of ARG profiles between honeybees and bumblebees inhabiting the same environments are limited. Moreover, the diversity of mobile genetic elements (MGEs) in bee gut microbiomes and their potential role in mediating the horizontal transfer of ARGs have not yet been fully elucidated. In this study, metagenomic sequencing of 48 gut samples from farmed Apis mellifera, Apis cerana, and Bombus terrestris across four regions in China revealed 127 ARG subtypes, which collectively conferred resistance to nine major antibiotic classes. We found that A. mellifera, which carried the highest load of ARGs, concurrently harbored the greatest abundance of MGEs among the three species. Although ARG abundance varied significantly by region, no consistent geographical pattern emerged across the bee species. Importantly, strong positive correlations were detected between the abundances of ARGs and MGEs, particularly between the insertion sequence gene Tn3 and plasmid gene IncQ1. Metagenome-assembled genome analyses further confirmed the co-occurrence of ARGs (sul2, aph(3″)-Ib, and aph(6)-Id) with MGEs (Tn3 and IncQ1) across the three bee species, providing direct evidence that horizontal gene transfer mediated by MGEs contributes to the dissemination of ARGs within bee gut microbiomes. Overall, these findings highlight the critical role of the bee microbiome as a reservoir for ARGs and as a bioindicator for environmental pollutants, providing important insights into the mechanisms of ARG dissemination in ecosystems.
Additional Links: PMID-42034426
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@article {pmid42034426,
year = {2026},
author = {Zhou, N and Wei, R and Yang, S and Hu, F and Feng, Y and Zheng, H},
title = {Antibiotic resistance gene profiles in the gut microbiomes of Apis cerana, Apis mellifera, and Bombus terrestris.},
journal = {Pesticide biochemistry and physiology},
volume = {220},
number = {},
pages = {107059},
doi = {10.1016/j.pestbp.2026.107059},
pmid = {42034426},
issn = {1095-9939},
mesh = {Animals ; Bees/microbiology ; *Gastrointestinal Microbiome/genetics ; *Drug Resistance, Microbial/genetics ; Anti-Bacterial Agents/pharmacology ; Metagenome ; China ; },
abstract = {The gut microbiota of honeybees has been increasingly recognized as a reservoir of antibiotic resistance genes (ARGs). However, comprehensive comparisons of ARG profiles between honeybees and bumblebees inhabiting the same environments are limited. Moreover, the diversity of mobile genetic elements (MGEs) in bee gut microbiomes and their potential role in mediating the horizontal transfer of ARGs have not yet been fully elucidated. In this study, metagenomic sequencing of 48 gut samples from farmed Apis mellifera, Apis cerana, and Bombus terrestris across four regions in China revealed 127 ARG subtypes, which collectively conferred resistance to nine major antibiotic classes. We found that A. mellifera, which carried the highest load of ARGs, concurrently harbored the greatest abundance of MGEs among the three species. Although ARG abundance varied significantly by region, no consistent geographical pattern emerged across the bee species. Importantly, strong positive correlations were detected between the abundances of ARGs and MGEs, particularly between the insertion sequence gene Tn3 and plasmid gene IncQ1. Metagenome-assembled genome analyses further confirmed the co-occurrence of ARGs (sul2, aph(3″)-Ib, and aph(6)-Id) with MGEs (Tn3 and IncQ1) across the three bee species, providing direct evidence that horizontal gene transfer mediated by MGEs contributes to the dissemination of ARGs within bee gut microbiomes. Overall, these findings highlight the critical role of the bee microbiome as a reservoir for ARGs and as a bioindicator for environmental pollutants, providing important insights into the mechanisms of ARG dissemination in ecosystems.},
}
MeSH Terms:
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Animals
Bees/microbiology
*Gastrointestinal Microbiome/genetics
*Drug Resistance, Microbial/genetics
Anti-Bacterial Agents/pharmacology
Metagenome
China
RevDate: 2026-04-25
The island biology of the host microbiome.
Trends in microbiology pii:S0966-842X(26)00040-5 [Epub ahead of print].
Microbiomes perform critical functions for their hosts, and understanding microbiome variation is important for both basic and applied science. However, host traits alone cannot explain the entirety of microbiome variation, because, alongside host traits, microbiomes are shaped by multiple ecological processes. Researchers have thus turned to theories of island biology, conceptualising animal hosts as islands and animal microbiomes as metacommunities that assemble within and disperse between host islands. To develop realistic models, this host-as-island metaphor must be examined by explicitly comparing geological and host islands. Here, we critically examine the host-as-island metaphor by evaluating how microbiome variation is shaped by the four metacommunity processes that explain biodiversity on geological islands: local interspecies interactions, local selection, dispersal, and stochasticity. Key differences between host islands and geological islands include the complexity of microbiome transmission networks arising from host mobility and sociality and the capacity of hosts to evolve to control their microbiomes. We conclude with discussions of how eco-evolutionary dynamics differ between geological islands and host islands, and the reciprocal relevance of island biology and microbiome science.
Additional Links: PMID-42034466
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PubMed:
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@article {pmid42034466,
year = {2026},
author = {Sarkar, A and Raulo, A and Stothart, MR and Ibata, NGO and Harty, S and Metcalf, CJE and Bohannan, BJM and Bennett, GM and Carmody, RN},
title = {The island biology of the host microbiome.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.03.001},
pmid = {42034466},
issn = {1878-4380},
abstract = {Microbiomes perform critical functions for their hosts, and understanding microbiome variation is important for both basic and applied science. However, host traits alone cannot explain the entirety of microbiome variation, because, alongside host traits, microbiomes are shaped by multiple ecological processes. Researchers have thus turned to theories of island biology, conceptualising animal hosts as islands and animal microbiomes as metacommunities that assemble within and disperse between host islands. To develop realistic models, this host-as-island metaphor must be examined by explicitly comparing geological and host islands. Here, we critically examine the host-as-island metaphor by evaluating how microbiome variation is shaped by the four metacommunity processes that explain biodiversity on geological islands: local interspecies interactions, local selection, dispersal, and stochasticity. Key differences between host islands and geological islands include the complexity of microbiome transmission networks arising from host mobility and sociality and the capacity of hosts to evolve to control their microbiomes. We conclude with discussions of how eco-evolutionary dynamics differ between geological islands and host islands, and the reciprocal relevance of island biology and microbiome science.},
}
RevDate: 2026-04-25
Antibiotic treatment reveals the contributions of the gut microbiome to CLN2 disease in the central and enteric nervous system.
Scientific reports pii:10.1038/s41598-026-49850-z [Epub ahead of print].
The Neuronal Ceroid Lipofuscinoses (NCLs) are fatal inherited lysosomal storage diseases, with pronounced neuron loss in the central nervous system (CNS). Gastrointestinal issues are frequently reported by people with NCLs, although mechanisms underlying these symptoms are poorly understood. We recently demonstrated degeneration occurs within the enteric nervous system (ENS) in several NCLs. Given that the gut microbiome has been shown to be altered a CLN2 mouse model (Tpp1[R207X/R207X]) and may potentially influence both CNS and ENS pathology, we investigated the long-term impact of modulating the gut microbiome in these mice. This was done by administering a VNAM antibiotic cocktail (vancomycin, neomycin, ampicillin, and metronidazole) for 1-week post-weaning, examining its effects at disease endstage. While VNAM treatment markedly altered the gut microbiome and caused significant loss of enteric neurons in wildtype mice, it did not exacerbate key pathological parameters in either bowel or brain of Tpp1[R207X/R207X] mice. These included histomorphometric changes in the small intestine and neurodegeneration of enteric neurons, or CNS neuropathology. However, we did find evidence for moderate protective effects of VNAM upon enteric neurons in the ileum, and upon CNS microglia, but all other pathologies were unaltered in Tpp1[R207X/R207X] mice. These findings suggest that intestinal and ENS pathology is primarily driven by TPP1-deficiency rather than changes in the gut microbiome. Indeed, these alterations to the gut microbiome may occur secondary to the impact of CLN2 disease upon the bowel.
Additional Links: PMID-42034784
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PubMed:
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@article {pmid42034784,
year = {2026},
author = {Ziółkowska, EA and Nix, P and Olszowy, B and Williams, LL and Eultgen, EM and Nowacka, A and Celorrio, M and Friess, SH and Heuckeroth, RO and Cooper, JD},
title = {Antibiotic treatment reveals the contributions of the gut microbiome to CLN2 disease in the central and enteric nervous system.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-49850-z},
pmid = {42034784},
issn = {2045-2322},
support = {R01 DK129691/NH/NIH HHS/United States ; R21 NS116574/NS/NINDS NIH HHS/United States ; },
abstract = {The Neuronal Ceroid Lipofuscinoses (NCLs) are fatal inherited lysosomal storage diseases, with pronounced neuron loss in the central nervous system (CNS). Gastrointestinal issues are frequently reported by people with NCLs, although mechanisms underlying these symptoms are poorly understood. We recently demonstrated degeneration occurs within the enteric nervous system (ENS) in several NCLs. Given that the gut microbiome has been shown to be altered a CLN2 mouse model (Tpp1[R207X/R207X]) and may potentially influence both CNS and ENS pathology, we investigated the long-term impact of modulating the gut microbiome in these mice. This was done by administering a VNAM antibiotic cocktail (vancomycin, neomycin, ampicillin, and metronidazole) for 1-week post-weaning, examining its effects at disease endstage. While VNAM treatment markedly altered the gut microbiome and caused significant loss of enteric neurons in wildtype mice, it did not exacerbate key pathological parameters in either bowel or brain of Tpp1[R207X/R207X] mice. These included histomorphometric changes in the small intestine and neurodegeneration of enteric neurons, or CNS neuropathology. However, we did find evidence for moderate protective effects of VNAM upon enteric neurons in the ileum, and upon CNS microglia, but all other pathologies were unaltered in Tpp1[R207X/R207X] mice. These findings suggest that intestinal and ENS pathology is primarily driven by TPP1-deficiency rather than changes in the gut microbiome. Indeed, these alterations to the gut microbiome may occur secondary to the impact of CLN2 disease upon the bowel.},
}
RevDate: 2026-04-26
Chronic kidney disease and cognitive impairment: The role of diet and gut microbiota.
Nutrition (Burbank, Los Angeles County, Calif.), 148:113135 pii:S0899-9007(26)00044-4 [Epub ahead of print].
Several important milestones have been achieved in recent years in the area of slowing the progression of chronic kidney disease (CKD). Consequently, additional facets of reducing quality of life (QoL) in CKD patients have emerged, including progressive cognitive impairment (CI) in up to 50% of patients. Accumulating evidence suggests that gut microbiome dysregulation may promote CI in a paradigm of kidney-brain-gut axis. Systemic inflammation, oxidative stress, uremic toxins and increased intestinal permeability ("leaky gut") are key components of the kidney-brain-gut axis dysfunction. Correcting this cross-stalk through dietary changes may improve brain function and prevent further kidney damage. Beneficial nutritional guidelines include plant-based (Mediterranean style) low-protein diet, substitution of animal protein with soy isolate, ketoanalogues of essential amino acids supplementation, modification of the gut microbiota through prebiotics, probiotics, synbiotics and metabiotics. Although being a subject of debate, there are many worthwhile areas for research in kidney-brain-gut axis dysfunction. In this review, we aimed to address knowledge gaps in studies of CI in CKD patients in the context of the kidney-brain-gut axis.
Additional Links: PMID-42034942
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PubMed:
Citation:
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@article {pmid42034942,
year = {2026},
author = {Milovanova, LY and Nezhdanov, KS and Milovanova, SY and Druzhinin, DS and Zakharov, VV and Kosivtsova, OV and Braga, VI and Volkov, AV and Moiseev, SV},
title = {Chronic kidney disease and cognitive impairment: The role of diet and gut microbiota.},
journal = {Nutrition (Burbank, Los Angeles County, Calif.)},
volume = {148},
number = {},
pages = {113135},
doi = {10.1016/j.nut.2026.113135},
pmid = {42034942},
issn = {1873-1244},
abstract = {Several important milestones have been achieved in recent years in the area of slowing the progression of chronic kidney disease (CKD). Consequently, additional facets of reducing quality of life (QoL) in CKD patients have emerged, including progressive cognitive impairment (CI) in up to 50% of patients. Accumulating evidence suggests that gut microbiome dysregulation may promote CI in a paradigm of kidney-brain-gut axis. Systemic inflammation, oxidative stress, uremic toxins and increased intestinal permeability ("leaky gut") are key components of the kidney-brain-gut axis dysfunction. Correcting this cross-stalk through dietary changes may improve brain function and prevent further kidney damage. Beneficial nutritional guidelines include plant-based (Mediterranean style) low-protein diet, substitution of animal protein with soy isolate, ketoanalogues of essential amino acids supplementation, modification of the gut microbiota through prebiotics, probiotics, synbiotics and metabiotics. Although being a subject of debate, there are many worthwhile areas for research in kidney-brain-gut axis dysfunction. In this review, we aimed to address knowledge gaps in studies of CI in CKD patients in the context of the kidney-brain-gut axis.},
}
RevDate: 2026-04-26
Exploring the links between nutrition, gut microbiome, and neurodevelopmental disorders.
Nutrition (Burbank, Los Angeles County, Calif.), 148:113030 pii:S0899-9007(25)00347-8 [Epub ahead of print].
Neurodevelopmental disorders (NDDs), such as autism spectrum disorder (ASD), emerge during early childhood, affecting cognitive and behavioral health and motor development. While genetic factors contribute to the onset of ASD, recent studies highlight the significant role of environmental factors, particularly nutrition, in influencing the severity and manifestation of symptoms, primarily through the gut microbiome. This review explores how dietary imbalances, such as the consumption of ultra-processed foods, disrupt gastrointestinal health and microbiome composition, which in turn impact neurodevelopmental outcomes. It further explores the gut-brain axis and how early-life exposures, along with dietary and environmental factors, play a significant role in shaping brain development. The review concludes by underscoring the potential of a deeper understanding of these interactions to pave the way for more effective interventions aimed at improving developmental outcomes in children with ASD and other related NDDs. Key findings reveal that specific gut microbiota imbalances, such as a reduction in Bifidobacterium, are commonly associated with ASD. Additionally, dietary patterns like the Mediterranean and ketogenic diets show promise in supporting cognitive function and promoting neurodevelopment. Maternal nutrition, stress, and epigenetic factors during early life are also shown to influence brain development, contributing to gut dysbiosis, neuroinflammation, and the development of NDDs. To enhance our understanding of NDDs, future research should focus on large-scale longitudinal studies, maternal nutrition, and integrative multi-omics approaches.
Additional Links: PMID-42034943
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@article {pmid42034943,
year = {2025},
author = {Chatzinikolaou, R and Rouskas, K and Argiriou, A},
title = {Exploring the links between nutrition, gut microbiome, and neurodevelopmental disorders.},
journal = {Nutrition (Burbank, Los Angeles County, Calif.)},
volume = {148},
number = {},
pages = {113030},
doi = {10.1016/j.nut.2025.113030},
pmid = {42034943},
issn = {1873-1244},
abstract = {Neurodevelopmental disorders (NDDs), such as autism spectrum disorder (ASD), emerge during early childhood, affecting cognitive and behavioral health and motor development. While genetic factors contribute to the onset of ASD, recent studies highlight the significant role of environmental factors, particularly nutrition, in influencing the severity and manifestation of symptoms, primarily through the gut microbiome. This review explores how dietary imbalances, such as the consumption of ultra-processed foods, disrupt gastrointestinal health and microbiome composition, which in turn impact neurodevelopmental outcomes. It further explores the gut-brain axis and how early-life exposures, along with dietary and environmental factors, play a significant role in shaping brain development. The review concludes by underscoring the potential of a deeper understanding of these interactions to pave the way for more effective interventions aimed at improving developmental outcomes in children with ASD and other related NDDs. Key findings reveal that specific gut microbiota imbalances, such as a reduction in Bifidobacterium, are commonly associated with ASD. Additionally, dietary patterns like the Mediterranean and ketogenic diets show promise in supporting cognitive function and promoting neurodevelopment. Maternal nutrition, stress, and epigenetic factors during early life are also shown to influence brain development, contributing to gut dysbiosis, neuroinflammation, and the development of NDDs. To enhance our understanding of NDDs, future research should focus on large-scale longitudinal studies, maternal nutrition, and integrative multi-omics approaches.},
}
RevDate: 2026-04-26
Metagenomic profiling of Poa alpigena rhizosphere and bulk soil microbiomes across differing land-use contexts in the Qinghai lake alpine wetland.
BMC microbiology pii:10.1186/s12866-026-04999-5 [Epub ahead of print].
Additional Links: PMID-42034975
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PubMed:
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@article {pmid42034975,
year = {2026},
author = {Wang, H and Chen, Z and Qi, L and Wang, Z and Xu, D and Mao, Y and Shen, Z and Chen, K},
title = {Metagenomic profiling of Poa alpigena rhizosphere and bulk soil microbiomes across differing land-use contexts in the Qinghai lake alpine wetland.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-04999-5},
pmid = {42034975},
issn = {1471-2180},
support = {This work was supported by the Natural Science Foundation Project of Anhui Provincial Universities (No. 2022AH052150 and 2024AH051553). Research on Ecosystem Changes in the Qinghai Lake Littoral Zone Under Water Level Rise and Their Impacts on Carbon Cycle (2023-ZJ-905T).//This work was supported by the Natural Science Foundation Project of Anhui Provincial Universities (No. 2022AH052150 and 2024AH051553). Research on Ecosystem Changes in the Qinghai Lake Littoral Zone Under Water Level Rise and Their Impacts on Carbon Cycle (2023-ZJ-905T)./ ; },
}
RevDate: 2026-04-26
Organ-on-chip (OoC) and nano-biomaterials: next generation of precision oral and dental healthcare research.
Journal of nanobiotechnology pii:10.1186/s12951-026-04410-5 [Epub ahead of print].
