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ESP: PubMed Auto Bibliography 14 Dec 2025 at 01:55 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2025-12-13
Resistant starch improves Parkinson's disease symptoms through restructuring of the gut microbiome and modulating inflammation.
Brain, behavior, and immunity pii:S0889-1591(25)00459-3 [Epub ahead of print].
Alterations in the gut microbiome and a "leaky" gut are associated with Parkinson's disease (PD), which implies the prospect of rebalancing via dietary intervention. Here, we investigate the impact of a diet rich in resistant starch on the gut microbiome through a multi-omics approach. We conducted a randomized, controlled trial with short-term and long-term phases involving 74 PD patients of three groups: conventional diet, supplementation with resistant starch, and high-fibre diet. Our findings reveal associations between dietary patterns and changes in the gut microbiome's taxonomic composition, functional potential, metabolic activity, and host inflammatory proteome response. Resistant starch supplementation led to an increase in Faecalibacterium species and short-chain fatty acids and a reduction of opportunistic pathogens. Long-term supplementation also increased blood APOA4 and HSPA5 and reduced symptoms of PD. Our study highlights the potential of dietary interventions to modulate the gut microbiome and improve the quality of life for PD patients.
Additional Links: PMID-41389850
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PubMed:
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@article {pmid41389850,
year = {2025},
author = {Petrov, VA and Schade, S and Laczny, CC and Hallqvist, J and May, P and Jäger, C and Aho, VTE and Hickl, O and Halder, R and Lang, E and Caussin, J and Lebrun, LA and Schulz, J and Unger, MM and Mills, K and Mollenhauer, B and Wilmes, P},
title = {Resistant starch improves Parkinson's disease symptoms through restructuring of the gut microbiome and modulating inflammation.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {106217},
doi = {10.1016/j.bbi.2025.106217},
pmid = {41389850},
issn = {1090-2139},
abstract = {Alterations in the gut microbiome and a "leaky" gut are associated with Parkinson's disease (PD), which implies the prospect of rebalancing via dietary intervention. Here, we investigate the impact of a diet rich in resistant starch on the gut microbiome through a multi-omics approach. We conducted a randomized, controlled trial with short-term and long-term phases involving 74 PD patients of three groups: conventional diet, supplementation with resistant starch, and high-fibre diet. Our findings reveal associations between dietary patterns and changes in the gut microbiome's taxonomic composition, functional potential, metabolic activity, and host inflammatory proteome response. Resistant starch supplementation led to an increase in Faecalibacterium species and short-chain fatty acids and a reduction of opportunistic pathogens. Long-term supplementation also increased blood APOA4 and HSPA5 and reduced symptoms of PD. Our study highlights the potential of dietary interventions to modulate the gut microbiome and improve the quality of life for PD patients.},
}
RevDate: 2025-12-13
Fluoride-induced gut dysbiosis in metabolic disorders: Mechanisms and public health implications.
Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS), 93:127806 pii:S0946-672X(25)00219-6 [Epub ahead of print].
AIM: This review explores the effects of fluoride exposure and metabolic alterations linked to obesity and diabetes, and highlights preventive and therapeutic approaches to mitigate fluoride-driven metabolic risks.
SUMMARY: While fluoride is beneficial to dental health, but excessive exposure disrupts gut microbiota composition, reducing short-chain fatty acids (SCFA) production and impairing intestinal barrier integrity. These disruptions alter the oxidative stress, inflammation and insulin resistance. Evidence from animal and human studies suggest a dose-dependent pattern, with depletion of beneficial bacteria such as Lactobacillus and Faecalibacterium and enrichment of pro-inflammatory microbes. Such microbial imbalances influence bile acid metabolism. lipopolysaccharide (LPS) translocation and glucose regulation. This review discusses potential microbiome modulating strategies include probiotics, prebiotics, synbiotics, fecal microbiota transplantation (FMT) and glucose lowering agents such as metformin and GLP-1 receptor agonists as possible therapeutic interventions to restore microbial balance and improve metabolic outcome However, the long-term and epigenetic effects of fluoride on intestinal and metabolic health remain unclear.
CONCLUSION: Since fluoride contaminates drinking water in areas with an endemic tendency, defluoridation, exposure monitoring, and public awareness are essential preventive strategies. Future mechanistic and clinical studies are necessary to elucidate the pathways linking fluoride metabolic disease progression.
Additional Links: PMID-41389504
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PubMed:
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@article {pmid41389504,
year = {2025},
author = {Meenakshi, S and Amrutha, TV and Abubakar, M and Prakash, V and Kumar, N and Murti, K},
title = {Fluoride-induced gut dysbiosis in metabolic disorders: Mechanisms and public health implications.},
journal = {Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)},
volume = {93},
number = {},
pages = {127806},
doi = {10.1016/j.jtemb.2025.127806},
pmid = {41389504},
issn = {1878-3252},
abstract = {AIM: This review explores the effects of fluoride exposure and metabolic alterations linked to obesity and diabetes, and highlights preventive and therapeutic approaches to mitigate fluoride-driven metabolic risks.
SUMMARY: While fluoride is beneficial to dental health, but excessive exposure disrupts gut microbiota composition, reducing short-chain fatty acids (SCFA) production and impairing intestinal barrier integrity. These disruptions alter the oxidative stress, inflammation and insulin resistance. Evidence from animal and human studies suggest a dose-dependent pattern, with depletion of beneficial bacteria such as Lactobacillus and Faecalibacterium and enrichment of pro-inflammatory microbes. Such microbial imbalances influence bile acid metabolism. lipopolysaccharide (LPS) translocation and glucose regulation. This review discusses potential microbiome modulating strategies include probiotics, prebiotics, synbiotics, fecal microbiota transplantation (FMT) and glucose lowering agents such as metformin and GLP-1 receptor agonists as possible therapeutic interventions to restore microbial balance and improve metabolic outcome However, the long-term and epigenetic effects of fluoride on intestinal and metabolic health remain unclear.
CONCLUSION: Since fluoride contaminates drinking water in areas with an endemic tendency, defluoridation, exposure monitoring, and public awareness are essential preventive strategies. Future mechanistic and clinical studies are necessary to elucidate the pathways linking fluoride metabolic disease progression.},
}
RevDate: 2025-12-13
DIETARY MANAGEMENT OF FUNCTIONAL CONSTIPATION IN DISORDERS OF GUT-BRAIN INTERACTION - A SCOPING REVIEW.
Clinical nutrition ESPEN pii:S2405-4577(25)03162-6 [Epub ahead of print].
BACKGROUND: Functional constipation is one of the most prevalent disorders of gut-brain interaction, but available dietary interventions haven't been comprehensively collated.
AIMS: The aim of this scoping review was to synthesise the current evidence surrounding dietary-based interventions used to manage functional constipation in adults and to identify any gaps among published dietary management strategies that could warrant further research, namely a systematic review.
METHODS: A comprehensive database search was conducted on MEDLINE, CINAHL and Web of Science capturing the notions of 'dietary management' and 'disorders of gut-brain interaction', from which two rounds of screening were performed.
RESULTS: Forty primary studies and twelve review papers were included in this review. These 52 papers non-exclusively cover a range of dietary domains including fibre supplementation (n=15), microbiome modulation using prebiotics, probiotics or synbiotics (n=26), functional foods (n=10), fluid intake (n=6) and other dietary approaches (n=7). Fiber supplementation with psyllium is the current strongest dietary recommendation, with emerging strong evidence backing functional fruits like kiwifruit and prunes. Meanwhile the efficacy for all other approaches cannot be accurately deduced due to limited well-designed studies or conflicting evidence. However, improvements to constipation severity or symptoms have been observed with probiotics with both Bifidobacterium and Lactobacillus components, galacto-oligosaccharides, partially hydrolysed guar gum and various synbiotic formulations.
CONCLUSIONS: This paper contributes to the growing research around functional constipation where the open-ended approach allowed for identification and synthesis of all nutrition strategies trialed in the literature. We recommend further studies to be conducted on prebiotics, probiotics and synbiotics to determine its potential role in constipation management for this cohort.
Additional Links: PMID-41390064
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PubMed:
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@article {pmid41390064,
year = {2025},
author = {Quan, V and Carey, S},
title = {DIETARY MANAGEMENT OF FUNCTIONAL CONSTIPATION IN DISORDERS OF GUT-BRAIN INTERACTION - A SCOPING REVIEW.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {102849},
doi = {10.1016/j.clnesp.2025.102849},
pmid = {41390064},
issn = {2405-4577},
abstract = {BACKGROUND: Functional constipation is one of the most prevalent disorders of gut-brain interaction, but available dietary interventions haven't been comprehensively collated.
AIMS: The aim of this scoping review was to synthesise the current evidence surrounding dietary-based interventions used to manage functional constipation in adults and to identify any gaps among published dietary management strategies that could warrant further research, namely a systematic review.
METHODS: A comprehensive database search was conducted on MEDLINE, CINAHL and Web of Science capturing the notions of 'dietary management' and 'disorders of gut-brain interaction', from which two rounds of screening were performed.
RESULTS: Forty primary studies and twelve review papers were included in this review. These 52 papers non-exclusively cover a range of dietary domains including fibre supplementation (n=15), microbiome modulation using prebiotics, probiotics or synbiotics (n=26), functional foods (n=10), fluid intake (n=6) and other dietary approaches (n=7). Fiber supplementation with psyllium is the current strongest dietary recommendation, with emerging strong evidence backing functional fruits like kiwifruit and prunes. Meanwhile the efficacy for all other approaches cannot be accurately deduced due to limited well-designed studies or conflicting evidence. However, improvements to constipation severity or symptoms have been observed with probiotics with both Bifidobacterium and Lactobacillus components, galacto-oligosaccharides, partially hydrolysed guar gum and various synbiotic formulations.
CONCLUSIONS: This paper contributes to the growing research around functional constipation where the open-ended approach allowed for identification and synthesis of all nutrition strategies trialed in the literature. We recommend further studies to be conducted on prebiotics, probiotics and synbiotics to determine its potential role in constipation management for this cohort.},
}
RevDate: 2025-12-13
A scoping review of the clinical outcomes and use of blenderized tube feeds and commercial food-based formulas in pediatrics.
Clinical nutrition ESPEN pii:S2405-4577(25)03158-4 [Epub ahead of print].
BACKGROUND & AIMS: Blenderized tube feeding (BTF) is the use of blended whole foods and liquids given into the gastrointestinal (GI) system via an enteral access device, such as a gastrostomy tube. With an increased interest among caregivers as well as clinicians in BTFs, variations have evolved including homemade BTFs (HBTFs), commercially prepared BTFs (CBTFs), and commercial food-based formula (CFBF). Convenient, ready-to-use alternatives to HBTFs, either CBTFs or CFBFs, are considered appealing by tube-fed patients and/or their caregivers, as well as health care providers. While CBTFs or CFBFs may offer similar benefits to HBTFs, research on these products has been sparse. This scoping review aims to map and summarize the currently available literature on CBTFs, CFBFs, or commercially blenderized feeds (CBFs) when undifferentiated in the study, as well as offer recommendations for clinical practice and future research.
METHODS: This scoping review was conducted in accordance with the Preferred Reporting Items for Systematic review and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR). A comprehensive search strategy was developed and applied across four databases: PubMed, Ovid MEDLINE(R), CINAHL, and Web of Science. Eligible studies were full-text, English language, articles that reported on the use of CBFs among the pediatric population receiving enteral nutrition.
RESULTS: Sixteen studies met the inclusion criteria. Key outcome themes identified included clinical outcomes (GI symptoms, stool patterns, growth and weight, GI microbiome, and emergency department visits and hospitalizations), nutritional adequacy, satisfaction and quality of life, and viscosity and the effects of the administration of CBFs.
CONCLUSIONS: Current evidence suggests that CBFs may improve GI tolerance, support greater gut microdiversity, reduce medical burdens, and enhance quality of life in pediatric patients receiving enteral nutrition. Nevertheless, the limited number and methodological heterogeneity of studies highlight the need for more rigorous research to determine the long-term safety, efficacy, and nutritional adequacy of these formulas.
Additional Links: PMID-41390062
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PubMed:
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@article {pmid41390062,
year = {2025},
author = {Ramuscak, AV and Martincevic, I and Hulst, JM},
title = {A scoping review of the clinical outcomes and use of blenderized tube feeds and commercial food-based formulas in pediatrics.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {102845},
doi = {10.1016/j.clnesp.2025.102845},
pmid = {41390062},
issn = {2405-4577},
abstract = {BACKGROUND & AIMS: Blenderized tube feeding (BTF) is the use of blended whole foods and liquids given into the gastrointestinal (GI) system via an enteral access device, such as a gastrostomy tube. With an increased interest among caregivers as well as clinicians in BTFs, variations have evolved including homemade BTFs (HBTFs), commercially prepared BTFs (CBTFs), and commercial food-based formula (CFBF). Convenient, ready-to-use alternatives to HBTFs, either CBTFs or CFBFs, are considered appealing by tube-fed patients and/or their caregivers, as well as health care providers. While CBTFs or CFBFs may offer similar benefits to HBTFs, research on these products has been sparse. This scoping review aims to map and summarize the currently available literature on CBTFs, CFBFs, or commercially blenderized feeds (CBFs) when undifferentiated in the study, as well as offer recommendations for clinical practice and future research.
METHODS: This scoping review was conducted in accordance with the Preferred Reporting Items for Systematic review and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR). A comprehensive search strategy was developed and applied across four databases: PubMed, Ovid MEDLINE(R), CINAHL, and Web of Science. Eligible studies were full-text, English language, articles that reported on the use of CBFs among the pediatric population receiving enteral nutrition.
RESULTS: Sixteen studies met the inclusion criteria. Key outcome themes identified included clinical outcomes (GI symptoms, stool patterns, growth and weight, GI microbiome, and emergency department visits and hospitalizations), nutritional adequacy, satisfaction and quality of life, and viscosity and the effects of the administration of CBFs.
CONCLUSIONS: Current evidence suggests that CBFs may improve GI tolerance, support greater gut microdiversity, reduce medical burdens, and enhance quality of life in pediatric patients receiving enteral nutrition. Nevertheless, the limited number and methodological heterogeneity of studies highlight the need for more rigorous research to determine the long-term safety, efficacy, and nutritional adequacy of these formulas.},
}
RevDate: 2025-12-13
Gellan gum-based nanocarriers for the delivery of anticancer agents: A review.
International journal of biological macromolecules pii:S0141-8130(25)10217-1 [Epub ahead of print].
Gellan gum (GG) is a naturally occurring anionic polysaccharide that has been used extensively in the delivery of anticancer agents. The application of GG as an effective delivery vehicle is prominently dependent on its adjustable physicochemical characteristics, biocompatibility, and biodegradability. GG has the capability of forming stable hydrogels and diverse nanostructures in physiological conditions. Hence, it is used in the development of multipurpose drug carriers that can effectively carry and deliver a broad spectrum of anticancer drugs at the site of action. Recently, the development of hybrid and composite GG-based systems, where GG is combined with synthetic polymers, nanoparticles, or bioactive peptides, has gained tremendous attention in the scientific community since they provide improved mechanical stability, pharmacokinetic properties, and synergistic biological effects, thereby expanding the therapeutic potential and versatility of GG nanocarriers. However, several obstacles must be addressed before its widespread clinical application can be fathomed. These include ensuring commercial-scale repeatability, long-term stability, precise control of drug release kinetics, and addressing regulatory complications. In addition, further research is required to maximize safety and effectiveness in the interactions of GG nanocarriers with biological settings, such as enzymatic degradation, immunological responses, and microbiome interactions. Interdisciplinary research integrating materials science, pharmacology, and clinical studies will be critical for its further applications. Continued research efforts and collaborative innovation are expected to establish GG-based delivery systems as the core platforms for next-generation anticancer therapies.
Additional Links: PMID-41390021
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PubMed:
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@article {pmid41390021,
year = {2025},
author = {Bora, S and Priya, B and Pooja, D and Kulhari, H},
title = {Gellan gum-based nanocarriers for the delivery of anticancer agents: A review.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {149660},
doi = {10.1016/j.ijbiomac.2025.149660},
pmid = {41390021},
issn = {1879-0003},
abstract = {Gellan gum (GG) is a naturally occurring anionic polysaccharide that has been used extensively in the delivery of anticancer agents. The application of GG as an effective delivery vehicle is prominently dependent on its adjustable physicochemical characteristics, biocompatibility, and biodegradability. GG has the capability of forming stable hydrogels and diverse nanostructures in physiological conditions. Hence, it is used in the development of multipurpose drug carriers that can effectively carry and deliver a broad spectrum of anticancer drugs at the site of action. Recently, the development of hybrid and composite GG-based systems, where GG is combined with synthetic polymers, nanoparticles, or bioactive peptides, has gained tremendous attention in the scientific community since they provide improved mechanical stability, pharmacokinetic properties, and synergistic biological effects, thereby expanding the therapeutic potential and versatility of GG nanocarriers. However, several obstacles must be addressed before its widespread clinical application can be fathomed. These include ensuring commercial-scale repeatability, long-term stability, precise control of drug release kinetics, and addressing regulatory complications. In addition, further research is required to maximize safety and effectiveness in the interactions of GG nanocarriers with biological settings, such as enzymatic degradation, immunological responses, and microbiome interactions. Interdisciplinary research integrating materials science, pharmacology, and clinical studies will be critical for its further applications. Continued research efforts and collaborative innovation are expected to establish GG-based delivery systems as the core platforms for next-generation anticancer therapies.},
}
RevDate: 2025-12-13
Aging of the Colon - A Mechanistic View.
Mechanisms of ageing and development pii:S0047-6374(25)00119-8 [Epub ahead of print].
The colon is one of the gastrointestinal organs most profoundly affected by aging. Recent advances in our understanding of both colonic physiology and the general mechanisms of aging have significantly expanded our knowledge of the types and underlying processes of colonic aging. In this review, we summarize current insights into the cellular and molecular mechanisms that drive physiological aging of the human colon. We examine the unique structural and functional features of key components of the colon, including the epithelium, local immune system, microbiome, enteric neurons, and smooth muscle cells, and explore how aging affects each of these cell populations, ultimately impacting overall colonic function. In the epithelium, increased mutational burden does not appear to be the primary driver of age-related dysfunction. Instead, dysregulation of signaling pathways such as EGF and Wnt is likely responsible for key phenotypic changes. Aged colonic neurons display protein misfolding and axonal dysfunction reminiscent of aging processes observed in the central nervous system. Similarly, smooth muscle cells exhibit impaired contractility, which is associated with disruptions in calcium homeostasis and deficits in cholinergic signaling. At the same time, age-related activation of the local immune system mirrors broader immunosenescence and may be further influenced by shifts in the gut microbiome, although a consistent aging-associated microbiome signature has yet to be identified. These multifaceted changes, combined with the colon's inherent regional and cellular complexity and the challenges of modeling human colonic aging, continue to fascinate but also pose substantial obstacles for research. Emerging experimental models and clinical strategies offer promising avenues for improving the prevention and treatment of age-associated colonic dysfunction.
Additional Links: PMID-41389945
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PubMed:
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@article {pmid41389945,
year = {2025},
author = {Hofmann, C and Geiger, H},
title = {Aging of the Colon - A Mechanistic View.},
journal = {Mechanisms of ageing and development},
volume = {},
number = {},
pages = {112143},
doi = {10.1016/j.mad.2025.112143},
pmid = {41389945},
issn = {1872-6216},
abstract = {The colon is one of the gastrointestinal organs most profoundly affected by aging. Recent advances in our understanding of both colonic physiology and the general mechanisms of aging have significantly expanded our knowledge of the types and underlying processes of colonic aging. In this review, we summarize current insights into the cellular and molecular mechanisms that drive physiological aging of the human colon. We examine the unique structural and functional features of key components of the colon, including the epithelium, local immune system, microbiome, enteric neurons, and smooth muscle cells, and explore how aging affects each of these cell populations, ultimately impacting overall colonic function. In the epithelium, increased mutational burden does not appear to be the primary driver of age-related dysfunction. Instead, dysregulation of signaling pathways such as EGF and Wnt is likely responsible for key phenotypic changes. Aged colonic neurons display protein misfolding and axonal dysfunction reminiscent of aging processes observed in the central nervous system. Similarly, smooth muscle cells exhibit impaired contractility, which is associated with disruptions in calcium homeostasis and deficits in cholinergic signaling. At the same time, age-related activation of the local immune system mirrors broader immunosenescence and may be further influenced by shifts in the gut microbiome, although a consistent aging-associated microbiome signature has yet to be identified. These multifaceted changes, combined with the colon's inherent regional and cellular complexity and the challenges of modeling human colonic aging, continue to fascinate but also pose substantial obstacles for research. Emerging experimental models and clinical strategies offer promising avenues for improving the prevention and treatment of age-associated colonic dysfunction.},
}
RevDate: 2025-12-13
Vaginal microbe media (VMM): a novel medium to culture Lactobacillus iners and other fastidious vaginal bacteria.
Journal of microbiological methods pii:S0167-7012(25)00274-X [Epub ahead of print].
A more comprehensive understanding of the bacterial species in the vaginal microbiome and their roles requires their cultivation as pure isolates. However, difficulty in culturing fastidious species, particularly in liquid media, has limited certain types of experimental approaches for studying these organisms. To address this challenge, Vaginal Microbe Medium (VMM) was developed to enable robust growth of Lactobacillus iners within a relatively short period (36 h). A simplified version with fewer components, named VMM2, was subsequently developed. L. iners strains grown in VMM and VMM2 reached higher optical densities in a shorter period compared to NYCIII, supplemented MRS and Columbia broth. Bacterial cells cultured in VMM and VMM2 were significantly longer than those grown in NYCIII. These results indicate that VMM and VMM2 provide superior growth conditions for L. iners as compared to currently available media. Both media also support the growth of a range of other vaginal bacterial species. The development of these media facilitates liquid culture of fastidious bacteria from the vaginal niche, enabling broader experimental capabilities and deeper insights into causal relationships within the microbiome.
Additional Links: PMID-41389846
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PubMed:
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@article {pmid41389846,
year = {2025},
author = {Roberts, LA and Gaboriau, DCA and MacIntyre, DA and Marchesi, JR},
title = {Vaginal microbe media (VMM): a novel medium to culture Lactobacillus iners and other fastidious vaginal bacteria.},
journal = {Journal of microbiological methods},
volume = {},
number = {},
pages = {107358},
doi = {10.1016/j.mimet.2025.107358},
pmid = {41389846},
issn = {1872-8359},
abstract = {A more comprehensive understanding of the bacterial species in the vaginal microbiome and their roles requires their cultivation as pure isolates. However, difficulty in culturing fastidious species, particularly in liquid media, has limited certain types of experimental approaches for studying these organisms. To address this challenge, Vaginal Microbe Medium (VMM) was developed to enable robust growth of Lactobacillus iners within a relatively short period (36 h). A simplified version with fewer components, named VMM2, was subsequently developed. L. iners strains grown in VMM and VMM2 reached higher optical densities in a shorter period compared to NYCIII, supplemented MRS and Columbia broth. Bacterial cells cultured in VMM and VMM2 were significantly longer than those grown in NYCIII. These results indicate that VMM and VMM2 provide superior growth conditions for L. iners as compared to currently available media. Both media also support the growth of a range of other vaginal bacterial species. The development of these media facilitates liquid culture of fastidious bacteria from the vaginal niche, enabling broader experimental capabilities and deeper insights into causal relationships within the microbiome.},
}
RevDate: 2025-12-13
Unravelling the role of the microbiome in Parkinson's disease.
The Lancet. Neurology, 25(1):7-8.
Additional Links: PMID-41389831
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PubMed:
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@article {pmid41389831,
year = {2026},
author = {McNamara, CG and Cryan, JF},
title = {Unravelling the role of the microbiome in Parkinson's disease.},
journal = {The Lancet. Neurology},
volume = {25},
number = {1},
pages = {7-8},
doi = {10.1016/S1474-4422(25)00452-1},
pmid = {41389831},
issn = {1474-4465},
}
RevDate: 2025-12-13
CmpDate: 2025-12-13
The gut microbiome, systemic inflammation, and autoimmunity in Parkinson's disease.
The Lancet. Neurology, 25(1):103-114.
Inflammation is a core feature of Parkinson's disease, extending beyond the CNS to include systemic immune activation. The gut microbiome is increasingly recognised as a key regulator of immune function in the gastrointestinal tract, peripheral circulation, and brain. In individuals with Parkinson's disease, gut microbial composition is altered, with reductions in anti-inflammatory taxa and increases in pro-inflammatory bacterial species. Preclinical studies have shown that microbiome alterations can promote α-synuclein aggregation and neuroinflammation, whereas human data suggest early involvement of the gut and immune system. Immune-mediated mechanisms in Parkinson's disease include activation of brain resident microglia and peripheral innate and adaptive immune cells. Emerging evidence suggests the gut microbiome modulates systemic immune activation, through autoreactive T cells that might drive neurodegeneration. An improved understanding of how the microbiome shapes inflammation and autoimmunity in Parkinson's disease could inform the development of therapies that target the immune system or the gut-brain axis.