Periodontitis and dental caries are the most widespread non-communicable oral disorders worldwide, affecting approximately 3.5 billion people worldwide. Nevertheless, existing in vitro models do not accurately emulate the intricate interactions between the oral microbiome, the host immune response, and the fluctuating physicochemical environment. This lack of physiologically realistic models makes it extremely difficult to understand disease mechanisms and to design effective therapies. While organ-on-a-chip technology has revolutionized biomedical research, its application in oral healthcare and dental precision medicine remains fragmented, often lacking the integration of functional materials necessary for precise monitoring and treatment. Herein, this review offers a comprehensive overview of the oral microenvironment, emphasizing the essential biophysical signals of the tooth surface, gingival crevice, and periodontal contact that must be replicated. We rigorously assess current oral-on-a-chip systems, pinpointing their deficiencies in replicating multi-tissue interactions and real-time monitoring. New oral-on-chip and organ-on-chip systems need to be made as a next-generation platform that combines microfluidics with advanced/ functional nanomaterials that bridge this gap. This suggested system incorporates sustainable, biodegradable, and bio- and nanomaterials with integrated nanosensors for real-time monitoring of pH and cytokines, providing a comprehensive solution for modeling oral illnesses. Our primary objective is to establish a framework for creating high-fidelity, sustained in vitro oral models that can expedite the advancement of precision oral healthcare.
Additional Links: PMID-42035068
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PubMed:
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@article {pmid42035068,
year = {2026},
author = {Wadan, AS and El-Gemaie, DSA and Bayoumi, AM and Zein, MM and El Sattar Ahmed, MA and El-Khawaga, AM and Nagy, MM},
title = {Organ-on-chip (OoC) and nano-biomaterials: next generation of precision oral and dental healthcare research.},
journal = {Journal of nanobiotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12951-026-04410-5},
pmid = {42035068},
issn = {1477-3155},
abstract = {Periodontitis and dental caries are the most widespread non-communicable oral disorders worldwide, affecting approximately 3.5 billion people worldwide. Nevertheless, existing in vitro models do not accurately emulate the intricate interactions between the oral microbiome, the host immune response, and the fluctuating physicochemical environment. This lack of physiologically realistic models makes it extremely difficult to understand disease mechanisms and to design effective therapies. While organ-on-a-chip technology has revolutionized biomedical research, its application in oral healthcare and dental precision medicine remains fragmented, often lacking the integration of functional materials necessary for precise monitoring and treatment. Herein, this review offers a comprehensive overview of the oral microenvironment, emphasizing the essential biophysical signals of the tooth surface, gingival crevice, and periodontal contact that must be replicated. We rigorously assess current oral-on-a-chip systems, pinpointing their deficiencies in replicating multi-tissue interactions and real-time monitoring. New oral-on-chip and organ-on-chip systems need to be made as a next-generation platform that combines microfluidics with advanced/ functional nanomaterials that bridge this gap. This suggested system incorporates sustainable, biodegradable, and bio- and nanomaterials with integrated nanosensors for real-time monitoring of pH and cytokines, providing a comprehensive solution for modeling oral illnesses. Our primary objective is to establish a framework for creating high-fidelity, sustained in vitro oral models that can expedite the advancement of precision oral healthcare.},
}
RevDate: 2026-04-26
Temporal dynamics shifts in multi-kingdom rumen microbiota and fermentation profiles of water buffalo under heat stress.
Animal microbiome pii:10.1186/s42523-026-00570-9 [Epub ahead of print].
Additional Links: PMID-42035169
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PubMed:
Citation:
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@article {pmid42035169,
year = {2026},
author = {Wu, Y and Li, J and Yu, J and Yang, C and Mao, S},
title = {Temporal dynamics shifts in multi-kingdom rumen microbiota and fermentation profiles of water buffalo under heat stress.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00570-9},
pmid = {42035169},
issn = {2524-4671},
support = {32361143788//National Natural Science Foundation of China/ ; },
}
RevDate: 2026-04-26
CmpDate: 2026-04-26
Biomimetic nanovesicles and nanotechnology for oral and maxillofacial diseases.
Discover nano, 21(1):.
Oral and maxillofacial diseases, such as dental caries, periodontal disease, and tissue defects, demonstrate limited therapeutic effect due to the oral cavity's complex microecological environment, intractable chronic inflammation, and the challenge of regenerating dental and periodontal tissues. Biomimetic nanovesicles (BNVs), including extracellular vesicles (EVs) and artificial nanovesicles (ANVs), play a beneficial therapeutic role in these diseases. BNVs are capable of delivering a variety of therapeutic agents, including RNAs, proteins, drugs, and nanoparticles, with their efficiency, specificity, and safety enhanced by nanotechnological modification and engineering. This review provides a comprehensive overview of BNV classification and characterization, summarizes their functional advantages in disease treatment, and highlights their applications in oral and maxillofacial disorders, particularly in microbiome modulation, immunoinflammatory regulation, and tissue regeneration. The opportunities and challenges of translating BNVs into clinical practice are also assessed.
Additional Links: PMID-42035387
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@article {pmid42035387,
year = {2026},
author = {Sun, J and Tang, S and Yan, J and Wang, J and Bai, R and Wang, X and Han, B and Yu, T},
title = {Biomimetic nanovesicles and nanotechnology for oral and maxillofacial diseases.},
journal = {Discover nano},
volume = {21},
number = {1},
pages = {},
pmid = {42035387},
issn = {2731-9229},
support = {2024YFC2510702//National Key Research and Development Program of China/ ; 2022YFA1206100//National Key Research and Development Program of China/ ; U21A2055//National Natural Science Foundation of China/ ; 52373123//National Natural Science Foundation of China/ ; Z211100002921066//Beijing Municipal Science Technology Commission/ ; F252067//Beijing Natural Science Foundation/ ; BJPSTP-2025-01//Beijing Physician Scientist Training Project/ ; },
abstract = {Oral and maxillofacial diseases, such as dental caries, periodontal disease, and tissue defects, demonstrate limited therapeutic effect due to the oral cavity's complex microecological environment, intractable chronic inflammation, and the challenge of regenerating dental and periodontal tissues. Biomimetic nanovesicles (BNVs), including extracellular vesicles (EVs) and artificial nanovesicles (ANVs), play a beneficial therapeutic role in these diseases. BNVs are capable of delivering a variety of therapeutic agents, including RNAs, proteins, drugs, and nanoparticles, with their efficiency, specificity, and safety enhanced by nanotechnological modification and engineering. This review provides a comprehensive overview of BNV classification and characterization, summarizes their functional advantages in disease treatment, and highlights their applications in oral and maxillofacial disorders, particularly in microbiome modulation, immunoinflammatory regulation, and tissue regeneration. The opportunities and challenges of translating BNVs into clinical practice are also assessed.},
}
RevDate: 2026-04-26
Integrative multi-kingdom gut microbiome analysis uncovers clinical signatures of major depressive disorder.
Journal of affective disorders pii:S0165-0327(26)00710-X [Epub ahead of print].
BACKGROUND: Accumulating evidence indicates that gut microbiome is significantly altered in major depressive disorder (MDD). However, most studies have focused on bacteria, while the functional and ecological contributions of eukaryotes, archaea, and viruses in MDD remain poorly understood.
METHODS: Fecal samples were collected from 121 first-episode, drug-naïve young adults with MDD and 117 healthy controls (HC) with matched demographic characteristics for shotgun metagenomic sequencing. Clinical data included the Hamilton Depression Scale (HAMD) and the MATRICS Consensus Cognitive Battery (MCCB). We systematically explored the multi-kingdom gut microbiome, functional genes, and metabolic pathways in MDD and their clinical associations, further assessing their diagnostic potential via machine learning.
RESULTS: MDD patients showed significant alterations in multi-kingdom microbiota diversity, accompanied by coordinated diversity relationships across microbial kingdoms relative to HC. In addition, we further identified 19 bacterial, 16 eukaryotic, 15 archaeal, and 10 viral species, as well as 22 functional genes and 32 metabolic pathways, that differed between groups. Importantly, five bacterial and four viral species were significantly associated with cognitive function, such as a positive correlation between Bifidobacterium pseudocatenulatum and attention/vigilance in MDD. Finally, validation demonstrated that a Random Forest model integrating multi-kingdom microbiota and functional features achieved superior diagnostic performance, significantly outperforming models based solely on bacterial features.
CONCLUSION: This study revealed extensive multi-kingdom microbial dysbiosis in MDD, providing deeper insight into disease-associated ecological disruption and highlighting the potential of microbial markers for enhancing clinical auxiliary diagnosis.
Additional Links: PMID-42035799
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PubMed:
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@article {pmid42035799,
year = {2026},
author = {Chen, S and Zhu, B and Lu, X and Huang, Y and Wang, S and Wang, W and Chen, G and Wu, X and Zhou, J and Wu, F and Wu, K},
title = {Integrative multi-kingdom gut microbiome analysis uncovers clinical signatures of major depressive disorder.},
journal = {Journal of affective disorders},
volume = {},
number = {},
pages = {121858},
doi = {10.1016/j.jad.2026.121858},
pmid = {42035799},
issn = {1573-2517},
abstract = {BACKGROUND: Accumulating evidence indicates that gut microbiome is significantly altered in major depressive disorder (MDD). However, most studies have focused on bacteria, while the functional and ecological contributions of eukaryotes, archaea, and viruses in MDD remain poorly understood.
METHODS: Fecal samples were collected from 121 first-episode, drug-naïve young adults with MDD and 117 healthy controls (HC) with matched demographic characteristics for shotgun metagenomic sequencing. Clinical data included the Hamilton Depression Scale (HAMD) and the MATRICS Consensus Cognitive Battery (MCCB). We systematically explored the multi-kingdom gut microbiome, functional genes, and metabolic pathways in MDD and their clinical associations, further assessing their diagnostic potential via machine learning.
RESULTS: MDD patients showed significant alterations in multi-kingdom microbiota diversity, accompanied by coordinated diversity relationships across microbial kingdoms relative to HC. In addition, we further identified 19 bacterial, 16 eukaryotic, 15 archaeal, and 10 viral species, as well as 22 functional genes and 32 metabolic pathways, that differed between groups. Importantly, five bacterial and four viral species were significantly associated with cognitive function, such as a positive correlation between Bifidobacterium pseudocatenulatum and attention/vigilance in MDD. Finally, validation demonstrated that a Random Forest model integrating multi-kingdom microbiota and functional features achieved superior diagnostic performance, significantly outperforming models based solely on bacterial features.
CONCLUSION: This study revealed extensive multi-kingdom microbial dysbiosis in MDD, providing deeper insight into disease-associated ecological disruption and highlighting the potential of microbial markers for enhancing clinical auxiliary diagnosis.},
}
RevDate: 2026-04-26
Integrated Multi-Omics Reveals Synergistic Hepatotoxicity of Ethanol and PFOS Co-Exposure.
Chemico-biological interactions pii:S0009-2797(26)00209-7 [Epub ahead of print].
Alcohol-associated liver disease (ALD) and exposure to per- and polyfluoroalkyl substances (PFAS) share key mechanisms of hepatotoxicity, yet their combined effects remain poorly characterized. We evaluated the impact of concurrent ethanol and perfluorooctanesulfonic acid (PFOS) exposure using a murine Lieber-DeCarli model characterized via multi-omic, spatial lipidomic, and metagenomic analyses. Exposure to PFOS resulted in rapid weight loss, while co-exposure led to decreased survival and pronounced hepatomegaly exceeding the effects of either exposure alone despite reduced cumulative ethanol intake. Histological analysis revealed enhanced hepatocellular injury with combined macrovesicular and microvesicular steatosis, consistent with impaired lipid handling and mitochondrial dysfunction. Transcriptomic and metabolomic profiling demonstrated disruption of xenobiotic metabolism, fatty acid β-oxidation, mitochondrial function, and bile acid transport, with PFOS acting as a dominant driver of metabolic stress and ethanol amplifying injury-related responses. Spatial lipidomics revealed hepatocyte-scale remodeling of membrane phospholipids, characterized by increased phosphatidic acid and depletion of phosphatidylinositol and phosphatidylserine under PFOS-containing conditions. Plasma metabolomics indicated systemic metabolic disturbance, including altered amino acid and redox pathways and depletion of microbiome-derived indole metabolites. Metagenomic analysis revealed reduced bacterial load and severe dysbiosis characterized by loss of commensal anaerobes, expansion of opportunistic taxa, and decreased microbial biosynthetic capacity. These findings indicate that PFOS increases susceptibility to alcohol-induced liver injury potentially through coordinated disruption of hepatic metabolism and gut-liver crosstalk, highlighting environmental PFAS exposure as a potential modifier of ALD severity.
Additional Links: PMID-42036057
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@article {pmid42036057,
year = {2026},
author = {Stem, AD and Alayyoub, M and Aalizadeh, R and Nikolopoulou, V and Lisgara, A and Shvartsman, A and Anitha, M and Patterson, A and Coble, R and Rushing, B and Sumner, S and Vasiliou, V},
title = {Integrated Multi-Omics Reveals Synergistic Hepatotoxicity of Ethanol and PFOS Co-Exposure.},
journal = {Chemico-biological interactions},
volume = {},
number = {},
pages = {112101},
doi = {10.1016/j.cbi.2026.112101},
pmid = {42036057},
issn = {1872-7786},
abstract = {Alcohol-associated liver disease (ALD) and exposure to per- and polyfluoroalkyl substances (PFAS) share key mechanisms of hepatotoxicity, yet their combined effects remain poorly characterized. We evaluated the impact of concurrent ethanol and perfluorooctanesulfonic acid (PFOS) exposure using a murine Lieber-DeCarli model characterized via multi-omic, spatial lipidomic, and metagenomic analyses. Exposure to PFOS resulted in rapid weight loss, while co-exposure led to decreased survival and pronounced hepatomegaly exceeding the effects of either exposure alone despite reduced cumulative ethanol intake. Histological analysis revealed enhanced hepatocellular injury with combined macrovesicular and microvesicular steatosis, consistent with impaired lipid handling and mitochondrial dysfunction. Transcriptomic and metabolomic profiling demonstrated disruption of xenobiotic metabolism, fatty acid β-oxidation, mitochondrial function, and bile acid transport, with PFOS acting as a dominant driver of metabolic stress and ethanol amplifying injury-related responses. Spatial lipidomics revealed hepatocyte-scale remodeling of membrane phospholipids, characterized by increased phosphatidic acid and depletion of phosphatidylinositol and phosphatidylserine under PFOS-containing conditions. Plasma metabolomics indicated systemic metabolic disturbance, including altered amino acid and redox pathways and depletion of microbiome-derived indole metabolites. Metagenomic analysis revealed reduced bacterial load and severe dysbiosis characterized by loss of commensal anaerobes, expansion of opportunistic taxa, and decreased microbial biosynthetic capacity. These findings indicate that PFOS increases susceptibility to alcohol-induced liver injury potentially through coordinated disruption of hepatic metabolism and gut-liver crosstalk, highlighting environmental PFAS exposure as a potential modifier of ALD severity.},
}
RevDate: 2026-04-26
CmpDate: 2026-04-26
Clearing the Noise: Seasonal Dynamics of Endophytic Bacteria in Fagus sylvatica Leaves Revealed by Application of PNA Clamps.
Physiologia plantarum, 178(3):e70897.
The characterization of the seasonal dynamics of endophytic bacteria in beech leaves can be hindered by co-amplification of chloroplast and mitochondrial plant DNA. This study applies established peptide nucleic acid (PNA) clamps to suppress host-derived amplification while resolving bacterial succession across the vegetative season. Chloroplast- and mitochondrion-specific PNAs inverted the proportion of host to bacterial reads, enabled the recovery of bacterial sequence variants, and increased alpha diversity accordingly. Beta-diversity analyses showed that, once host contamination was removed, samples displayed a clear seasonal trajectory. Early-season leaves contained high abundances of Pseudomonas together with taxa likely introduced through plant-insect-microbe interactions. As leaves matured, the microbiome shifted toward a more stable composition dominated by well-established genera. The transition from early transient taxa to the later enrichment of phyllosphere-adapted and nutrient-cycling genera demonstrates that beech leaves host a temporally structured microbiome shaped by leaf development and seasonal environmental stress.
Additional Links: PMID-42036304
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@article {pmid42036304,
year = {2026},
author = {Giubilei, I and Turco, S and Cardacino, A and Mahawar, L and Albrectsen, BR and Mazzaglia, A},
title = {Clearing the Noise: Seasonal Dynamics of Endophytic Bacteria in Fagus sylvatica Leaves Revealed by Application of PNA Clamps.},
journal = {Physiologia plantarum},
volume = {178},
number = {3},
pages = {e70897},
doi = {10.1111/ppl.70897},
pmid = {42036304},
issn = {1399-3054},
support = {CN00000022//Agritech National Research Center/ ; },
mesh = {*Plant Leaves/microbiology ; *Fagus/microbiology ; Seasons ; *Endophytes/physiology/genetics ; *Bacteria/genetics/classification ; Microbiota ; },
abstract = {The characterization of the seasonal dynamics of endophytic bacteria in beech leaves can be hindered by co-amplification of chloroplast and mitochondrial plant DNA. This study applies established peptide nucleic acid (PNA) clamps to suppress host-derived amplification while resolving bacterial succession across the vegetative season. Chloroplast- and mitochondrion-specific PNAs inverted the proportion of host to bacterial reads, enabled the recovery of bacterial sequence variants, and increased alpha diversity accordingly. Beta-diversity analyses showed that, once host contamination was removed, samples displayed a clear seasonal trajectory. Early-season leaves contained high abundances of Pseudomonas together with taxa likely introduced through plant-insect-microbe interactions. As leaves matured, the microbiome shifted toward a more stable composition dominated by well-established genera. The transition from early transient taxa to the later enrichment of phyllosphere-adapted and nutrient-cycling genera demonstrates that beech leaves host a temporally structured microbiome shaped by leaf development and seasonal environmental stress.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Plant Leaves/microbiology
*Fagus/microbiology
Seasons
*Endophytes/physiology/genetics
*Bacteria/genetics/classification
Microbiota
RevDate: 2026-04-26
Metagenomic insights into urolithin formation from rambutan rind extract by rat faecal-derived microbiome.
Applied microbiology and biotechnology pii:10.1007/s00253-026-13841-x [Epub ahead of print].
Ellagitannins and ellagic acid are microbially converted into urolithins, metabolites associated with antioxidant, anti-inflammatory, and mitochondrial-related activities. Although several human-derived urolithin-producing strains and their associated enzymes have recently been characterised, the diversity of microbial strategies across host systems remains poorly understood. This study investigated urolithin production in the Sprague-Dawley rat faecal-derived microbial communities supplemented with rambutan rind extract, an ellagitannin-rich agricultural by-product containing 35-40% geraniin. Rambutan rind extract supplementation was associated with reduced isobutyric acid levels at study endpoint. Ex vivo anaerobic fermentation of hydrolysed rambutan rind extract (113 µM ellagic acid equivalent) resulted in the formation of urolithin C (9.4 ± 0.6 µM) and Isourolithin A (12.5 ± 0.6 µM) by day 9. Shotgun metagenomics analysis revealed very low relative abundance of Actinobacteria (< 0.009%), despite this phylum encompassing most previously characterised urolithin-producing taxa. Canonical ellagic acid degradation genes and the MetaCyc EA degradation pathway were not detected. Comparative pathway analysis indicated overlap in general metabolic pathways with Ellagibacter isourolithinifaciens DSM 104140[T] reflecting shared metabolic frameworks rather than conserved urolithin biosynthetic pathways, with highly divergent homologues (Eadh1, Eadh2, Eadh3, and Ucdh). Together, these findings demonstrate that rambutan rind extract can support urolithin formation in rat faecal-derived microbial consortia and highlight functional associations consistent with alternative or yet-uncharacterised microbial strategies for ellagitannin biotransformation. These findings support a discovery-driven framework for investigating urolithin biotransformation in non-human gut microbiomes using ellagitannin-rich agricultural substrates. KEY POINTS: • Rambutan rind extract supports urolithin formation in rat-derived gut microbiota. • Substrate concentration influences urolithin production under ex vivo conditions. • Rat gut microbiota shows homologues' divergence in urolithin-associated proteins.
Additional Links: PMID-42036496
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@article {pmid42036496,
year = {2026},
author = {Tow, WK and Teh, CSJ and Ooi, CW and Lee, RFS and Krishnasamy, M and Palanisamy, UD and Sundralingam, U},
title = {Metagenomic insights into urolithin formation from rambutan rind extract by rat faecal-derived microbiome.},
journal = {Applied microbiology and biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00253-026-13841-x},
pmid = {42036496},
issn = {1432-0614},
abstract = {Ellagitannins and ellagic acid are microbially converted into urolithins, metabolites associated with antioxidant, anti-inflammatory, and mitochondrial-related activities. Although several human-derived urolithin-producing strains and their associated enzymes have recently been characterised, the diversity of microbial strategies across host systems remains poorly understood. This study investigated urolithin production in the Sprague-Dawley rat faecal-derived microbial communities supplemented with rambutan rind extract, an ellagitannin-rich agricultural by-product containing 35-40% geraniin. Rambutan rind extract supplementation was associated with reduced isobutyric acid levels at study endpoint. Ex vivo anaerobic fermentation of hydrolysed rambutan rind extract (113 µM ellagic acid equivalent) resulted in the formation of urolithin C (9.4 ± 0.6 µM) and Isourolithin A (12.5 ± 0.6 µM) by day 9. Shotgun metagenomics analysis revealed very low relative abundance of Actinobacteria (< 0.009%), despite this phylum encompassing most previously characterised urolithin-producing taxa. Canonical ellagic acid degradation genes and the MetaCyc EA degradation pathway were not detected. Comparative pathway analysis indicated overlap in general metabolic pathways with Ellagibacter isourolithinifaciens DSM 104140[T] reflecting shared metabolic frameworks rather than conserved urolithin biosynthetic pathways, with highly divergent homologues (Eadh1, Eadh2, Eadh3, and Ucdh). Together, these findings demonstrate that rambutan rind extract can support urolithin formation in rat faecal-derived microbial consortia and highlight functional associations consistent with alternative or yet-uncharacterised microbial strategies for ellagitannin biotransformation. These findings support a discovery-driven framework for investigating urolithin biotransformation in non-human gut microbiomes using ellagitannin-rich agricultural substrates. KEY POINTS: • Rambutan rind extract supports urolithin formation in rat-derived gut microbiota. • Substrate concentration influences urolithin production under ex vivo conditions. • Rat gut microbiota shows homologues' divergence in urolithin-associated proteins.},
}
RevDate: 2026-04-26
Itching to know: the Microbiome, Allergic Disease, and Antimicrobial Chemicals.
Current environmental health reports, 13(1):.
Additional Links: PMID-42036511
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Citation:
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@article {pmid42036511,
year = {2026},
author = {Laue, HE and Fleury, ES and Romano, ME and Hoen, AG and Braun, JM},
title = {Itching to know: the Microbiome, Allergic Disease, and Antimicrobial Chemicals.},
journal = {Current environmental health reports},
volume = {13},
number = {1},
pages = {},
pmid = {42036511},
issn = {2196-5412},
support = {K99/R00 ES034086/ES/NIEHS NIH HHS/United States ; R03 ES035140/ES/NIEHS NIH HHS/United States ; R01 ES032836/ES/NIEHS NIH HHS/United States ; },
}
RevDate: 2026-04-26
CmpDate: 2026-04-27
Antibiotic-induced Microbiome Depletion Selectively Reduces Baseline Hypothalamic Oxytocin Signaling without Affecting MDMA-induced Oxytocin Response in Rats.
Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology, 24(2):402-407.
OBJECTIVE: To determine whether antibiotic-induced microbiome depletion influences baseline or 3,4-methylenedioxymethamphetamine (MDMA)-induced oxytocin signaling in rats.
METHODS: Male Wistar rats received broad-spectrum antibiotics (ABX) or water for 7 days, followed by a single oral administration of MDMA (30 mg/kg). Plasma oxytocin levels were measured by ELISA, and oxytocin-immunoreactivity in the paraventricular (PVN) and supraoptic (SON) nuclei were quantified by immunofluorescence.
RESULTS: ABX treatment induced marked cecal enlargement without affecting body weight, confirming microbiome disruption while maintaining systemic stability. Peripheral oxytocin concentrations were unchanged; however, baseline central oxytocin expression in both the PVN and SON was significantly reduced after ABX treatment. MDMA increased central oxytocin expression, and this response was not significantly altered by microbiome depletion. Similarly, MDMA-induced peripheral oxytocin levels did not differ between control and ABX-treated rats.
CONCLUSION: Antibiotic-induced microbiome depletion selectively attenuates baseline central oxytocin signaling while leaving peripheral oxytocin regulation intact. In contrast, MDMA-induced oxytocin responses in both the brain and circulation are preserved despite microbiome disruption. These findings suggest that gut microbiota contribute to central oxytocin homeostasis under basal conditions but are not essential for acute MDMA-induced oxytocin activation.
Additional Links: PMID-42036749
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PubMed:
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@article {pmid42036749,
year = {2026},
author = {Yue, Y and Cai, Y and Murayama, R and Ding, X and Wan, X and Liu, G and Hashimoto, H and Anzai, N and Hashimoto, K},
title = {Antibiotic-induced Microbiome Depletion Selectively Reduces Baseline Hypothalamic Oxytocin Signaling without Affecting MDMA-induced Oxytocin Response in Rats.},
journal = {Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology},
volume = {24},
number = {2},
pages = {402-407},
doi = {10.9758/cpn.25.1381},
pmid = {42036749},
issn = {1738-1088},
abstract = {OBJECTIVE: To determine whether antibiotic-induced microbiome depletion influences baseline or 3,4-methylenedioxymethamphetamine (MDMA)-induced oxytocin signaling in rats.
METHODS: Male Wistar rats received broad-spectrum antibiotics (ABX) or water for 7 days, followed by a single oral administration of MDMA (30 mg/kg). Plasma oxytocin levels were measured by ELISA, and oxytocin-immunoreactivity in the paraventricular (PVN) and supraoptic (SON) nuclei were quantified by immunofluorescence.
RESULTS: ABX treatment induced marked cecal enlargement without affecting body weight, confirming microbiome disruption while maintaining systemic stability. Peripheral oxytocin concentrations were unchanged; however, baseline central oxytocin expression in both the PVN and SON was significantly reduced after ABX treatment. MDMA increased central oxytocin expression, and this response was not significantly altered by microbiome depletion. Similarly, MDMA-induced peripheral oxytocin levels did not differ between control and ABX-treated rats.
CONCLUSION: Antibiotic-induced microbiome depletion selectively attenuates baseline central oxytocin signaling while leaving peripheral oxytocin regulation intact. In contrast, MDMA-induced oxytocin responses in both the brain and circulation are preserved despite microbiome disruption. These findings suggest that gut microbiota contribute to central oxytocin homeostasis under basal conditions but are not essential for acute MDMA-induced oxytocin activation.},
}
RevDate: 2026-04-27
The mosquito midgut harbors stable bacteria that enhance host hemolymph immunity.
Pest management science [Epub ahead of print].
BACKGROUND: Mosquito symbionts have the potential to control mosquito-borne diseases by reducing vector competence through direct or indirect interactions with pathogens. However, the microbiome of field-collected mosquitoes is often unstable, and it remains unclear whether certain symbiont species can both colonize their hosts stably and modulate host immunity. In this study, we collected second-instar Aedes albopictus and Culex pipiens larvae from field water sources in Hong Kong and reared them to fourth-instar larvae and adults under laboratory conditions. We investigated microbiome changes from water to mosquito midguts and identified stable bacterial species (≥ 0.01% relative abundance) across mosquito stages using 16S rRNA-based bacteriome analysis. We further isolated symbiotic bacteria on culture plates, screened stable species by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, and evaluated their functional potential.
RESULTS: Mosquito microbiomes were influenced by water source, developmental stage, and host species. Taxonomically, Proteobacteria and Bacteroidetes dominated mosquito midguts. Each mosquito species maintained four stable bacterial species (≥ 0.01% relative abundance) throughout development. We confirmed culturable Comamonas thiooxydans as a stable symbiont of Culex pipiens and Vibrionimonas magnilacihabitans in Aedes albopictus. Genomic predictions suggested their involvement in antimicrobial peptide synthesis. Functionally, these bacteria enhanced host survival and increased hemolymph antimicrobial activity against Erwinia carotovora subspecies carotovora 15 (ECC15), but not across mosquito species.
CONCLUSION: Our findings suggest that mosquitoes harbor generally unstable bacterial communities with only a few species-specific stable symbionts, which may contribute to host survival and immune function. © 2026 Society of Chemical Industry.
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@article {pmid42036782,
year = {2026},
author = {Song, B and Zeb, J},
title = {The mosquito midgut harbors stable bacteria that enhance host hemolymph immunity.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.70720},
pmid = {42036782},
issn = {1526-4998},
support = {//City University of Hong Kong and the University of Hong Kong./ ; },
abstract = {BACKGROUND: Mosquito symbionts have the potential to control mosquito-borne diseases by reducing vector competence through direct or indirect interactions with pathogens. However, the microbiome of field-collected mosquitoes is often unstable, and it remains unclear whether certain symbiont species can both colonize their hosts stably and modulate host immunity. In this study, we collected second-instar Aedes albopictus and Culex pipiens larvae from field water sources in Hong Kong and reared them to fourth-instar larvae and adults under laboratory conditions. We investigated microbiome changes from water to mosquito midguts and identified stable bacterial species (≥ 0.01% relative abundance) across mosquito stages using 16S rRNA-based bacteriome analysis. We further isolated symbiotic bacteria on culture plates, screened stable species by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, and evaluated their functional potential.
RESULTS: Mosquito microbiomes were influenced by water source, developmental stage, and host species. Taxonomically, Proteobacteria and Bacteroidetes dominated mosquito midguts. Each mosquito species maintained four stable bacterial species (≥ 0.01% relative abundance) throughout development. We confirmed culturable Comamonas thiooxydans as a stable symbiont of Culex pipiens and Vibrionimonas magnilacihabitans in Aedes albopictus. Genomic predictions suggested their involvement in antimicrobial peptide synthesis. Functionally, these bacteria enhanced host survival and increased hemolymph antimicrobial activity against Erwinia carotovora subspecies carotovora 15 (ECC15), but not across mosquito species.
CONCLUSION: Our findings suggest that mosquitoes harbor generally unstable bacterial communities with only a few species-specific stable symbionts, which may contribute to host survival and immune function. © 2026 Society of Chemical Industry.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
A Bait-and-Switch Strategy Links Phenotypes to Genes Coding for Polymer-Degrading Enzymes in Intact Microbiomes.
Microbial biotechnology, 19(4):e70359.
Natural microbial communities, with their vast diversity and complexity, are among the richest sources of untapped novel enzymes. Identifying novel enzymes can be challenging because microbiomes often lack clear, measurable phenotypes, unlike laboratory cultures where enzymatic activity can be linked to genetic elements. These constraints have left much of the functional diversity within microbiomes inaccessible to enzyme discovery efforts. Here, we present a genotype/phenotype association framework directly on microbial communities for enzyme discovery. For this, we developed a 'bait-and-switch' treatment strategy that generates measurable dual phenotypes directly within intact microbiomes. Using soil microbiomes as a test system, we applied chitin-rich compost as 'bait' to enrich chitin-degrading organisms, followed by glucose addition to functionally 'switch' the community. This treatment produced a distinct phenotypic signature: prevalence of known chitin degradation genes increases during the bait phase, and their transcripts are rapidly downregulated during the switch phase. By performing hypothesis-free association analysis of protein domains with this dual phenotype, we identified the glycoside hydrolase 18 as the most significantly associated protein domain. Experimental validation confirmed chitinase activity in 63% of tested enzymes, including candidates from unculturable bacteria and those with previously uncharacterized domain architectures. This species-independent, reference-free approach to discover novel enzymes has broad applications in microbiome engineering, biopolymer processing and systems biology, offering a generalizable strategy for functional gene discovery in complex microbial systems.
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PubMed:
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@article {pmid42036837,
year = {2026},
author = {Yancey, CE and Brumfield, KD and Buss, JA and Colwell, RR and Ettwiller, L},
title = {A Bait-and-Switch Strategy Links Phenotypes to Genes Coding for Polymer-Degrading Enzymes in Intact Microbiomes.},
journal = {Microbial biotechnology},
volume = {19},
number = {4},
pages = {e70359},
doi = {10.1111/1751-7915.70359},
pmid = {42036837},
issn = {1751-7915},
support = {//New England Biolabs/ ; OCE1839171//National Science Foundation/ ; CCF1918749//National Science Foundation/ ; CBET1751854//National Science Foundation/ ; R01ES030317A/ES/NIEHS NIH HHS/United States ; 80NSSC20K0814/NASA/NASA/United States ; 80NSSC22K1044/NASA/NASA/United States ; },
mesh = {*Microbiota ; *Chitin/metabolism ; Soil Microbiology ; *Bacteria/enzymology/genetics/classification ; Phenotype ; Chitinases/genetics/metabolism ; Genetic Association Studies ; },
abstract = {Natural microbial communities, with their vast diversity and complexity, are among the richest sources of untapped novel enzymes. Identifying novel enzymes can be challenging because microbiomes often lack clear, measurable phenotypes, unlike laboratory cultures where enzymatic activity can be linked to genetic elements. These constraints have left much of the functional diversity within microbiomes inaccessible to enzyme discovery efforts. Here, we present a genotype/phenotype association framework directly on microbial communities for enzyme discovery. For this, we developed a 'bait-and-switch' treatment strategy that generates measurable dual phenotypes directly within intact microbiomes. Using soil microbiomes as a test system, we applied chitin-rich compost as 'bait' to enrich chitin-degrading organisms, followed by glucose addition to functionally 'switch' the community. This treatment produced a distinct phenotypic signature: prevalence of known chitin degradation genes increases during the bait phase, and their transcripts are rapidly downregulated during the switch phase. By performing hypothesis-free association analysis of protein domains with this dual phenotype, we identified the glycoside hydrolase 18 as the most significantly associated protein domain. Experimental validation confirmed chitinase activity in 63% of tested enzymes, including candidates from unculturable bacteria and those with previously uncharacterized domain architectures. This species-independent, reference-free approach to discover novel enzymes has broad applications in microbiome engineering, biopolymer processing and systems biology, offering a generalizable strategy for functional gene discovery in complex microbial systems.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Microbiota
*Chitin/metabolism
Soil Microbiology
*Bacteria/enzymology/genetics/classification
Phenotype
Chitinases/genetics/metabolism
Genetic Association Studies
RevDate: 2026-04-27
Oral PHGG ameliorates atopic dermatitis-like dermatitis with concurrent modulation of colonic IgA and cecal microbiota: implications for the gut-skin axis.
Journal of the science of food and agriculture [Epub ahead of print].
BACKGROUND: Atopic dermatitis (AD) is increasingly recognized as a systemic inflammatory disorder linked to intestinal immune and microbiome dysregulation. However, whether dietary galactomannan fibers can mitigate AD through coordinated modulation of the gut-skin axis remains unexplored. This study investigated the anti-atopic potential of orally administered partially hydrolyzed guar gum (PHGG), a low-viscosity, fermentable galactomannan enriched in low-mass oligosaccharides (mannose/galactose ratio of 1.87).