Additional Links: PMID-41389810
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PubMed:
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@article {pmid41389810,
year = {2026},
author = {de Castro Fonseca, M and Zanetti, L and Fanourakis, S and Sulzer, DL and Mazmanian, SK},
title = {The gut microbiome, systemic inflammation, and autoimmunity in Parkinson's disease.},
journal = {The Lancet. Neurology},
volume = {25},
number = {1},
pages = {103-114},
doi = {10.1016/S1474-4422(25)00382-5},
pmid = {41389810},
issn = {1474-4465},
mesh = {Humans ; *Parkinson Disease/immunology/microbiology ; *Gastrointestinal Microbiome/immunology/physiology ; *Autoimmunity/immunology/physiology ; *Inflammation/immunology ; Animals ; },
abstract = {Inflammation is a core feature of Parkinson's disease, extending beyond the CNS to include systemic immune activation. The gut microbiome is increasingly recognised as a key regulator of immune function in the gastrointestinal tract, peripheral circulation, and brain. In individuals with Parkinson's disease, gut microbial composition is altered, with reductions in anti-inflammatory taxa and increases in pro-inflammatory bacterial species. Preclinical studies have shown that microbiome alterations can promote α-synuclein aggregation and neuroinflammation, whereas human data suggest early involvement of the gut and immune system. Immune-mediated mechanisms in Parkinson's disease include activation of brain resident microglia and peripheral innate and adaptive immune cells. Emerging evidence suggests the gut microbiome modulates systemic immune activation, through autoreactive T cells that might drive neurodegeneration. An improved understanding of how the microbiome shapes inflammation and autoimmunity in Parkinson's disease could inform the development of therapies that target the immune system or the gut-brain axis.},
}
MeSH Terms:
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Humans
*Parkinson Disease/immunology/microbiology
*Gastrointestinal Microbiome/immunology/physiology
*Autoimmunity/immunology/physiology
*Inflammation/immunology
Animals
RevDate: 2025-12-13
A neuroprotective effect of newly isolated probiotic bacterium Lactobacillus acidophilus SLAM_LAA02 in a rotenone-induced mouse model of Parkinson's disease.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 194:118896 pii:S0753-3322(25)01090-X [Epub ahead of print].
The gut microbiota plays a pivotal role in maintaining host health and has increasingly been linked to the pathogenesis of neurodegenerative diseases through the microbiota-gut-brain axis. Parkinson's disease (PD), characterized by dopaminergic dysfunction, neuro inflammation, and pathological alpha-synuclein (α-synuclein) aggregation, is frequently accompanied by gut microbial dysbiosis. Probiotics isolated from human infants could offer distinct neuroprotective and immunomodulatory benefits, yet their effects on integrated gut-brain axis models remain underexplored. In this study, we investigated the therapeutic potential of Lactobacillus acidophilus SLAM_LAA02 (L. acidophilus SLAM_LAA02), a novel infant-derived strain, in modulating PD-related behavioral and neuropathological features via modulation of the gut-brain axis. Following comprehensive safety and functional assessments, we first assessed L. acidophilus SLAM_LAA02 in Caenorhabditis elegans, where supplementation extended lifespan, enhanced antimicrobial defense, improved behavioral responses, and reduced α-synuclein expression in transgenic worms. We then evaluated its effects in a rotenone-induced mouse model that reflects early-stage PD-like features. L. acidophilus SLAM_LAA02 administration ameliorated motor dysfunction, modulated neuroinflammatory signaling, restored gut microbial diversity, and improved intestinal barrier-associated outcomes. These changes were accompanied by a notable reduction in α-synuclein expression and upregulated neuroprotective gene expression, including brain-derived neurotrophic factor (BDNF). Together, these findings suggest that L. acidophilus SLAM_LAA02 exhibits neuroprotective and gut-modulating properties across complementary model systems, supporting its potential as a promising probiotic candidate for alleviating early PD-related dysfunctions through the gut-brain axis.
Additional Links: PMID-41389626
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PubMed:
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@article {pmid41389626,
year = {2025},
author = {Kim, Y and Seo, E and Kang, A and Kang, MG and Jang, KB and Oh, S and Kim, Y},
title = {A neuroprotective effect of newly isolated probiotic bacterium Lactobacillus acidophilus SLAM_LAA02 in a rotenone-induced mouse model of Parkinson's disease.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {194},
number = {},
pages = {118896},
doi = {10.1016/j.biopha.2025.118896},
pmid = {41389626},
issn = {1950-6007},
abstract = {The gut microbiota plays a pivotal role in maintaining host health and has increasingly been linked to the pathogenesis of neurodegenerative diseases through the microbiota-gut-brain axis. Parkinson's disease (PD), characterized by dopaminergic dysfunction, neuro inflammation, and pathological alpha-synuclein (α-synuclein) aggregation, is frequently accompanied by gut microbial dysbiosis. Probiotics isolated from human infants could offer distinct neuroprotective and immunomodulatory benefits, yet their effects on integrated gut-brain axis models remain underexplored. In this study, we investigated the therapeutic potential of Lactobacillus acidophilus SLAM_LAA02 (L. acidophilus SLAM_LAA02), a novel infant-derived strain, in modulating PD-related behavioral and neuropathological features via modulation of the gut-brain axis. Following comprehensive safety and functional assessments, we first assessed L. acidophilus SLAM_LAA02 in Caenorhabditis elegans, where supplementation extended lifespan, enhanced antimicrobial defense, improved behavioral responses, and reduced α-synuclein expression in transgenic worms. We then evaluated its effects in a rotenone-induced mouse model that reflects early-stage PD-like features. L. acidophilus SLAM_LAA02 administration ameliorated motor dysfunction, modulated neuroinflammatory signaling, restored gut microbial diversity, and improved intestinal barrier-associated outcomes. These changes were accompanied by a notable reduction in α-synuclein expression and upregulated neuroprotective gene expression, including brain-derived neurotrophic factor (BDNF). Together, these findings suggest that L. acidophilus SLAM_LAA02 exhibits neuroprotective and gut-modulating properties across complementary model systems, supporting its potential as a promising probiotic candidate for alleviating early PD-related dysfunctions through the gut-brain axis.},
}
RevDate: 2025-12-13
From bias to reliable insight: Rethinking feature importance in microbiome analytics.
Additional Links: PMID-41389588
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PubMed:
Citation:
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@article {pmid41389588,
year = {2025},
author = {Oka, S and Yoshida, K and Takefuji, Y},
title = {From bias to reliable insight: Rethinking feature importance in microbiome analytics.},
journal = {Veterinary microbiology},
volume = {312},
number = {},
pages = {110838},
doi = {10.1016/j.vetmic.2025.110838},
pmid = {41389588},
issn = {1873-2542},
}
RevDate: 2025-12-13
Integrative multi-omics elucidates the impact of microalgae on growth, quality, phytohormones, and rhizosphere microbiome of Angelica sinensis.
Microbiological research, 304:128418 pii:S0944-5013(25)00377-5 [Epub ahead of print].
Microalgae have recently been recognized as sustainable biofertilizers that improve soil fertility while enhancing crop performance. However, their roles in regulating medicinal plant growth and quality, as well as the underlying ecological mechanisms, remain poorly understood. In this study, we systematically assessed the effects of three representative microalgae-Anabaena cylindrica (AC), Phormidium tenue (PT), and Chlorella vulgaris (CV)-on the growth, quality, hormonal regulation, soil nutrient dynamics, and rhizosphere microbiome of Angelica sinensis. Field inoculation trials demonstrated that all three microalgae significantly promoted biomass accumulation and increased antioxidant capacity. AC and CV further enhanced the accumulation of ferulic acid and flavonoids, which are two key quality determinants. Microalgal inoculation significantly altered rhizosphere soil properties by increasing total organic carbon and alkali-hydrolyzable nitrogen, with AC uniquely elevating available phosphorus and iron. Metagenomic analysis revealed that AC and PT stimulated nitrification while suppressing denitrification, thereby reducing nitrogen loss and stabilizing the soil nitrogen pools. Distinct microbial taxa, including Rhodanobacter, Streptomyces, and Pseudomonas, were identified as the major contributors to carbon and nitrogen cycling. Hormone metabolomics showed that microalgal inoculation reprogrammed A. sinensis phytohormone profiles in a species-specific manner. Partial least squares path modeling suggested that AC and CV promote ferulic acid biosynthesis through distinct mechanisms, with AC associated with reduced investment in C-mineralization processes and CV associated with lower salicylic acid levels, whereas PT enhances biomass accumulation mainly by stimulating N-cycle processes. Collectively, this study provides integrated evidence linking microalgae-mediated nutrient cycling, rhizosphere microbiome shifts and hormonal regulation to enhanced quality formation in A. sinensis.
Additional Links: PMID-41389554
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PubMed:
Citation:
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@article {pmid41389554,
year = {2025},
author = {Yang, T and Zhan, Y and Sha, J and Zhao, J and Wang, C and Peng, T and Zhang, L},
title = {Integrative multi-omics elucidates the impact of microalgae on growth, quality, phytohormones, and rhizosphere microbiome of Angelica sinensis.},
journal = {Microbiological research},
volume = {304},
number = {},
pages = {128418},
doi = {10.1016/j.micres.2025.128418},
pmid = {41389554},
issn = {1618-0623},
abstract = {Microalgae have recently been recognized as sustainable biofertilizers that improve soil fertility while enhancing crop performance. However, their roles in regulating medicinal plant growth and quality, as well as the underlying ecological mechanisms, remain poorly understood. In this study, we systematically assessed the effects of three representative microalgae-Anabaena cylindrica (AC), Phormidium tenue (PT), and Chlorella vulgaris (CV)-on the growth, quality, hormonal regulation, soil nutrient dynamics, and rhizosphere microbiome of Angelica sinensis. Field inoculation trials demonstrated that all three microalgae significantly promoted biomass accumulation and increased antioxidant capacity. AC and CV further enhanced the accumulation of ferulic acid and flavonoids, which are two key quality determinants. Microalgal inoculation significantly altered rhizosphere soil properties by increasing total organic carbon and alkali-hydrolyzable nitrogen, with AC uniquely elevating available phosphorus and iron. Metagenomic analysis revealed that AC and PT stimulated nitrification while suppressing denitrification, thereby reducing nitrogen loss and stabilizing the soil nitrogen pools. Distinct microbial taxa, including Rhodanobacter, Streptomyces, and Pseudomonas, were identified as the major contributors to carbon and nitrogen cycling. Hormone metabolomics showed that microalgal inoculation reprogrammed A. sinensis phytohormone profiles in a species-specific manner. Partial least squares path modeling suggested that AC and CV promote ferulic acid biosynthesis through distinct mechanisms, with AC associated with reduced investment in C-mineralization processes and CV associated with lower salicylic acid levels, whereas PT enhances biomass accumulation mainly by stimulating N-cycle processes. Collectively, this study provides integrated evidence linking microalgae-mediated nutrient cycling, rhizosphere microbiome shifts and hormonal regulation to enhanced quality formation in A. sinensis.},
}
RevDate: 2025-12-13
Gut microbiota and nutritional interventions in alcohol-associated liver disease: Mechanisms and therapeutic advances.
Nutrition research (New York, N.Y.), 145:8-24 pii:S0271-5317(25)00140-X [Epub ahead of print].
Alcohol-associated liver disease (ALD) is a leading cause of liver-related morbidity and mortality worldwide. Despite growing awareness of its burden, treatment options remain limited, with abstinence as the only widely accepted intervention. Recent research underscores the critical role of the gut-liver axis and nutritional status, particularly dietary protein, in modulating ALD pathogenesis and progression. This review aims to integrate current knowledge on the interplay between gut microbiota, dietary protein, and alcohol-induced liver injury, and to evaluate microbiota-targeted therapeutic strategies, including fecal microbiota transplantation (FMT), within this context. We examine how chronic alcohol intake reshapes the gut microbiome, impairs barrier function, and alters microbial metabolism. We discuss how dietary protein, based on source, quantity, and amino acid composition, influences microbial ecology and metabolite profiles, with plant and dairy proteins emerging as beneficial. The review also highlights advances in FMT, which shows promise in improving outcomes in severe alcoholic hepatitis. However, its efficacy is modulated by donor microbial composition and recipient compatibility, both of which may be influenced by diet. Furthermore, we address emerging evidence on the role of fungal and viral communities, which remain understudied contributors to ALD. Despite substantial progress, significant knowledge gaps persist. These include the need for clinical validation of preclinical findings, deeper exploration of nonbacterial microbiota, and a lack of personalized, nutrition-based interventions. Addressing these gaps through integrative, multiomic approaches will be essential to advancing precision therapeutics in ALD.
Additional Links: PMID-41389450
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PubMed:
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@article {pmid41389450,
year = {2025},
author = {Mittal, A and Sharma, S},
title = {Gut microbiota and nutritional interventions in alcohol-associated liver disease: Mechanisms and therapeutic advances.},
journal = {Nutrition research (New York, N.Y.)},
volume = {145},
number = {},
pages = {8-24},
doi = {10.1016/j.nutres.2025.11.004},
pmid = {41389450},
issn = {1879-0739},
abstract = {Alcohol-associated liver disease (ALD) is a leading cause of liver-related morbidity and mortality worldwide. Despite growing awareness of its burden, treatment options remain limited, with abstinence as the only widely accepted intervention. Recent research underscores the critical role of the gut-liver axis and nutritional status, particularly dietary protein, in modulating ALD pathogenesis and progression. This review aims to integrate current knowledge on the interplay between gut microbiota, dietary protein, and alcohol-induced liver injury, and to evaluate microbiota-targeted therapeutic strategies, including fecal microbiota transplantation (FMT), within this context. We examine how chronic alcohol intake reshapes the gut microbiome, impairs barrier function, and alters microbial metabolism. We discuss how dietary protein, based on source, quantity, and amino acid composition, influences microbial ecology and metabolite profiles, with plant and dairy proteins emerging as beneficial. The review also highlights advances in FMT, which shows promise in improving outcomes in severe alcoholic hepatitis. However, its efficacy is modulated by donor microbial composition and recipient compatibility, both of which may be influenced by diet. Furthermore, we address emerging evidence on the role of fungal and viral communities, which remain understudied contributors to ALD. Despite substantial progress, significant knowledge gaps persist. These include the need for clinical validation of preclinical findings, deeper exploration of nonbacterial microbiota, and a lack of personalized, nutrition-based interventions. Addressing these gaps through integrative, multiomic approaches will be essential to advancing precision therapeutics in ALD.},
}
RevDate: 2025-12-13
Impact of Sinus Surgery on Bacteriome Composition in Patients With Chronic Rhinosinusitis With Nasal Polyps.
International forum of allergy & rhinology [Epub ahead of print].
Additional Links: PMID-41389146
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PubMed:
Citation:
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@article {pmid41389146,
year = {2025},
author = {Vorobeva, M and iAkushev, A and Chen, CC and Orihara, M and Akbar, N and Colley, P and Sehanobish, E and Chung, CHY and Scott, A and O'Brien, E and Chang, CB and Kita, H and Voyich, J and Knoop, K and Jerschow, E},
title = {Impact of Sinus Surgery on Bacteriome Composition in Patients With Chronic Rhinosinusitis With Nasal Polyps.},
journal = {International forum of allergy & rhinology},
volume = {},
number = {},
pages = {},
doi = {10.1002/alr.70082},
pmid = {41389146},
issn = {2042-6984},
support = {R21AI171306 to E.J./TR/NCATS NIH HHS/United States ; CTSA 5KL2TR001071/TR/NCATS NIH HHS/United States ; /NH/NIH HHS/United States ; },
}
RevDate: 2025-12-13
CmpDate: 2025-12-13
Neuroinflammatory Mechanisms and Therapeutic Targets in Oxaliplatin-Induced Peripheral Neuropathy: a Comprehensive Review.
Neurotoxicity research, 43(6):52.
Oxaliplatin-induced peripheral neuropathy (OIPN) is a severe, dose-limiting complication that significantly reduces quality of life in cancer patients, with no effective preventive or therapeutic options currently available. There is increasing evidence that neuroinflammation plays a central role in OIPN initiation and progression. This review provides a critical and up-to-date analysis of recent studies on the molecular mechanisms of oxaliplatin-induced neuroinflammation, with a particular focus on the integration of mitochondrial dysfunction, immune-mediated inflammation, glial activation, microRNA dysregulation, and gut-nerve axis disruption. Recent findings demonstrate that oxaliplatin disrupts mitochondrial dynamics, increases oxidative stress, and impairs blood-nerve barrier integrity, triggering neuroinflammatory responses. Neuroinflammation in OIPN is mediated through the activation of several key signaling pathways, including MAPK, NF-κB, Wnt/β-catenin, TLR4, and mTOR, which lead to increased production of pro-inflammatory cytokines and activation of glial cells. Furthermore, emerging evidence has identified dysregulation of the gut-nerve axis and alterations in gut microbiota composition as contributing factors that exacerbate oxaliplatin-induced neuroinflammation and neuropathic pain. Various pharmacological and plant-derived compounds, such as naringin, baicalein, and puerarin, as well as selective inhibitors of inflammatory pathways, have shown promising neuroprotective effects in animal models by attenuating inflammatory responses and alleviating neuropathic symptoms. By synthesizing these converging lines of evidence, this review further outlines potential future directions, including the development of combination therapies targeting multiple inflammatory pathways, microbiome-based interventions, and the translation of preclinical findings into well-designed clinical trials.
Additional Links: PMID-41389089
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Citation:
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@article {pmid41389089,
year = {2025},
author = {Dehghani, S and Khorsandi, H and Hosseinzadegan, R and Rahimi, H and Mottaghi, M and Fallahpour, S and Fazayel, SMA and Bayat, A and Namini, NJ and Karimi, A and Morovatshoar, R and Mobinikhaledi, M and Behfar, Q and Ghasemi, M},
title = {Neuroinflammatory Mechanisms and Therapeutic Targets in Oxaliplatin-Induced Peripheral Neuropathy: a Comprehensive Review.},
journal = {Neurotoxicity research},
volume = {43},
number = {6},
pages = {52},
pmid = {41389089},
issn = {1476-3524},
mesh = {Humans ; *Oxaliplatin/adverse effects/toxicity ; Animals ; *Peripheral Nervous System Diseases/chemically induced/drug therapy/metabolism ; *Neuroinflammatory Diseases/chemically induced/drug therapy/metabolism ; *Antineoplastic Agents/adverse effects/toxicity ; },
abstract = {Oxaliplatin-induced peripheral neuropathy (OIPN) is a severe, dose-limiting complication that significantly reduces quality of life in cancer patients, with no effective preventive or therapeutic options currently available. There is increasing evidence that neuroinflammation plays a central role in OIPN initiation and progression. This review provides a critical and up-to-date analysis of recent studies on the molecular mechanisms of oxaliplatin-induced neuroinflammation, with a particular focus on the integration of mitochondrial dysfunction, immune-mediated inflammation, glial activation, microRNA dysregulation, and gut-nerve axis disruption. Recent findings demonstrate that oxaliplatin disrupts mitochondrial dynamics, increases oxidative stress, and impairs blood-nerve barrier integrity, triggering neuroinflammatory responses. Neuroinflammation in OIPN is mediated through the activation of several key signaling pathways, including MAPK, NF-κB, Wnt/β-catenin, TLR4, and mTOR, which lead to increased production of pro-inflammatory cytokines and activation of glial cells. Furthermore, emerging evidence has identified dysregulation of the gut-nerve axis and alterations in gut microbiota composition as contributing factors that exacerbate oxaliplatin-induced neuroinflammation and neuropathic pain. Various pharmacological and plant-derived compounds, such as naringin, baicalein, and puerarin, as well as selective inhibitors of inflammatory pathways, have shown promising neuroprotective effects in animal models by attenuating inflammatory responses and alleviating neuropathic symptoms. By synthesizing these converging lines of evidence, this review further outlines potential future directions, including the development of combination therapies targeting multiple inflammatory pathways, microbiome-based interventions, and the translation of preclinical findings into well-designed clinical trials.},
}
MeSH Terms:
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Humans
*Oxaliplatin/adverse effects/toxicity
Animals
*Peripheral Nervous System Diseases/chemically induced/drug therapy/metabolism
*Neuroinflammatory Diseases/chemically induced/drug therapy/metabolism
*Antineoplastic Agents/adverse effects/toxicity
RevDate: 2025-12-13
Androgen-Deprivation Therapy and Dietary Habits Influence the Gut Microbial Environment in Patients With High-Risk Localized Prostate Cancer.
The Prostate [Epub ahead of print].
BACKGROUND: The aim of this study is to investigate the relationship between the gut microbial profiles, occurrence of side effects, total testosterone (TS) levels, and pretreatment dietary habits among patients with high-risk localized prostate cancer who were subjected to androgen-deprivation therapy (ADT).
METHODS: This prospective study included patients diagnosed with high-risk localized prostate cancer who underwent ADT between March 2021 and August 2022. The correlation between the pre- and post (after 3 months)-ADT gut microbial profiles, laboratory tests, body consumption data, and pretreatment dietary habits was analyzed.
RESULTS: No significant differences were observed in the alpha- and beta-diversities of the gut microbiota during pre- and post-ADT. The relative abundance of genus Ruminococcus 2 (p = 0.013) and genus [Eubacterium] ruminantium group (p = 0.043) were significantly higher during post-ADT compared with those during pre-ADT. Twenty percent of the patients with a post-ADT TS level of < 20 ng/dL had a significantly high proportion of genus Ruminococccus 2, whereas no significant proportion was observed in patients with a TS level of ≥ 20 ng/dL. In terms of the impact of the pretreatment dietary habits on the changes of the gut microbiota, genus Romboutsia and genus Fusicatenibacter showed a positive correlation with n-6 polyunsaturated fatty acid intake, whereas the amounts of genus Ruminococcus 2 and genus Veillonella showed a negative correlation with n-3 polyunsaturated fatty acids.
CONCLUSIONS: Short-term ADT was found to increase the proportion of gut genus Ruminococcus 2 in patients with advanced prostate cancer, which was associated with low TS levels and showed a negative correlation with n-3 polyunsaturated fatty acid intake. Further validation is important to identify specific changes in the gut microbiota during ADT in patients with prostate cancer.
Additional Links: PMID-41389040
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PubMed:
Citation:
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@article {pmid41389040,
year = {2025},
author = {Ishida, M and Narita, S and Sato, H and Sekine, Y and Kobayashi, M and Kashima, S and Yamamoto, R and Numakura, K and Saito, M and Takahashi, Y and Funahashi, K and Yamauchi, Y and Fukuda, S and Habuchi, T},
title = {Androgen-Deprivation Therapy and Dietary Habits Influence the Gut Microbial Environment in Patients With High-Risk Localized Prostate Cancer.},
journal = {The Prostate},
volume = {},
number = {},
pages = {},
doi = {10.1002/pros.70109},
pmid = {41389040},
issn = {1097-0045},
support = {22K09464//MEXT/JSPS (Kakenhi)/ ; 23K19665//MEXT/JSPS (Kakenhi)/ ; 25K02770//MEXT/JSPS (Kakenhi)/ ; },
abstract = {BACKGROUND: The aim of this study is to investigate the relationship between the gut microbial profiles, occurrence of side effects, total testosterone (TS) levels, and pretreatment dietary habits among patients with high-risk localized prostate cancer who were subjected to androgen-deprivation therapy (ADT).
METHODS: This prospective study included patients diagnosed with high-risk localized prostate cancer who underwent ADT between March 2021 and August 2022. The correlation between the pre- and post (after 3 months)-ADT gut microbial profiles, laboratory tests, body consumption data, and pretreatment dietary habits was analyzed.
RESULTS: No significant differences were observed in the alpha- and beta-diversities of the gut microbiota during pre- and post-ADT. The relative abundance of genus Ruminococcus 2 (p = 0.013) and genus [Eubacterium] ruminantium group (p = 0.043) were significantly higher during post-ADT compared with those during pre-ADT. Twenty percent of the patients with a post-ADT TS level of < 20 ng/dL had a significantly high proportion of genus Ruminococccus 2, whereas no significant proportion was observed in patients with a TS level of ≥ 20 ng/dL. In terms of the impact of the pretreatment dietary habits on the changes of the gut microbiota, genus Romboutsia and genus Fusicatenibacter showed a positive correlation with n-6 polyunsaturated fatty acid intake, whereas the amounts of genus Ruminococcus 2 and genus Veillonella showed a negative correlation with n-3 polyunsaturated fatty acids.
CONCLUSIONS: Short-term ADT was found to increase the proportion of gut genus Ruminococcus 2 in patients with advanced prostate cancer, which was associated with low TS levels and showed a negative correlation with n-3 polyunsaturated fatty acid intake. Further validation is important to identify specific changes in the gut microbiota during ADT in patients with prostate cancer.},
}
RevDate: 2025-12-13
Antibiotics Alter Duodenal Immune Populations Upon Gluten Exposure in Mice: Implications for Non-Coeliac Gluten Sensitivity.
American journal of physiology. Gastrointestinal and liver physiology [Epub ahead of print].
A growing proportion of the non-celiac population experience adverse symptoms to gluten. The pathogenesis of non-celiac gluten sensitivity (NCGS) is unclear, but elevated duodenal eosinophils and altered mucosa-associated microbiota (MAM) populations have been reported. Given the microbiome's role in gluten digestion and its susceptibility to antibiotics, we hypothesised that altering the microbiome with antibiotics would modify immune responses to gluten in mice. BALB/C mice consuming gluten-free chow received amoxicillin/clavulanate (5mg/kg) or PBS-vehicle daily for 5-days. Mice were then treated with a 3mg wheat-gluten suspension, or vehicle, on days 4 and 5 before sacrifice on day 7. Duodenal immune cells were analysed by histology and flow cytometry, while the duodenal MAM and faecal microbiome were characterised via 16S rRNA and shotgun metagenomic sequencing, respectively. Antibiotic treatment followed by gluten reintroduction significantly reduced Staphylococcus in the duodenal MAM, enriched Bacteroides in faeces, and resulted in altered microbial carbohydrate and lipid metabolism, compared to vehicle controls. Treatment with antibiotics and gluten also increased duodenal eosinophils, which positively correlated with the genus Blautia. Flow cytometry revealed that sequential antibiotic and gluten treatment resulted in a greater proportion of active eosinophils and epithelial γδ T-cells, compared to vehicle control mice. This study demonstrated that modulating the microbiome with antibiotics was sufficient to alter the immune response to gluten in mice, suggesting that the microbiome may determine the capacity for gluten to induce immune responses. These findings contribute valuable insights into possible microbial mechanisms underlying NCGS, such as altered gluten metabolism or production of immunomodulatory metabolites.