RESULTS: In TNF-α/IFN-γ-stimulated HaCaT keratinocytes, PHGG (100-400 μg mL[-1]) suppressed IL-6, IL-8, and MCP-1 secretion and down-regulated AD-relevant mediators, including TARC, MDC, RANTES, and TSLP. In TNF-α-challenged Caco-2 cells, PHGG reduced IL-8 and MCP-1 and partially restored barrier-associated transcripts (TJP1, TJP2, OCLN, CLDN1) and MUC2. In 2,4-dinitrochlorobenzene (DNCB)-induced AD BALB/c mice, oral PHGG (100-400 mg kg[-1] d[-1]) attenuated lesion severity, epidermal hyperplasia, collagen loss, and mast cell infiltration without adverse effects on body weight or organ weights. PHGG reduced circulating immunoglobulins and inflammatory cytokines, suppressed skin type 2 helper T-cell (Th2)-associated mediators, and restored colonic immune homeostasis, as evidenced by increased immunoglobulin A (IgA) and decreased interleukin 1 beta (IL-1β) and IL-6. Cecal 16S rRNA profiling revealed that PHGG shifted dysbiotic microbial signatures toward fiber-responsive Bacteroidales lineages (e.g., Muribaculaceae, Alistipes, Rikenellaceae) and partially normalized community structure in beta-diversity analyses.
CONCLUSION: These findings demonstrate that oligosaccharide-enriched PHGG ameliorates AD-like inflammation through concurrent modulation of cutaneous immune responses, colonic mucosal immunity, and gut microbial community structure, supporting a gut-skin axis mechanism. Future studies quantifying microbial metabolites are warranted to establish causal mediators of gut-to-skin signaling. © 2026 The Author(s). Journal of the Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
Additional Links: PMID-42036885
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@article {pmid42036885,
year = {2026},
author = {Kakooza, D and Yu, H and Jeong, J and Shin, JC and Kim, WJ and Moon, SK and Kim, H},
title = {Oral PHGG ameliorates atopic dermatitis-like dermatitis with concurrent modulation of colonic IgA and cecal microbiota: implications for the gut-skin axis.},
journal = {Journal of the science of food and agriculture},
volume = {},
number = {},
pages = {},
doi = {10.1002/jsfa.70676},
pmid = {42036885},
issn = {1097-0010},
support = {RS-2026-25497299//National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT)/ ; 2018R1A6A1A03025159//Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education/ ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) is increasingly recognized as a systemic inflammatory disorder linked to intestinal immune and microbiome dysregulation. However, whether dietary galactomannan fibers can mitigate AD through coordinated modulation of the gut-skin axis remains unexplored. This study investigated the anti-atopic potential of orally administered partially hydrolyzed guar gum (PHGG), a low-viscosity, fermentable galactomannan enriched in low-mass oligosaccharides (mannose/galactose ratio of 1.87).
RESULTS: In TNF-α/IFN-γ-stimulated HaCaT keratinocytes, PHGG (100-400 μg mL[-1]) suppressed IL-6, IL-8, and MCP-1 secretion and down-regulated AD-relevant mediators, including TARC, MDC, RANTES, and TSLP. In TNF-α-challenged Caco-2 cells, PHGG reduced IL-8 and MCP-1 and partially restored barrier-associated transcripts (TJP1, TJP2, OCLN, CLDN1) and MUC2. In 2,4-dinitrochlorobenzene (DNCB)-induced AD BALB/c mice, oral PHGG (100-400 mg kg[-1] d[-1]) attenuated lesion severity, epidermal hyperplasia, collagen loss, and mast cell infiltration without adverse effects on body weight or organ weights. PHGG reduced circulating immunoglobulins and inflammatory cytokines, suppressed skin type 2 helper T-cell (Th2)-associated mediators, and restored colonic immune homeostasis, as evidenced by increased immunoglobulin A (IgA) and decreased interleukin 1 beta (IL-1β) and IL-6. Cecal 16S rRNA profiling revealed that PHGG shifted dysbiotic microbial signatures toward fiber-responsive Bacteroidales lineages (e.g., Muribaculaceae, Alistipes, Rikenellaceae) and partially normalized community structure in beta-diversity analyses.
CONCLUSION: These findings demonstrate that oligosaccharide-enriched PHGG ameliorates AD-like inflammation through concurrent modulation of cutaneous immune responses, colonic mucosal immunity, and gut microbial community structure, supporting a gut-skin axis mechanism. Future studies quantifying microbial metabolites are warranted to establish causal mediators of gut-to-skin signaling. © 2026 The Author(s). Journal of the Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.},
}
RevDate: 2026-04-27
Metal-organic frameworks for pesticide remediation: From adsorption and photocatalysis to health-relevant risk reduction.
Pest management science [Epub ahead of print].
Conventional remediation strategies implicitly assume that efficient pollutant removal equates to effective health-risk mitigation; however, growing epidemiological and microbiome evidence challenges this assumption, particularly for pesticide exposure. Accumulating studies demonstrate that pesticide residues and their transformation products can disrupt gut microbial homeostasis and metabolic regulation, indicating that removal efficiency alone is insufficient to evaluate remediation success. Against this backdrop, this review advances a risk-oriented paradigm for pesticide remediation by redefining metal-organic frameworks (MOFs) from high-performance adsorbents or photocatalysts into exposure-modulating materials bridging environmental decontamination with human health protection. We summarize recent progress in MOF design for pesticide adsorption and photocatalytic degradation, emphasizing structure-function relationships governing molecular recognition, pore confinement, surface chemistry and degradation-pathway control. Beyond performance metrics, this work examines how MOF-enabled adsorption and photocatalysis shape transformation-product profiles determining biological perturbation potential. Evidence linking pesticide exposure to gut microbiota dysbiosis and metabolic disorders underscores the health relevance of pathway-selective remediation. Finally, we outline future directions toward health-relevant remediation, advocating a shift from pollutant-centric efficiency metrics to risk relevant endpoints considering exposure profiles and biological disruption. By coupling programmable molecular selectivity with pathway-controlled degradation, MOFs emerge as enabling platforms for next-generation remediation strategies advancing environmental sustainability and human health protection. © 2026 Society of Chemical Industry.
Additional Links: PMID-42036926
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PubMed:
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@article {pmid42036926,
year = {2026},
author = {Dong, X and Chu, Y and Yi, X and Meng, D and Fu, J and Tong, Z and Sun, M and Duan, J},
title = {Metal-organic frameworks for pesticide remediation: From adsorption and photocatalysis to health-relevant risk reduction.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.70856},
pmid = {42036926},
issn = {1526-4998},
support = {32372609//National Natural Science Foundation of China/ ; 32302414//National Natural Science Foundation of China/ ; 2023YFD1400900//National Key Research and Development Program of China/ ; },
abstract = {Conventional remediation strategies implicitly assume that efficient pollutant removal equates to effective health-risk mitigation; however, growing epidemiological and microbiome evidence challenges this assumption, particularly for pesticide exposure. Accumulating studies demonstrate that pesticide residues and their transformation products can disrupt gut microbial homeostasis and metabolic regulation, indicating that removal efficiency alone is insufficient to evaluate remediation success. Against this backdrop, this review advances a risk-oriented paradigm for pesticide remediation by redefining metal-organic frameworks (MOFs) from high-performance adsorbents or photocatalysts into exposure-modulating materials bridging environmental decontamination with human health protection. We summarize recent progress in MOF design for pesticide adsorption and photocatalytic degradation, emphasizing structure-function relationships governing molecular recognition, pore confinement, surface chemistry and degradation-pathway control. Beyond performance metrics, this work examines how MOF-enabled adsorption and photocatalysis shape transformation-product profiles determining biological perturbation potential. Evidence linking pesticide exposure to gut microbiota dysbiosis and metabolic disorders underscores the health relevance of pathway-selective remediation. Finally, we outline future directions toward health-relevant remediation, advocating a shift from pollutant-centric efficiency metrics to risk relevant endpoints considering exposure profiles and biological disruption. By coupling programmable molecular selectivity with pathway-controlled degradation, MOFs emerge as enabling platforms for next-generation remediation strategies advancing environmental sustainability and human health protection. © 2026 Society of Chemical Industry.},
}
RevDate: 2026-04-27
Scalp microbiome differences in subjects with self-reported hair loss: A quantitative approach to microbial dysbiosis.
International journal of cosmetic science [Epub ahead of print].
OBJECTIVE: Hair loss is a common issue that affects a large proportion of the population, leading to lower self-confidence and quality of life. Microbial dysbiosis of the scalp has been shown to be associated with several different disorders leading to hair loss. Though several 'microbiome friendly cosmetic treatments are currently on the market, there is no agreement on the best technique for assessing dysbiosis, leading to a lack of scientific rigour for quantifying the effective treatments. To help address this, the association between self-perceived hair loss and the scalp microbiome in an African-American cohort (n = 36) was investigated.
METHODS: Using a self-controlled design, swabs were collected from both 'sparse' and 'normal' scalp sites. The scalp microbiome was characterized via 16S rRNA gene sequencing and a dysbiosis score was calculated based on the proportion of all taxa within the samples. Further, we identified the taxa that contributed most to abnormal or dysbiotic hair sites using a machine learning random forest classifier and a negative binomial mixed-effects model.
RESULTS: The dysbiosis index is sensitive to participants' self-assessment of hair loss and interindividual variation. We found a core set of operational taxonomic units (OTUs) assigned to 7 genera that significantly contributed to increased scalp dysbiosis.
CONCLUSION: This study demonstrates that self-perceived hair loss is associated with significant and measurable alterations in the scalp microbiome, making the reported dysbiosis index a practical tool that may be used to assess microbiome changes following cosmetic or medical interventions for hair loss and other microbiome-associated disorders.
Additional Links: PMID-42037062
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@article {pmid42037062,
year = {2026},
author = {Malas, J and Reczek, S and Porter, I and Lenzy, YM and Barbosa, V and Porter, C and Hampton-Marcell, J},
title = {Scalp microbiome differences in subjects with self-reported hair loss: A quantitative approach to microbial dysbiosis.},
journal = {International journal of cosmetic science},
volume = {},
number = {},
pages = {},
doi = {10.1111/ics.70101},
pmid = {42037062},
issn = {1468-2494},
abstract = {OBJECTIVE: Hair loss is a common issue that affects a large proportion of the population, leading to lower self-confidence and quality of life. Microbial dysbiosis of the scalp has been shown to be associated with several different disorders leading to hair loss. Though several 'microbiome friendly cosmetic treatments are currently on the market, there is no agreement on the best technique for assessing dysbiosis, leading to a lack of scientific rigour for quantifying the effective treatments. To help address this, the association between self-perceived hair loss and the scalp microbiome in an African-American cohort (n = 36) was investigated.
METHODS: Using a self-controlled design, swabs were collected from both 'sparse' and 'normal' scalp sites. The scalp microbiome was characterized via 16S rRNA gene sequencing and a dysbiosis score was calculated based on the proportion of all taxa within the samples. Further, we identified the taxa that contributed most to abnormal or dysbiotic hair sites using a machine learning random forest classifier and a negative binomial mixed-effects model.
RESULTS: The dysbiosis index is sensitive to participants' self-assessment of hair loss and interindividual variation. We found a core set of operational taxonomic units (OTUs) assigned to 7 genera that significantly contributed to increased scalp dysbiosis.
CONCLUSION: This study demonstrates that self-perceived hair loss is associated with significant and measurable alterations in the scalp microbiome, making the reported dysbiosis index a practical tool that may be used to assess microbiome changes following cosmetic or medical interventions for hair loss and other microbiome-associated disorders.},
}
RevDate: 2026-04-27
The Allium cepa Derived Compound Propyl Propane Thiosulfonate (PTSO) Improves Tumorigenesis Due to Its Immunomodulatory Effect: A Preclinical Study.
Phytotherapy research : PTR [Epub ahead of print].
Allium-derived organosulfur compounds offer significant health benefits. Specifically, PTSO, an organosulfur compound extracted from Allium cepa, has demonstrated immunomodulatory and prebiotic properties. However, its effects on tumorigenesis and gut dysbiosis in colitis-associated colorectal cancer (CAC) remain unexplored. This study aimed to investigate the impact of two PTSO formulations, free (FP) and encapsulated (EP), on a murine model of CAC focusing on their impact on the immune system and gut microbiome. The antitumor effect of PTSO was characterized in vitro in HCT116 cells and in a CAC murine model induced by the administration of azoxymethane and dextran sulfate sodium. FP and EP were administered orally throughout the assay and 5-fluorouracil was used as a control. FP and EP were effective in reducing tumor burden, with EP showing a greater positive impact on tumorigenesis by reducing both tumor number and size, likely due to enhanced bioavailability. PTSO induced apoptosis through oxidative stress mechanisms and modulated key pathways like STAT3, PI3K/mTOR, and Wnt/β-catenin. Additionally, PTSO, especially EP, exhibited an immunomodulatory effect on myeloid and lymphoid populations and hindered the release of cytokines that prompted inflammation and cancer progression. PTSO also enhanced gut barrier integrity, increased the abundance of beneficial bacteria, like Akkermansia, Leuconostoc mesenteroides, and Weissella confusa, and the release of short-chain fatty acids (SCFAs). This study highlights the potential of PTSO, particularly in its encapsulated form, as a promising therapeutic agent for CRC by targeting both tumor growth and the underlying inflammatory processes while restoring gut microbiota balance.
Additional Links: PMID-42037123
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PubMed:
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@article {pmid42037123,
year = {2026},
author = {Rodríguez-Sojo, MJ and Hidalgo-García, L and Molina-Tijeras, JA and López-Escanez, L and Gbati, L and Vezza, T and Diez-Echave, P and Ruiz-Malagón, AJ and García-García, J and García, F and Baños, A and Gil-Martínez, L and López-Posadas, R and Neurath, MF and Gálvez, J and Rodríguez-Cabezas, ME and Rodríguez-Nogales, A},
title = {The Allium cepa Derived Compound Propyl Propane Thiosulfonate (PTSO) Improves Tumorigenesis Due to Its Immunomodulatory Effect: A Preclinical Study.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.70334},
pmid = {42037123},
issn = {1099-1573},
support = {CULTUREDMEAT-Project-MIG-20201012//Centro para el Desarrollo Tecnológico Industrial/ ; PI19/01058//Instituto de Salud Carlos III/ ; PI20/01447//Instituto de Salud Carlos III/ ; IFI21/00030//Instituto de Salud Carlos III/ ; CD23/00102//Instituto de Salud Carlos III/ ; CD23/00117//Instituto de Salud Carlos III/ ; CD22/00112//Instituto de Salud Carlos III/ ; CP22/00153//Instituto de Salud Carlos III/ ; },
abstract = {Allium-derived organosulfur compounds offer significant health benefits. Specifically, PTSO, an organosulfur compound extracted from Allium cepa, has demonstrated immunomodulatory and prebiotic properties. However, its effects on tumorigenesis and gut dysbiosis in colitis-associated colorectal cancer (CAC) remain unexplored. This study aimed to investigate the impact of two PTSO formulations, free (FP) and encapsulated (EP), on a murine model of CAC focusing on their impact on the immune system and gut microbiome. The antitumor effect of PTSO was characterized in vitro in HCT116 cells and in a CAC murine model induced by the administration of azoxymethane and dextran sulfate sodium. FP and EP were administered orally throughout the assay and 5-fluorouracil was used as a control. FP and EP were effective in reducing tumor burden, with EP showing a greater positive impact on tumorigenesis by reducing both tumor number and size, likely due to enhanced bioavailability. PTSO induced apoptosis through oxidative stress mechanisms and modulated key pathways like STAT3, PI3K/mTOR, and Wnt/β-catenin. Additionally, PTSO, especially EP, exhibited an immunomodulatory effect on myeloid and lymphoid populations and hindered the release of cytokines that prompted inflammation and cancer progression. PTSO also enhanced gut barrier integrity, increased the abundance of beneficial bacteria, like Akkermansia, Leuconostoc mesenteroides, and Weissella confusa, and the release of short-chain fatty acids (SCFAs). This study highlights the potential of PTSO, particularly in its encapsulated form, as a promising therapeutic agent for CRC by targeting both tumor growth and the underlying inflammatory processes while restoring gut microbiota balance.},
}
RevDate: 2026-04-27
Short-Term Promotion of Beneficial Skin Commensal Staphylococcus Species Growth by PS-B1, a Postbiotic Composed of Lactic Acid Bacteria-Fermented Soy Milk.
Microbiology and immunology [Epub ahead of print].
Postbiotics, defined as non-viable microbial cells, their components, or metabolites, are emerging functional ingredients that can modulate host health, including skin barrier function, immune responses, and microbial balance. The human skin microbiome plays a critical role in maintaining skin health, and the selective stimulation of beneficial commensals is of growing interest for cosmetic applications. PS-B1, a postbiotic derived from lactic acid bacteria during soy fermentation, is already used in beverages and cosmetics, but its direct effects on skin-resident bacteria have not been fully elucidated. In this study, we evaluated the effects of preservative-containing and preservative-free PS-B1 on the growth of twelve Staphylococcus strains and seven Cutibacterium acnes strains in vitro. The preservative-containing PS-B1 showed strong growth inhibition for all strains at higher concentrations. In contrast, the preservative-free PS-B1 significantly promoted the growth of Staphylococcus epidermidis, Staphylococcus hominis, and Staphylococcus lugdunensis, while Staphylococcus warneri was the only strain exhibiting growth inhibition. Other species showed no notable changes. Additionally, all C. acnes strains displayed slight growth enhancement. These results indicate that preservative-free PS-B1 selectively stimulates beneficial skin commensals, particularly S. hominis, revealing a previously unrecognized potential of PS-B1 to support a balanced skin microbiome.