Additional Links: PMID-41389008
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PubMed:
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@article {pmid41389008,
year = {2025},
author = {Pryor, JC and Hoedt, EC and Soh, WS and Fowler, S and Caban, S and Minahan, K and Sherwin, S and Nieva, C and McCarthy, H and Horvat, J and Hedley, KE and Duncanson, K and Burns, GL and Talley, NJ and Keely, S},
title = {Antibiotics Alter Duodenal Immune Populations Upon Gluten Exposure in Mice: Implications for Non-Coeliac Gluten Sensitivity.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00159.2025},
pmid = {41389008},
issn = {1522-1547},
support = {2004860//DHAC | National Health and Medical Research Council (NHMRC)/ ; 2035319//DHAC | National Health and Medical Research Council (NHMRC)/ ; 1170893//DHAC | National Health and Medical Research Council (NHMRC)/ ; },
abstract = {A growing proportion of the non-celiac population experience adverse symptoms to gluten. The pathogenesis of non-celiac gluten sensitivity (NCGS) is unclear, but elevated duodenal eosinophils and altered mucosa-associated microbiota (MAM) populations have been reported. Given the microbiome's role in gluten digestion and its susceptibility to antibiotics, we hypothesised that altering the microbiome with antibiotics would modify immune responses to gluten in mice. BALB/C mice consuming gluten-free chow received amoxicillin/clavulanate (5mg/kg) or PBS-vehicle daily for 5-days. Mice were then treated with a 3mg wheat-gluten suspension, or vehicle, on days 4 and 5 before sacrifice on day 7. Duodenal immune cells were analysed by histology and flow cytometry, while the duodenal MAM and faecal microbiome were characterised via 16S rRNA and shotgun metagenomic sequencing, respectively. Antibiotic treatment followed by gluten reintroduction significantly reduced Staphylococcus in the duodenal MAM, enriched Bacteroides in faeces, and resulted in altered microbial carbohydrate and lipid metabolism, compared to vehicle controls. Treatment with antibiotics and gluten also increased duodenal eosinophils, which positively correlated with the genus Blautia. Flow cytometry revealed that sequential antibiotic and gluten treatment resulted in a greater proportion of active eosinophils and epithelial γδ T-cells, compared to vehicle control mice. This study demonstrated that modulating the microbiome with antibiotics was sufficient to alter the immune response to gluten in mice, suggesting that the microbiome may determine the capacity for gluten to induce immune responses. These findings contribute valuable insights into possible microbial mechanisms underlying NCGS, such as altered gluten metabolism or production of immunomodulatory metabolites.},
}
RevDate: 2025-12-13
Cross-talk within plant niches: endophytic and arbuscular mycorrhizal fungi for sustainable crop production.
FEMS microbiology reviews pii:8379428 [Epub ahead of print].
World agriculture depends in part on the crop-associated microbiome for improved plant growth, health, and productivity. In particular, endophytic fungi (EF) with plant growth-promoting activities fulfill some of these roles and are central as bioinoculant agents. In the case of arbuscular mycorrhizal fungi (AMF), they form a symbiosis with their host plants, enhancing the uptake of water, phosphorus, nitrogen, and other micronutrients, while the plants provide them with photosynthates. This work reviews the differences in the colonization of internal plant niches between these beneficial fungi, as well as other distinctive ecological traits. It also explores mechanisms of seedborne vertical transmission in AMF and their classification. Genomic and transcriptomic advances in fungal endophytes are highlighted, shedding light on genes and expression profiles that define their lifestyle and plant associations. In addition, recent studies on their abilities to promote plant growth are analyzed, especially focusing on Trichoderma spp., Epichloë spp., Serendipita indica (formerly Piriformospora indica), and entomopathogens like Beauveria spp. and Metarhizium spp. Finally, the multiple interactions among EF, AMF, and other members of the plant microbiome-notably plant growth-promoting bacteria (PGPB)-are discussed, emphasizing how these organisms synergistically benefit the host. A deeper understanding of these fungi and their plant-beneficial effects should facilitate commercialization and help farmers achieve sustainable production, especially under challenges posed by global climate change.
Additional Links: PMID-41388904
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PubMed:
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@article {pmid41388904,
year = {2025},
author = {Orozco-Mosqueda, MDC and Glick, BR and Santoyo, G},
title = {Cross-talk within plant niches: endophytic and arbuscular mycorrhizal fungi for sustainable crop production.},
journal = {FEMS microbiology reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsre/fuaf063},
pmid = {41388904},
issn = {1574-6976},
abstract = {World agriculture depends in part on the crop-associated microbiome for improved plant growth, health, and productivity. In particular, endophytic fungi (EF) with plant growth-promoting activities fulfill some of these roles and are central as bioinoculant agents. In the case of arbuscular mycorrhizal fungi (AMF), they form a symbiosis with their host plants, enhancing the uptake of water, phosphorus, nitrogen, and other micronutrients, while the plants provide them with photosynthates. This work reviews the differences in the colonization of internal plant niches between these beneficial fungi, as well as other distinctive ecological traits. It also explores mechanisms of seedborne vertical transmission in AMF and their classification. Genomic and transcriptomic advances in fungal endophytes are highlighted, shedding light on genes and expression profiles that define their lifestyle and plant associations. In addition, recent studies on their abilities to promote plant growth are analyzed, especially focusing on Trichoderma spp., Epichloë spp., Serendipita indica (formerly Piriformospora indica), and entomopathogens like Beauveria spp. and Metarhizium spp. Finally, the multiple interactions among EF, AMF, and other members of the plant microbiome-notably plant growth-promoting bacteria (PGPB)-are discussed, emphasizing how these organisms synergistically benefit the host. A deeper understanding of these fungi and their plant-beneficial effects should facilitate commercialization and help farmers achieve sustainable production, especially under challenges posed by global climate change.},
}
RevDate: 2025-12-13
CmpDate: 2025-12-13
Unraveling the oral microbiome's role in Alzheimer's disease: From pathophysiology to therapeutic potential.
Alzheimer's & dementia : the journal of the Alzheimer's Association, 21(12):e71011.
Oral dysbiosis contributes to Alzheimer's disease (AD) by promoting neuroinflammation. Pathobionts such as Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum release virulence factors that induce amyloid beta aggregation and tau hyperphosphorylation, while the loss of commensals like Streptococcus salivarius and Neisseria spp. impairs anti-inflammatory protection, worsening neuronal damage. P. gingivalis is strongly linked to an increased risk of AD, especially in individuals with systemic conditions like diabetes, hypertension, and chronic kidney disease. Its presence in brain tissue correlates with a higher likelihood of AD, while salivary Veillonella and periodontal pathogens in gingival crevicular fluid show potential as non-invasive biomarkers for early AD detection. Therapeutic strategies targeting the oral microbiota, such as gingipain inhibitors, antimicrobials, probiotics, and prebiotics, show promise for mitigating AD risk. However, causal mechanisms and clinical efficacy remain to be fully established. Maintaining microbial balance through preventive and targeted modulation represents an innovative approach to reducing AD susceptibility. HIGHLIGHTS: We identified Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum as key oral pathogens driving Alzheimer's disease (AD) via gingipain-induced amyloid beta aggregation, systemic inflammation, and blood-brain barrier disruption. Our study revealed diabetes, hypertension, and chronic kidney disease (CKD) amplify AD risk through shared oral dysbiosis, with uremic toxins (CKD) and hyperglycemia (diabetes) exacerbating neuroinflammation. We propose Veillonella in saliva and Porphyromonas gingivalis in gingival crevicular fluid as non-invasive AD biomarkers, correlating with 6 to 10× higher AD risk when detected in brain tissue. Gingipain inhibitors (e.g., COR388), nitrate-reducing probiotics, and integrated dental-neurology care are promising interventions to disrupt the oral-brain axis. We advocate for oral microbiome screening in high-risk populations (apolipoprotein E ε4 carriers, diabetics) and interdisciplinary approaches to AD prevention.
Additional Links: PMID-41388822
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PubMed:
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@article {pmid41388822,
year = {2025},
author = {Rozenblum, G and Ait-Aissa, K and Zahran, G and Alipour, M and Sahyoun, AM and Munkhsaikhan, U and Kassan, A and Ishrat, T and Wang, Q and Abidi, AH and Kassan, M},
title = {Unraveling the oral microbiome's role in Alzheimer's disease: From pathophysiology to therapeutic potential.},
journal = {Alzheimer's & dementia : the journal of the Alzheimer's Association},
volume = {21},
number = {12},
pages = {e71011},
doi = {10.1002/alz.71011},
pmid = {41388822},
issn = {1552-5279},
mesh = {Humans ; *Alzheimer Disease/microbiology/physiopathology ; *Microbiota/physiology ; *Mouth/microbiology ; *Dysbiosis/microbiology/complications ; Fusobacterium nucleatum ; Amyloid beta-Peptides/metabolism ; },
abstract = {Oral dysbiosis contributes to Alzheimer's disease (AD) by promoting neuroinflammation. Pathobionts such as Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum release virulence factors that induce amyloid beta aggregation and tau hyperphosphorylation, while the loss of commensals like Streptococcus salivarius and Neisseria spp. impairs anti-inflammatory protection, worsening neuronal damage. P. gingivalis is strongly linked to an increased risk of AD, especially in individuals with systemic conditions like diabetes, hypertension, and chronic kidney disease. Its presence in brain tissue correlates with a higher likelihood of AD, while salivary Veillonella and periodontal pathogens in gingival crevicular fluid show potential as non-invasive biomarkers for early AD detection. Therapeutic strategies targeting the oral microbiota, such as gingipain inhibitors, antimicrobials, probiotics, and prebiotics, show promise for mitigating AD risk. However, causal mechanisms and clinical efficacy remain to be fully established. Maintaining microbial balance through preventive and targeted modulation represents an innovative approach to reducing AD susceptibility. HIGHLIGHTS: We identified Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum as key oral pathogens driving Alzheimer's disease (AD) via gingipain-induced amyloid beta aggregation, systemic inflammation, and blood-brain barrier disruption. Our study revealed diabetes, hypertension, and chronic kidney disease (CKD) amplify AD risk through shared oral dysbiosis, with uremic toxins (CKD) and hyperglycemia (diabetes) exacerbating neuroinflammation. We propose Veillonella in saliva and Porphyromonas gingivalis in gingival crevicular fluid as non-invasive AD biomarkers, correlating with 6 to 10× higher AD risk when detected in brain tissue. Gingipain inhibitors (e.g., COR388), nitrate-reducing probiotics, and integrated dental-neurology care are promising interventions to disrupt the oral-brain axis. We advocate for oral microbiome screening in high-risk populations (apolipoprotein E ε4 carriers, diabetics) and interdisciplinary approaches to AD prevention.},
}
MeSH Terms:
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Humans
*Alzheimer Disease/microbiology/physiopathology
*Microbiota/physiology
*Mouth/microbiology
*Dysbiosis/microbiology/complications
Fusobacterium nucleatum
Amyloid beta-Peptides/metabolism
RevDate: 2025-12-13
CmpDate: 2025-12-13
Skin and gut microbiome in atopic dermatitis: Mechanisms and therapeutic opportunities.
Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology, 36(12):e70265.
The pathogenesis of atopic dermatitis (AD) comprises a combination of genetic, immune, and microbial factors. An imbalance in skin and gut microbiota composition, termed dysbiosis, may contribute to AD pathogenesis and severity through overgrowth of pathogenic microbes and suppression of healthy commensal colonization. These, in turn, promote barrier disruption and pro-inflammatory responses. The skin and gut microbiota composition plays crucial roles in AD, namely as early predictive biomarkers of AD onset; indicators of treatment response; and as future novel therapeutics such as probiotics, fecal, and skin microbiota transplantation. Such interventions aim to directly "reset" and restore a healthy microbial equilibrium, thereby fundamentally repairing barrier function, regulating immune homeostasis, and establishing new adjunctive pathways for the long-term management of AD.
Additional Links: PMID-41388767
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PubMed:
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@article {pmid41388767,
year = {2025},
author = {Hou, B and Shao, H and Yuan, D and Tham, EH},
title = {Skin and gut microbiome in atopic dermatitis: Mechanisms and therapeutic opportunities.},
journal = {Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology},
volume = {36},
number = {12},
pages = {e70265},
doi = {10.1111/pai.70265},
pmid = {41388767},
issn = {1399-3038},
support = {//National Medical Research Council/ ; },
mesh = {Humans ; *Dermatitis, Atopic/therapy/microbiology/immunology ; *Gastrointestinal Microbiome/immunology ; *Skin/microbiology/immunology ; *Dysbiosis/immunology/therapy ; Probiotics/therapeutic use ; Animals ; Fecal Microbiota Transplantation ; },
abstract = {The pathogenesis of atopic dermatitis (AD) comprises a combination of genetic, immune, and microbial factors. An imbalance in skin and gut microbiota composition, termed dysbiosis, may contribute to AD pathogenesis and severity through overgrowth of pathogenic microbes and suppression of healthy commensal colonization. These, in turn, promote barrier disruption and pro-inflammatory responses. The skin and gut microbiota composition plays crucial roles in AD, namely as early predictive biomarkers of AD onset; indicators of treatment response; and as future novel therapeutics such as probiotics, fecal, and skin microbiota transplantation. Such interventions aim to directly "reset" and restore a healthy microbial equilibrium, thereby fundamentally repairing barrier function, regulating immune homeostasis, and establishing new adjunctive pathways for the long-term management of AD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dermatitis, Atopic/therapy/microbiology/immunology
*Gastrointestinal Microbiome/immunology
*Skin/microbiology/immunology
*Dysbiosis/immunology/therapy
Probiotics/therapeutic use
Animals
Fecal Microbiota Transplantation
RevDate: 2025-12-13
CmpDate: 2025-12-13
Osteopontin: a central hub in the pathogenesis and therapeutic intervention of liver disease.
Annals of medicine, 57(1):2596538.
BACKGROUND: Osteopontin (OPN) is a phosphorylated glycoprotein implicated in inflammation and tissue remodeling. Its expression is significantly elevated in various liver diseases, but its precise pathophysiological roles remain complex and context-dependent.
OBJECTIVE: This review systematically examines the mechanisms of OPN in multiple liver diseases, including acute liver injury, alcoholic liver disease, viral hepatitis, metabolic-associated fatty liver disease, and hepatocellular carcinoma. It focuses on its cell-type-specific functions and explores its potential as a diagnostic biomarker and therapeutic target.
RESULTS: OPN exhibits a dual role in liver pathophysiology. It promotes disease progression by activating hepatic stellate cells to drive fibrosis, enhancing collagen deposition, and facilitating HCC invasion and metastasis. Conversely, OPN also demonstrates protective functions. Intestinal OPN preserves gut barrier integrity and microbiome homeostasis, ameliorating alcohol-induced liver injury. Notably, a recent identified mechanism reveals that macrophage-derived OPN activates the OSM-STAT3-ARG2 signaling axis in hepatocytes, enhancing fatty acid oxidation and attenuating hepatic steatosis in MAFLD. Furthermore, OPN shows promise as a clinical biomarker for detecting early-stage HCC and assessing liver fibrosis, potentially outperforming alpha-fetoprotein.
CONCLUSION: Osteopontin serves as a central signaling hub in liver diseases, where it effectively integrates inflammatory, metabolic and fibrogenic networks. Harnessing its therapeutic potential represents the cornerstone for developing future OPN-targeted therapies. This strategic approach will create new avenues for liver disease treatment, enabling precise interventions tailored to specific disease contexts.
Additional Links: PMID-41388723
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PubMed:
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@article {pmid41388723,
year = {2025},
author = {Yang, J and Yao, Y and Zhou, Z},
title = {Osteopontin: a central hub in the pathogenesis and therapeutic intervention of liver disease.},
journal = {Annals of medicine},
volume = {57},
number = {1},
pages = {2596538},
doi = {10.1080/07853890.2025.2596538},
pmid = {41388723},
issn = {1365-2060},
mesh = {*Osteopontin/metabolism ; Humans ; *Liver Diseases/metabolism/therapy/pathology ; Liver Neoplasms/metabolism/pathology ; Liver/pathology/metabolism ; Animals ; Biomarkers/metabolism ; Carcinoma, Hepatocellular/metabolism ; Signal Transduction ; Hepatic Stellate Cells/metabolism ; Disease Progression ; },
abstract = {BACKGROUND: Osteopontin (OPN) is a phosphorylated glycoprotein implicated in inflammation and tissue remodeling. Its expression is significantly elevated in various liver diseases, but its precise pathophysiological roles remain complex and context-dependent.
OBJECTIVE: This review systematically examines the mechanisms of OPN in multiple liver diseases, including acute liver injury, alcoholic liver disease, viral hepatitis, metabolic-associated fatty liver disease, and hepatocellular carcinoma. It focuses on its cell-type-specific functions and explores its potential as a diagnostic biomarker and therapeutic target.
RESULTS: OPN exhibits a dual role in liver pathophysiology. It promotes disease progression by activating hepatic stellate cells to drive fibrosis, enhancing collagen deposition, and facilitating HCC invasion and metastasis. Conversely, OPN also demonstrates protective functions. Intestinal OPN preserves gut barrier integrity and microbiome homeostasis, ameliorating alcohol-induced liver injury. Notably, a recent identified mechanism reveals that macrophage-derived OPN activates the OSM-STAT3-ARG2 signaling axis in hepatocytes, enhancing fatty acid oxidation and attenuating hepatic steatosis in MAFLD. Furthermore, OPN shows promise as a clinical biomarker for detecting early-stage HCC and assessing liver fibrosis, potentially outperforming alpha-fetoprotein.
CONCLUSION: Osteopontin serves as a central signaling hub in liver diseases, where it effectively integrates inflammatory, metabolic and fibrogenic networks. Harnessing its therapeutic potential represents the cornerstone for developing future OPN-targeted therapies. This strategic approach will create new avenues for liver disease treatment, enabling precise interventions tailored to specific disease contexts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Osteopontin/metabolism
Humans
*Liver Diseases/metabolism/therapy/pathology
Liver Neoplasms/metabolism/pathology
Liver/pathology/metabolism
Animals
Biomarkers/metabolism
Carcinoma, Hepatocellular/metabolism
Signal Transduction
Hepatic Stellate Cells/metabolism
Disease Progression
RevDate: 2025-12-13
The endophytic Pseudomonas sp. JBR1 alleviates salt stress through integrated host-microbiome mechanisms.
Plant physiology pii:8379226 [Epub ahead of print].
Soil salinity is a major abiotic stress that restricts plant growth and agricultural productivity worldwide. Here, we characterized Pseudomonas sp. JBR1, an endophytic bacterium isolated from the halophyte Carex pumila, and evaluated its capacity to enhance salt tolerance in non-halophytic plants. Inoculation with strain JBR1 markedly improved growth of Arabidopsis (Arabidopsis thaliana) and Brassica rapa under saline conditions by reducing reactive oxygen species (ROS) accumulation, enhancing antioxidant enzyme activity, improving Na[+]/K[+] ion homeostasis, and stimulating auxin accumulation in roots. In addition to these direct physiological effects, strain JBR1 markedly altered rhizosphere microbial communities. 16S rRNA amplicon sequencing revealed increased microbial diversity and enrichment of beneficial taxa, particularly Streptomyces and Pseudomonas. Predictive functional profiling indicated upregulation of bacterial motility, chemotaxis, and signal transduction pathways in strain JBR1-treated plants, suggesting enhanced microbial colonization and plant-microbe interactions. These results demonstrate that strain JBR1 confers salt tolerance through a dual mechanism: direct modulation of host physiology and indirect restructuring of the rhizosphere microbiome. The synergistic effects of strain JBR1 highlight its potential as a microbial bioinoculant to improve crop resilience in saline soils and support sustainable agriculture.
Additional Links: PMID-41388648
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PubMed:
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@article {pmid41388648,
year = {2025},
author = {Peng, Y and Youn, C and Seo, J and Park, EJ and Jang, IC and Kim, CY and Lee, J},
title = {The endophytic Pseudomonas sp. JBR1 alleviates salt stress through integrated host-microbiome mechanisms.},
journal = {Plant physiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/plphys/kiaf646},
pmid = {41388648},
issn = {1532-2548},
abstract = {Soil salinity is a major abiotic stress that restricts plant growth and agricultural productivity worldwide. Here, we characterized Pseudomonas sp. JBR1, an endophytic bacterium isolated from the halophyte Carex pumila, and evaluated its capacity to enhance salt tolerance in non-halophytic plants. Inoculation with strain JBR1 markedly improved growth of Arabidopsis (Arabidopsis thaliana) and Brassica rapa under saline conditions by reducing reactive oxygen species (ROS) accumulation, enhancing antioxidant enzyme activity, improving Na[+]/K[+] ion homeostasis, and stimulating auxin accumulation in roots. In addition to these direct physiological effects, strain JBR1 markedly altered rhizosphere microbial communities. 16S rRNA amplicon sequencing revealed increased microbial diversity and enrichment of beneficial taxa, particularly Streptomyces and Pseudomonas. Predictive functional profiling indicated upregulation of bacterial motility, chemotaxis, and signal transduction pathways in strain JBR1-treated plants, suggesting enhanced microbial colonization and plant-microbe interactions. These results demonstrate that strain JBR1 confers salt tolerance through a dual mechanism: direct modulation of host physiology and indirect restructuring of the rhizosphere microbiome. The synergistic effects of strain JBR1 highlight its potential as a microbial bioinoculant to improve crop resilience in saline soils and support sustainable agriculture.},
}
RevDate: 2025-12-13
Evacuation Dysfunction Does Not Impact Breath Test Results.
Neurogastroenterology and motility [Epub ahead of print].
BACKGROUND: Evacuation dysfunction affects gastrointestinal motility, yet its effect on small bowel microbiota is unknown. We aimed to compare the glucose breath test (GBT) and lactulose breath test (LBT) outcomes in patients with or without evacuation dysfunction based on high-resolution anorectal manometry (HR-ARM) and balloon expulsion test (BET).
METHODS: We conducted a retrospective review of patients who received a HR-ARM and either a GBT or LBT from 2018 to 2024.
KEY RESULTS: We studied 344 patients who underwent GBT and 144 who underwent LBT. Clinical characteristics between the two groups were comparable. Abnormal BET was observed in 53% of patients. Rates of abnormal breath tests were comparable among patients with or without abnormal BET. Patients with positive vs. negative breath tests had similar anorectal pressures, rectal sensory function, and BET results. There were significantly more negative breath tests in GBT (64%) versus LBT (35%), with higher rates of small intestinal bacterial overgrowth (SIBO) in LBT versus GBT (SIBO only: 20.1% vs. 7.6%; SIBO+IMO: 21.5% vs. 5.5%; p < 0.001).
CONCLUSIONS AND INFERENCES: The presence of evacuation dysfunction does not impact the results of the breath test. HR-ARM and BET demonstrate a high diagnostic yield in identifying the etiology of abdominal bloating in patients with chronic constipation or IBS without diarrhea, whereas hydrogen breath tests have a low diagnostic yield in this context. The specificity and sensitivity of LBT in this patient population remain less certain.
Additional Links: PMID-41388564
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PubMed:
Citation:
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@article {pmid41388564,
year = {2025},
author = {Soetaert, C and Itani, M and Triadafilopoulos, G and Spencer, S and Nguyen, L and Neshatian, L},
title = {Evacuation Dysfunction Does Not Impact Breath Test Results.},
journal = {Neurogastroenterology and motility},
volume = {},
number = {},
pages = {e70211},
doi = {10.1111/nmo.70211},
pmid = {41388564},
issn = {1365-2982},
support = {//Belgian American Educational Foundation/ ; },
abstract = {BACKGROUND: Evacuation dysfunction affects gastrointestinal motility, yet its effect on small bowel microbiota is unknown. We aimed to compare the glucose breath test (GBT) and lactulose breath test (LBT) outcomes in patients with or without evacuation dysfunction based on high-resolution anorectal manometry (HR-ARM) and balloon expulsion test (BET).
METHODS: We conducted a retrospective review of patients who received a HR-ARM and either a GBT or LBT from 2018 to 2024.
KEY RESULTS: We studied 344 patients who underwent GBT and 144 who underwent LBT. Clinical characteristics between the two groups were comparable. Abnormal BET was observed in 53% of patients. Rates of abnormal breath tests were comparable among patients with or without abnormal BET. Patients with positive vs. negative breath tests had similar anorectal pressures, rectal sensory function, and BET results. There were significantly more negative breath tests in GBT (64%) versus LBT (35%), with higher rates of small intestinal bacterial overgrowth (SIBO) in LBT versus GBT (SIBO only: 20.1% vs. 7.6%; SIBO+IMO: 21.5% vs. 5.5%; p < 0.001).
CONCLUSIONS AND INFERENCES: The presence of evacuation dysfunction does not impact the results of the breath test. HR-ARM and BET demonstrate a high diagnostic yield in identifying the etiology of abdominal bloating in patients with chronic constipation or IBS without diarrhea, whereas hydrogen breath tests have a low diagnostic yield in this context. The specificity and sensitivity of LBT in this patient population remain less certain.},
}
RevDate: 2025-12-13
MCSPACE: inferring microbiome spatiotemporal dynamics from high-throughput co-localization data.
Microbiome pii:10.1186/s40168-025-02279-4 [Epub ahead of print].
BACKGROUND: Recent advances in high-throughput approaches for estimating co-localization of microbes, such as SAMPL-seq, allow characterization of the biogeography of the gut microbiome longitudinally and at an unprecedented scale. However, these high-dimensional data are complex and have unique noise properties.