Additional Links: PMID-42037251
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@article {pmid42037251,
year = {2026},
author = {Funatsu, O and Ishii, H and Shimatsu, R and Shimokawa, Y and Asahina, A and Dekio, I},
title = {Short-Term Promotion of Beneficial Skin Commensal Staphylococcus Species Growth by PS-B1, a Postbiotic Composed of Lactic Acid Bacteria-Fermented Soy Milk.},
journal = {Microbiology and immunology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1348-0421.70057},
pmid = {42037251},
issn = {1348-0421},
abstract = {Postbiotics, defined as non-viable microbial cells, their components, or metabolites, are emerging functional ingredients that can modulate host health, including skin barrier function, immune responses, and microbial balance. The human skin microbiome plays a critical role in maintaining skin health, and the selective stimulation of beneficial commensals is of growing interest for cosmetic applications. PS-B1, a postbiotic derived from lactic acid bacteria during soy fermentation, is already used in beverages and cosmetics, but its direct effects on skin-resident bacteria have not been fully elucidated. In this study, we evaluated the effects of preservative-containing and preservative-free PS-B1 on the growth of twelve Staphylococcus strains and seven Cutibacterium acnes strains in vitro. The preservative-containing PS-B1 showed strong growth inhibition for all strains at higher concentrations. In contrast, the preservative-free PS-B1 significantly promoted the growth of Staphylococcus epidermidis, Staphylococcus hominis, and Staphylococcus lugdunensis, while Staphylococcus warneri was the only strain exhibiting growth inhibition. Other species showed no notable changes. Additionally, all C. acnes strains displayed slight growth enhancement. These results indicate that preservative-free PS-B1 selectively stimulates beneficial skin commensals, particularly S. hominis, revealing a previously unrecognized potential of PS-B1 to support a balanced skin microbiome.},
}
RevDate: 2026-04-27
Genome-resolved insights into arsenic-impacted paddy soil and microcosm-derived microbiomes from West Bengal, India.
Microbiology resource announcements [Epub ahead of print].
This study reports 32 metagenome-assembled genomes (MAGs) reconstructed from arsenic (As)-impacted paddy soils of West Bengal, India, and microcosms from these soil samples. These MAGs, represented by 10 bacterial and 2 archaeal phyla, provided critical insights into the metabolic and biogeochemical potential of microbiomes in a highly As-impacted agroecosystem.
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@article {pmid42037351,
year = {2026},
author = {Chakraborty, S and Mukherjee, D and Sar, P},
title = {Genome-resolved insights into arsenic-impacted paddy soil and microcosm-derived microbiomes from West Bengal, India.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0005926},
doi = {10.1128/mra.00059-26},
pmid = {42037351},
issn = {2576-098X},
abstract = {This study reports 32 metagenome-assembled genomes (MAGs) reconstructed from arsenic (As)-impacted paddy soils of West Bengal, India, and microcosms from these soil samples. These MAGs, represented by 10 bacterial and 2 archaeal phyla, provided critical insights into the metabolic and biogeochemical potential of microbiomes in a highly As-impacted agroecosystem.},
}
RevDate: 2026-04-27
Gut microbiome associations with acute malnutrition relapse in South Sudan.
Microbiology spectrum [Epub ahead of print].
Severe acute malnutrition (SAM) is a leading cause of childhood morbidity and mortality that is defined by anthropometric measurements, weight-for-height z score, and mid-upper arm circumference (MUAC) falling significantly below healthy standards. While treatments for SAM and our understanding of this disease have advanced, children experiencing SAM frequently relapse to acute malnutrition (AM) following anthropometric recovery. Little is known about the contribution of the gut microbiome to AM relapse. We hypothesized that features of the gut microbiome, including microbial composition, antimicrobial resistance gene carriage, and predicted microbial functional pathways, of children discharged from treatment for uncomplicated SAM in South Sudan, may be associated with AM relapse at 1-month follow-up. Overall, broad microbiome profiles at discharge were not associated with AM relapse. We evaluated the associations of microbiome features with AM relapse 1-month post-recovery using mixed linear effect models. We identified associations between higher MUAC, which may be a proxy for future health trajectories, and increased Sutterella wadsworthensis and trimethoprim-resistant dihydrofolate reductase antimicrobial resistance genes. These findings suggest that the gut microbiome at discharge of children treated for uncomplicated SAM has limited predictive value as a standalone diagnostic tool for identifying relapse risk at 1 month.IMPORTANCESevere acute malnutrition (SAM) is a devastating illness that impacts the morbidity and mortality of millions of children worldwide. Community-based management of acute malnutrition (CMAM) is the standard of care in South Sudan and many other low-resource settings for children presenting with SAM. Despite this intervention, children treated for SAM under CMAM frequently relapse to acute malnutrition (AM) following treatment. With advancements in our understanding of malnutrition, there has been a strong and growing interest in developing microbiome-based strategies to treat, prevent, and predict relapse to AM following treatment for SAM. Our work characterizes gut microbiome features of children from a geographic area that is traditionally underrepresented in gut microbiome research and shows that in isolation, a child's gut microbiome at discharge likely holds low predictive value for relapse to AM post-CMAM treatment; however, we identified key microbes and microbial features meriting further research.
Additional Links: PMID-42037384
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@article {pmid42037384,
year = {2026},
author = {Yang, K and King, S and Marshak, A and D'Mello-Guyett, L and Grignard, L and Knee, J and Wong, G and Zhao, L and Lamaka, NG and Save, D and Gose, M and Myers, A and Trehan, I and Cumming, O and Stobaugh, H and Schwartz, DJ},
title = {Gut microbiome associations with acute malnutrition relapse in South Sudan.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0358725},
doi = {10.1128/spectrum.03587-25},
pmid = {42037384},
issn = {2165-0497},
abstract = {Severe acute malnutrition (SAM) is a leading cause of childhood morbidity and mortality that is defined by anthropometric measurements, weight-for-height z score, and mid-upper arm circumference (MUAC) falling significantly below healthy standards. While treatments for SAM and our understanding of this disease have advanced, children experiencing SAM frequently relapse to acute malnutrition (AM) following anthropometric recovery. Little is known about the contribution of the gut microbiome to AM relapse. We hypothesized that features of the gut microbiome, including microbial composition, antimicrobial resistance gene carriage, and predicted microbial functional pathways, of children discharged from treatment for uncomplicated SAM in South Sudan, may be associated with AM relapse at 1-month follow-up. Overall, broad microbiome profiles at discharge were not associated with AM relapse. We evaluated the associations of microbiome features with AM relapse 1-month post-recovery using mixed linear effect models. We identified associations between higher MUAC, which may be a proxy for future health trajectories, and increased Sutterella wadsworthensis and trimethoprim-resistant dihydrofolate reductase antimicrobial resistance genes. These findings suggest that the gut microbiome at discharge of children treated for uncomplicated SAM has limited predictive value as a standalone diagnostic tool for identifying relapse risk at 1 month.IMPORTANCESevere acute malnutrition (SAM) is a devastating illness that impacts the morbidity and mortality of millions of children worldwide. Community-based management of acute malnutrition (CMAM) is the standard of care in South Sudan and many other low-resource settings for children presenting with SAM. Despite this intervention, children treated for SAM under CMAM frequently relapse to acute malnutrition (AM) following treatment. With advancements in our understanding of malnutrition, there has been a strong and growing interest in developing microbiome-based strategies to treat, prevent, and predict relapse to AM following treatment for SAM. Our work characterizes gut microbiome features of children from a geographic area that is traditionally underrepresented in gut microbiome research and shows that in isolation, a child's gut microbiome at discharge likely holds low predictive value for relapse to AM post-CMAM treatment; however, we identified key microbes and microbial features meriting further research.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
The Role of Biotics in Rosacea: A Narrative Review.
Cureus, 18(3):e105799.
Rosacea is a chronic inflammatory dermatosis affecting the central face of adults, characterized by persistent erythema, flushing, papules, pustules, telangiectasias, and, in some cases, phymatous changes. Its pathogenesis involves a multifactorial interplay of immune dysregulation, neurovascular alterations, genetic predisposition, and disturbances of the skin and gut microbiota. Increasing interest in the gut-skin axis has prompted investigation into microbiota-targeted therapies, including probiotics, prebiotics, postbiotics, and synbiotics. This narrative review evaluates current evidence regarding the role of biotics in rosacea. A literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science using combinations of the terms "rosacea," "gut-skin axis," "probiotics," "prebiotics," "postbiotics," and "synbiotics." Clinical trials, observational studies, and relevant mechanistic investigations published in English were considered. Available data suggest that certain probiotic strains, administered orally or topically, may improve inflammatory lesions, erythema, and skin barrier function, particularly as adjuncts to standard therapy. However, findings are characterized by significant heterogeneity in strains, dosages, study design, outcome measures, and treatment duration. Evidence supporting the use of prebiotics, postbiotics, and synbiotics in rosacea remains limited and, in many cases, extrapolated from related inflammatory conditions or preclinical models. Although microbiota modulation represents a promising therapeutic avenue, current evidence is insufficient to establish standardized clinical recommendations. Larger, well-designed randomized controlled trials with standardized endpoints and long-term follow-up are required to clarify their efficacy, optimal formulations, and safety.
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@article {pmid42037847,
year = {2026},
author = {Avendaño-Pérez, AL and Orozco-Covarrubias, L and Saez-de-Ocariz, M},
title = {The Role of Biotics in Rosacea: A Narrative Review.},
journal = {Cureus},
volume = {18},
number = {3},
pages = {e105799},
pmid = {42037847},
issn = {2168-8184},
abstract = {Rosacea is a chronic inflammatory dermatosis affecting the central face of adults, characterized by persistent erythema, flushing, papules, pustules, telangiectasias, and, in some cases, phymatous changes. Its pathogenesis involves a multifactorial interplay of immune dysregulation, neurovascular alterations, genetic predisposition, and disturbances of the skin and gut microbiota. Increasing interest in the gut-skin axis has prompted investigation into microbiota-targeted therapies, including probiotics, prebiotics, postbiotics, and synbiotics. This narrative review evaluates current evidence regarding the role of biotics in rosacea. A literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science using combinations of the terms "rosacea," "gut-skin axis," "probiotics," "prebiotics," "postbiotics," and "synbiotics." Clinical trials, observational studies, and relevant mechanistic investigations published in English were considered. Available data suggest that certain probiotic strains, administered orally or topically, may improve inflammatory lesions, erythema, and skin barrier function, particularly as adjuncts to standard therapy. However, findings are characterized by significant heterogeneity in strains, dosages, study design, outcome measures, and treatment duration. Evidence supporting the use of prebiotics, postbiotics, and synbiotics in rosacea remains limited and, in many cases, extrapolated from related inflammatory conditions or preclinical models. Although microbiota modulation represents a promising therapeutic avenue, current evidence is insufficient to establish standardized clinical recommendations. Larger, well-designed randomized controlled trials with standardized endpoints and long-term follow-up are required to clarify their efficacy, optimal formulations, and safety.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Diet-induced metabolic and faecal microbiome responses in pet dogs fed a minimally processed versus extruded kibble diet.
Frontiers in veterinary science, 13:1734572.
INTRODUCTION: The extent to which food is processed influences gut functions, such as digestion, nutrient uptake, and microbiome response, with the potential to impact immuno-metabolic health. Despite known associations between ultra-processed food (UPF) intake and chronic diseases in humans, mechanistic links explaining inferred health risks remain unclear. Health risks associated with chronic disease are also a concern for companion animals such as dogs, where nutritionally complete dry processed foods constitute a major component of contemporary pet dog diets. A challenge is that nutrition is complex and even diets based on nutritionally complete processed foods typically vary in multiple dimensions.
METHODS: Here, we use a randomised, cross-over design to compare short-term effects of two commercially available nutritionally complete canine diets-an extruded kibble diet (EKD) and a mildly cooked, minimally processed diet (MPD). We assigned 24 healthy dogs to one of two groups: all dogs remained on their at-home diet for 1 week, before transitioning to (1) MPD or (2) EKD for 2 weeks each. One dog was removed from the study due to health complications, and the remaining 23 dogs completed both dietary treatment periods. Glycaemic, hormonal, and gut microbiome responses were captured from pre- and post-prandial blood samples and time series of 12 faecal samples from each dog.
RESULTS: The experimental diets resulted in distinct physiological and gut microbiome responses. MPD was associated with improved faecal consistency (FCS 2.24 ± 0.67, p = 0.005), lower pre- and post-prandial gastric inhibitory polypeptide (GIP, p < 0.001) and peptide YY (PYY, p < 0.05), and reduced post-prandial glycaemic response compared to EKD (AUC, p = 0.009). Diet was the strongest predictor of microbial response despite between-dog differences, with higher alpha diversity associated with MPD and greater within-individual community turnover following transition to MPD in both treatment groups (Group 1, p < 0.001; Group 2, p < 0.05).
CONCLUSION: These data show the feasibility of testing diet formulations in pet dogs and understanding the role of host-microbiome interactions in responses to food. The demonstration of distinct outcomes highlights the need for further studies on long-term feeding to better understand mechanisms and implications for health in community pets.
Additional Links: PMID-42038049
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@article {pmid42038049,
year = {2026},
author = {Campbell, L and Thompson, M and Muir, M and Raubenheimer, D and Holmes, A},
title = {Diet-induced metabolic and faecal microbiome responses in pet dogs fed a minimally processed versus extruded kibble diet.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1734572},
pmid = {42038049},
issn = {2297-1769},
abstract = {INTRODUCTION: The extent to which food is processed influences gut functions, such as digestion, nutrient uptake, and microbiome response, with the potential to impact immuno-metabolic health. Despite known associations between ultra-processed food (UPF) intake and chronic diseases in humans, mechanistic links explaining inferred health risks remain unclear. Health risks associated with chronic disease are also a concern for companion animals such as dogs, where nutritionally complete dry processed foods constitute a major component of contemporary pet dog diets. A challenge is that nutrition is complex and even diets based on nutritionally complete processed foods typically vary in multiple dimensions.
METHODS: Here, we use a randomised, cross-over design to compare short-term effects of two commercially available nutritionally complete canine diets-an extruded kibble diet (EKD) and a mildly cooked, minimally processed diet (MPD). We assigned 24 healthy dogs to one of two groups: all dogs remained on their at-home diet for 1 week, before transitioning to (1) MPD or (2) EKD for 2 weeks each. One dog was removed from the study due to health complications, and the remaining 23 dogs completed both dietary treatment periods. Glycaemic, hormonal, and gut microbiome responses were captured from pre- and post-prandial blood samples and time series of 12 faecal samples from each dog.
RESULTS: The experimental diets resulted in distinct physiological and gut microbiome responses. MPD was associated with improved faecal consistency (FCS 2.24 ± 0.67, p = 0.005), lower pre- and post-prandial gastric inhibitory polypeptide (GIP, p < 0.001) and peptide YY (PYY, p < 0.05), and reduced post-prandial glycaemic response compared to EKD (AUC, p = 0.009). Diet was the strongest predictor of microbial response despite between-dog differences, with higher alpha diversity associated with MPD and greater within-individual community turnover following transition to MPD in both treatment groups (Group 1, p < 0.001; Group 2, p < 0.05).
CONCLUSION: These data show the feasibility of testing diet formulations in pet dogs and understanding the role of host-microbiome interactions in responses to food. The demonstration of distinct outcomes highlights the need for further studies on long-term feeding to better understand mechanisms and implications for health in community pets.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Associations of cord blood biomarkers with infant colic and excessive crying.
Frontiers in pediatrics, 14:1767660.
INTRODUCTION: There are currently no known biomarkers associated with the diagnosis of infant colic, a common early disorder of gut brain interaction (DGBI) that has been found to predict adverse health outcomes, including atopy, migraines and other DGBIs. Infant colic manifests as unsoothable crying and is perceived to be associated with abdominal pain, differentiating it from other crying behaviors. Prior studies have postulated it may involve microbial dysbiosis as well as immunological and neurological dysregulation. The aim of our study was to investigate the associations of cord blood biomarkers at birth with parent reports of colic and excessive crying behaviors at 6 months of age.
METHODS: We used available data from Project Viva a pre-birth cohort based in the greater Boston, MA area. All infants were born between 1999 and 2002.
RESULTS: Among participants with information on infant colic and cord blood biomarkers (n = 405), we found higher trans fatty acids and an increased abundance of Gammaproteobacteria signature in cord blood from infants with colic and those with excessive crying without colic, compared to those unaffected by colic. The majority of inflammatory and immune system cord blood biomarkers previously measured, including metabolites and cytokine stimulation, showed no association with either colic or excessive crying.
DISCUSSION: This exploratory study examined cord blood biomarkers of inflammation or immune dysregulation to support the underlying mechanism of infant colic, and identified trans fatty acid levels and Gammaproteobacteria microbial signatures as possible candidate predictors. On the other hand, we also found a lack of association with most of the cord blood immune and neurological biomarkers that we assessed. In turn, we propose that colic biomarkers may be present closer to its manifestation as a clinical condition of early infancy.
Additional Links: PMID-42038231
PubMed:
Citation:
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@article {pmid42038231,
year = {2026},
author = {Simonin, EM and Switkowski, KM and Rifas-Shiman, SL and Nadeau, KC and Oken, E and Lightdale, JR},
title = {Associations of cord blood biomarkers with infant colic and excessive crying.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1767660},
pmid = {42038231},
issn = {2296-2360},
abstract = {INTRODUCTION: There are currently no known biomarkers associated with the diagnosis of infant colic, a common early disorder of gut brain interaction (DGBI) that has been found to predict adverse health outcomes, including atopy, migraines and other DGBIs. Infant colic manifests as unsoothable crying and is perceived to be associated with abdominal pain, differentiating it from other crying behaviors. Prior studies have postulated it may involve microbial dysbiosis as well as immunological and neurological dysregulation. The aim of our study was to investigate the associations of cord blood biomarkers at birth with parent reports of colic and excessive crying behaviors at 6 months of age.
METHODS: We used available data from Project Viva a pre-birth cohort based in the greater Boston, MA area. All infants were born between 1999 and 2002.
RESULTS: Among participants with information on infant colic and cord blood biomarkers (n = 405), we found higher trans fatty acids and an increased abundance of Gammaproteobacteria signature in cord blood from infants with colic and those with excessive crying without colic, compared to those unaffected by colic. The majority of inflammatory and immune system cord blood biomarkers previously measured, including metabolites and cytokine stimulation, showed no association with either colic or excessive crying.
DISCUSSION: This exploratory study examined cord blood biomarkers of inflammation or immune dysregulation to support the underlying mechanism of infant colic, and identified trans fatty acid levels and Gammaproteobacteria microbial signatures as possible candidate predictors. On the other hand, we also found a lack of association with most of the cord blood immune and neurological biomarkers that we assessed. In turn, we propose that colic biomarkers may be present closer to its manifestation as a clinical condition of early infancy.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Lactoferrin combined with Bifidobacterium animalis subsp. lactis BB-12 improves respiratory tract infections and modulates Gut microbiome function in children: a randomized, double-blind, placebo-controlled trial.
Frontiers in pediatrics, 14:1778240.
OBJECTIVES AND STUDY: To explore the effects and mechanisms of lactoferrin combined with Bifidobacterium animalis subsp. lactis BB-12 on Respiratory tract infections (RTIs) in healthy children through a randomized, double-blind, placebo-controlled trial.
METHODS: Eligible healthy children aged 0-6 years were randomized into intervention group (IG, n = 60, receiving lactoferrin and probiotic for 3 months) and control group (CG, n = 34, receiving placebo). The study primarily assessed changes in the incidence and severity of RTIs, and monitored gastrointestinal adverse events. Fecal samples were collected pre- and post-intervention to analyze gut microbiota composition and metabolomic profiles, including short-chain fatty acids (SCFAs).
RESULTS: After the intervention, the incidence of RTIs showed no significant difference between groups (55% vs. 61.8%, p = 0.52), but both the RTI severity score (3.0 vs. 4.0, p < 0.05) and mean duration per RTI episode (3.54 d vs. 5.27 d, p < 0.05) were significantly lower in the IG. No serious adverse events were reported, and the incidence of indigestion was significantly reduced in the IG compared with the CG (8.3% vs. 23.5%, p = 0.04). The intervention significantly altered phylogenetic diversity (PD-whole tree within IG: p = 0.0011; baseline between IG and CG: p = 0.63; post-intervention between IG and CG: p = 0.029) and community structure (weighted UniFrac within IG: 0.012; between IG and CG at 3 months: p = 0.036 vs. baseline p = 0.01). The gut microbiota in the intervention group exhibited a trend toward greater stability over time. Integrated microbiome-metabolite analysis showed attenuation of fatty acid oxidation-and energy metabolism-related metabolic drivers after intervention, together with no significant changes in fecal SCFA levels.
CONCLUSIONS: The intervention improved clinical outcomes and induced phylogenetic restructuring of the gut microbiota rather than changes in overall abundance, accompanied by a shift toward greater stability in gut microbial structure and energy metabolic patterns.
CLINICAL TRIAL REGISTRATION: identifier ChiCTR2500111308.
Additional Links: PMID-42038244
PubMed:
Citation:
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@article {pmid42038244,
year = {2026},
author = {Shi, Z and Zhu, H and Tao, X and Liu, F and Zhao, L and Zhang, J and Zhang, J},
title = {Lactoferrin combined with Bifidobacterium animalis subsp. lactis BB-12 improves respiratory tract infections and modulates Gut microbiome function in children: a randomized, double-blind, placebo-controlled trial.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1778240},
pmid = {42038244},
issn = {2296-2360},
abstract = {OBJECTIVES AND STUDY: To explore the effects and mechanisms of lactoferrin combined with Bifidobacterium animalis subsp. lactis BB-12 on Respiratory tract infections (RTIs) in healthy children through a randomized, double-blind, placebo-controlled trial.
METHODS: Eligible healthy children aged 0-6 years were randomized into intervention group (IG, n = 60, receiving lactoferrin and probiotic for 3 months) and control group (CG, n = 34, receiving placebo). The study primarily assessed changes in the incidence and severity of RTIs, and monitored gastrointestinal adverse events. Fecal samples were collected pre- and post-intervention to analyze gut microbiota composition and metabolomic profiles, including short-chain fatty acids (SCFAs).
RESULTS: After the intervention, the incidence of RTIs showed no significant difference between groups (55% vs. 61.8%, p = 0.52), but both the RTI severity score (3.0 vs. 4.0, p < 0.05) and mean duration per RTI episode (3.54 d vs. 5.27 d, p < 0.05) were significantly lower in the IG. No serious adverse events were reported, and the incidence of indigestion was significantly reduced in the IG compared with the CG (8.3% vs. 23.5%, p = 0.04). The intervention significantly altered phylogenetic diversity (PD-whole tree within IG: p = 0.0011; baseline between IG and CG: p = 0.63; post-intervention between IG and CG: p = 0.029) and community structure (weighted UniFrac within IG: 0.012; between IG and CG at 3 months: p = 0.036 vs. baseline p = 0.01). The gut microbiota in the intervention group exhibited a trend toward greater stability over time. Integrated microbiome-metabolite analysis showed attenuation of fatty acid oxidation-and energy metabolism-related metabolic drivers after intervention, together with no significant changes in fecal SCFA levels.
CONCLUSIONS: The intervention improved clinical outcomes and induced phylogenetic restructuring of the gut microbiota rather than changes in overall abundance, accompanied by a shift toward greater stability in gut microbial structure and energy metabolic patterns.
CLINICAL TRIAL REGISTRATION: identifier ChiCTR2500111308.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Sparse regression, classification, and microbial network estimation in QIIME2 with q2-classo and q2-gglasso.
ArXiv pii:2604.15520.
MOTIVATION: Statistical analysis of microbial count data derived from 16S rRNA or metagenomics sequencing poses unique challenges due to the sparse, compositional, and high-dimensional nature of the data. While QIIME 2 already provides many tools for data pre-processing and analysis, plugins for statistical regression, classification, and microbial network estimation tailored to compositional count data are relatively scarce.
RESULTS: We present q2-classo and q2-gglasso, two novel QIIME 2 plugins that implement penalized regression, classification, and graphical modeling approaches for microbial compositional data. q2-classo enables the prediction of a continuous or binary outcome of interest using compositional microbiome data as predictors. Both sparse log-contrast regression and classification, as well as tree-aggregated log-contrast models are available. q2-gglasso enables the estimation of taxon-taxon association networks through sparse graphical model estimation, such as, e.g., the SPIEC-EASI framework, as well as adaptive and latent graphical models. The latent model can decompose taxon-taxon associations into a sparse direct interaction matrix and a latent (low-rank) matrix which enables robust principal component embedding of a data set. Within the QIIME 2 ecosystem we demonstrate their application on the Atacama soil microbiome dataset, illustrating robust model selection, classification, and microbial network estimation with covariates and latent factors.
AVAILABILITY: The software is freely available under the BSD-3-Clause License. Source code is available at https://github.com/bio-datascience/q2-gglasso and https://github.com/bio-datascience/q2-classo-latest, with installation through QIIME 2 and Docker.
Additional Links: PMID-42038418
Full Text:
PubMed:
Citation:
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@article {pmid42038418,
year = {2026},
author = {Vlasovets, O and Schaipp, F and Simpson, L and Bolyen, E and Caporaso, JG and Mueller, CL},
title = {Sparse regression, classification, and microbial network estimation in QIIME2 with q2-classo and q2-gglasso.},
journal = {ArXiv},
volume = {},
number = {},
pages = {},
pmid = {42038418},
issn = {2331-8422},
abstract = {MOTIVATION: Statistical analysis of microbial count data derived from 16S rRNA or metagenomics sequencing poses unique challenges due to the sparse, compositional, and high-dimensional nature of the data. While QIIME 2 already provides many tools for data pre-processing and analysis, plugins for statistical regression, classification, and microbial network estimation tailored to compositional count data are relatively scarce.
RESULTS: We present q2-classo and q2-gglasso, two novel QIIME 2 plugins that implement penalized regression, classification, and graphical modeling approaches for microbial compositional data. q2-classo enables the prediction of a continuous or binary outcome of interest using compositional microbiome data as predictors. Both sparse log-contrast regression and classification, as well as tree-aggregated log-contrast models are available. q2-gglasso enables the estimation of taxon-taxon association networks through sparse graphical model estimation, such as, e.g., the SPIEC-EASI framework, as well as adaptive and latent graphical models. The latent model can decompose taxon-taxon associations into a sparse direct interaction matrix and a latent (low-rank) matrix which enables robust principal component embedding of a data set. Within the QIIME 2 ecosystem we demonstrate their application on the Atacama soil microbiome dataset, illustrating robust model selection, classification, and microbial network estimation with covariates and latent factors.
AVAILABILITY: The software is freely available under the BSD-3-Clause License. Source code is available at https://github.com/bio-datascience/q2-gglasso and https://github.com/bio-datascience/q2-classo-latest, with installation through QIIME 2 and Docker.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Age-related alterations in fatty acid metabolism: a clinical study of erythrocyte and plasma profiles in a population from Brandenburg, Germany.
Frontiers in aging, 7:1725187.
INTRODUCTION: Aging is accompanied by changes in lipid metabolism that may influence cellular homeostasis and risk for age-related disease. Circulating polyunsaturated fatty acid (PUFA) status is increasingly recognized as an important marker of metabolic health and may shift with age. Product-to-precursor ratios of fatty acids, including PUFA are commonly used as proxy indices of desaturation and elongation but do not directly reflect enzyme activity.
METHODS: In this cross-sectional study, plasma and erythrocyte fatty acid profiles were measured by gas chromatography-flame ionization detection (GC-FID) in patients (n = 1277) from a metabolic disease clinic in Brandenburg, Germany. Participants were stratified into five age groups (≤ 34, 35-44, 45-54, 55-64, ≥ 65 years) and differences between groups were assessed using statistical tests.
RESULTS: Participants aged ≥ 65 years had higher total omega-3 (n-3) and lower total omega-6 (n-6) PUFA levels in both matrices. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) increased with age, whereas linoleic acid (LA) and dihomo-gamma-linolenic acid (DGLA) decreased. Ratio-based indices showed consistent age associations. The delta-5-desaturase index (D5D) and arachidonic acid (AA)/LA ratio were positively associated with age, while elongation of very long chain fatty acids (ELOVL)2 and ELOVL6 were inversely associated.
DISCUSSION: Overall, blood PUFA profiles and multiple ratio-based indices showed consistent, age-related trends in this clinical cohort. Interpretation is limited by the cross-sectional design and the lack of key determinants of PUFA status (e.g., diet, clinical covariates, genetic information and gut/microbiome factors). Nevertheless, these results underscore age-related shifts in PUFA composition and enzymatic proxy indices, providing new insights into lipid metabolism across the lifespan.
Additional Links: PMID-42038449
PubMed:
Citation:
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@article {pmid42038449,
year = {2026},
author = {Yu, Y and Wang, C and Wang, R and Chen, Y and Wei, Z and Xiao, Y and Elbelt, U and Pietzner, A and Weylandt, KH},
title = {Age-related alterations in fatty acid metabolism: a clinical study of erythrocyte and plasma profiles in a population from Brandenburg, Germany.},
journal = {Frontiers in aging},
volume = {7},
number = {},
pages = {1725187},
pmid = {42038449},
issn = {2673-6217},
abstract = {INTRODUCTION: Aging is accompanied by changes in lipid metabolism that may influence cellular homeostasis and risk for age-related disease. Circulating polyunsaturated fatty acid (PUFA) status is increasingly recognized as an important marker of metabolic health and may shift with age. Product-to-precursor ratios of fatty acids, including PUFA are commonly used as proxy indices of desaturation and elongation but do not directly reflect enzyme activity.
METHODS: In this cross-sectional study, plasma and erythrocyte fatty acid profiles were measured by gas chromatography-flame ionization detection (GC-FID) in patients (n = 1277) from a metabolic disease clinic in Brandenburg, Germany. Participants were stratified into five age groups (≤ 34, 35-44, 45-54, 55-64, ≥ 65 years) and differences between groups were assessed using statistical tests.
RESULTS: Participants aged ≥ 65 years had higher total omega-3 (n-3) and lower total omega-6 (n-6) PUFA levels in both matrices. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) increased with age, whereas linoleic acid (LA) and dihomo-gamma-linolenic acid (DGLA) decreased. Ratio-based indices showed consistent age associations. The delta-5-desaturase index (D5D) and arachidonic acid (AA)/LA ratio were positively associated with age, while elongation of very long chain fatty acids (ELOVL)2 and ELOVL6 were inversely associated.
DISCUSSION: Overall, blood PUFA profiles and multiple ratio-based indices showed consistent, age-related trends in this clinical cohort. Interpretation is limited by the cross-sectional design and the lack of key determinants of PUFA status (e.g., diet, clinical covariates, genetic information and gut/microbiome factors). Nevertheless, these results underscore age-related shifts in PUFA composition and enzymatic proxy indices, providing new insights into lipid metabolism across the lifespan.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Associations among diet, gut microbiota, and hypertension: a cross-sectional study in Thai subjects.
PeerJ, 14:e21135.
Background: Although the link between the gut microbiota and hypertension has been investigated, its specific role in the increasing prevalence of this disease in Thailand, influenced by changing dietary patterns, remains unexplored. This cohort study investigated the association between the gut microbiome and hypertension-related dietary habits in Thai subjects. Methods: The fecal microbiomes of 31 Thai adults, including non-hypertensive (NHT, n = 12) and hypertensive (HT, n = 19) subjects, were grouped and analyzed according to their dietary and medical records. Alpha and beta diversity analyses were performed to determine significant differences (p < 0.05) in microbial diversity between groups. Variations in the microbiome profiles were identified using Linear Discriminant Analysis Effect Size (LEfSe) based on a linear discriminant analysis score > 2.0 (p < 0.05). Multiple Factor Analysis (MFA) was employed to integrate anthropometric data, dietary consumption, and gut microbiome, enabling the visualization of features driving overall variation. Functional profiles of the gut microbiome were predicted using PICRUSt2 based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) categories. Differential abundance and microbial-functional associations were evaluated using ALDEx2 and HAllA, respectively. Results: Our exploratory analysis suggests that hypertension-related differences are strongly associated with host factors (age and clinical profiles) rather than diet or microbial composition. Key taxonomic signatures of the HT group include the expansion of Phascolarctobacterium and depletion of Alistipes, which relates to anthropometric and blood profiles. Functional analysis revealed a profound restructuring of the gut ecosystem in the HT group, characterized by functional dysbiosis where microbial-functional association patterns shift distinct from changes abundance. Conclusions: These findings suggest that the gut microbiota's potential role in hypertension may involve altered interaction dynamics, which may provide a new perspective for targeted interventions in the Thai population.
Additional Links: PMID-42038454
PubMed:
Citation:
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@article {pmid42038454,
year = {2026},
author = {Therdtatha, P and Buakhao, T and Kullawong, N and Jinatham, V and Vichasilp, T and Nakayama, J and Popluechai, S},
title = {Associations among diet, gut microbiota, and hypertension: a cross-sectional study in Thai subjects.},
journal = {PeerJ},
volume = {14},
number = {},
pages = {e21135},
pmid = {42038454},
issn = {2167-8359},
mesh = {Humans ; *Gastrointestinal Microbiome ; Thailand/epidemiology ; Male ; Cross-Sectional Studies ; *Hypertension/microbiology/epidemiology ; Female ; Middle Aged ; *Diet ; Adult ; Feces/microbiology ; Aged ; Feeding Behavior ; Southeast Asian People ; },
abstract = {Background: Although the link between the gut microbiota and hypertension has been investigated, its specific role in the increasing prevalence of this disease in Thailand, influenced by changing dietary patterns, remains unexplored. This cohort study investigated the association between the gut microbiome and hypertension-related dietary habits in Thai subjects. Methods: The fecal microbiomes of 31 Thai adults, including non-hypertensive (NHT, n = 12) and hypertensive (HT, n = 19) subjects, were grouped and analyzed according to their dietary and medical records. Alpha and beta diversity analyses were performed to determine significant differences (p < 0.05) in microbial diversity between groups. Variations in the microbiome profiles were identified using Linear Discriminant Analysis Effect Size (LEfSe) based on a linear discriminant analysis score > 2.0 (p < 0.05). Multiple Factor Analysis (MFA) was employed to integrate anthropometric data, dietary consumption, and gut microbiome, enabling the visualization of features driving overall variation. Functional profiles of the gut microbiome were predicted using PICRUSt2 based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) categories. Differential abundance and microbial-functional associations were evaluated using ALDEx2 and HAllA, respectively. Results: Our exploratory analysis suggests that hypertension-related differences are strongly associated with host factors (age and clinical profiles) rather than diet or microbial composition. Key taxonomic signatures of the HT group include the expansion of Phascolarctobacterium and depletion of Alistipes, which relates to anthropometric and blood profiles. Functional analysis revealed a profound restructuring of the gut ecosystem in the HT group, characterized by functional dysbiosis where microbial-functional association patterns shift distinct from changes abundance. Conclusions: These findings suggest that the gut microbiota's potential role in hypertension may involve altered interaction dynamics, which may provide a new perspective for targeted interventions in the Thai population.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
Thailand/epidemiology
Male
Cross-Sectional Studies
*Hypertension/microbiology/epidemiology
Female
Middle Aged
*Diet
Adult
Feces/microbiology
Aged
Feeding Behavior
Southeast Asian People
RevDate: 2026-04-27
CmpDate: 2026-04-27
Chronic Kidney disease and cognitive frailty in aging: molecular crosstalk and clinical implications.
Frontiers in aging neuroscience, 18:1778574.
BACKGROUND: Chronic kidney disease (CKD) and cognitive frailty frequently co-occur in older adults, compounding adverse health outcomes and placing substantial strain on healthcare systems.