RESULTS: To address these challenges, we developed MCSPACE, a probabilistic AI method that infers, from microbiome co-localization data, spatially coherent assemblages of taxa, their dynamics over time, and their responses to perturbations. To evaluate MCSPACE's capabilities, we generated the largest longitudinal microbiome co-localization dataset to date, profiling spatial relationships of microbes in the guts of mice subjected to serial dietary perturbations over 76 days. Analyses of these data and two existing human longitudinal datasets demonstrated superior benchmarking performance of MCSPACE over existing methods and moreover yielded insights into the spatiotemporal structuring of the gut microbiome, including identifying temporally persistent and dynamic microbial assemblages in the human gut, and shifts in assemblages in the murine gut induced by specific dietary components.
CONCLUSIONS: Our results highlight the utility of MCSPACE, which we make available to the community as an open-source software tool, for elucidating the dynamics of microbiome biogeography and gaining insights into the role of spatial relationships in host-microbial ecosystem function. Video Abstract.
Additional Links: PMID-41388559
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PubMed:
Citation:
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@article {pmid41388559,
year = {2025},
author = {Uppal, G and Urtecho, G and Richardson, M and Comba, IY and Lee, J and Moody, T and Wang, HH and Gerber, GK},
title = {MCSPACE: inferring microbiome spatiotemporal dynamics from high-throughput co-localization data.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02279-4},
pmid = {41388559},
issn = {2049-2618},
support = {Hanna H. Gray Postdoctoral Fellowship (GT15182)/HHMI/Howard Hughes Medical Institute/United States ; MTM2 2025512//National Science Foundation/ ; R01GM130777//NIH NIGMS/ ; Research Infrastructure Program//Massachusetts Life Sciences Center/ ; President's Scholar Award//Brigham and Women's Hospital/ ; },
abstract = {BACKGROUND: Recent advances in high-throughput approaches for estimating co-localization of microbes, such as SAMPL-seq, allow characterization of the biogeography of the gut microbiome longitudinally and at an unprecedented scale. However, these high-dimensional data are complex and have unique noise properties.
RESULTS: To address these challenges, we developed MCSPACE, a probabilistic AI method that infers, from microbiome co-localization data, spatially coherent assemblages of taxa, their dynamics over time, and their responses to perturbations. To evaluate MCSPACE's capabilities, we generated the largest longitudinal microbiome co-localization dataset to date, profiling spatial relationships of microbes in the guts of mice subjected to serial dietary perturbations over 76 days. Analyses of these data and two existing human longitudinal datasets demonstrated superior benchmarking performance of MCSPACE over existing methods and moreover yielded insights into the spatiotemporal structuring of the gut microbiome, including identifying temporally persistent and dynamic microbial assemblages in the human gut, and shifts in assemblages in the murine gut induced by specific dietary components.
CONCLUSIONS: Our results highlight the utility of MCSPACE, which we make available to the community as an open-source software tool, for elucidating the dynamics of microbiome biogeography and gaining insights into the role of spatial relationships in host-microbial ecosystem function. Video Abstract.},
}
RevDate: 2025-12-13
Early upregulation of alpha-7 nicotinic acetylcholine receptor in limbic system correlates with gut dysbiosis in mice exposed to binge ethanol.
Alcohol, clinical & experimental research [Epub ahead of print].
BACKGROUND: Alcohol use disorder (AUD) causes neuroinflammation and disrupts the gut microbiome through bidirectional communication between the brain and gut. However, it remains unclear whether the brain or gut responds first to alcohol exposure. We hypothesized that brain regions respond to alcohol first, preceding changes in the gut microbiome.
METHODS: B6 mice were given ethanol (EtOH; 5 g/kg/day, 42%v/v, i.g.) at various time points. Fecal samples were collected prior to the first EtOH injection (Day 0), at 24 h following the first, second, and third injections (Day 1, Day 2, and Day 3, respectively), and at 96 h after the third injection (Day 6). Brain regions, central amygdala (CeA), hypothalamus (Hyp), and nucleus accumbens (NAc) were isolated at 2 min, 12 h, 24 h, and 192 h following the first and third doses of binge EtOH, respectively. mRNA or protein expression levels of TNF-α, IL-1β, P2Y12, ITGβ2, and α7nAChR were analyzed by qRT-PCR and western blot, respectively. Fecal microbial composition and abundance were assessed using 16S rRNA metagenomic sequencing.
RESULTS: Data revealed increased TNF-α expression in the Amg, Hyp, and NAc and increased IL-1β expression in the Amg and NAc, 12 h after the first EtOH injection. α7nAChR expression in the CeA, Hyp, and NAc was also upregulated at 24 h after the third EtOH dose, compared to the control group. α7nAChR expression in the Hyp was observed at 2 min after the first EtOH dose. CHRNA7 mRNA levels were upregulated 24 h after the third EtOH dose. ITGβ2 showed an increasing trend in the Amg at 12 h after the first dose, followed by a significant reduction at 24 h, and 192 h after the third dose. 16S rRNA sequencing revealed a significant difference in β-diversity on Day 6. The relative abundance of the Prevotellaceae family was higher in EtOH-treated mice compared to controls at Day 3 and Day 6.
CONCLUSION: This study showed that brain inflammation, indicated by α7nAChR upregulation, occurred before EtOH-induced gut dysbiosis, supporting an anterograde sequence of events.
Additional Links: PMID-41388485
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@article {pmid41388485,
year = {2025},
author = {Khan, MAS and Bishir, M and Huang, W and Chidambaram, SB and Chang, SL},
title = {Early upregulation of alpha-7 nicotinic acetylcholine receptor in limbic system correlates with gut dysbiosis in mice exposed to binge ethanol.},
journal = {Alcohol, clinical & experimental research},
volume = {},
number = {},
pages = {},
doi = {10.1111/acer.70210},
pmid = {41388485},
issn = {2993-7175},
support = {AA029925/AA/NIAAA NIH HHS/United States ; },
abstract = {BACKGROUND: Alcohol use disorder (AUD) causes neuroinflammation and disrupts the gut microbiome through bidirectional communication between the brain and gut. However, it remains unclear whether the brain or gut responds first to alcohol exposure. We hypothesized that brain regions respond to alcohol first, preceding changes in the gut microbiome.
METHODS: B6 mice were given ethanol (EtOH; 5 g/kg/day, 42%v/v, i.g.) at various time points. Fecal samples were collected prior to the first EtOH injection (Day 0), at 24 h following the first, second, and third injections (Day 1, Day 2, and Day 3, respectively), and at 96 h after the third injection (Day 6). Brain regions, central amygdala (CeA), hypothalamus (Hyp), and nucleus accumbens (NAc) were isolated at 2 min, 12 h, 24 h, and 192 h following the first and third doses of binge EtOH, respectively. mRNA or protein expression levels of TNF-α, IL-1β, P2Y12, ITGβ2, and α7nAChR were analyzed by qRT-PCR and western blot, respectively. Fecal microbial composition and abundance were assessed using 16S rRNA metagenomic sequencing.
RESULTS: Data revealed increased TNF-α expression in the Amg, Hyp, and NAc and increased IL-1β expression in the Amg and NAc, 12 h after the first EtOH injection. α7nAChR expression in the CeA, Hyp, and NAc was also upregulated at 24 h after the third EtOH dose, compared to the control group. α7nAChR expression in the Hyp was observed at 2 min after the first EtOH dose. CHRNA7 mRNA levels were upregulated 24 h after the third EtOH dose. ITGβ2 showed an increasing trend in the Amg at 12 h after the first dose, followed by a significant reduction at 24 h, and 192 h after the third dose. 16S rRNA sequencing revealed a significant difference in β-diversity on Day 6. The relative abundance of the Prevotellaceae family was higher in EtOH-treated mice compared to controls at Day 3 and Day 6.
CONCLUSION: This study showed that brain inflammation, indicated by α7nAChR upregulation, occurred before EtOH-induced gut dysbiosis, supporting an anterograde sequence of events.},
}
RevDate: 2025-12-13
CmpDate: 2025-12-13
Fetal programming by the parental microbiome of offspring behavior, and DNA methylation and gene expression within the hippocampus.
Microbiome, 13(1):254.
BACKGROUND: The microorganisms colonizing the gastrointestinal tract of animals, collectively referred to as the gut microbiome, affect numerous host behaviors dependent on the central nervous system (CNS). Studies comparing germ-free mice to normally colonized mice have demonstrated influences of the microbiome on anxiety-related behaviors, voluntary activity, and gene expression in the CNS. Additionally, there is epidemiologic evidence supporting an intergenerational influence of the maternal microbiome on neurodevelopment of offspring and behavior later in life. There is limited experimental evidence however directly linking the maternal microbiome to long-term neurodevelopmental outcomes, or knowledge regarding mechanisms responsible for such effects.
RESULTS: Here we show that that the maternal microbiome has a dominant influence on several offspring phenotypes including anxiety-related behavior, voluntary activity, and body weight. Adverse outcomes in offspring were associated with features of the maternal microbiome including bile salt hydrolase activity gene expression (bsh), abundance of certain bile acids, and hepatic expression of Slc10a1. In cross-foster experiments, offspring resembled their birth dam phenotypically, despite faithful colonization in the postnatal period with the surrogate dam microbiome. Genome-wide DNA methylation analysis of hippocampal DNA identified microbiome-associated differences in DNA methylation of 196 loci in total, 176 of which show conserved profiles between mother and offspring. Further, single-cell transcriptional analysis revealed accompanying differences in expression of several differentially methylated genes within certain hippocampal cell clusters, and vascular expression of genes associated with bile acid transport. Inferred cell-to-cell communication in the hippocampus based on coordinated ligand-receptor expression revealed differences in expression of neuropeptides associated with satiety.
CONCLUSIONS: Collectively, these data provide proof-of-principle that the maternal gut microbiome has a dominant influence on the neurodevelopment underlying certain offspring behaviors and activities, and selectively affects genome DNA methylation and gene expression in the offspring hippocampus in conjunction with that neurodevelopment. Video Abstract.
Additional Links: PMID-41388434
PubMed:
Citation:
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@article {pmid41388434,
year = {2025},
author = {Gustafson, KL and Busi, SB and McAdams, ZL and McCorkle, RE and Khodakivskyi, P and Bivens, NJ and Davis, DJ and Raju, M and Coghill, LM and Goun, EA and Amos-Landgraf, J and Franklin, CL and Wilmes, P and Cortese, R and Ericsson, AC},
title = {Fetal programming by the parental microbiome of offspring behavior, and DNA methylation and gene expression within the hippocampus.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {254},
pmid = {41388434},
issn = {2049-2618},
support = {U42 OD010918/NH/NIH HHS/United States ; R03 OD028259-01/NH/NIH HHS/United States ; },
mesh = {Animals ; Female ; *Hippocampus/metabolism ; *DNA Methylation ; Mice ; *Gastrointestinal Microbiome ; Pregnancy ; *Fetal Development/genetics ; Male ; Behavior, Animal ; Mice, Inbred C57BL ; Anxiety/microbiology ; },
abstract = {BACKGROUND: The microorganisms colonizing the gastrointestinal tract of animals, collectively referred to as the gut microbiome, affect numerous host behaviors dependent on the central nervous system (CNS). Studies comparing germ-free mice to normally colonized mice have demonstrated influences of the microbiome on anxiety-related behaviors, voluntary activity, and gene expression in the CNS. Additionally, there is epidemiologic evidence supporting an intergenerational influence of the maternal microbiome on neurodevelopment of offspring and behavior later in life. There is limited experimental evidence however directly linking the maternal microbiome to long-term neurodevelopmental outcomes, or knowledge regarding mechanisms responsible for such effects.
RESULTS: Here we show that that the maternal microbiome has a dominant influence on several offspring phenotypes including anxiety-related behavior, voluntary activity, and body weight. Adverse outcomes in offspring were associated with features of the maternal microbiome including bile salt hydrolase activity gene expression (bsh), abundance of certain bile acids, and hepatic expression of Slc10a1. In cross-foster experiments, offspring resembled their birth dam phenotypically, despite faithful colonization in the postnatal period with the surrogate dam microbiome. Genome-wide DNA methylation analysis of hippocampal DNA identified microbiome-associated differences in DNA methylation of 196 loci in total, 176 of which show conserved profiles between mother and offspring. Further, single-cell transcriptional analysis revealed accompanying differences in expression of several differentially methylated genes within certain hippocampal cell clusters, and vascular expression of genes associated with bile acid transport. Inferred cell-to-cell communication in the hippocampus based on coordinated ligand-receptor expression revealed differences in expression of neuropeptides associated with satiety.
CONCLUSIONS: Collectively, these data provide proof-of-principle that the maternal gut microbiome has a dominant influence on the neurodevelopment underlying certain offspring behaviors and activities, and selectively affects genome DNA methylation and gene expression in the offspring hippocampus in conjunction with that neurodevelopment. Video Abstract.},
}
MeSH Terms:
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Animals
Female
*Hippocampus/metabolism
*DNA Methylation
Mice
*Gastrointestinal Microbiome
Pregnancy
*Fetal Development/genetics
Male
Behavior, Animal
Mice, Inbred C57BL
Anxiety/microbiology
RevDate: 2025-12-13
Environmental and skin-nasal microbiome variation in South African children with atopic dermatitis.
BMC microbiology pii:10.1186/s12866-025-04589-x [Epub ahead of print].
BACKGROUND: Atopic dermatitis (AD) in early childhood is associated with microbial dysbiosis. Skin and nasal microbiomes have been linked to AD severity; this relationship has not yet been studied in an African cohort. Here, we aimed to explore how urban and rural stratification, disease severity, and inter-site bacterial overlap shape the skin and nasal microbiomes of South African children with AD.
METHODS: Children were recruited from urban Cape Town (CT) and rural Umtata (UM), South Africa. We profiled the skin and nasal microbiomes of 183 children (84 healthy controls and 99 with AD; ages 9-37 months), totaling 462 samples, including both lesional and non-lesional skin sites in children with AD, in a cross-sectional study design. Using 16S rRNA V4-V5 sequencing for its accessibility, we applied random forest (RF) models to classify AD status based on amplicon sequence variants (ASVs) and analyzed microbiome composition and diversity by region.
RESULTS: We found that RF models could predict AD status using both skin and nasal microbiomes (AUCs: skin = 0.69-0.79; nasal = 0.65), strongly driven by both Streptococcus and Staphylococcus. The correlations between skin and nasal microbiomes were significantly stronger in children with AD compared to controls, with higher correlations observed in rural UM (healthy r = 0.45 to AD r = 0.67) compared to urban CT (healthy r = 0.27 to AD r = 0.65). The skin microbiome diversity was higher in children from rural UM with healthy skin than in those from urban CT (p = 0.004). However, children with AD in both groups showed significant alterations in their microbiome, with those in rural UM exhibiting greater beta diversity changes (p = 0.001-0.002) than their urban CT counterparts (p = 0.002-0.349).
CONCLUSION: In South African children with AD, skin-nasal microbiomes reflect shared reservoirs, and differences in the AD microbiome were observed between environmental regions. These findings highlight the need for geographically diverse studies incorporating skin and mucocutaneous sampling to better understand pediatric AD.
Additional Links: PMID-41388368
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PubMed:
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@article {pmid41388368,
year = {2025},
author = {Chen, Y and Nguyen, AD and Lunjani, N and Ndhlovu, G and Kaul, D and De Pessemier, B and Nakatsuji, T and Madzinga, M and Sovershaeva, E and Hlela, C and Levin, M and Mankahla, A and Hightower, G and Callewaert, C and Knight, R and Gallo, RL and Dupont, CL and Dube, F},
title = {Environmental and skin-nasal microbiome variation in South African children with atopic dermatitis.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-025-04589-x},
pmid = {41388368},
issn = {1471-2180},
support = {HREC/REF: 451/2014/GF/NIH HHS/United States ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) in early childhood is associated with microbial dysbiosis. Skin and nasal microbiomes have been linked to AD severity; this relationship has not yet been studied in an African cohort. Here, we aimed to explore how urban and rural stratification, disease severity, and inter-site bacterial overlap shape the skin and nasal microbiomes of South African children with AD.
METHODS: Children were recruited from urban Cape Town (CT) and rural Umtata (UM), South Africa. We profiled the skin and nasal microbiomes of 183 children (84 healthy controls and 99 with AD; ages 9-37 months), totaling 462 samples, including both lesional and non-lesional skin sites in children with AD, in a cross-sectional study design. Using 16S rRNA V4-V5 sequencing for its accessibility, we applied random forest (RF) models to classify AD status based on amplicon sequence variants (ASVs) and analyzed microbiome composition and diversity by region.
RESULTS: We found that RF models could predict AD status using both skin and nasal microbiomes (AUCs: skin = 0.69-0.79; nasal = 0.65), strongly driven by both Streptococcus and Staphylococcus. The correlations between skin and nasal microbiomes were significantly stronger in children with AD compared to controls, with higher correlations observed in rural UM (healthy r = 0.45 to AD r = 0.67) compared to urban CT (healthy r = 0.27 to AD r = 0.65). The skin microbiome diversity was higher in children from rural UM with healthy skin than in those from urban CT (p = 0.004). However, children with AD in both groups showed significant alterations in their microbiome, with those in rural UM exhibiting greater beta diversity changes (p = 0.001-0.002) than their urban CT counterparts (p = 0.002-0.349).
CONCLUSION: In South African children with AD, skin-nasal microbiomes reflect shared reservoirs, and differences in the AD microbiome were observed between environmental regions. These findings highlight the need for geographically diverse studies incorporating skin and mucocutaneous sampling to better understand pediatric AD.},
}
RevDate: 2025-12-13
Standardizing microbiome research: interlaboratory validation of SOPs for sample preparation and DNA extraction from food and environmental ecosystems.
Environmental microbiome pii:10.1186/s40793-025-00833-z [Epub ahead of print].
BACKGROUND: Microbiome research has expanded rapidly, however, lack of standardized and validated protocols for microbiome sampling and DNA extraction has hindered the reproducibility and comparability of studies. The SUS-MIRRI.IT project aimed to prepare and validate Standard Operating Procedures (SOPs) for microbiome analysis across diverse ecosystems, including fermented foods, soils, waters, and more. To validate these protocols, 15 Italian research units (RUs) participated in an interlaboratory trial on 120 samples (liquid and solid fermented foods, waters, and soils). Metataxonomic sequencing was performed using 16S rRNA gene amplicon sequencing to assess the reproducibility of the protocols. The interlaboratory trial involved distributing homogenized samples to participating RUs and evaluating performance both between and within RUs. This was done by comparing results obtained from DNA extraction and amplicon-based sequencing.
RESULTS: The results demonstrated high reproducibility of the procedures suggested in the SOPs across different sample types, with no significant differences in microbial diversity or composition between biological replicates or research units. DNA recovery was generally consistent, with minor variations observed in solid samples.
CONCLUSIONS: This study underlines the importance of standardized protocols in microbiome research. The validated Standard Operating Procedures developed by the SUS-MIRRI.IT project demonstrate robustness and reproducibility across diverse ecosystems, providing a foundation for future microbiome studies. The adoption of these protocols will enhance data comparability and support large-scale meta-analyses in food systems microbiome research.
Additional Links: PMID-41388332
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PubMed:
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@article {pmid41388332,
year = {2025},
author = {Ferrocino, I and Ferrara, M and Garello, M and Turchetti, B and Andreolli, M and Arena, MP and Alduina, R and Aloi, F and Bevivino, A and Bruno, E and Capozzi, V and Coronas, R and De Vero, L and Di Renzo, T and Franzetti, A and Gaglio, R and Gallo, G and Gullo, M and Guarcello, R and Giavalisco, M and Lampis, S and Mugnai, G and Quatrini, P and Reale, A and Sbarra, F and Sannino, C and Spadaro, D and Tatangelo, V and Visca, A and Zara, G and Zotta, T and Varese, GC and Cocolin, L},
title = {Standardizing microbiome research: interlaboratory validation of SOPs for sample preparation and DNA extraction from food and environmental ecosystems.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-025-00833-z},
pmid = {41388332},
issn = {2524-6372},
support = {IR0000005//Ministero dell'Università e della Ricerca/ ; },
abstract = {BACKGROUND: Microbiome research has expanded rapidly, however, lack of standardized and validated protocols for microbiome sampling and DNA extraction has hindered the reproducibility and comparability of studies. The SUS-MIRRI.IT project aimed to prepare and validate Standard Operating Procedures (SOPs) for microbiome analysis across diverse ecosystems, including fermented foods, soils, waters, and more. To validate these protocols, 15 Italian research units (RUs) participated in an interlaboratory trial on 120 samples (liquid and solid fermented foods, waters, and soils). Metataxonomic sequencing was performed using 16S rRNA gene amplicon sequencing to assess the reproducibility of the protocols. The interlaboratory trial involved distributing homogenized samples to participating RUs and evaluating performance both between and within RUs. This was done by comparing results obtained from DNA extraction and amplicon-based sequencing.
RESULTS: The results demonstrated high reproducibility of the procedures suggested in the SOPs across different sample types, with no significant differences in microbial diversity or composition between biological replicates or research units. DNA recovery was generally consistent, with minor variations observed in solid samples.
CONCLUSIONS: This study underlines the importance of standardized protocols in microbiome research. The validated Standard Operating Procedures developed by the SUS-MIRRI.IT project demonstrate robustness and reproducibility across diverse ecosystems, providing a foundation for future microbiome studies. The adoption of these protocols will enhance data comparability and support large-scale meta-analyses in food systems microbiome research.},
}
RevDate: 2025-12-12
Green manure-induced shifts in nematode communities associated with soil bacterial and fungal biomes.
Scientific reports pii:10.1038/s41598-025-31442-y [Epub ahead of print].
Green manures are widely used to enhance soil health and suppress plant-parasitic nematodes, and their effects on the broader soil food web have been studied. Beyond direct suppression, the role of green manures in supporting and sustaining soil food webs has attracted increasing attention. In this study, we evaluated the use of DNA sequencing to identify various nematode genera and their microbial associates in a field trial using oat (Avena sativa) and hairy vetch (Vicia villosa) as green manures. Nematode index analysis revealed that the oat treatment promoted a structured nematode community. Furthermore, the nematode community structure observed in the oat treatment was linked to specific bacterial and fungal genera. Several beneficial fungi were identified, indicating that oats, used as a green manure, actively enhanced the microbiome. Our results showed that enriching the micro-food web through organic fertilizers can help in the detection of beneficial microorganisms, with the nematode index serving as a potential indicator.
Additional Links: PMID-41387949
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PubMed:
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@article {pmid41387949,
year = {2025},
author = {Sudo, A and Yoshimura, D and Daimon, H and Sato, S and Asamizu, E},
title = {Green manure-induced shifts in nematode communities associated with soil bacterial and fungal biomes.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-025-31442-y},
pmid = {41387949},
issn = {2045-2322},
abstract = {Green manures are widely used to enhance soil health and suppress plant-parasitic nematodes, and their effects on the broader soil food web have been studied. Beyond direct suppression, the role of green manures in supporting and sustaining soil food webs has attracted increasing attention. In this study, we evaluated the use of DNA sequencing to identify various nematode genera and their microbial associates in a field trial using oat (Avena sativa) and hairy vetch (Vicia villosa) as green manures. Nematode index analysis revealed that the oat treatment promoted a structured nematode community. Furthermore, the nematode community structure observed in the oat treatment was linked to specific bacterial and fungal genera. Several beneficial fungi were identified, indicating that oats, used as a green manure, actively enhanced the microbiome. Our results showed that enriching the micro-food web through organic fertilizers can help in the detection of beneficial microorganisms, with the nematode index serving as a potential indicator.},
}
RevDate: 2025-12-12
Deoxycholic acid derived from the gut microbiota involved in the regulation of adaptive thermogenesis in response to dietary protein restriction in plateau pika.
Microbiome pii:10.1186/s40168-025-02233-4 [Epub ahead of print].
BACKGROUND: Most winter-active mammals experience protein restriction. Gut microbiota is a key regulator of host energy homeostasis during nutrient deficiency, yet cross talk between microbiota and factors (e.g., hormones, signaling molecules) that regulate host energy metabolism in a low-protein (LP) context has not been studied sufficiently.
RESULT: The LP diet triggered the hepatic FGF21 adaptive metabolic pathway, which increased thermogenesis and reduced body weight, and this adaptive response was dependent on the composition and function of gut microbiota. Specifically, the LP diet induced a reshaping of the gut microbiota, altering its metabolic profile to increase deoxycholic acid levels and thereby increasing UCP1-induced thermogenesis of brown adipose tissue in an FGF21-dependent manner. Fecal transplantation with LP-associated microbiota increased thermogenesis through activation of GCN2-eIF2α-FGF21 signaling. Supplementation of the LP diet with yak fecal bacteria in plateau pika reduced UCP1-associated thermogenesis by altering the gut microbiome, decreasing deoxycholic acid production, suppressing activation of GCN2-eIF2α-FGF21 signaling, and alleviating LP-induced weight loss.
CONCLUSIONS: Our study reveals an association between the gut microbiota and LP diet-associated regulation of FGF21 signaling and thermogenesis and further demonstrates that this relationship is influenced by interspecies microbial transfer, indicating a critical mechanism whereby horizontal microbial exchange between sympatric species enhances host energy homeostasis. These findings provide novel insights into our understanding of the adaptations of mammals to high-elevation environments. Video Abstract.
Additional Links: PMID-41387927
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PubMed:
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@article {pmid41387927,
year = {2025},
author = {Shi, F and Yang, Z and Zhang, L and Zou, D and Yu, J and Guo, N and Ren, S and Tang, X and Gu, C and Xu, R and Ru, Y and Zhang, Y and Wang, D},
title = {Deoxycholic acid derived from the gut microbiota involved in the regulation of adaptive thermogenesis in response to dietary protein restriction in plateau pika.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02233-4},
pmid = {41387927},
issn = {2049-2618},
support = {32301301//National Natural Science Foundation of China/ ; 32330012//National Natural Science Foundation of China/ ; 23-2-1-26-zyyd-jch//Natural Science Foundation of Qingdao/ ; ZR2024QC355//Natural Science Foundation of Shandong/ ; },
abstract = {BACKGROUND: Most winter-active mammals experience protein restriction. Gut microbiota is a key regulator of host energy homeostasis during nutrient deficiency, yet cross talk between microbiota and factors (e.g., hormones, signaling molecules) that regulate host energy metabolism in a low-protein (LP) context has not been studied sufficiently.
RESULT: The LP diet triggered the hepatic FGF21 adaptive metabolic pathway, which increased thermogenesis and reduced body weight, and this adaptive response was dependent on the composition and function of gut microbiota. Specifically, the LP diet induced a reshaping of the gut microbiota, altering its metabolic profile to increase deoxycholic acid levels and thereby increasing UCP1-induced thermogenesis of brown adipose tissue in an FGF21-dependent manner. Fecal transplantation with LP-associated microbiota increased thermogenesis through activation of GCN2-eIF2α-FGF21 signaling. Supplementation of the LP diet with yak fecal bacteria in plateau pika reduced UCP1-associated thermogenesis by altering the gut microbiome, decreasing deoxycholic acid production, suppressing activation of GCN2-eIF2α-FGF21 signaling, and alleviating LP-induced weight loss.
CONCLUSIONS: Our study reveals an association between the gut microbiota and LP diet-associated regulation of FGF21 signaling and thermogenesis and further demonstrates that this relationship is influenced by interspecies microbial transfer, indicating a critical mechanism whereby horizontal microbial exchange between sympatric species enhances host energy homeostasis. These findings provide novel insights into our understanding of the adaptations of mammals to high-elevation environments. Video Abstract.},
}
RevDate: 2025-12-12
Multiomics insights into rumen microbiome and function in grazing lambs: implications for nutrient absorption and grassland sustainability.
Microbiome pii:10.1186/s40168-025-02200-z [Epub ahead of print].
BACKGROUND: The center of sustainable development of grassland husbandry is the balance between forage intake and growth characteristics of animals, and one of the keys to restricting the conversion efficiency of forage intake is the digestibility of forage produced by rumen microorganisms. Thus, the interaction between grass intake and rumen microbial fermentation is a key driver of both ruminant productivity and grassland ecosystem health. However, interactions between grass species, supplementary feeding, rumen microbiome, and rumen epithelium function, remain poorly understood.
RESULTS: We employed metagenomic and metatranscriptomic analyses, coupled with single-cell RNA sequencing (scRNA-seq) of rumen wall and serum metabolomics, to investigate how the rumen microbiome regulates grass intake and host metabolism. In a two-factor (grazing intensity and concentrate supplementation) experiment with 72 lambs, supplementary feeding under moderate grazing increased dry matter intake but decreased grass consumption of Artemisia tanacetifolia. These shifts correlated with contrasting trends between metagenomic and metatranscriptomic profiles of Lachnospiraceae. scRNA-seq revealed an increased abundance of basal cells (BCs), terminally differentiated keratinocytes (TDKs), and differentiated keratinocytes (DKs) in the supplemented group, with solute carrier genes (e.g., SLC16A1) involved in short chain fatty acids (SCFAs) transport enriched in basal cells. We also identified interactions between the rumen microbiome and host epithelial cells, influencing gene expression and localization, which in turn mediated the animal serum nutrient metabolism, particularly in B vitamin, bile acids, and amino acids.
CONCLUSIONS: Our study identified key microbiome and epithelial cell subtypes involved in grass digestion and SCFAs metabolism in the rumen. This novel link between ruminal microbial function, epithelial cell cluster-based genes, and host metabolism provides critical insights into mechanisms underlying the interaction between grass intake and supplementary feeding for optimizing ruminant management strategies in sustainable grazing systems. Video Abstract.
Additional Links: PMID-41387926
Publisher:
PubMed:
Citation:
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@article {pmid41387926,
year = {2025},
author = {Ma, X and Wang, B and Xu, M and Zhang, Y and Liu, N and Teng, L and Li, Z and Yang, H and Xie, X and Zhang, B and Wang, Z and Wang, Y and Liu, J and Bao, J and Luo, H},
title = {Multiomics insights into rumen microbiome and function in grazing lambs: implications for nutrient absorption and grassland sustainability.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02200-z},
pmid = {41387926},
issn = {2049-2618},
support = {32192463//The Major Program of National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: The center of sustainable development of grassland husbandry is the balance between forage intake and growth characteristics of animals, and one of the keys to restricting the conversion efficiency of forage intake is the digestibility of forage produced by rumen microorganisms. Thus, the interaction between grass intake and rumen microbial fermentation is a key driver of both ruminant productivity and grassland ecosystem health. However, interactions between grass species, supplementary feeding, rumen microbiome, and rumen epithelium function, remain poorly understood.
RESULTS: We employed metagenomic and metatranscriptomic analyses, coupled with single-cell RNA sequencing (scRNA-seq) of rumen wall and serum metabolomics, to investigate how the rumen microbiome regulates grass intake and host metabolism. In a two-factor (grazing intensity and concentrate supplementation) experiment with 72 lambs, supplementary feeding under moderate grazing increased dry matter intake but decreased grass consumption of Artemisia tanacetifolia. These shifts correlated with contrasting trends between metagenomic and metatranscriptomic profiles of Lachnospiraceae. scRNA-seq revealed an increased abundance of basal cells (BCs), terminally differentiated keratinocytes (TDKs), and differentiated keratinocytes (DKs) in the supplemented group, with solute carrier genes (e.g., SLC16A1) involved in short chain fatty acids (SCFAs) transport enriched in basal cells. We also identified interactions between the rumen microbiome and host epithelial cells, influencing gene expression and localization, which in turn mediated the animal serum nutrient metabolism, particularly in B vitamin, bile acids, and amino acids.
CONCLUSIONS: Our study identified key microbiome and epithelial cell subtypes involved in grass digestion and SCFAs metabolism in the rumen. This novel link between ruminal microbial function, epithelial cell cluster-based genes, and host metabolism provides critical insights into mechanisms underlying the interaction between grass intake and supplementary feeding for optimizing ruminant management strategies in sustainable grazing systems. Video Abstract.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Assessing the impact of bariatric surgery on cardiovascular risk in type 2 diabetes: a systematic review and meta-analysis using OMICs data.
Diabetology & metabolic syndrome, 17(1):448.
Type 2 diabetes (T2D) is a complex, multifactorial metabolic disorder, and while bariatric surgery has emerged as a promising intervention for obesity-related T2D with significant metabolic benefits, its long-term durability and potential for remission vary among patients. This systematic review and meta-analysis explore how omics modalities-such as genomics, epigenomics, transcriptomics, metabolomics, proteomics, and gut microbiome-can reveal potential biomarkers linked to cardiovascular disease (CVD) of T2D patients who undergo bariatric surgery. Following PRISMA 2020 guidelines, a systematic search in PubMed identified 49 eligible studies. The meta-analysis of eight proteomic biomarkers, showed significant post-surgery improvements in total cholesterol (mean difference (MD) 0.44 (95% CI: 0.06-0.82), p = 0.02), triglycerides (MD 1.00 (0.77-1.24), p < 0.00001), LDL cholesterol (MD 0.27 (0.02, 0.52), p = 0.03), HDL cholesterol (MD -0.22 (-0.30, -0.15), p < 0.00001), hsCRP (MD 0.64 (0.44, 0.84), p < 0.00001), C peptide levels (MD 1.29 (0.96, 1.61), p < 0.0001), and IL-6 (MD 1.84 (0.85, 2.84), p = 0.0003). These findings highlight the value of integrated omics in developing personalized diagnostics, predicting disease risks, and designing targeted therapies. The present study is the first systematic review presenting the omics disciplines that offer a comprehensive view of the effectiveness of bariatric surgery in managing T2D, subsequently reducing the risk of CVD.
Additional Links: PMID-41387897
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Citation:
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@article {pmid41387897,
year = {2025},
author = {Almazrouei, B and Mousa, M and Al Dain Marzouka, N and Barajas-Gamboa, JS and Abril, C and Al Safar, H},
title = {Assessing the impact of bariatric surgery on cardiovascular risk in type 2 diabetes: a systematic review and meta-analysis using OMICs data.},
journal = {Diabetology & metabolic syndrome},
volume = {17},
number = {1},
pages = {448},
pmid = {41387897},
issn = {1758-5996},
support = {8434000344//This work was supported by The Abu Dhabi Department of Education and Knowledge (ADEK)/ ; },
abstract = {Type 2 diabetes (T2D) is a complex, multifactorial metabolic disorder, and while bariatric surgery has emerged as a promising intervention for obesity-related T2D with significant metabolic benefits, its long-term durability and potential for remission vary among patients. This systematic review and meta-analysis explore how omics modalities-such as genomics, epigenomics, transcriptomics, metabolomics, proteomics, and gut microbiome-can reveal potential biomarkers linked to cardiovascular disease (CVD) of T2D patients who undergo bariatric surgery. Following PRISMA 2020 guidelines, a systematic search in PubMed identified 49 eligible studies. The meta-analysis of eight proteomic biomarkers, showed significant post-surgery improvements in total cholesterol (mean difference (MD) 0.44 (95% CI: 0.06-0.82), p = 0.02), triglycerides (MD 1.00 (0.77-1.24), p < 0.00001), LDL cholesterol (MD 0.27 (0.02, 0.52), p = 0.03), HDL cholesterol (MD -0.22 (-0.30, -0.15), p < 0.00001), hsCRP (MD 0.64 (0.44, 0.84), p < 0.00001), C peptide levels (MD 1.29 (0.96, 1.61), p < 0.0001), and IL-6 (MD 1.84 (0.85, 2.84), p = 0.0003). These findings highlight the value of integrated omics in developing personalized diagnostics, predicting disease risks, and designing targeted therapies. The present study is the first systematic review presenting the omics disciplines that offer a comprehensive view of the effectiveness of bariatric surgery in managing T2D, subsequently reducing the risk of CVD.},
}
RevDate: 2025-12-12
SIMBA-GNN: mechanistic graph learning for microbiome prediction.
NPJ systems biology and applications pii:10.1038/s41540-025-00631-w [Epub ahead of print].
Predicting how gut microbial communities assemble and change requires models that capture the underlying mechanisms driving interspecies interactions, not just taxonomic correlations. We present SIMBA, a simulation-augmented graph neural network that integrates mechanistic insights from metabolic simulations with edge-aware graph transformers to predict microbial community composition. Using a high-fiber dietary cohort mapped to metabolic networks, we ran thousands of pairwise simulations to infer cross-feeding probabilities, pathway activity fingerprints, and microbe-microbe functional similarity. These signals instantiate a global microbe-metabolite-pathway graph for learning. A custom heterogeneous graph transformer incorporates scalar edge attributes into attention. It is trained through a multi-stage pipeline combining self-supervised learning, supervised pretraining on simulated graphs, and fine-tuning on experimental microbial abundance data. Each individual's microbiome is represented as a sample-specific instantiation of the shared mechanistic graph derived from metabolic simulations, where only the set of microbes detected in that individual varies. SIMBA learns from this mechanistic prior to predict microbial presence and relative abundance across individuals, enabling hypothesis-driven exploration of microbial ecosystems.
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@article {pmid41387745,
year = {2025},
author = {Aminian-Dehkordi, J and Parsa, M and Dickson, A and Mofrad, MRK},
title = {SIMBA-GNN: mechanistic graph learning for microbiome prediction.},
journal = {NPJ systems biology and applications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41540-025-00631-w},
pmid = {41387745},
issn = {2056-7189},
abstract = {Predicting how gut microbial communities assemble and change requires models that capture the underlying mechanisms driving interspecies interactions, not just taxonomic correlations. We present SIMBA, a simulation-augmented graph neural network that integrates mechanistic insights from metabolic simulations with edge-aware graph transformers to predict microbial community composition. Using a high-fiber dietary cohort mapped to metabolic networks, we ran thousands of pairwise simulations to infer cross-feeding probabilities, pathway activity fingerprints, and microbe-microbe functional similarity. These signals instantiate a global microbe-metabolite-pathway graph for learning. A custom heterogeneous graph transformer incorporates scalar edge attributes into attention. It is trained through a multi-stage pipeline combining self-supervised learning, supervised pretraining on simulated graphs, and fine-tuning on experimental microbial abundance data. Each individual's microbiome is represented as a sample-specific instantiation of the shared mechanistic graph derived from metabolic simulations, where only the set of microbes detected in that individual varies. SIMBA learns from this mechanistic prior to predict microbial presence and relative abundance across individuals, enabling hypothesis-driven exploration of microbial ecosystems.},
}
RevDate: 2025-12-12
Association between the gut microbiome and neurodevelopmental outcomes in infants with congenital heart disease: A prospective cohort study.
JPEN. Journal of parenteral and enteral nutrition [Epub ahead of print].
BACKGROUND: Children with congenital heart disease are at risk for poor neurodevelopment. The gut microbiome may influence neurodevelopmental outcomes through the gut-brain axis. This study investigated the association of early-life gut microbiome with neurodevelopmental outcomes.
METHODS: A prospective cohort study was conducted in the cardiac intensive care unit. Fecal samples were collected before surgery, after surgery, and before discharge. Neurodevelopmental testing used Bayley Scales of Infant and Toddler Development between 9 and 12 months. Microbial data of the 16S ribosomal RNA V4 region were processed. Microbiome data were analyzed using Quantitative Insights Into Microbial Ecology 2 and MicrobiomeAnalyst 2.0.
RESULTS: Twenty-four patients were analyzed: 15 (62.5%) were male and 12 (50%) were White. Children with lower cognitive (Chao1 P = 0.024) and language scores (Chao1 P = 0.018) had lower alpha diversity; beta diversity showed marginally significant dissimilarities (Jaccard P = 0.102 and P = 0.051, respectively). Lower cognitive scores were associated with less Parabacteroides (P = 0.031), Bacteroides (P = 0.041), and Bifidobacterium (P = 0.047), and lower language scores were associated with less Bifidobacterium (P = 0.044) and Enterococcus (P = 0.024). Lower motor scores were associated with less Rothia (P = 0.017) but a higher abundance of Serratia (P < 0.001), Acinetobacter (P = 0.016), and Proteus (P = 0.013).
CONCLUSION: Children with congenital heart disease with lower cognitive and language scores had lower diversity and less anti-inflammatory flora (eg, Bifidobacterium), whereas those with lower motor scores had a higher abundance of pro-inflammatory flora (eg, Serratia, Acinetobacter, and Proteus). Further studies are needed to understand the longitudinal effect of gut microbial dysbiosis on neurodevelopment in children with congenital heart disease.
Additional Links: PMID-41387715
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PubMed:
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@article {pmid41387715,
year = {2025},
author = {Fundora, MP and Dressner, L and Calamaro, C and Brown, AM and John, AS and Keiffer, R and Alexander, N and Huang, H and Gillespie, S and Denning, PW and Sanders-Lewis, K and Bai, J},
title = {Association between the gut microbiome and neurodevelopmental outcomes in infants with congenital heart disease: A prospective cohort study.},
journal = {JPEN. Journal of parenteral and enteral nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpen.70038},
pmid = {41387715},
issn = {1941-2444},
support = {UL1-TR002378//The Imagine, Innovate and Impact (I3) Award from the Emory University School of Medicine, Georgia CTSA NIH award/ ; },
abstract = {BACKGROUND: Children with congenital heart disease are at risk for poor neurodevelopment. The gut microbiome may influence neurodevelopmental outcomes through the gut-brain axis. This study investigated the association of early-life gut microbiome with neurodevelopmental outcomes.
METHODS: A prospective cohort study was conducted in the cardiac intensive care unit. Fecal samples were collected before surgery, after surgery, and before discharge. Neurodevelopmental testing used Bayley Scales of Infant and Toddler Development between 9 and 12 months. Microbial data of the 16S ribosomal RNA V4 region were processed. Microbiome data were analyzed using Quantitative Insights Into Microbial Ecology 2 and MicrobiomeAnalyst 2.0.
RESULTS: Twenty-four patients were analyzed: 15 (62.5%) were male and 12 (50%) were White. Children with lower cognitive (Chao1 P = 0.024) and language scores (Chao1 P = 0.018) had lower alpha diversity; beta diversity showed marginally significant dissimilarities (Jaccard P = 0.102 and P = 0.051, respectively). Lower cognitive scores were associated with less Parabacteroides (P = 0.031), Bacteroides (P = 0.041), and Bifidobacterium (P = 0.047), and lower language scores were associated with less Bifidobacterium (P = 0.044) and Enterococcus (P = 0.024). Lower motor scores were associated with less Rothia (P = 0.017) but a higher abundance of Serratia (P < 0.001), Acinetobacter (P = 0.016), and Proteus (P = 0.013).
CONCLUSION: Children with congenital heart disease with lower cognitive and language scores had lower diversity and less anti-inflammatory flora (eg, Bifidobacterium), whereas those with lower motor scores had a higher abundance of pro-inflammatory flora (eg, Serratia, Acinetobacter, and Proteus). Further studies are needed to understand the longitudinal effect of gut microbial dysbiosis on neurodevelopment in children with congenital heart disease.},
}
RevDate: 2025-12-12
A young child formula with Limosilactobacillus reuteri and GOS modulates gut microbiome and enhances bone and muscle development: a randomized trial.
Nature communications pii:10.1038/s41467-025-66930-2 [Epub ahead of print].
In this randomized, double-blind controlled trial, 182 Filipino children aged 2-3 years received either an experimental young child formula (EYCF) containing a combination of Limosilactobacillus reuteri DSM 17938 and galacto-oligosaccharides (GOS; n = 91) or a minimally fortified milk (CM; n = 91) for 6 months. Primary outcome was tibia speed of sound and secondary outcomes were muscle strength, blood vitamin D levels, bone turnover markers, gut microbiota, fecal calcium fatty acid soaps and gastro-intestinal tolerance. Compared to CM, those in the EYCF group showed increased tibia speed of sound after 3 and 6 months. The intervention remodeled the stool microbiome composition, assessed by shotgun metagenomics, with enrichment of L. reuteri and higher bifidobacteria presence in the EYCF group. Increased L. reuteri abundance after 6 months of EYCF consumption associates with higher bone quality and muscle strength. Stool metabolomics show 45 metabolites modulated by EYCF consumption and associated to microbiome compositional changes, leading to enrichment of tryptophane and indole metabolism. In summary, consumption of EYCF containing a L. reuteri + GOS synbiotic improves musculoskeletal development in toddlers via modulation of microbiota composition and function. These results provide insights on gut-musculoskeletal crosstalk during early life. Clinicaltrial.gov NCT04799028.
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@article {pmid41387706,
year = {2025},
author = {Bonnet, N and Capeding, MR and Siegwald, L and Garcia-Garcera, M and Desgeorges, T and Tytgat, HLP and Krattinger, LF and Lebumfacil, J and Phee, LC and Moll, JM and Gudjonsson, A and Rodriguez-Garcia, P and Baruchet, M and Feige, JN and Jankovic, I and Chen, Y and Egli, D and Horcajada, MN},
title = {A young child formula with Limosilactobacillus reuteri and GOS modulates gut microbiome and enhances bone and muscle development: a randomized trial.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-025-66930-2},
pmid = {41387706},
issn = {2041-1723},
abstract = {In this randomized, double-blind controlled trial, 182 Filipino children aged 2-3 years received either an experimental young child formula (EYCF) containing a combination of Limosilactobacillus reuteri DSM 17938 and galacto-oligosaccharides (GOS; n = 91) or a minimally fortified milk (CM; n = 91) for 6 months. Primary outcome was tibia speed of sound and secondary outcomes were muscle strength, blood vitamin D levels, bone turnover markers, gut microbiota, fecal calcium fatty acid soaps and gastro-intestinal tolerance. Compared to CM, those in the EYCF group showed increased tibia speed of sound after 3 and 6 months. The intervention remodeled the stool microbiome composition, assessed by shotgun metagenomics, with enrichment of L. reuteri and higher bifidobacteria presence in the EYCF group. Increased L. reuteri abundance after 6 months of EYCF consumption associates with higher bone quality and muscle strength. Stool metabolomics show 45 metabolites modulated by EYCF consumption and associated to microbiome compositional changes, leading to enrichment of tryptophane and indole metabolism. In summary, consumption of EYCF containing a L. reuteri + GOS synbiotic improves musculoskeletal development in toddlers via modulation of microbiota composition and function. These results provide insights on gut-musculoskeletal crosstalk during early life. Clinicaltrial.gov NCT04799028.},
}
RevDate: 2025-12-12
Microbial Allies in the Olive Canopy: Endophyte Composition, Drivers, and their Role in Plant Protection.
Microbial ecology pii:10.1007/s00248-025-02676-0 [Epub ahead of print].
The olive tree (Olea europaea L.) hosts diverse endophytic microbial communities that contribute to its resilience, productivity, and adaptation to environmental stressors. Since the temperature increases caused by global climate change primarily affects the aerial part of the plant, this review synthesizes current knowledge on the diversity, composition, and ecological drivers of olive phyllosphere endophytes, with a focus on bacterial and fungal communities. We highlight the role of host-related factors-including plant genotype, organ specificity, age, and phenological stage-in shaping microbiota structure across spatial and temporal scales. Genotype consistently emerges as a major determinant of microbial composition, while leaves and twigs harbor distinct yet overlapping communities. Geographic location, environmental variables, and seasonal shifts significantly influence microbial assemblages, with closer sites often supporting more similar communities. We also discuss the impact of agricultural practices and biotic and abiotic stressors on microbiota stability and function. Notably, several cultivable taxa-including Bacillus, Paenibacillus, Pantoea, Aureobasidium, and Penicillium-exhibit antagonistic activity against key olive pathogens, underscoring their potential as biological control agents. We conclude by emphasizing the need for functional studies to elucidate the roles of keystone endophytes and to inform microbiome-based strategies for sustainable olive cultivation.
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@article {pmid41387646,
year = {2025},
author = {Crucitti, D and Carimi, F and Caruso, T and Pacifico, D},
title = {Microbial Allies in the Olive Canopy: Endophyte Composition, Drivers, and their Role in Plant Protection.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-025-02676-0},
pmid = {41387646},
issn = {1432-184X},
abstract = {The olive tree (Olea europaea L.) hosts diverse endophytic microbial communities that contribute to its resilience, productivity, and adaptation to environmental stressors. Since the temperature increases caused by global climate change primarily affects the aerial part of the plant, this review synthesizes current knowledge on the diversity, composition, and ecological drivers of olive phyllosphere endophytes, with a focus on bacterial and fungal communities. We highlight the role of host-related factors-including plant genotype, organ specificity, age, and phenological stage-in shaping microbiota structure across spatial and temporal scales. Genotype consistently emerges as a major determinant of microbial composition, while leaves and twigs harbor distinct yet overlapping communities. Geographic location, environmental variables, and seasonal shifts significantly influence microbial assemblages, with closer sites often supporting more similar communities. We also discuss the impact of agricultural practices and biotic and abiotic stressors on microbiota stability and function. Notably, several cultivable taxa-including Bacillus, Paenibacillus, Pantoea, Aureobasidium, and Penicillium-exhibit antagonistic activity against key olive pathogens, underscoring their potential as biological control agents. We conclude by emphasizing the need for functional studies to elucidate the roles of keystone endophytes and to inform microbiome-based strategies for sustainable olive cultivation.},
}
RevDate: 2025-12-12
Bidirectional relations between the maternal and infant gut microbiome and behavior.
Pediatric research [Epub ahead of print].
BACKGROUND: An infant's mother is one of the first sources of neonatal microbial colonization, and infant-maternal dyad microbial variations have been linked to childhood behavioral traits and mental health outcomes. However, how the gut microbiome influences mental health, including potential bidirectional relations between mother and child, remains poorly understood.
METHOD: Using metagenomic sequencing and behavioral questionnaires, we examined within-person and between-person (mother-infant dyad) associations between the gut microbiota and behavior across the first year of postnatal life (N = 121 dyads; N = 514 stool samples).
RESULTS: There were rapid changes in taxa diversity and gut microbiota composition for infants, whereas the maternal microbiome remains relatively constant. Gut microbes and functional terms (e.g., antibiotic resistance genes and virulence factors) were associated with infant temperament but not maternal depression symptoms. Whereas maternal depression was not associated with any maternal taxa or functional terms.
CONCLUSIONS: Our findings provide evidence for complex within- and between-person relations between maternal and infant gut microbiomes and behavioral traits.
IMPACT: How the gut microbiome influences maternal mental health and infant behavior remains poorly understood. We measured mothers' and infants' gut microbiota composition and behavior across the first year of the infant's life. Individual taxa from the infant, but not the maternal, gut were associated with infant behavioral temperament. Our findings provide evidence for complex bidirectional gut-behavior associations between mothers and infants.
Additional Links: PMID-41387551
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@article {pmid41387551,
year = {2025},
author = {Kelsey, C and Moulder, R and Yancey, H and Prescott, S and McCulloch, JA and Trinchieri, G and Dreisbach, C and Alhusen, J and Grossmann, T},
title = {Bidirectional relations between the maternal and infant gut microbiome and behavior.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {41387551},
issn = {1530-0447},
abstract = {BACKGROUND: An infant's mother is one of the first sources of neonatal microbial colonization, and infant-maternal dyad microbial variations have been linked to childhood behavioral traits and mental health outcomes. However, how the gut microbiome influences mental health, including potential bidirectional relations between mother and child, remains poorly understood.