SUMMARY: This review outlines the molecular pathways that link CKD to cognitive decline, including chronic inflammation, oxidative stress, vascular dysfunction, hormonal dysregulation, and interactions along the gut-kidney-brain axis. Recent advances in neuroimaging offer objective biomarkers of brain atrophy, white matter injury, and disrupted functional connectivity.
KEY MESSAGES: Multi-omics and single-cell technologies are uncovering cell-type-specific mechanisms and candidate biomarkers, paving the way for precision medicine approaches. Emerging strategies include integrated geriatric-nephrology care models and targeted interventions, such as SGLT2 inhibitors, IL-6 antagonists, microbiome modulation, and structured exercise programs. Bioengineering and artificial intelligence now enable the integration of multimodal data to support risk prediction, disease monitoring, and individualized therapeutic planning. Future priorities should focus on longitudinal cohort studies, interventional trials with cognitive endpoints, and the development of rigorously validated AI-driven predictive models. Effectively addressing CKD-related cognitive frailty will require translating molecular insights into clinical practice to mitigate vulnerability in aging populations.
Additional Links: PMID-42038696
PubMed:
Citation:
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@article {pmid42038696,
year = {2026},
author = {Cao, Y and Wang, Z and Xue, J and Wang, L and Qin, W and Sun, Q and Chang, J},
title = {Chronic Kidney disease and cognitive frailty in aging: molecular crosstalk and clinical implications.},
journal = {Frontiers in aging neuroscience},
volume = {18},
number = {},
pages = {1778574},
pmid = {42038696},
issn = {1663-4365},
abstract = {BACKGROUND: Chronic kidney disease (CKD) and cognitive frailty frequently co-occur in older adults, compounding adverse health outcomes and placing substantial strain on healthcare systems.
SUMMARY: This review outlines the molecular pathways that link CKD to cognitive decline, including chronic inflammation, oxidative stress, vascular dysfunction, hormonal dysregulation, and interactions along the gut-kidney-brain axis. Recent advances in neuroimaging offer objective biomarkers of brain atrophy, white matter injury, and disrupted functional connectivity.
KEY MESSAGES: Multi-omics and single-cell technologies are uncovering cell-type-specific mechanisms and candidate biomarkers, paving the way for precision medicine approaches. Emerging strategies include integrated geriatric-nephrology care models and targeted interventions, such as SGLT2 inhibitors, IL-6 antagonists, microbiome modulation, and structured exercise programs. Bioengineering and artificial intelligence now enable the integration of multimodal data to support risk prediction, disease monitoring, and individualized therapeutic planning. Future priorities should focus on longitudinal cohort studies, interventional trials with cognitive endpoints, and the development of rigorously validated AI-driven predictive models. Effectively addressing CKD-related cognitive frailty will require translating molecular insights into clinical practice to mitigate vulnerability in aging populations.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Pangenomics-Driven Reverse Vaccinology for the Discovery of New Vaccine Candidates Against Bordetella pertussis.
Bioinformatics and biology insights, 20:11779322261442522.
Despite widespread vaccination, pertussis resurgence persists due to waning immunity and emerging resistant strains in Bordetella pertussis. This study employs a pangenomics-driven reverse vaccinology approach to identify novel vaccine candidates. Analyzing 160 genomes revealed a closed pan-genome, with approximately 60% conserved genes, including 3389 core genes of which 1312 participate in pathogen-specific pathways. Non-homologous proteins were identified by comparison against human and microbiome proteomes, yielding 205 candidates. Essentiality assessment via the Database of Essential Genes (DEG) refined this to 63 non-homologous essential proteins. A multi-criteria selection process evaluated purifiability based on physicochemical properties and transmembrane helices, accessibility (extracellular or secreted localization), and immunogenicity through antigenicity prediction and B-cell epitope mapping. This pipeline culminated in 11 high-potential vaccine targets. The in silico methodology offers rapidity, cost-effectiveness, and reduced side effects compared with conventional vaccinology, though experimental validation is essential for confirmation.
Additional Links: PMID-42038770
PubMed:
Citation:
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@article {pmid42038770,
year = {2026},
author = {Abdelouahab, M and Idrissa, D},
title = {Pangenomics-Driven Reverse Vaccinology for the Discovery of New Vaccine Candidates Against Bordetella pertussis.},
journal = {Bioinformatics and biology insights},
volume = {20},
number = {},
pages = {11779322261442522},
pmid = {42038770},
issn = {1177-9322},
abstract = {Despite widespread vaccination, pertussis resurgence persists due to waning immunity and emerging resistant strains in Bordetella pertussis. This study employs a pangenomics-driven reverse vaccinology approach to identify novel vaccine candidates. Analyzing 160 genomes revealed a closed pan-genome, with approximately 60% conserved genes, including 3389 core genes of which 1312 participate in pathogen-specific pathways. Non-homologous proteins were identified by comparison against human and microbiome proteomes, yielding 205 candidates. Essentiality assessment via the Database of Essential Genes (DEG) refined this to 63 non-homologous essential proteins. A multi-criteria selection process evaluated purifiability based on physicochemical properties and transmembrane helices, accessibility (extracellular or secreted localization), and immunogenicity through antigenicity prediction and B-cell epitope mapping. This pipeline culminated in 11 high-potential vaccine targets. The in silico methodology offers rapidity, cost-effectiveness, and reduced side effects compared with conventional vaccinology, though experimental validation is essential for confirmation.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Recent perspectives on precision-targeting therapy against oral biofilm.
Journal of oral microbiology, 18(1):2662093.
BACKGROUND: Oral biofilm-derived diseases pose a significant clinical challenge due to their persistent nature and increasing drug resistance, contributing to a substantial global economic burden. Conventional treatments-such as mechanical debridement, antiseptic agents, and laser therapy-though partially effective, often lack specificity, resulting in non-targeted microbial killing and disruption of the ecological balance.
OBJECTIVE: This review provides an updated overview of the application of precision antimicrobial therapies against oral biofilms, with a particular focus on pH-responsive materials and bacteriophage-based strategies.
DESIGN: A comprehensive literature search was conducted across PubMed and Google Scholar databases from January 2016 to January 2026. A total of 84 full-text articles were included for qualitative synthesis.
RESULTS: The collective findings demonstrate that multiple precision-targeting strategies-spanning from bacteriophage therapy to pH-responsive antimicrobial materials-exhibit distinct advantages in combating oral biofilms.
CONCLUSION: The common core principle underpinning these approaches lies in their 'precision-targeting' capability: the ability to identify and interfere with specific targets or biological processes. This attribute not only significantly enhances therapeutic efficacy but also paves the way for developing personalized, microbiome-preserving strategies for the prevention and management of oral diseases.
Additional Links: PMID-42038981
PubMed:
Citation:
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@article {pmid42038981,
year = {2026},
author = {Wu, L and Tu, Y and Xiao, S and Zeng, J and Sun, G and Li, Y},
title = {Recent perspectives on precision-targeting therapy against oral biofilm.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2662093},
pmid = {42038981},
issn = {2000-2297},
abstract = {BACKGROUND: Oral biofilm-derived diseases pose a significant clinical challenge due to their persistent nature and increasing drug resistance, contributing to a substantial global economic burden. Conventional treatments-such as mechanical debridement, antiseptic agents, and laser therapy-though partially effective, often lack specificity, resulting in non-targeted microbial killing and disruption of the ecological balance.
OBJECTIVE: This review provides an updated overview of the application of precision antimicrobial therapies against oral biofilms, with a particular focus on pH-responsive materials and bacteriophage-based strategies.
DESIGN: A comprehensive literature search was conducted across PubMed and Google Scholar databases from January 2016 to January 2026. A total of 84 full-text articles were included for qualitative synthesis.
RESULTS: The collective findings demonstrate that multiple precision-targeting strategies-spanning from bacteriophage therapy to pH-responsive antimicrobial materials-exhibit distinct advantages in combating oral biofilms.
CONCLUSION: The common core principle underpinning these approaches lies in their 'precision-targeting' capability: the ability to identify and interfere with specific targets or biological processes. This attribute not only significantly enhances therapeutic efficacy but also paves the way for developing personalized, microbiome-preserving strategies for the prevention and management of oral diseases.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
The prairie vole gut-brain-microbiota-axis: a narrative review.
Gut microbiome (Cambridge, England), 7:e4.
The microbiota-gut-brain axis (MGBA) has garnered considerable attention for its role in health, disease, and higher psychological processes. One area of particular importance is the relationship between the MGBA and stress. Although numerous animal models are suitable for research on stress, the number suitable for research on the impact of social stressors with translatability to humans is limited. The prairie vole is regarded as an ideal organism for probing the impact of social stress, as these animals not only exhibit social behaviours rare in mammals but also lack many drawbacks that come with using non-human primates. Moreover, the neurophysiological basis of their social behaviours is well characterized, and numerous studies have examined the impact of social stress, particularly social isolation, on these animals. However, only a limited number of studies have examined the prairie vole gastrointestinal system, intestinal microbiome, or MGBA. Consequently, this leaves ample opportunity for future research. In this review article, we summarize basic aspects of prairie vole ecology, behaviour, and neurophysiology, then review the limited but valuable body of research examining the gastrointestinal system and microbiome of prairie voles. Additionally, we note potential challenges and opportunities for future MGBA research utilizing prairie voles.
Additional Links: PMID-42039085
PubMed:
Citation:
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@article {pmid42039085,
year = {2026},
author = {Nuccio, DA and Grippo, A and Singh, P},
title = {The prairie vole gut-brain-microbiota-axis: a narrative review.},
journal = {Gut microbiome (Cambridge, England)},
volume = {7},
number = {},
pages = {e4},
pmid = {42039085},
issn = {2632-2897},
abstract = {The microbiota-gut-brain axis (MGBA) has garnered considerable attention for its role in health, disease, and higher psychological processes. One area of particular importance is the relationship between the MGBA and stress. Although numerous animal models are suitable for research on stress, the number suitable for research on the impact of social stressors with translatability to humans is limited. The prairie vole is regarded as an ideal organism for probing the impact of social stress, as these animals not only exhibit social behaviours rare in mammals but also lack many drawbacks that come with using non-human primates. Moreover, the neurophysiological basis of their social behaviours is well characterized, and numerous studies have examined the impact of social stress, particularly social isolation, on these animals. However, only a limited number of studies have examined the prairie vole gastrointestinal system, intestinal microbiome, or MGBA. Consequently, this leaves ample opportunity for future research. In this review article, we summarize basic aspects of prairie vole ecology, behaviour, and neurophysiology, then review the limited but valuable body of research examining the gastrointestinal system and microbiome of prairie voles. Additionally, we note potential challenges and opportunities for future MGBA research utilizing prairie voles.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
A perfect storm: the immunological and pathophysiological landscape of pediatric post-COVID-19 condition.
Frontiers in immunology, 17:1794596.
Pediatric Post-COVID Condition (PPCC) represents a significant and complex long-term sequela of SARS-CoV-2 infection, affecting a subset of children and adolescents even after mild acute disease. While acute COVID-19 is generally milder in children due to a more robust innate immune response, the mechanisms driving the persistence of symptoms in PPCC remain incompletely understood and likely multifactorial. This narrative review synthesizes current epidemiological data and explores the "perfect storm" of immunological and pathophysiological alterations underpinning the condition. We examine critical hypotheses including a dysregulated immune response characterized by altered T-cell subsets, monocyte activation, and autoantibody production. We discuss the potential role of persistent SARS-CoV-2 viral reservoirs in "sanctuary sites" like the gastrointestinal tract and the reactivation of latent viruses such as Epstein-Barr virus (EBV). Furthermore, the review details downstream pathogenic pathways, including vascular endothelial inflammation (thrombo-inflammation), neuroinflammation, and metabolic dysfunctions affecting the mitochondria and tryptophan-kynurenine pathway. Finally, we address the role of microbiome dysbiosis in perpetuating systemic inflammation and the gut-lung axis dysfunction. Given the heterogeneity of clinical presentations, we conclude that PPCC is likely a syndrome of overlapping biological phenotypes. Future research must prioritize identifying these specific biological endotypes to develop targeted diagnostic and therapeutic strategies for the pediatric population.
Additional Links: PMID-42039182
PubMed:
Citation:
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@article {pmid42039182,
year = {2026},
author = {Lap, CR and van Houten, M and Bogaert, D and Biesbroek, G},
title = {A perfect storm: the immunological and pathophysiological landscape of pediatric post-COVID-19 condition.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1794596},
pmid = {42039182},
issn = {1664-3224},
mesh = {Humans ; *COVID-19/immunology/complications/virology/epidemiology ; *SARS-CoV-2/immunology ; Child ; Gastrointestinal Microbiome/immunology ; Dysbiosis/immunology ; Adolescent ; Immunity, Innate ; Post-Acute COVID-19 Syndrome ; },
abstract = {Pediatric Post-COVID Condition (PPCC) represents a significant and complex long-term sequela of SARS-CoV-2 infection, affecting a subset of children and adolescents even after mild acute disease. While acute COVID-19 is generally milder in children due to a more robust innate immune response, the mechanisms driving the persistence of symptoms in PPCC remain incompletely understood and likely multifactorial. This narrative review synthesizes current epidemiological data and explores the "perfect storm" of immunological and pathophysiological alterations underpinning the condition. We examine critical hypotheses including a dysregulated immune response characterized by altered T-cell subsets, monocyte activation, and autoantibody production. We discuss the potential role of persistent SARS-CoV-2 viral reservoirs in "sanctuary sites" like the gastrointestinal tract and the reactivation of latent viruses such as Epstein-Barr virus (EBV). Furthermore, the review details downstream pathogenic pathways, including vascular endothelial inflammation (thrombo-inflammation), neuroinflammation, and metabolic dysfunctions affecting the mitochondria and tryptophan-kynurenine pathway. Finally, we address the role of microbiome dysbiosis in perpetuating systemic inflammation and the gut-lung axis dysfunction. Given the heterogeneity of clinical presentations, we conclude that PPCC is likely a syndrome of overlapping biological phenotypes. Future research must prioritize identifying these specific biological endotypes to develop targeted diagnostic and therapeutic strategies for the pediatric population.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*COVID-19/immunology/complications/virology/epidemiology
*SARS-CoV-2/immunology
Child
Gastrointestinal Microbiome/immunology
Dysbiosis/immunology
Adolescent
Immunity, Innate
Post-Acute COVID-19 Syndrome
RevDate: 2026-04-27
CmpDate: 2026-04-27
What is the impact of the virome and mycobiome on female reproductive tract health? A systematic scoping review.
Frontiers in immunology, 17:1749584.
BACKGROUND: Traditional research on the female reproductive tract (FRT) microbiome has focused on the dominance of bacteria, particularly Lactobacillus, as a marker of health. This bacteriocentric paradigm, however, cannot fully explain clinical enigmas like the high recurrence of bacterial vaginosis (BV) or the persistence of HPV infection. This review introduces a new pan-microbiome framework that highlights the overlooked roles of the virome and mycobiome as the ecosystem's neglected components.
METHODS: We conducted a systematic scoping review following the PRISMA-ScR guidelines. We searched PubMed, Embase, and Web of Science databases for studies published up to October 2025. Inclusion criteria focused on original research and metagenomic studies examining the female reproductive tract (FRT) virome, mycobiome, and bacteriome, specifically their interactions and clinical associations with bacterial vaginosis (BV) and HPV persistence. Data were extracted and synthesized to evaluate the pan-microbiome framework.
RESULTS: The virome and mycobiome, despite their low biomass, are increasingly recognized as potential ecosystem modulators. Bacteriophages, for instance, are proposed to act as community "modulators," either through lytic cycles that maintain bacterial diversity or lysogenic cycles that may contribute to stabilizing pathogenic biofilms in dysbiosis like BV by introducing virulence genes. Similarly, fungi like Candida can transition from harmless commensals to pathogens when the protective bacterial balance is disturbed.
CONCLUSION: FRT health is an emergent property of the complex interactions among bacteria, viruses, and fungi. A comprehensive understanding requires a pan-microbiome perspective. Future therapeutic strategies should move beyond a "one-bug, one-drug" approach toward "ecosystem restoration," using targeted methods like phage therapy or vaginal microbiota transplantation to attempt to restore the balance of the entire microbial community.
Additional Links: PMID-42039195
PubMed:
Citation:
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hide bibtex listing
@article {pmid42039195,
year = {2026},
author = {Liu, Y and Liao, X and Chen, Q and Wang, H and Dai, H},
title = {What is the impact of the virome and mycobiome on female reproductive tract health? A systematic scoping review.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1749584},
pmid = {42039195},
issn = {1664-3224},
mesh = {Female ; Humans ; *Virome ; *Mycobiome ; *Vaginosis, Bacterial/microbiology/virology ; *Microbiota ; Papillomavirus Infections/microbiology/virology ; Vagina/microbiology/virology ; *Reproductive Health ; *Genitalia, Female/microbiology/virology ; Bacteriophages ; },
abstract = {BACKGROUND: Traditional research on the female reproductive tract (FRT) microbiome has focused on the dominance of bacteria, particularly Lactobacillus, as a marker of health. This bacteriocentric paradigm, however, cannot fully explain clinical enigmas like the high recurrence of bacterial vaginosis (BV) or the persistence of HPV infection. This review introduces a new pan-microbiome framework that highlights the overlooked roles of the virome and mycobiome as the ecosystem's neglected components.
METHODS: We conducted a systematic scoping review following the PRISMA-ScR guidelines. We searched PubMed, Embase, and Web of Science databases for studies published up to October 2025. Inclusion criteria focused on original research and metagenomic studies examining the female reproductive tract (FRT) virome, mycobiome, and bacteriome, specifically their interactions and clinical associations with bacterial vaginosis (BV) and HPV persistence. Data were extracted and synthesized to evaluate the pan-microbiome framework.