METHOD: Using metagenomic sequencing and behavioral questionnaires, we examined within-person and between-person (mother-infant dyad) associations between the gut microbiota and behavior across the first year of postnatal life (N = 121 dyads; N = 514 stool samples).
RESULTS: There were rapid changes in taxa diversity and gut microbiota composition for infants, whereas the maternal microbiome remains relatively constant. Gut microbes and functional terms (e.g., antibiotic resistance genes and virulence factors) were associated with infant temperament but not maternal depression symptoms. Whereas maternal depression was not associated with any maternal taxa or functional terms.
CONCLUSIONS: Our findings provide evidence for complex within- and between-person relations between maternal and infant gut microbiomes and behavioral traits.
IMPACT: How the gut microbiome influences maternal mental health and infant behavior remains poorly understood. We measured mothers' and infants' gut microbiota composition and behavior across the first year of the infant's life. Individual taxa from the infant, but not the maternal, gut were associated with infant behavioral temperament. Our findings provide evidence for complex bidirectional gut-behavior associations between mothers and infants.},
}
RevDate: 2025-12-12
CRISPR-engineered microbiome: living therapeutics revolutionize blood cancer immunotherapy.
NPJ biofilms and microbiomes pii:10.1038/s41522-025-00882-9 [Epub ahead of print].
Blood cancers such as leukemia, lymphoma, and myeloma remain refractory in many patients due to immune escape, antigen heterogeneity, and therapy‑related toxicities. To address these challenges, we review recent strategies that harness CRISPR‑engineered gut commensals as precision "living therapeutics" to modulate host immunity and directly target malignant clones. We frame this review around three principal themes: (1) mechanistic strategies whereby CRISPR-engineered commensals modulate host immunity and directly antagonize malignant clones; (2) the enabling technologies and delivery/containment platforms, CRISPR variants, phage/LNP delivery, genetic circuits and biocontainment, that make living therapeutics feasible; and (3) translational progress, outstanding technical and safety barriers, and ethical/regulatory challenges that must be addressed for clinical deployment. To illustrate these themes, we discuss three concrete therapeutic modalities: engineered microbial secretion of immunomodulators, targeted delivery of tumor-lytic payloads, and engineered production of anticancer metabolites, and how these are enabled by contemporary CRISPR and synthetic-biology toolkits. Selected preclinical models report substantial antitumor effects, often >60% tumor reduction in rodent studies, and restoration of CAR-T cell function in controlled settings; however, effect sizes vary across models, and human translation remains unproven. We also analyze key technical barriers, strain stability, biocontainment, off‑target effects, and propose solutions, including auxotrophic kill-switches and AI‑guided strain optimization. Finally, we outline future directions, from in situ phage delivery to multi‑omics-driven patient stratification. CRISPR‑microbiome editing represents a paradigm shift in hematologic oncology, offering localized, sustained therapy with reduced systemic toxicity.
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@article {pmid41387457,
year = {2025},
author = {Cheng, F and Soleimani Samarkhazan, H and Khazaei, Y},
title = {CRISPR-engineered microbiome: living therapeutics revolutionize blood cancer immunotherapy.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-025-00882-9},
pmid = {41387457},
issn = {2055-5008},
abstract = {Blood cancers such as leukemia, lymphoma, and myeloma remain refractory in many patients due to immune escape, antigen heterogeneity, and therapy‑related toxicities. To address these challenges, we review recent strategies that harness CRISPR‑engineered gut commensals as precision "living therapeutics" to modulate host immunity and directly target malignant clones. We frame this review around three principal themes: (1) mechanistic strategies whereby CRISPR-engineered commensals modulate host immunity and directly antagonize malignant clones; (2) the enabling technologies and delivery/containment platforms, CRISPR variants, phage/LNP delivery, genetic circuits and biocontainment, that make living therapeutics feasible; and (3) translational progress, outstanding technical and safety barriers, and ethical/regulatory challenges that must be addressed for clinical deployment. To illustrate these themes, we discuss three concrete therapeutic modalities: engineered microbial secretion of immunomodulators, targeted delivery of tumor-lytic payloads, and engineered production of anticancer metabolites, and how these are enabled by contemporary CRISPR and synthetic-biology toolkits. Selected preclinical models report substantial antitumor effects, often >60% tumor reduction in rodent studies, and restoration of CAR-T cell function in controlled settings; however, effect sizes vary across models, and human translation remains unproven. We also analyze key technical barriers, strain stability, biocontainment, off‑target effects, and propose solutions, including auxotrophic kill-switches and AI‑guided strain optimization. Finally, we outline future directions, from in situ phage delivery to multi‑omics-driven patient stratification. CRISPR‑microbiome editing represents a paradigm shift in hematologic oncology, offering localized, sustained therapy with reduced systemic toxicity.},
}
RevDate: 2025-12-12
Microbiome analysis of 940 lung cancers in never-smokers reveals lack of clinically relevant associations.
Nature communications pii:10.1038/s41467-025-66780-y [Epub ahead of print].
In spite of the growing interest in the microbiome in human cancer, there are currently only small-scale lung cancer microbiome studies conducted directly on tissue. As part of the Sherlock-Lung study, we studied the microbiomes of 940 lung cancers (4090 samples) in never smokers (LCINS) directly from lung tissue using three data types: 16S rRNA gene sequencing (16S), whole-genome sequencing (WGS) with paired blood, and RNA-seq. We observe very low biomass and few microbiome associations in LCINS using 16S and WGS tissue. Using RNA-seq, we observe more total microbial reads, and decreased relative abundance of several commensal bacteria at the genus and species levels in tumors relative to paired normal lung tissue. Among all datasets, we see no consistent associations between the lung tissue microbiome, or circulating bacterial DNA, and any available demographic and clinical features, including age, sex, genetic ancestry, second-hand tobacco smoking exposure, LCINS histology, stage, and overall survival. We also observe no microbiome associations with any human genomic alterations within the same samples. Every null result should be interpreted with caution given the possibility of future methodological breakthroughs. However, all together, using multiple data types in nearly 1000 patients, we find no substantive role for the lung cancer microbiome in treatment-naïve LCINS.
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@article {pmid41387456,
year = {2025},
author = {McElderry, JP and Zhang, T and Zhao, W and Hoang, PH and Anyaso-Samuel, S and Sang, J and Khandekar, A and Hartman, C and Colón-Matos, FJ and Miraftab, M and Saha, M and Lee, O and Sharma, S and Jones, KM and Zhu, B and Díaz-Gay, M and Mas, L and Rodriguez, OGA and Edell, ES and Santamaría, JM and Schabath, MB and Yendamuri, S and Manczuk, M and Lissowska, J and Świątkowska, B and Mukeria, A and Shangina, O and Zaridze, D and Holcatova, I and Janout, V and Mates, D and Ognjanovic, S and Savic, M and Kontic, M and Bossé, Y and Gould Rothberg, BE and Christiani, DC and Gaborieau, V and Brennan, P and Liu, G and Hofman, P and Wong, MP and Leung, KC and Chen, CY and Hsiung, CA and Rothman, N and Leduc, C and Baine, MK and Travis, WD and Sholl, LM and Joubert, P and Homer, R and Yang, SR and Lan, Q and Nowak, MA and Wedge, DC and Alexandrov, LB and Chanock, SJ and Vogtmann, E and Abnet, CC and Shi, J and Landi, MT},
title = {Microbiome analysis of 940 lung cancers in never-smokers reveals lack of clinically relevant associations.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-025-66780-y},
pmid = {41387456},
issn = {2041-1723},
support = {ZIACP101231//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; U01CA209414//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01ES032547-01, R01CA269919-01, and 1U01CA290479-01//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; P30-CA076292//Moffitt Cancer Center (Moffitt)/ ; DOH97-TD-G-111-029, DOH98-TD-G-111-018, DOH99-TD-G-111-015//Ministry of Health and Welfare (Ministry of Health and Welfare, Taiwan)/ ; },
abstract = {In spite of the growing interest in the microbiome in human cancer, there are currently only small-scale lung cancer microbiome studies conducted directly on tissue. As part of the Sherlock-Lung study, we studied the microbiomes of 940 lung cancers (4090 samples) in never smokers (LCINS) directly from lung tissue using three data types: 16S rRNA gene sequencing (16S), whole-genome sequencing (WGS) with paired blood, and RNA-seq. We observe very low biomass and few microbiome associations in LCINS using 16S and WGS tissue. Using RNA-seq, we observe more total microbial reads, and decreased relative abundance of several commensal bacteria at the genus and species levels in tumors relative to paired normal lung tissue. Among all datasets, we see no consistent associations between the lung tissue microbiome, or circulating bacterial DNA, and any available demographic and clinical features, including age, sex, genetic ancestry, second-hand tobacco smoking exposure, LCINS histology, stage, and overall survival. We also observe no microbiome associations with any human genomic alterations within the same samples. Every null result should be interpreted with caution given the possibility of future methodological breakthroughs. However, all together, using multiple data types in nearly 1000 patients, we find no substantive role for the lung cancer microbiome in treatment-naïve LCINS.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Gut Prevotella stercorea associates with protection against infection in rural African children.
Nature communications, 16(1):11101.
Understanding how the gut microbiome confers immune protection in early life remains a fundamental challenge, particularly in high-infection-burden, underrepresented populations. Here, we analyse longitudinal stool microbiome and illness data from 633 Gambian children aged 7-37 months enroled in a randomised, double-blind iron supplementation trial (NCT02941081). The primary endpoint was correction of iron deficiency anaemia, and the secondary endpoint was diarrhoea incidence and other adverse events; IHAT was non-inferior to ferrous sulphate for iron correction and showed fewer moderate-to-severe diarrhoea episodes. Using 16S rRNA sequencing at three timepoints (Days 1, 15, and 85), we find that children who remained infection-free harboured a consistently higher relative abundance of Prevotella stercorea, a keystone taxon of non-industrialised gut ecologies. In contrast, Escherichia coli and other opportunistic pathogens were enriched in children who developed infections. These taxonomic signatures were temporally stable and embedded within distinct, co-occurring microbial networks. Strikingly, higher P. stercorea abundance was inversely associated with both infection frequency and duration, with the greatest differences observed in children aged 1-2 years, potentially explaining their increased infectious risk. Our findings reveal a Prevotella-dominated enterotype associated with reduced infection risk, with implications for vaccine responsiveness, child survival, and microbiota-targeted interventions in global child health.
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@article {pmid41387413,
year = {2025},
author = {Ofordile, O and Pereira, DIA and Prentice, AM and Wagner, J},
title = {Gut Prevotella stercorea associates with protection against infection in rural African children.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {11101},
pmid = {41387413},
issn = {2041-1723},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics/immunology ; *Prevotella/genetics/isolation & purification ; Child, Preschool ; Infant ; Rural Population ; Male ; Female ; Gambia/epidemiology ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Double-Blind Method ; Diarrhea/microbiology/epidemiology ; Anemia, Iron-Deficiency/drug therapy/microbiology ; Iron/therapeutic use ; Escherichia coli/isolation & purification ; Ferrous Compounds ; },
abstract = {Understanding how the gut microbiome confers immune protection in early life remains a fundamental challenge, particularly in high-infection-burden, underrepresented populations. Here, we analyse longitudinal stool microbiome and illness data from 633 Gambian children aged 7-37 months enroled in a randomised, double-blind iron supplementation trial (NCT02941081). The primary endpoint was correction of iron deficiency anaemia, and the secondary endpoint was diarrhoea incidence and other adverse events; IHAT was non-inferior to ferrous sulphate for iron correction and showed fewer moderate-to-severe diarrhoea episodes. Using 16S rRNA sequencing at three timepoints (Days 1, 15, and 85), we find that children who remained infection-free harboured a consistently higher relative abundance of Prevotella stercorea, a keystone taxon of non-industrialised gut ecologies. In contrast, Escherichia coli and other opportunistic pathogens were enriched in children who developed infections. These taxonomic signatures were temporally stable and embedded within distinct, co-occurring microbial networks. Strikingly, higher P. stercorea abundance was inversely associated with both infection frequency and duration, with the greatest differences observed in children aged 1-2 years, potentially explaining their increased infectious risk. Our findings reveal a Prevotella-dominated enterotype associated with reduced infection risk, with implications for vaccine responsiveness, child survival, and microbiota-targeted interventions in global child health.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/genetics/immunology
*Prevotella/genetics/isolation & purification
Child, Preschool
Infant
Rural Population
Male
Female
Gambia/epidemiology
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Double-Blind Method
Diarrhea/microbiology/epidemiology
Anemia, Iron-Deficiency/drug therapy/microbiology
Iron/therapeutic use
Escherichia coli/isolation & purification
Ferrous Compounds
RevDate: 2025-12-12
Gut Bacterium Lysinibacillus Sphaericus Exacerbates Aspirin-induced Intestinal Injury by Production of Carboxylesterase EstB.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Aspirin provides long-term health benefits but can cause gastrointestinal toxicity, and the role of gut microbiota in aspirin metabolism and enterotoxicity remains unclear. In this study, the contribution and mechanisms of microbiota-aspirin interactions in intestinal injury are investigated. In a mouse model, aspirin-induced enteropathy is found to be more severe in microbiota-replete than in microbiota-depleted mice, implicating a detrimental role of gut microbiota. Co-cultivation experiments revealed that gut microbes facilitated the biotransformation of aspirin into salicylic acid, a metabolite more harmful than aspirin itself in disrupting epithelial cell integrity and renewal, both in vitro and in vivo. Through metagenomic screening, selective bacterial interrogation, and functional validation, Lysinibacillus sphaericus is identified as the culprit bacterium, and its secreted carboxylesterase EstB as the key enzyme catalyzing aspirin hydrolysis to salicylic acid. Importantly, inhibition of microbial EstB with the dietary compound flavanomarein abrogated aspirin biotransformation and prevented intestinal injury. Together, these findings reveal L. sphaericus and EstB as central drivers of aspirin enterotoxicity, highlight the functional importance of gut microbiota in drug metabolism, and suggest microbiota- and metabolite-guided precision prevention strategies.
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@article {pmid41387308,
year = {2025},
author = {Zhao, Z and Li, Q and Bai, X and Zhai, E and Dai, W and Qian, Y and Zhang, T and Huang, Z and Huang, Z and Meng, F and Chen, J and Zuo, T and Cai, S and Zhao, R},
title = {Gut Bacterium Lysinibacillus Sphaericus Exacerbates Aspirin-induced Intestinal Injury by Production of Carboxylesterase EstB.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e17747},
doi = {10.1002/advs.202517747},
pmid = {41387308},
issn = {2198-3844},
support = {82100626//National Natural Science Foundation of China/ ; 82173239//National Natural Science Foundation of China/ ; 32470958//National Natural Science Foundation of China/ ; 82403246//National Natural Science Foundation of China/ ; 823B2010//National Natural Science Foundation of China/ ; 202206010014//Special Project of Guangzhou Science and Technology Innovation Development/ ; },
abstract = {Aspirin provides long-term health benefits but can cause gastrointestinal toxicity, and the role of gut microbiota in aspirin metabolism and enterotoxicity remains unclear. In this study, the contribution and mechanisms of microbiota-aspirin interactions in intestinal injury are investigated. In a mouse model, aspirin-induced enteropathy is found to be more severe in microbiota-replete than in microbiota-depleted mice, implicating a detrimental role of gut microbiota. Co-cultivation experiments revealed that gut microbes facilitated the biotransformation of aspirin into salicylic acid, a metabolite more harmful than aspirin itself in disrupting epithelial cell integrity and renewal, both in vitro and in vivo. Through metagenomic screening, selective bacterial interrogation, and functional validation, Lysinibacillus sphaericus is identified as the culprit bacterium, and its secreted carboxylesterase EstB as the key enzyme catalyzing aspirin hydrolysis to salicylic acid. Importantly, inhibition of microbial EstB with the dietary compound flavanomarein abrogated aspirin biotransformation and prevented intestinal injury. Together, these findings reveal L. sphaericus and EstB as central drivers of aspirin enterotoxicity, highlight the functional importance of gut microbiota in drug metabolism, and suggest microbiota- and metabolite-guided precision prevention strategies.},
}
RevDate: 2025-12-12
The tumor microbiome and cancer immunotherapy: A systematic review of a new frontier beyond the gut.
Bulletin du cancer pii:S0007-4551(25)00507-7 [Epub ahead of print].
BACKGROUND: While the gut microbiome is known to modulate systemic immunity and response to immune checkpoint inhibitors, the role of tumor-resident microbiota remains underexplored. Recent evidence suggests that these local microbial communities may influence intratumoral immunity and therapeutic outcomes.
METHODS: A systematic review compliant with PRISMA guidelines was conducted to evaluate the impact of tumor-associated bacteria on anti-tumor immune responses. Four databases (PubMed, Scopus, Web of Science and EMBASE) were searched for studies published between January 2010 and April 2025. Eligible studies characterized non-intestinal microbiota within tumor tissue and assessed immune endpoints such as T cell infiltration, cytokine profiles, PD-L1 expression, or immune checkpoint inhibitors responsiveness. Due to endpoint heterogeneity, no meta-analysis was performed. Seventeen studies met inclusion criteria.
RESULTS: In tumors including melanoma, pancreatic, esophageal, gastric, breast, lung, and colorectal cancers, intratumoral bacteria modulated immune responses and immune checkpoint inhibitors efficacy. Three recurring mechanisms emerged: immune activation via antigen presentation and Th1 polarization; immune suppression through regulatory T cell recruitment and stromal remodeling; and checkpoint modulation and T cell exhaustion via microbial signaling. These effects were spatially structured and tumor-context dependent.
CONCLUSION: Tumor-local microbiota represents a distinct and actionable component of the tumor-immune microenvironment. Incorporating microbial profiling into immuno-oncology strategies may enhance biomarker discovery, patient stratification, and development of microbiome-based therapies. Further research is warranted to map spatial microbial heterogeneity, validate functional mechanisms, and translate findings into clinical applications in precision immunotherapy.
Additional Links: PMID-41387030
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PubMed:
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@article {pmid41387030,
year = {2025},
author = {Barjij, I and Meliani, M},
title = {The tumor microbiome and cancer immunotherapy: A systematic review of a new frontier beyond the gut.},
journal = {Bulletin du cancer},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.bulcan.2025.09.006},
pmid = {41387030},
issn = {1769-6917},
abstract = {BACKGROUND: While the gut microbiome is known to modulate systemic immunity and response to immune checkpoint inhibitors, the role of tumor-resident microbiota remains underexplored. Recent evidence suggests that these local microbial communities may influence intratumoral immunity and therapeutic outcomes.
METHODS: A systematic review compliant with PRISMA guidelines was conducted to evaluate the impact of tumor-associated bacteria on anti-tumor immune responses. Four databases (PubMed, Scopus, Web of Science and EMBASE) were searched for studies published between January 2010 and April 2025. Eligible studies characterized non-intestinal microbiota within tumor tissue and assessed immune endpoints such as T cell infiltration, cytokine profiles, PD-L1 expression, or immune checkpoint inhibitors responsiveness. Due to endpoint heterogeneity, no meta-analysis was performed. Seventeen studies met inclusion criteria.
RESULTS: In tumors including melanoma, pancreatic, esophageal, gastric, breast, lung, and colorectal cancers, intratumoral bacteria modulated immune responses and immune checkpoint inhibitors efficacy. Three recurring mechanisms emerged: immune activation via antigen presentation and Th1 polarization; immune suppression through regulatory T cell recruitment and stromal remodeling; and checkpoint modulation and T cell exhaustion via microbial signaling. These effects were spatially structured and tumor-context dependent.
CONCLUSION: Tumor-local microbiota represents a distinct and actionable component of the tumor-immune microenvironment. Incorporating microbial profiling into immuno-oncology strategies may enhance biomarker discovery, patient stratification, and development of microbiome-based therapies. Further research is warranted to map spatial microbial heterogeneity, validate functional mechanisms, and translate findings into clinical applications in precision immunotherapy.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Design biology and mind-body health.
Journal, genetic engineering & biotechnology, 23(4):100621.
Recent advances in design biology, including artificial cells, DNA nanostructures, artificial intelligence (AI)-driven molecular design, biofoundries, and next-generation genome editing, are transforming the health sciences of mind and body (HS-MB). Moving beyond traditional observational paradigms, these technologies enable predictive and design-oriented strategies for regulating stress, emotional health, achieving immune homeostasis, and managing lifestyle-related disorders. Psychological and social factors profoundly influence core physiological systems, including neuroendocrine (hypothalamic-pituitary-adrenal [HPA]) axis and cortisol rhythm, autonomic (vagal tone and heart rate variability), immune (cytokine balance and inflammatory control), metabolic (glucose-insulin regulation), and sleep-circadian systems. Artificial cells serve as controllable models for neurotransmitter signaling, immune interactions, and gut-brain communication, while DNA origami provides programmable nanocarriers that complement lipid nanoparticles (LNPs). Genome-editing innovations-such as prime, base, and epigenome editing-facilitate precise and reversible modulation of psychiatric risk genes, particularly when combined with induced pluripotent stem cell (iPSC) and brain-organoid models. Biofoundries integrate AI into Design-Build-Test-Learn (DBTL) cycles, automating molecular discovery and optimization. Ethical and regulatory considerations, including AI transparency, biocontainment, and dual-use governance, must be incorporated from the outset. Collectively, design biology, when strategically aligned with HS-MB, establishes a foundational framework for twenty-first-century medicine that bridges molecular engineering and holistic well-being.
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@article {pmid41386887,
year = {2025},
author = {Kumagai, K and Chiba, A and Yajima, H},
title = {Design biology and mind-body health.},
journal = {Journal, genetic engineering & biotechnology},
volume = {23},
number = {4},
pages = {100621},
doi = {10.1016/j.jgeb.2025.100621},
pmid = {41386887},
issn = {2090-5920},
abstract = {Recent advances in design biology, including artificial cells, DNA nanostructures, artificial intelligence (AI)-driven molecular design, biofoundries, and next-generation genome editing, are transforming the health sciences of mind and body (HS-MB). Moving beyond traditional observational paradigms, these technologies enable predictive and design-oriented strategies for regulating stress, emotional health, achieving immune homeostasis, and managing lifestyle-related disorders. Psychological and social factors profoundly influence core physiological systems, including neuroendocrine (hypothalamic-pituitary-adrenal [HPA]) axis and cortisol rhythm, autonomic (vagal tone and heart rate variability), immune (cytokine balance and inflammatory control), metabolic (glucose-insulin regulation), and sleep-circadian systems. Artificial cells serve as controllable models for neurotransmitter signaling, immune interactions, and gut-brain communication, while DNA origami provides programmable nanocarriers that complement lipid nanoparticles (LNPs). Genome-editing innovations-such as prime, base, and epigenome editing-facilitate precise and reversible modulation of psychiatric risk genes, particularly when combined with induced pluripotent stem cell (iPSC) and brain-organoid models. Biofoundries integrate AI into Design-Build-Test-Learn (DBTL) cycles, automating molecular discovery and optimization. Ethical and regulatory considerations, including AI transparency, biocontainment, and dual-use governance, must be incorporated from the outset. Collectively, design biology, when strategically aligned with HS-MB, establishes a foundational framework for twenty-first-century medicine that bridges molecular engineering and holistic well-being.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
A metagenomic exploration of microbial distribution among the pond sediment, shrimp (Penaeus monodon) tissue and pond water: A special focus on nutrient cycling and shrimp viral pathogens.
Journal, genetic engineering & biotechnology, 23(4):100568.
Penaeus monodon, a major shrimp species cultivated in Eastern Asia, has faced setbacks in aquaculture due to disease outbreaks. Metagenomic studies offer insights into the pond microbiome, revealing its critical roles in nutrient cycling, water quality, and disease control. This study investigated microbial communities in sediment, water, and shrimp samples from an aquaculture pond in Chaital, West Bengal, India. Shotgun metagenomic sequencing and bioinformatics analyses were used to assess taxonomic and functional profiles, focusing on nutrient cycling genes and viral populations. Sediments showed the highest microbial diversity, contributing to organic matter decomposition and ecological stability. Water microbes played roles in oxygenation and pathogen suppression, while shrimp tissues hosted microbes aiding digestion and immunity. Pathogenic viruses, especially Whispovirus (White Spot Syndrome Virus), dominated shrimp tissues. Functional gene analysis identified key pathways in carbon, nitrogen, and sulfur cycling. Integrating water quality data with microbiome profiles could help identify bioindicators and predict pathogen risks.
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@article {pmid41386833,
year = {2025},
author = {Sarkar, A and Patra, RK and Muthaiyan, M and Mallik, A},
title = {A metagenomic exploration of microbial distribution among the pond sediment, shrimp (Penaeus monodon) tissue and pond water: A special focus on nutrient cycling and shrimp viral pathogens.},
journal = {Journal, genetic engineering & biotechnology},
volume = {23},
number = {4},
pages = {100568},
doi = {10.1016/j.jgeb.2025.100568},
pmid = {41386833},
issn = {2090-5920},
abstract = {Penaeus monodon, a major shrimp species cultivated in Eastern Asia, has faced setbacks in aquaculture due to disease outbreaks. Metagenomic studies offer insights into the pond microbiome, revealing its critical roles in nutrient cycling, water quality, and disease control. This study investigated microbial communities in sediment, water, and shrimp samples from an aquaculture pond in Chaital, West Bengal, India. Shotgun metagenomic sequencing and bioinformatics analyses were used to assess taxonomic and functional profiles, focusing on nutrient cycling genes and viral populations. Sediments showed the highest microbial diversity, contributing to organic matter decomposition and ecological stability. Water microbes played roles in oxygenation and pathogen suppression, while shrimp tissues hosted microbes aiding digestion and immunity. Pathogenic viruses, especially Whispovirus (White Spot Syndrome Virus), dominated shrimp tissues. Functional gene analysis identified key pathways in carbon, nitrogen, and sulfur cycling. Integrating water quality data with microbiome profiles could help identify bioindicators and predict pathogen risks.},
}
RevDate: 2025-12-12
Rising temperature and atmospheric CO2 combine to antagonistically alter Cd mobility and biogeochemistry in an agricultural soil.
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(25)01882-2 [Epub ahead of print].
Soil cadmium (Cd) contamination threatens ecosystems and crop safety. Understanding how individual climate change factors influence soil Cd bioavailability is essential for mechanistic understanding and future risk assessments. This study examined individual and combined effects of elevated temperature (+4°C) and doubled atmospheric CO2 (800 ppmv) on soil Cd bioavailability, biogeochemistry, and greenhouse gas emissions in agricultural soils with native (0.13 mg Cd kg-[1]) and high Cd (1.5 mg Cd kg[-1]). Elevated temperature increased porewater Cd up to 50% relative to ambient, while doubled atmospheric CO2 did not alter porewater Cd. Combined future conditions increased porewater Cd by 30% relative to ambient indicating an antagonistic interaction. Doubled atmospheric CO2 enhanced microbial nitrogen fixation and reduced ammonium oxidation, increasing ammonium concentrations up to 10-fold relative to ambient. Elevated temperature stimulated microbiome activity and ammonium oxidation, leading to 1.7-fold more CO2 and 5.5-fold more N2O compared to ambient, both exceeding levels observed under combined future climate. These contrasting single-factor responses highlight the non-additive nature of combined climate factor effects. Warming alone overestimated and CO2 alone underestimated the combined impact on Cd mobility and soil biogeochemistry. Simulating multiple climate drivers is therefore essential for accurate environmental prediction and sustainable Cd management under climate change.
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@article {pmid41386516,
year = {2025},
author = {Drabesch, S and Mueller, S and Leon Ninin, JM and Planer-Friedrich, B and Kappler, A and Muehe, EM},
title = {Rising temperature and atmospheric CO2 combine to antagonistically alter Cd mobility and biogeochemistry in an agricultural soil.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {127508},
doi = {10.1016/j.envpol.2025.127508},
pmid = {41386516},
issn = {1873-6424},
abstract = {Soil cadmium (Cd) contamination threatens ecosystems and crop safety. Understanding how individual climate change factors influence soil Cd bioavailability is essential for mechanistic understanding and future risk assessments. This study examined individual and combined effects of elevated temperature (+4°C) and doubled atmospheric CO2 (800 ppmv) on soil Cd bioavailability, biogeochemistry, and greenhouse gas emissions in agricultural soils with native (0.13 mg Cd kg-[1]) and high Cd (1.5 mg Cd kg[-1]). Elevated temperature increased porewater Cd up to 50% relative to ambient, while doubled atmospheric CO2 did not alter porewater Cd. Combined future conditions increased porewater Cd by 30% relative to ambient indicating an antagonistic interaction. Doubled atmospheric CO2 enhanced microbial nitrogen fixation and reduced ammonium oxidation, increasing ammonium concentrations up to 10-fold relative to ambient. Elevated temperature stimulated microbiome activity and ammonium oxidation, leading to 1.7-fold more CO2 and 5.5-fold more N2O compared to ambient, both exceeding levels observed under combined future climate. These contrasting single-factor responses highlight the non-additive nature of combined climate factor effects. Warming alone overestimated and CO2 alone underestimated the combined impact on Cd mobility and soil biogeochemistry. Simulating multiple climate drivers is therefore essential for accurate environmental prediction and sustainable Cd management under climate change.},
}
RevDate: 2025-12-12
Uncovering novel endocannabinoidome-gut microbiome-brain axis-based therapeutic targets in a Fragile X Syndrome mouse model.
Progress in neuro-psychopharmacology & biological psychiatry pii:S0278-5846(25)00329-X [Epub ahead of print].
BACKGROUND: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition associated with increased risk of psychiatric, gastrointestinal, and metabolic comorbidities. Recent studies highlight the bidirectional role of the gut microbiome (GM) and endocannabinoidome (eCBome) in the eCBome-GM-brain axis, suggesting its therapeutic potential for ASD and comorbidities.
METHODS: We investigated the eCBome-GM-brain axis in the Fragile X Messenger Ribonucleoprotein 1 (Fmr1[-/y]) mouse model, known as a genetic model of ASD, to identify therapeutic targets. Fecal GM composition was analysed via 16S rDNA sequencing, brain eCBome profile via HPLC-MS/MS and qRT-PCR, and fecal short chain fatty acids via GC-FID.
RESULTS: Significant eCBome-GM-brain axis dysregulation was observed in Fmr1[-/y] compared to WT mice. GM analyses revealed gut dysbiosis, increased permeability, and inflammation. Specifically, elevated Akkermansia and Eubacterium siraeum-linked to gut barrier dysfunction-and Ruminococcus and Clostridium, associated with ASD severity, were identified. Concurrently, decreased levels of the gut health biomarker Roseburia and the taxa Helicobacter and Anaeroplasma were observed. Brain region-specific eCBome alterations underscored neuroinflammation. In the HPC, reduced anti-inflammatory dihomogamma-linolenic acid (DGLA) was accompanied by elevated pro-inflammatory 12-hydroxy-heptadecatrienoic acid, a mediator of microglial activation. In the PFC, decreased DGLA, 1/2-linoleoylglycerol, and linoleic acid N-linoleoyl-ethanolamine suggested neuroinflammation; elevated prostaglandin D2, a marker of autophagy impairment, underscores further mechanisms of dysfunction. Upregulation of cannabinoid type 2 and PPAR-γ receptor genes in the PFC suggested a compensatory response to neuroinflammation. Correlations between eCBome and GM alterations highlighted links between dysbiosis, systemic inflammation, and neurodevelopmental atypicalities.
CONCLUSIONS: The Fmr1[-/y] ASD mouse model harbors significant eCBome-GM-brain axis alterations. This study highlights specific GM taxa and eCBome components as potential therapeutic targets for clinical validation in Fragile X Syndrome and ASD.
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@article {pmid41386393,
year = {2025},
author = {Campanale, A and Mir, HD and Dumais, E and Inserra, A and Flamand, N and Chakravarty, M and Gantois, I and Siddiqui, N and Sonenberg, N and Gobbi, G and Silvestri, C and Di Marzo, V},
title = {Uncovering novel endocannabinoidome-gut microbiome-brain axis-based therapeutic targets in a Fragile X Syndrome mouse model.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111575},
doi = {10.1016/j.pnpbp.2025.111575},
pmid = {41386393},
issn = {1878-4216},
abstract = {BACKGROUND: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition associated with increased risk of psychiatric, gastrointestinal, and metabolic comorbidities. Recent studies highlight the bidirectional role of the gut microbiome (GM) and endocannabinoidome (eCBome) in the eCBome-GM-brain axis, suggesting its therapeutic potential for ASD and comorbidities.
METHODS: We investigated the eCBome-GM-brain axis in the Fragile X Messenger Ribonucleoprotein 1 (Fmr1[-/y]) mouse model, known as a genetic model of ASD, to identify therapeutic targets. Fecal GM composition was analysed via 16S rDNA sequencing, brain eCBome profile via HPLC-MS/MS and qRT-PCR, and fecal short chain fatty acids via GC-FID.
RESULTS: Significant eCBome-GM-brain axis dysregulation was observed in Fmr1[-/y] compared to WT mice. GM analyses revealed gut dysbiosis, increased permeability, and inflammation. Specifically, elevated Akkermansia and Eubacterium siraeum-linked to gut barrier dysfunction-and Ruminococcus and Clostridium, associated with ASD severity, were identified. Concurrently, decreased levels of the gut health biomarker Roseburia and the taxa Helicobacter and Anaeroplasma were observed. Brain region-specific eCBome alterations underscored neuroinflammation. In the HPC, reduced anti-inflammatory dihomogamma-linolenic acid (DGLA) was accompanied by elevated pro-inflammatory 12-hydroxy-heptadecatrienoic acid, a mediator of microglial activation. In the PFC, decreased DGLA, 1/2-linoleoylglycerol, and linoleic acid N-linoleoyl-ethanolamine suggested neuroinflammation; elevated prostaglandin D2, a marker of autophagy impairment, underscores further mechanisms of dysfunction. Upregulation of cannabinoid type 2 and PPAR-γ receptor genes in the PFC suggested a compensatory response to neuroinflammation. Correlations between eCBome and GM alterations highlighted links between dysbiosis, systemic inflammation, and neurodevelopmental atypicalities.
CONCLUSIONS: The Fmr1[-/y] ASD mouse model harbors significant eCBome-GM-brain axis alterations. This study highlights specific GM taxa and eCBome components as potential therapeutic targets for clinical validation in Fragile X Syndrome and ASD.},
}
RevDate: 2025-12-12
Making Waves: Advancing environmental risk assessment through the quantification of marine microbial sensitivity thresholds.
Water research, 290:125102 pii:S0043-1354(25)02005-6 [Epub ahead of print].
Microbial communities play a vital role in maintaining marine ecosystem health, yet they remain largely excluded from environmental risk assessments and water quality guideline development. Traditional ecotoxicological and regulatory frameworks predominantly rely on single-species toxicity data from eukaryotes, overlooking microbial responses to environmental stressors. However, microbial communities often respond rapidly to environmental change and can serve as sensitive early indicators of ecological disturbance. Advances in high-throughput sequencing and bioinformatics enable comprehensive assessment of microbial responses across multiple levels of biological organisation. Despite these capabilities, standardised methodologies for deriving quantitative microbial sensitivity thresholds remain lacking. This paper synthesises recent progress and emerging approaches in microbial ecotoxicology to support the incorporation of microbial endpoints into environmental regulatory frameworks. We highlight the potential of combining 16S rRNA gene amplicon sequencing of viable cells with microbial load quantification and advanced Bayesian concentration-response modelling to resolve microbial stress responses and quantify sensitivity thresholds at both community and taxon levels. These thresholds can inform cumulative prokaryotic sensitivity distributions, enabling the derivation of guideline values for microbiomes in alignment with existing approaches used for eukaryotic species. Establishing robust microbial sensitivity thresholds represents a critical step toward incorporating prokaryotes into environmental quality guidelines, improving ecological realism, and enabling earlier, more holistic detection of ecosystem degradation.
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@article {pmid41386080,
year = {2025},
author = {Thomas, MC and Fisher, R and Luter, HM and Negri, AP},
title = {Making Waves: Advancing environmental risk assessment through the quantification of marine microbial sensitivity thresholds.},
journal = {Water research},
volume = {290},
number = {},
pages = {125102},
doi = {10.1016/j.watres.2025.125102},
pmid = {41386080},
issn = {1879-2448},
abstract = {Microbial communities play a vital role in maintaining marine ecosystem health, yet they remain largely excluded from environmental risk assessments and water quality guideline development. Traditional ecotoxicological and regulatory frameworks predominantly rely on single-species toxicity data from eukaryotes, overlooking microbial responses to environmental stressors. However, microbial communities often respond rapidly to environmental change and can serve as sensitive early indicators of ecological disturbance. Advances in high-throughput sequencing and bioinformatics enable comprehensive assessment of microbial responses across multiple levels of biological organisation. Despite these capabilities, standardised methodologies for deriving quantitative microbial sensitivity thresholds remain lacking. This paper synthesises recent progress and emerging approaches in microbial ecotoxicology to support the incorporation of microbial endpoints into environmental regulatory frameworks. We highlight the potential of combining 16S rRNA gene amplicon sequencing of viable cells with microbial load quantification and advanced Bayesian concentration-response modelling to resolve microbial stress responses and quantify sensitivity thresholds at both community and taxon levels. These thresholds can inform cumulative prokaryotic sensitivity distributions, enabling the derivation of guideline values for microbiomes in alignment with existing approaches used for eukaryotic species. Establishing robust microbial sensitivity thresholds represents a critical step toward incorporating prokaryotes into environmental quality guidelines, improving ecological realism, and enabling earlier, more holistic detection of ecosystem degradation.},
}
RevDate: 2025-12-12
Synergistic response of arbuscular mycorrhizal fungi and hyphosphere microbiome to arsenic contamination in agricultural soils.
The New phytologist [Epub ahead of print].
Arbuscular mycorrhizal fungi (AMF) can modulate arsenic (As) bioavailability through hyphal interactions with microbes. However, whether AMF hyphae assemble a core hyphosphere microbiome adapted to As stress and how this shapes in situ As transformation are still unknown. We conducted field experiments across agricultural soils with an As gradient (21-172 mg kg[-1]), using in situ mesh devices to collect hyphosphere and nonhyphosphere soils during a 98-d wheat growth period. We integrated 16S rRNA and ITS gene sequencing, PICRUSt2-based functional prediction, co-inertia and co-occurrence analyses, and sequential As extraction to investigate the hyphosphere microbiome's structure, functional potential, and AMF-microbe interactions. AMF hyphae significantly increased microbial diversity and niche breadth in the hyphosphere and reshaped community composition. Co-inertia and network analyses showed stronger associations under high As stress. We identified 100 ASVs as a core hyphosphere microbiome - dominated by Proteobacteria, Bacteroidetes, and Verrucomicrobia - rich in arsC, arsH, and arsB/ACR3 genes. Network modules formed by these taxa correlated positively with bioavailable As, suggesting adaptive potential under stress. This study provides the first field-based evidence that AMF hyphae selectively recruit a core microbiome with potential As-transforming functions, offering microbial targets for AMF-assisted remediation of As-contaminated soils.
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@article {pmid41387248,
year = {2025},
author = {Ji, C and Wu, T and Tian, Y and Li, J and Dong, J and Xing, S and Chen, H and Yang, D and Ouyang, S and Li, J and Huang, Y and Hao, Z and Zhang, X and Chen, B and Zhu, Y},
title = {Synergistic response of arbuscular mycorrhizal fungi and hyphosphere microbiome to arsenic contamination in agricultural soils.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.70782},
pmid = {41387248},
issn = {1469-8137},
support = {2023YFF1306004//National Key Research and Development Program of China/ ; 42377299//National Natural Science Foundation of China/ ; 42177109//National Natural Science Foundation of China/ ; U21A2024//National Natural Science Foundation of China/ ; 52504193//National Natural Science Foundation of China/ ; },
abstract = {Arbuscular mycorrhizal fungi (AMF) can modulate arsenic (As) bioavailability through hyphal interactions with microbes. However, whether AMF hyphae assemble a core hyphosphere microbiome adapted to As stress and how this shapes in situ As transformation are still unknown. We conducted field experiments across agricultural soils with an As gradient (21-172 mg kg[-1]), using in situ mesh devices to collect hyphosphere and nonhyphosphere soils during a 98-d wheat growth period. We integrated 16S rRNA and ITS gene sequencing, PICRUSt2-based functional prediction, co-inertia and co-occurrence analyses, and sequential As extraction to investigate the hyphosphere microbiome's structure, functional potential, and AMF-microbe interactions. AMF hyphae significantly increased microbial diversity and niche breadth in the hyphosphere and reshaped community composition. Co-inertia and network analyses showed stronger associations under high As stress. We identified 100 ASVs as a core hyphosphere microbiome - dominated by Proteobacteria, Bacteroidetes, and Verrucomicrobia - rich in arsC, arsH, and arsB/ACR3 genes. Network modules formed by these taxa correlated positively with bioavailable As, suggesting adaptive potential under stress. This study provides the first field-based evidence that AMF hyphae selectively recruit a core microbiome with potential As-transforming functions, offering microbial targets for AMF-assisted remediation of As-contaminated soils.},
}
RevDate: 2025-12-12
The Gut Microbiota Regulates Motor Deficits via Butyrate in a Gnal[+/-] Mouse Model of DYT25 Dystonia.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Dystonia is the third most common movement disorder, following essential tremor and Parkinson's disease. The underlying mechanisms behind dystonia are still one of the crucial unsolved research topics. Gnal haploinsufficient (Gnal[+/-]) mice are used as a model of DTY25 dystonia to investigate the mechanistic relationship between gut microbiota and dystonia. The present study unveiled Gnal[+/-] mice exhibit significant motor deficits of dystonia, along with a marked gut microbiota dysbiosis. Analysis of the gut microbiota composition and function reveals that Gnal[+/-] mice have decreased butyrate-producing bacteria abundance (such as Lachnospiraceae_NK4A136, Blautia, and Butyricicoccus) and disrupted butanoate metabolism. The targeted metabolomics analysis indicates that the Gnal[+/-] mice exhibit decreased butyrate levels in feces and serum. The colonization of antibiotic-treated wild-type mice with fecal microbiota from Gnal[+/-] mice is sufficient to induce motor deficit symptoms. Oral administration of sodium butyrate ameliorated motor deficits in the Gnal[+/-] mouse model of DYT25 dystonia. Striatal single-nucleus RNA sequencing reveals cell-type-specific gene expression changes, suggesting that butyrate modulates neurotransmitter pathways, particularly GABA signaling. This is confirmed by restored striatal GABA levels after butyrate supplementation. In sum, gut microbiome contributes to dystonia pathogenesis, and butyrate supplementation alleviates the motor deficits of dystonia in Gnal[+/-] mice.
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@article {pmid41387123,
year = {2025},
author = {Guo, J and Kang, SG and Huang, K and Tong, T},
title = {The Gut Microbiota Regulates Motor Deficits via Butyrate in a Gnal[+/-] Mouse Model of DYT25 Dystonia.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e12942},
doi = {10.1002/advs.202512942},
pmid = {41387123},
issn = {2198-3844},
abstract = {Dystonia is the third most common movement disorder, following essential tremor and Parkinson's disease. The underlying mechanisms behind dystonia are still one of the crucial unsolved research topics. Gnal haploinsufficient (Gnal[+/-]) mice are used as a model of DTY25 dystonia to investigate the mechanistic relationship between gut microbiota and dystonia. The present study unveiled Gnal[+/-] mice exhibit significant motor deficits of dystonia, along with a marked gut microbiota dysbiosis. Analysis of the gut microbiota composition and function reveals that Gnal[+/-] mice have decreased butyrate-producing bacteria abundance (such as Lachnospiraceae_NK4A136, Blautia, and Butyricicoccus) and disrupted butanoate metabolism. The targeted metabolomics analysis indicates that the Gnal[+/-] mice exhibit decreased butyrate levels in feces and serum. The colonization of antibiotic-treated wild-type mice with fecal microbiota from Gnal[+/-] mice is sufficient to induce motor deficit symptoms. Oral administration of sodium butyrate ameliorated motor deficits in the Gnal[+/-] mouse model of DYT25 dystonia. Striatal single-nucleus RNA sequencing reveals cell-type-specific gene expression changes, suggesting that butyrate modulates neurotransmitter pathways, particularly GABA signaling. This is confirmed by restored striatal GABA levels after butyrate supplementation. In sum, gut microbiome contributes to dystonia pathogenesis, and butyrate supplementation alleviates the motor deficits of dystonia in Gnal[+/-] mice.},
}
RevDate: 2025-12-12
Root-driven microbiome memory enhances plant disease resistance.
Trends in plant science pii:S1360-1385(25)00356-5 [Epub ahead of print].
Root-driven microbiome memory imprints biological and chemical legacies in soil, boosting plant disease resistance across generations. In a recent study, Wu et al. found flavonoids acting as key mediators, recruiting protective microbes and lowering pathogen severity beyond one crop cycle. Here, we highlight this concept, its limitations, and opportunities for sustainable disease resistance in agriculture.
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@article {pmid41387111,
year = {2025},
author = {Araujo, ASF and Pereira, APA and de Medeiros, EV and Mendes, LW},
title = {Root-driven microbiome memory enhances plant disease resistance.},
journal = {Trends in plant science},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tplants.2025.12.002},
pmid = {41387111},
issn = {1878-4372},
abstract = {Root-driven microbiome memory imprints biological and chemical legacies in soil, boosting plant disease resistance across generations. In a recent study, Wu et al. found flavonoids acting as key mediators, recruiting protective microbes and lowering pathogen severity beyond one crop cycle. Here, we highlight this concept, its limitations, and opportunities for sustainable disease resistance in agriculture.},
}
RevDate: 2025-12-12
Immune Functions of the Esophagus.
The Journal of allergy and clinical immunology pii:S0091-6749(25)01184-4 [Epub ahead of print].
The esophagus has long been regarded as a simple conduit for food transport. A new paradigm now recognizes it as an immune organ actively involved in environmental sensing, antigen tolerance, and neuroimmune signaling to maintain mucosal homeostasis. The stratified squamous epithelium provides a vital physical barrier, supported by transmembrane mucins and regulated by post-translational modifications, including citrullination mediated by esophagus-enriched peptidyl arginine deiminases. A unique esophageal microbiome, established early in life, shapes epithelial differentiation, gene expression, and immune development and response. Pattern recognition receptors and enriched interleukin 1 (IL-1) family cytokines, including the alarmins IL-33 and thymic stromal lymphopoietin (TSLP), orchestrate rapid immune responses to diverse environmental stimuli, such as allergens. The protease-antiprotease balance, controlled by serine and cysteine proteases, notably kallikreins, and the inhibitors SERPINs and SPINKs, regulates cytokine activity and barrier integrity. Neuroimmune circuits link innate immune activation, sensory perception, and barrier regulation. Disruption of these pathways, including genetic variants in barrier components, proteases, and immune regulators, contributes to disease susceptibility and pathogenesis. Thus, the esophagus is now understood to be an environmental sensing immune organ with functions in health and disease.
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@article {pmid41386478,
year = {2025},
author = {Rochman, M and Rothenberg, ME},
title = {Immune Functions of the Esophagus.},
journal = {The Journal of allergy and clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaci.2025.12.001},
pmid = {41386478},
issn = {1097-6825},
abstract = {The esophagus has long been regarded as a simple conduit for food transport. A new paradigm now recognizes it as an immune organ actively involved in environmental sensing, antigen tolerance, and neuroimmune signaling to maintain mucosal homeostasis. The stratified squamous epithelium provides a vital physical barrier, supported by transmembrane mucins and regulated by post-translational modifications, including citrullination mediated by esophagus-enriched peptidyl arginine deiminases. A unique esophageal microbiome, established early in life, shapes epithelial differentiation, gene expression, and immune development and response. Pattern recognition receptors and enriched interleukin 1 (IL-1) family cytokines, including the alarmins IL-33 and thymic stromal lymphopoietin (TSLP), orchestrate rapid immune responses to diverse environmental stimuli, such as allergens. The protease-antiprotease balance, controlled by serine and cysteine proteases, notably kallikreins, and the inhibitors SERPINs and SPINKs, regulates cytokine activity and barrier integrity. Neuroimmune circuits link innate immune activation, sensory perception, and barrier regulation. Disruption of these pathways, including genetic variants in barrier components, proteases, and immune regulators, contributes to disease susceptibility and pathogenesis. Thus, the esophagus is now understood to be an environmental sensing immune organ with functions in health and disease.},
}
RevDate: 2025-12-12
Multi-omics reveals gut microbiota-mediated environmental adaptation in Mallards and domesticated Shaoxing ducks.
Poultry science, 105(1):106177 pii:S0032-5791(25)01417-8 [Epub ahead of print].
Gut microbiota remodeling is a critical component of the domestication syndrome. However, the structural and functional consequences of domestication on gut microbiomes in ducks remain poorly understood. Understanding how domestication and associated ecological transitions influence gut microbial communities can shed light on host adaptation mechanisms. We performed integrated metagenomic and metabolomic analyses of the ileal and cecal microbiota from Mallards and Shaoxing ducks-two ecotypes of Anas platyrhynchos representing wild and domesticated lineages-to investigate microbial community structure, functional capacity, and host-microbe metabolic interactions. Principal coordinates analysis (PCoA) revealed distinct microbial stratification between intestinal compartments (ileum vs. cecum), with domestication-associated divergence observed primarily in the cecum. Metabolomic profiles were relatively stable across both segments and populations. Mallards harbored a more diverse and metabolically versatile gut microbiota, with significant enrichment in pathways related to carbohydrate, amino acid, and vitamin metabolism. The genus Gemmiger emerged as a key functional contributor, supporting branched-chain amino acid biosynthesis, coenzyme activation, and carbohydrate utilization, thus reflecting enhanced metabolic adaptability. In Shaoxing ducks, the gut microbiome was enriched in the glucagon signaling pathway and glucose-regulatory metabolites such as l-carnitine, myo-inositol, and quinate. Butyricicoccus sp017886875 was identified as a candidate taxon associated with glucose homeostasis. Additionally, immune-related pathways, including the NOD-like receptor signaling and antigen processing and presentation, were significantly enriched and linked to Anaerobiospirillum and Parabasalia, respectively. Co-enrichment of anti-inflammatory metabolites suggests the presence of a host-microbiota feedback mechanism that mitigates inflammation while maintaining immune readiness. These findings reveal that gut microbiota contribute to population-specific environmental adaptation in ducks, with distinct microbiome and functional traits associated with domestication history. The study highlights microbiota-mediated host adaptation as a key feature of domestication-related ecological transitions.