RESULTS: The virome and mycobiome, despite their low biomass, are increasingly recognized as potential ecosystem modulators. Bacteriophages, for instance, are proposed to act as community "modulators," either through lytic cycles that maintain bacterial diversity or lysogenic cycles that may contribute to stabilizing pathogenic biofilms in dysbiosis like BV by introducing virulence genes. Similarly, fungi like Candida can transition from harmless commensals to pathogens when the protective bacterial balance is disturbed.
CONCLUSION: FRT health is an emergent property of the complex interactions among bacteria, viruses, and fungi. A comprehensive understanding requires a pan-microbiome perspective. Future therapeutic strategies should move beyond a "one-bug, one-drug" approach toward "ecosystem restoration," using targeted methods like phage therapy or vaginal microbiota transplantation to attempt to restore the balance of the entire microbial community.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
Humans
*Virome
*Mycobiome
*Vaginosis, Bacterial/microbiology/virology
*Microbiota
Papillomavirus Infections/microbiology/virology
Vagina/microbiology/virology
*Reproductive Health
*Genitalia, Female/microbiology/virology
Bacteriophages
RevDate: 2026-04-27
CmpDate: 2026-04-27
Targeted intestinal barrier repair via probiotic-derived engineered outer membrane vesicles: A 3A1M strategy with antioxidant, anti-inflammatory, anti-ferroptotic, and microbiome modulation effects.
Acta pharmaceutica Sinica. B, 16(4):2527-2552.
Intestinal barrier disruption, driven by oxidative stress, ferroptosis, immune imbalance, and gut microbiota dysbiosis, plays a crucial role in inflammatory bowel disease (IBD) pathogenesis. Current treatments are often ineffective and cause side effects, emphasizing the need for novel therapies. Here, we have developed an engineered probiotic-derived outer membrane vesicle (OMV), GDO@CM, combining antioxidant gallic acid (GA) and anti-inflammatory H2S for targeted intestinal barrier repair. Constructed from Escherichia coli Nissle 1917 (EcN)-derived OMVs, GA and diallyl trisulfide (DATS) are incorporated into the hydrophilic inner cavity and lipid bilayer, respectively, while mannose-decorated chitosan (CM) is electrostatically attached to the OMVs surface, enhancing stability and enabling targeted delivery to damaged colonic lesions. GDO@CM efficiently enters activated immune cells and epithelial cells, where GA scavenges reactive oxygen species and inhibits ferroptosis, while H2S amplifies anti-inflammatory effects. OMVs further synergize with GA and DATS to suppress pathogenic bacteria. These combined actions facilitate effective barrier repair and alleviate IBD symptoms. Single-cell RNA sequencing reveals that GDO@CM reduces inflammation, increases the proportion of reparative M2 macrophages and intestinal stem cells, and promotes epithelial cell proliferation via the APP/CD74 axis. Our findings establish GDO@CM as a promising multi-target therapeutic for IBD, offering a novel strategy for intestinal barrier restoration.
Additional Links: PMID-42039264
PubMed:
Citation:
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@article {pmid42039264,
year = {2026},
author = {Yu, L and Zhang, H and Shi, C and Zhou, Q and Li, J and Lu, B and Lu, H and Jin, T and Zhu, Y and Zuo, T and Xu, M and Su, M and Zhang, Y and Shubhra, QTH and Hu, X and Deng, H and Cai, X},
title = {Targeted intestinal barrier repair via probiotic-derived engineered outer membrane vesicles: A 3A1M strategy with antioxidant, anti-inflammatory, anti-ferroptotic, and microbiome modulation effects.},
journal = {Acta pharmaceutica Sinica. B},
volume = {16},
number = {4},
pages = {2527-2552},
pmid = {42039264},
issn = {2211-3835},
abstract = {Intestinal barrier disruption, driven by oxidative stress, ferroptosis, immune imbalance, and gut microbiota dysbiosis, plays a crucial role in inflammatory bowel disease (IBD) pathogenesis. Current treatments are often ineffective and cause side effects, emphasizing the need for novel therapies. Here, we have developed an engineered probiotic-derived outer membrane vesicle (OMV), GDO@CM, combining antioxidant gallic acid (GA) and anti-inflammatory H2S for targeted intestinal barrier repair. Constructed from Escherichia coli Nissle 1917 (EcN)-derived OMVs, GA and diallyl trisulfide (DATS) are incorporated into the hydrophilic inner cavity and lipid bilayer, respectively, while mannose-decorated chitosan (CM) is electrostatically attached to the OMVs surface, enhancing stability and enabling targeted delivery to damaged colonic lesions. GDO@CM efficiently enters activated immune cells and epithelial cells, where GA scavenges reactive oxygen species and inhibits ferroptosis, while H2S amplifies anti-inflammatory effects. OMVs further synergize with GA and DATS to suppress pathogenic bacteria. These combined actions facilitate effective barrier repair and alleviate IBD symptoms. Single-cell RNA sequencing reveals that GDO@CM reduces inflammation, increases the proportion of reparative M2 macrophages and intestinal stem cells, and promotes epithelial cell proliferation via the APP/CD74 axis. Our findings establish GDO@CM as a promising multi-target therapeutic for IBD, offering a novel strategy for intestinal barrier restoration.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
A microbiota-derived bile acid overcomes antibiotic-induced hyporesponsiveness to immune checkpoint therapy by enhancing CD8 [+] T cell antitumor immunity.
bioRxiv : the preprint server for biology pii:2026.04.15.718788.
UNLABELLED: Gut microbiota are critical determinants of effective immune checkpoint therapy (ICT), yet the microbial mediators and host mechanisms that enhance antitumor immunity remain poorly understood. Here, we identify the microbiota-derived bile acid taurodeoxycholic acid (TDCA) as a metabolite associated with immune checkpoint therapy (ICT) response. TDCA administration alone is sufficient to overcome antibiotic-induced ICT hyporesponsiveness across multiple murine tumor models. Mechanistically, TDCA directly enhances CD8[+] T cell-mediated antitumor immunity, increasing cytotoxicity. These effects required signaling through the bile acid receptor TGR5. Together, these findings reveal TDCA as a gut microbial metabolite that restores ICT efficacy after antibiotic disruption by directly augmenting CD8[+] T cell anti-tumor activity. This work supports metabolite replacement as a therapeutic strategy to mitigate antibiotic-associated loss of cancer immunotherapy response.
SIGNIFICANCE: TDCA is a microbiota-derived metabolite that restores immune checkpoint therapy efficacy after antibiotic disruption by directly enhancing CD8⁺ T-cell-mediated anti-tumor immunity through bile acid receptor TGR5 signaling. Our findings suggest that supplementation with defined microbial metabolites can mitigate antibiotic-associated loss of immunotherapy response without requiring broader microbiome reconstitution.
Additional Links: PMID-42039389
Full Text:
Publisher:
PubMed:
Citation:
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@article {pmid42039389,
year = {2026},
author = {Li, W and Zarek, CM and Wang, H and Gan, S and Sabaiefard, P and Del Valle, P and Kim, J and Poulides, N and Coughlin, LA and Lichterman, JN and Zhang, C and Chiu, RS and Srinivasan, T and Velasquez, MJ and Raman, I and Maddox, VJ and McDonald, J and Kittler, R and Raj, P and Li, XV and Zhan, X and Liao, C and Xavier, JB and Koh, AY},
title = {A microbiota-derived bile acid overcomes antibiotic-induced hyporesponsiveness to immune checkpoint therapy by enhancing CD8 [+] T cell antitumor immunity.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.15.718788},
pmid = {42039389},
issn = {2692-8205},
abstract = {UNLABELLED: Gut microbiota are critical determinants of effective immune checkpoint therapy (ICT), yet the microbial mediators and host mechanisms that enhance antitumor immunity remain poorly understood. Here, we identify the microbiota-derived bile acid taurodeoxycholic acid (TDCA) as a metabolite associated with immune checkpoint therapy (ICT) response. TDCA administration alone is sufficient to overcome antibiotic-induced ICT hyporesponsiveness across multiple murine tumor models. Mechanistically, TDCA directly enhances CD8[+] T cell-mediated antitumor immunity, increasing cytotoxicity. These effects required signaling through the bile acid receptor TGR5. Together, these findings reveal TDCA as a gut microbial metabolite that restores ICT efficacy after antibiotic disruption by directly augmenting CD8[+] T cell anti-tumor activity. This work supports metabolite replacement as a therapeutic strategy to mitigate antibiotic-associated loss of cancer immunotherapy response.
SIGNIFICANCE: TDCA is a microbiota-derived metabolite that restores immune checkpoint therapy efficacy after antibiotic disruption by directly enhancing CD8⁺ T-cell-mediated anti-tumor immunity through bile acid receptor TGR5 signaling. Our findings suggest that supplementation with defined microbial metabolites can mitigate antibiotic-associated loss of immunotherapy response without requiring broader microbiome reconstitution.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Distinct prokaryotic gut microbiome and proviral-immune axes of pathophysiology in Sickle Cell Disease.
bioRxiv : the preprint server for biology pii:2026.04.13.718288.
Sickle cell disease (SCD) is a chronic, inherited condition rising across the globe. Prior studies revealed a direct link between the gut microbiome and disease micropathology via aged-like (ANs) neutrophils in mouse models. In SCD patients community-level shifts in the gut microbiome included decreases in diversity and the Firmicutes/Bacteroides (F:B) ratio, coupled to a loss of short chain fatty acid producing microbes and a shift to non-canonical butyrate production and aerobic fatty acid oxidation pathways. ANs and the proviral microbiome associate with multiple blood cytokines, while bacterial gut microbiome features largely do not. Prophages depleted of genes related to lysis, transcriptional regulation, and host takeover were enriched in SCD patient guts, pointing to domestication of these elements, and 25% of prophages were shared at high identity between study patients. In sum, we identify a viral-immune axis in SCD pathophysiology and targetable functional alterations to the gut microbiome in a heterogeneous chronic disease both affected by and effecting microbiome composition and function.
Additional Links: PMID-42039437
Full Text:
Publisher:
PubMed:
Citation:
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@article {pmid42039437,
year = {2026},
author = {Flamholz, ZN and De Los Santos, J and Ireland, K and Keenan, J and Kazmi, JS and Mahant, AM and Correa, A and Frenette, PS and Herold, BC and Manwani, D and Kelly, L},
title = {Distinct prokaryotic gut microbiome and proviral-immune axes of pathophysiology in Sickle Cell Disease.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.13.718288},
pmid = {42039437},
issn = {2692-8205},
abstract = {Sickle cell disease (SCD) is a chronic, inherited condition rising across the globe. Prior studies revealed a direct link between the gut microbiome and disease micropathology via aged-like (ANs) neutrophils in mouse models. In SCD patients community-level shifts in the gut microbiome included decreases in diversity and the Firmicutes/Bacteroides (F:B) ratio, coupled to a loss of short chain fatty acid producing microbes and a shift to non-canonical butyrate production and aerobic fatty acid oxidation pathways. ANs and the proviral microbiome associate with multiple blood cytokines, while bacterial gut microbiome features largely do not. Prophages depleted of genes related to lysis, transcriptional regulation, and host takeover were enriched in SCD patient guts, pointing to domestication of these elements, and 25% of prophages were shared at high identity between study patients. In sum, we identify a viral-immune axis in SCD pathophysiology and targetable functional alterations to the gut microbiome in a heterogeneous chronic disease both affected by and effecting microbiome composition and function.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
16S rRNA k-mer composition encodes microbial functional potential.
bioRxiv : the preprint server for biology pii:2026.04.16.718937.
16S rRNA amplicon sequencing is widely used to profile microbiome taxonomic composition and functional potential. Most 16S rRNA-based analysis methods depend on comparing sequenced reads against reference marker genes from previously characterized organisms. Thus, method accuracy declines in environments dominated by uncharacterized microbes. We uncovered a direct link between 16S rRNA and genome-encoded functions. Using fully sequenced bacterial genomes, we show that (i) whole-genome k-mer composition is predictive of functions encoded in the genome and (ii) 16S rRNA k-mer profiles reflect their source genome k-mer compositions. Leveraging these relationships, we developed embeRNA, a neural network-based framework that predicts functions directly from 16S rRNA k-mer embeddings, without taxonomy assignment or phylogenetic placement. Furthermore, by producing per-function probability scores rather than categorical assignments, embeRNA allows users to adapt decision thresholds to match study goals and sample characteristics, e.g. balancing precision vs. recall or accounting for community novelty. We trained embeRNA on a large collection of bacterial function-omes and evaluated it using a stringent "novel microbes" benchmark, where all test 16S rRNA sequences were dissimilar to those seen in training (all <97% identical). On this test set of phylogenetically novel organisms, embeRNA outperformed reference-based methods overall and achieved significantly better performance for the "hard to label" set of functions. In testing on soil metagenomes with paired 16S rRNA amplicon and whole metagenome shotgun (WMS) sequencing data, embeRNA recovered most WMS-inferred functions and yielded abundance profiles strongly correlated with WMS results. Together, our results indicate that 16S rRNA k-mer composition carries substantial functional signal and that 16S amplicon data can be used to complement WMS-based inference to broaden functional characterization of microbiomes, particularly in understudied environments.
Additional Links: PMID-42039480
Full Text:
Publisher:
PubMed:
Citation:
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@article {pmid42039480,
year = {2026},
author = {Liu, J and De Paolis Kaluza, MC and Bromberg, Y},
title = {16S rRNA k-mer composition encodes microbial functional potential.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.16.718937},
pmid = {42039480},
issn = {2692-8205},
abstract = {16S rRNA amplicon sequencing is widely used to profile microbiome taxonomic composition and functional potential. Most 16S rRNA-based analysis methods depend on comparing sequenced reads against reference marker genes from previously characterized organisms. Thus, method accuracy declines in environments dominated by uncharacterized microbes. We uncovered a direct link between 16S rRNA and genome-encoded functions. Using fully sequenced bacterial genomes, we show that (i) whole-genome k-mer composition is predictive of functions encoded in the genome and (ii) 16S rRNA k-mer profiles reflect their source genome k-mer compositions. Leveraging these relationships, we developed embeRNA, a neural network-based framework that predicts functions directly from 16S rRNA k-mer embeddings, without taxonomy assignment or phylogenetic placement. Furthermore, by producing per-function probability scores rather than categorical assignments, embeRNA allows users to adapt decision thresholds to match study goals and sample characteristics, e.g. balancing precision vs. recall or accounting for community novelty. We trained embeRNA on a large collection of bacterial function-omes and evaluated it using a stringent "novel microbes" benchmark, where all test 16S rRNA sequences were dissimilar to those seen in training (all <97% identical). On this test set of phylogenetically novel organisms, embeRNA outperformed reference-based methods overall and achieved significantly better performance for the "hard to label" set of functions. In testing on soil metagenomes with paired 16S rRNA amplicon and whole metagenome shotgun (WMS) sequencing data, embeRNA recovered most WMS-inferred functions and yielded abundance profiles strongly correlated with WMS results. Together, our results indicate that 16S rRNA k-mer composition carries substantial functional signal and that 16S amplicon data can be used to complement WMS-based inference to broaden functional characterization of microbiomes, particularly in understudied environments.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Ketogenic diet synergistic reprogramming of both host and microbiome promotes tissue regeneration.
bioRxiv : the preprint server for biology pii:2026.04.11.717958.
Nutrition influences host physiological processes, yet how diets reshape host physiology, microbial functions, or host-microbe interactions to promote regeneration remains poorly explored. Here, we show that a ketogenic diet (KD), enriched in fats and low in carbohydrates, reprograms both skin microbial and immune functions to promote tissue repair. KD enhances IL-17A activity in γδ T cells and mucosal-associated invariant T (MAIT) cells, accelerating tissue repair, while KD-induced skin lipidomic alterations enhance both the abundance and metabolic output of Staphylococcus epidermidis . Metatranscriptomic and lipidomic analyses revealed increased riboflavin biosynthesis and sphingomyelinase (Sph)-dependent ceramide production in S. epidermidis under KD conditions. Genetic depletion of microbial ribD, a key enzyme for riboflavin biosynthesis, or of sph compromised the ability of the bacteria to promote tissue repair. Thus, host nutritional status drives tissue regeneration by synergistically rewiring host and microbial functions, providing new insights into how diet can be harnessed to regulate host physiology.
Additional Links: PMID-42039490
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PubMed:
Citation:
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@article {pmid42039490,
year = {2026},
author = {Nagai, M and Band, V and Chi, L and Smelkinson, M and Schwarz, B and Brandes, NT and Burns, A and Perez-Chaparro, PJ and McCauley, KE and Corral, D and Bouladoux, N and Link, VM and Zheng, L and Constantinides, MG and Otto, M and Moutsopoulos, NM and Belkaid, Y},
title = {Ketogenic diet synergistic reprogramming of both host and microbiome promotes tissue regeneration.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.11.717958},
pmid = {42039490},
issn = {2692-8205},
abstract = {Nutrition influences host physiological processes, yet how diets reshape host physiology, microbial functions, or host-microbe interactions to promote regeneration remains poorly explored. Here, we show that a ketogenic diet (KD), enriched in fats and low in carbohydrates, reprograms both skin microbial and immune functions to promote tissue repair. KD enhances IL-17A activity in γδ T cells and mucosal-associated invariant T (MAIT) cells, accelerating tissue repair, while KD-induced skin lipidomic alterations enhance both the abundance and metabolic output of Staphylococcus epidermidis . Metatranscriptomic and lipidomic analyses revealed increased riboflavin biosynthesis and sphingomyelinase (Sph)-dependent ceramide production in S. epidermidis under KD conditions. Genetic depletion of microbial ribD, a key enzyme for riboflavin biosynthesis, or of sph compromised the ability of the bacteria to promote tissue repair. Thus, host nutritional status drives tissue regeneration by synergistically rewiring host and microbial functions, providing new insights into how diet can be harnessed to regulate host physiology.},
}
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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.
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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.
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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.
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Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.