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@article {pmid41385957,
year = {2025},
author = {Zhang, C and Wang, X and Wang, L and Li, P and Bao, Y and Zhang, Z and Jiang, Z and Feng, C and Chen, L},
title = {Multi-omics reveals gut microbiota-mediated environmental adaptation in Mallards and domesticated Shaoxing ducks.},
journal = {Poultry science},
volume = {105},
number = {1},
pages = {106177},
doi = {10.1016/j.psj.2025.106177},
pmid = {41385957},
issn = {1525-3171},
abstract = {Gut microbiota remodeling is a critical component of the domestication syndrome. However, the structural and functional consequences of domestication on gut microbiomes in ducks remain poorly understood. Understanding how domestication and associated ecological transitions influence gut microbial communities can shed light on host adaptation mechanisms. We performed integrated metagenomic and metabolomic analyses of the ileal and cecal microbiota from Mallards and Shaoxing ducks-two ecotypes of Anas platyrhynchos representing wild and domesticated lineages-to investigate microbial community structure, functional capacity, and host-microbe metabolic interactions. Principal coordinates analysis (PCoA) revealed distinct microbial stratification between intestinal compartments (ileum vs. cecum), with domestication-associated divergence observed primarily in the cecum. Metabolomic profiles were relatively stable across both segments and populations. Mallards harbored a more diverse and metabolically versatile gut microbiota, with significant enrichment in pathways related to carbohydrate, amino acid, and vitamin metabolism. The genus Gemmiger emerged as a key functional contributor, supporting branched-chain amino acid biosynthesis, coenzyme activation, and carbohydrate utilization, thus reflecting enhanced metabolic adaptability. In Shaoxing ducks, the gut microbiome was enriched in the glucagon signaling pathway and glucose-regulatory metabolites such as l-carnitine, myo-inositol, and quinate. Butyricicoccus sp017886875 was identified as a candidate taxon associated with glucose homeostasis. Additionally, immune-related pathways, including the NOD-like receptor signaling and antigen processing and presentation, were significantly enriched and linked to Anaerobiospirillum and Parabasalia, respectively. Co-enrichment of anti-inflammatory metabolites suggests the presence of a host-microbiota feedback mechanism that mitigates inflammation while maintaining immune readiness. These findings reveal that gut microbiota contribute to population-specific environmental adaptation in ducks, with distinct microbiome and functional traits associated with domestication history. The study highlights microbiota-mediated host adaptation as a key feature of domestication-related ecological transitions.},
}
RevDate: 2025-12-12
Effects of Phthalate Exposure on Oral Microbiome Diversity and Enrichment of Gemella and Streptococcus.
International dental journal, 76(1):109292 pii:S0020-6539(25)08575-2 [Epub ahead of print].
AIMS: Phthalates are endocrine-disrupting plasticizers widely used in consumer products, but their effects on oral microbiome diversity remain unclear. To examine associations between phthalate exposure and oral microbiome characteristics.
METHODS: Data were obtained from the 2009 to 2012 cycles of the National Health and Nutrition Examination Survey. Oral microbiome diversity was assessed via 16S rRNA gene sequencing of oral rinse samples. Urinary phthalate metabolites were measured by high performance liquid chromatography-electrospray ionization-tandem mass spectrometry and normalized to uric creatinine. Three microbiome indices were evaluated: α-diversity, β-diversity, and relative abundance. Linear regression and Permutational Multivariate Analysis of Variancetest were employed to examine associations between phthalate exposure and α-diversity and microbial composition, and to assess differences in β-diversity across phthalate exposure tertiles.
RESULTS: Higher concentrations of mono (carboxyoctyl) phthalate (MCOP) and mono-isononyl phthalate (MiNP) were significantly associated with reduced α-diversity (Observed ASVs: β = -0.096 and -0.098; Faith's Phylogenetic Diversity: β = -0.097 and -0.092; Shannon-Weiner index: β = -0.109 and -0.126; Simpson Index: β = -0.078 and -0.110, respectively, with all P < .05). β-diversity, including Bray-Curtis dissimilarity, unweighted UniFrac distance, and weighted UniFrac distance, significantly differed across phthalate exposure tertiles for most phthalates, except for mono-n-butyl phthalate (MBP) and mono-isobutyl phthalate (MiBP). At the genus level, Mono (carboxynonyl) phthalate (MCNP) was positively associated with Gemella (β = 0.099, P = .026), and MiNP with Streptococcus (β = 0.089, P = .026).
CONCLUSIONS: Pphthalate exposure is associated with alterations in oral microbiome diversity and composition, highlighting potential microbiome-mediated pathways underlying phthalate-related health effects.
CLINICAL RELEVANCE: phthalate exposure alters oral microbiome diversity, suggesting a potential mechanism linking plasticizers to adverse health outcomes.
Additional Links: PMID-41385919
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PubMed:
Citation:
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@article {pmid41385919,
year = {2025},
author = {Pan, Q and Zuo, C and Zhao, Y and Zhao, Y and Zhou, Z and Dang, H and Wang, H and Li, S and Liu, F},
title = {Effects of Phthalate Exposure on Oral Microbiome Diversity and Enrichment of Gemella and Streptococcus.},
journal = {International dental journal},
volume = {76},
number = {1},
pages = {109292},
doi = {10.1016/j.identj.2025.109292},
pmid = {41385919},
issn = {1875-595X},
abstract = {AIMS: Phthalates are endocrine-disrupting plasticizers widely used in consumer products, but their effects on oral microbiome diversity remain unclear. To examine associations between phthalate exposure and oral microbiome characteristics.
METHODS: Data were obtained from the 2009 to 2012 cycles of the National Health and Nutrition Examination Survey. Oral microbiome diversity was assessed via 16S rRNA gene sequencing of oral rinse samples. Urinary phthalate metabolites were measured by high performance liquid chromatography-electrospray ionization-tandem mass spectrometry and normalized to uric creatinine. Three microbiome indices were evaluated: α-diversity, β-diversity, and relative abundance. Linear regression and Permutational Multivariate Analysis of Variancetest were employed to examine associations between phthalate exposure and α-diversity and microbial composition, and to assess differences in β-diversity across phthalate exposure tertiles.
RESULTS: Higher concentrations of mono (carboxyoctyl) phthalate (MCOP) and mono-isononyl phthalate (MiNP) were significantly associated with reduced α-diversity (Observed ASVs: β = -0.096 and -0.098; Faith's Phylogenetic Diversity: β = -0.097 and -0.092; Shannon-Weiner index: β = -0.109 and -0.126; Simpson Index: β = -0.078 and -0.110, respectively, with all P < .05). β-diversity, including Bray-Curtis dissimilarity, unweighted UniFrac distance, and weighted UniFrac distance, significantly differed across phthalate exposure tertiles for most phthalates, except for mono-n-butyl phthalate (MBP) and mono-isobutyl phthalate (MiBP). At the genus level, Mono (carboxynonyl) phthalate (MCNP) was positively associated with Gemella (β = 0.099, P = .026), and MiNP with Streptococcus (β = 0.089, P = .026).
CONCLUSIONS: Pphthalate exposure is associated with alterations in oral microbiome diversity and composition, highlighting potential microbiome-mediated pathways underlying phthalate-related health effects.
CLINICAL RELEVANCE: phthalate exposure alters oral microbiome diversity, suggesting a potential mechanism linking plasticizers to adverse health outcomes.},
}
RevDate: 2025-12-12
Disentangling the molecular mechanisms of disease suppression by endophytic Flavobacterium sp. 98.
Microbiological research, 304:128415 pii:S0944-5013(25)00374-X [Epub ahead of print].
Endophytic microorganisms colonize internal plant tissues and enhance host resistance to pathogens. We previously showed that endophytic Flavobacterium sp. 98 (Fl98) protects sugar beet against the fungal root pathogen Rhizoctonia solani via biosynthetic gene cluster 298 (BGC298). However, the molecular mechanisms underlying this protection remained poorly understood. Here, comparative metabolomic analyses revealed that knockout of BGC298 led to reduced production of the antifungal compound 5,6-dimethylbenzimidazole (DMB) in Fl98. We hypothesized that BGC298 is involved in regulating DMB biosynthesis and therefore contributes to Fl98's disease suppression as a novel protective mechanism. Subsequent site-directed mutagenesis of the DMB-synthase gene bluB abolished DMB production by Fl98, and both ΔBGC298 and ΔbluB mutants were compromised in protecting sugar beet seedlings in greenhouse bioassays. Bioinformatic analyses further indicated that bluB is widespread across Flavobacterium, while BGC298 is limited to a small subset of plant-associated strains. Together, our findings highlight the pivotal role of BGC298 and DMB biosynthesis in plant protection by endophytic Flavobacterium sp. 98.
Additional Links: PMID-41385904
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PubMed:
Citation:
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@article {pmid41385904,
year = {2025},
author = {Pan, X and Elsayed, SS and van Wezel, GP and Raaijmakers, JM and Carrión, VJ},
title = {Disentangling the molecular mechanisms of disease suppression by endophytic Flavobacterium sp. 98.},
journal = {Microbiological research},
volume = {304},
number = {},
pages = {128415},
doi = {10.1016/j.micres.2025.128415},
pmid = {41385904},
issn = {1618-0623},
abstract = {Endophytic microorganisms colonize internal plant tissues and enhance host resistance to pathogens. We previously showed that endophytic Flavobacterium sp. 98 (Fl98) protects sugar beet against the fungal root pathogen Rhizoctonia solani via biosynthetic gene cluster 298 (BGC298). However, the molecular mechanisms underlying this protection remained poorly understood. Here, comparative metabolomic analyses revealed that knockout of BGC298 led to reduced production of the antifungal compound 5,6-dimethylbenzimidazole (DMB) in Fl98. We hypothesized that BGC298 is involved in regulating DMB biosynthesis and therefore contributes to Fl98's disease suppression as a novel protective mechanism. Subsequent site-directed mutagenesis of the DMB-synthase gene bluB abolished DMB production by Fl98, and both ΔBGC298 and ΔbluB mutants were compromised in protecting sugar beet seedlings in greenhouse bioassays. Bioinformatic analyses further indicated that bluB is widespread across Flavobacterium, while BGC298 is limited to a small subset of plant-associated strains. Together, our findings highlight the pivotal role of BGC298 and DMB biosynthesis in plant protection by endophytic Flavobacterium sp. 98.},
}
RevDate: 2025-12-12
Environmental and Microbial Drivers of Global Rhizosphere Resistome Assembly.
Journal of agricultural and food chemistry [Epub ahead of print].
Soil serves as a critical reservoir for antibiotic resistance genes (ARGs); however, the ecological mechanisms driving ARG assembly at the plant-soil interface remain poorly understood. In this study, we analyzed 383 metagenomic samples and identified 4803 predicted ARGs, which were classified into two distinct clusters. The ARG-abundant cluster exhibited higher rhizospheric ARG abundance and diversity but posed a relatively lower health risk compared to the ARG-scarce cluster. Warm and nutrient-rich soils promote diverse resistomes shaped by complex microbial interactions, whereas humid environments promote more homogeneously predicted ARG compositions. Environmental variables such as the temperature and nitrogen were found to indirectly influence resistome composition by modulating microbial diversity. Notably, relatively high proportions of high-risk predicted ARGs were detected in grains and raw-eat vegetables, highlighting a potential threat to public health. Our findings underscore the importance of incorporating both environmental and microbial perspectives into agricultural practices to mitigate ARG dissemination in soil.
Additional Links: PMID-41385764
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PubMed:
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@article {pmid41385764,
year = {2025},
author = {Yang, H and Yu, Y and Cui, R and Zhang, Q and Chen, B and Zhang, Z and Xu, N and Sun, L and Lu, T and Qian, H},
title = {Environmental and Microbial Drivers of Global Rhizosphere Resistome Assembly.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c11060},
pmid = {41385764},
issn = {1520-5118},
abstract = {Soil serves as a critical reservoir for antibiotic resistance genes (ARGs); however, the ecological mechanisms driving ARG assembly at the plant-soil interface remain poorly understood. In this study, we analyzed 383 metagenomic samples and identified 4803 predicted ARGs, which were classified into two distinct clusters. The ARG-abundant cluster exhibited higher rhizospheric ARG abundance and diversity but posed a relatively lower health risk compared to the ARG-scarce cluster. Warm and nutrient-rich soils promote diverse resistomes shaped by complex microbial interactions, whereas humid environments promote more homogeneously predicted ARG compositions. Environmental variables such as the temperature and nitrogen were found to indirectly influence resistome composition by modulating microbial diversity. Notably, relatively high proportions of high-risk predicted ARGs were detected in grains and raw-eat vegetables, highlighting a potential threat to public health. Our findings underscore the importance of incorporating both environmental and microbial perspectives into agricultural practices to mitigate ARG dissemination in soil.},
}
RevDate: 2025-12-12
Diversity of necrophagous flies and microbiome profiling of Phumosia promittens as a rainforest health indicator.
AMB Express pii:10.1186/s13568-025-01994-3 [Epub ahead of print].
Necrophagous flies play a critical role in decomposition and serve as bioindicators of environmental health and pollution. Malaysia's tropical rainforest ecosystems may host many necrophagous fly species, including unique blowflies and their associated bacteria. However, in many forest reserve areas, the diversity of these flies remains poorly studied. This study examines the diversity of necrophagous flies and their associated surface bacteria community, with a particular focus on Phumosia promittens (Walker in J Proc Linn Soc Lond Zool 4:90-96, 1859) in the Bangi Forest Reserve, Universiti Kebangsaan Malaysia. Sampling was conducted across three plots using baited traps, and collected flies were morphologically identified and processed under sterile conditions. Surface bacteria from P. promittens were isolated and analysed through metagenomic analysis targeting the 16S rRNA (V3-V4) amplicon sequencing gene to characterise their microbial communities comprehensively. Among 2,528 individuals collected, Chrysomya megacephala (Fabricius) was the most dominant species overall, while P. promittens was the most abundant among native forest species, suggesting their ecological adaptability and potential as a bioindicator of healthy rainforest. Shannon-Wiener and Simpson's diversity of flies in the study location were 0.67 ± 0.11 and 0.29 ± 0.06, respectively. Meanwhile, the Shannon-Wiener and Simpson's diversity of bacteria from P. promittens were 5.64 ± 0.70 and 0.96 ± 0.02, respectively. Bacterial microbiome analysis revealed the presence of core genera, including Wohlfahrtiimonas, Dysgonomonas, Vagococcus, and Ignatzschineria, which are implicated in both ecological symbiosis and public health concerns. These bacteria may contribute to nutrient cycling, such as heavy metals and antibiotics. Notably, several of these genera are emerging zoonotic pathogens with antimicrobial resistance, highlighting the dual role of necrophagous flies as ecosystem contributors and disease vectors. The findings underscore the importance of monitoring native fly species and their microbiota to assess the integrity of forest ecosystems and potential public health risks.
Additional Links: PMID-41385173
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PubMed:
Citation:
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@article {pmid41385173,
year = {2025},
author = {Othman, AA and Mohamed Zain, NI and Eshak, Z and Adman, MA and Abd Latif, Z and Aboshanab, KM and Ahmad, A},
title = {Diversity of necrophagous flies and microbiome profiling of Phumosia promittens as a rainforest health indicator.},
journal = {AMB Express},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13568-025-01994-3},
pmid = {41385173},
issn = {2191-0855},
abstract = {Necrophagous flies play a critical role in decomposition and serve as bioindicators of environmental health and pollution. Malaysia's tropical rainforest ecosystems may host many necrophagous fly species, including unique blowflies and their associated bacteria. However, in many forest reserve areas, the diversity of these flies remains poorly studied. This study examines the diversity of necrophagous flies and their associated surface bacteria community, with a particular focus on Phumosia promittens (Walker in J Proc Linn Soc Lond Zool 4:90-96, 1859) in the Bangi Forest Reserve, Universiti Kebangsaan Malaysia. Sampling was conducted across three plots using baited traps, and collected flies were morphologically identified and processed under sterile conditions. Surface bacteria from P. promittens were isolated and analysed through metagenomic analysis targeting the 16S rRNA (V3-V4) amplicon sequencing gene to characterise their microbial communities comprehensively. Among 2,528 individuals collected, Chrysomya megacephala (Fabricius) was the most dominant species overall, while P. promittens was the most abundant among native forest species, suggesting their ecological adaptability and potential as a bioindicator of healthy rainforest. Shannon-Wiener and Simpson's diversity of flies in the study location were 0.67 ± 0.11 and 0.29 ± 0.06, respectively. Meanwhile, the Shannon-Wiener and Simpson's diversity of bacteria from P. promittens were 5.64 ± 0.70 and 0.96 ± 0.02, respectively. Bacterial microbiome analysis revealed the presence of core genera, including Wohlfahrtiimonas, Dysgonomonas, Vagococcus, and Ignatzschineria, which are implicated in both ecological symbiosis and public health concerns. These bacteria may contribute to nutrient cycling, such as heavy metals and antibiotics. Notably, several of these genera are emerging zoonotic pathogens with antimicrobial resistance, highlighting the dual role of necrophagous flies as ecosystem contributors and disease vectors. The findings underscore the importance of monitoring native fly species and their microbiota to assess the integrity of forest ecosystems and potential public health risks.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Lipid nanoparticle-based mRNA platforms for mucosal HIV vaccines: formulation advances, immune mechanisms, and translational pathways.
Archives of microbiology, 208(1):68.
Developing an effective HIV vaccine remains a major challenge in modern medicine. The majority of HIV transmissions occur across mucosal surfaces, yet the mucosal immune protection provided by current systemic vaccination strategies is limited. However, the potential of lipid nanoparticle (LNP)-based messenger RNA (mRNA) vaccines to revolutionize HIV prevention is a source of hope and optimism. Additionally, circular RNA (circRNA) represents an emergent platform that may offer potential for mucosal HIV vaccine development. This review examines the relationship between mRNA-LNP formulation science and mucosal immunology, with a focus on how adjuvant design, device engineering, and delivery methods interact to influence protective outcomes. We summarize the most recent research on mucosal delivery methods, including nasal, vaginal, rectal, and pulmonary routes, as well as formulation techniques to overcome obstacles such as mucus penetration, enzymatic breakdown, and epithelial absorption. We also examine how mRNA design (including nucleoside modification status) and prime-boost regimens influence the desired immunological outcomes, such as the induction of mucosal secretory IgA (SIgA), tissue-resident memory T cells (TRM), and a balanced systemic-local immune response. The microbiome and mucosal inflammation are examined in relation to safety, tolerability, and regulatory considerations. We stress the importance of future research priorities, including integrated prime-boost schedules, adjuvant tuning, and early human trials, to engage the audience and commit to the advancement of HIV prevention. We also highlight translational roadblocks, such as the lack of standardized mucosal assays, limited preclinical challenge data, and manufacturing challenges. When combined, mucosal delivery of mRNA vaccines made with LNP presents a promising strategy for preventing HIV by focusing immune responses at viral entry points.
Additional Links: PMID-41385014
PubMed:
Citation:
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@article {pmid41385014,
year = {2025},
author = {Sawaran Singh, NS and Gataa, IS and Saleh, LH and Ganesan, S and Kavitha, V and Maharana, L and Sharma, R and Latipova, M and Madatova, N and Jumanazarov, D and Smerat, A},
title = {Lipid nanoparticle-based mRNA platforms for mucosal HIV vaccines: formulation advances, immune mechanisms, and translational pathways.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {68},
pmid = {41385014},
issn = {1432-072X},
mesh = {*AIDS Vaccines/immunology/administration & dosage ; Humans ; *HIV Infections/prevention & control/immunology ; *Nanoparticles/chemistry/administration & dosage ; Immunity, Mucosal ; *RNA, Messenger/immunology/administration & dosage/genetics ; Animals ; *Lipids/chemistry ; Adjuvants, Immunologic ; Mucous Membrane/immunology ; Administration, Mucosal ; Liposomes ; },
abstract = {Developing an effective HIV vaccine remains a major challenge in modern medicine. The majority of HIV transmissions occur across mucosal surfaces, yet the mucosal immune protection provided by current systemic vaccination strategies is limited. However, the potential of lipid nanoparticle (LNP)-based messenger RNA (mRNA) vaccines to revolutionize HIV prevention is a source of hope and optimism. Additionally, circular RNA (circRNA) represents an emergent platform that may offer potential for mucosal HIV vaccine development. This review examines the relationship between mRNA-LNP formulation science and mucosal immunology, with a focus on how adjuvant design, device engineering, and delivery methods interact to influence protective outcomes. We summarize the most recent research on mucosal delivery methods, including nasal, vaginal, rectal, and pulmonary routes, as well as formulation techniques to overcome obstacles such as mucus penetration, enzymatic breakdown, and epithelial absorption. We also examine how mRNA design (including nucleoside modification status) and prime-boost regimens influence the desired immunological outcomes, such as the induction of mucosal secretory IgA (SIgA), tissue-resident memory T cells (TRM), and a balanced systemic-local immune response. The microbiome and mucosal inflammation are examined in relation to safety, tolerability, and regulatory considerations. We stress the importance of future research priorities, including integrated prime-boost schedules, adjuvant tuning, and early human trials, to engage the audience and commit to the advancement of HIV prevention. We also highlight translational roadblocks, such as the lack of standardized mucosal assays, limited preclinical challenge data, and manufacturing challenges. When combined, mucosal delivery of mRNA vaccines made with LNP presents a promising strategy for preventing HIV by focusing immune responses at viral entry points.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*AIDS Vaccines/immunology/administration & dosage
Humans
*HIV Infections/prevention & control/immunology
*Nanoparticles/chemistry/administration & dosage
Immunity, Mucosal
*RNA, Messenger/immunology/administration & dosage/genetics
Animals
*Lipids/chemistry
Adjuvants, Immunologic
Mucous Membrane/immunology
Administration, Mucosal
Liposomes
RevDate: 2025-12-12
CmpDate: 2025-12-12
Phage therapy and the microbiome in hematologic malignancies: opportunities, mechanisms, and early evidence.
Journal of cancer research and clinical oncology, 152(1):8.
Hematologic malignancies remain among the most difficult cancers to treat, challenged by profound heterogeneity, treatment-induced immune dysfunction, and the frequent emergence of drug resistance. Beyond tumor-intrinsic mechanisms, dysbiosis of the gut microbiome is increasingly recognized as a critical determinant of therapeutic outcomes, shaping hematopoiesis, immune responses, and drug metabolism. Bacteriophage (phage) therapy has re-emerged as a precision tool capable of selectively eradicating pathogenic taxa while preserving commensal short-chain fatty acid-producing communities. Preclinical and early human studies demonstrate that phages can recalibrate microbial ecosystems, disrupt antibiotic-tolerant biofilms, and enrich metabolites such as butyrate that support mucosal integrity and immune balance. Mechanistically, phage DNA enriched with CpG motifs engages Toll-like receptor 9, activating dendritic cells and enhancing cytotoxic T lymphocyte responses, suggesting dual benefits in infection control and anti-tumor immunity. Emerging applications extend further, with engineered phages serving as vectors for CRISPR-Cas gene editing, targeted cytokine delivery, and nanocarrier platforms for leukemia therapy. Despite translational promise, major hurdles persist, including immunogenicity, horizontal gene transfer, resistance evolution, and regulatory uncertainty. Addressing these challenges through GMP-compliant manufacturing, metagenomics-guided personalization, and AI-optimized cocktail design could establish phage therapy as a microbiome-informed adjunct to overcome drug resistance in blood cancers. However, direct clinical evidence of phage therapy efficacy in hematologic malignancies remains limited, and current data are largely derived from preclinical and compassionate-use contexts.
Additional Links: PMID-41384994
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@article {pmid41384994,
year = {2025},
author = {Zhang, J and Liu, J and Bayani, A},
title = {Phage therapy and the microbiome in hematologic malignancies: opportunities, mechanisms, and early evidence.},
journal = {Journal of cancer research and clinical oncology},
volume = {152},
number = {1},
pages = {8},
pmid = {41384994},
issn = {1432-1335},
mesh = {Humans ; *Hematologic Neoplasms/therapy/microbiology/immunology ; *Phage Therapy/methods ; Animals ; *Bacteriophages ; *Gastrointestinal Microbiome ; *Microbiota ; },
abstract = {Hematologic malignancies remain among the most difficult cancers to treat, challenged by profound heterogeneity, treatment-induced immune dysfunction, and the frequent emergence of drug resistance. Beyond tumor-intrinsic mechanisms, dysbiosis of the gut microbiome is increasingly recognized as a critical determinant of therapeutic outcomes, shaping hematopoiesis, immune responses, and drug metabolism. Bacteriophage (phage) therapy has re-emerged as a precision tool capable of selectively eradicating pathogenic taxa while preserving commensal short-chain fatty acid-producing communities. Preclinical and early human studies demonstrate that phages can recalibrate microbial ecosystems, disrupt antibiotic-tolerant biofilms, and enrich metabolites such as butyrate that support mucosal integrity and immune balance. Mechanistically, phage DNA enriched with CpG motifs engages Toll-like receptor 9, activating dendritic cells and enhancing cytotoxic T lymphocyte responses, suggesting dual benefits in infection control and anti-tumor immunity. Emerging applications extend further, with engineered phages serving as vectors for CRISPR-Cas gene editing, targeted cytokine delivery, and nanocarrier platforms for leukemia therapy. Despite translational promise, major hurdles persist, including immunogenicity, horizontal gene transfer, resistance evolution, and regulatory uncertainty. Addressing these challenges through GMP-compliant manufacturing, metagenomics-guided personalization, and AI-optimized cocktail design could establish phage therapy as a microbiome-informed adjunct to overcome drug resistance in blood cancers. However, direct clinical evidence of phage therapy efficacy in hematologic malignancies remains limited, and current data are largely derived from preclinical and compassionate-use contexts.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Hematologic Neoplasms/therapy/microbiology/immunology
*Phage Therapy/methods
Animals
*Bacteriophages
*Gastrointestinal Microbiome
*Microbiota
RevDate: 2025-12-12
LinkML: An Open Data Modeling Framework.
GigaScience pii:8378082 [Epub ahead of print].
BACKGROUND: Scientific research relies on well-structured, standardized data; however, much of it is stored in formats such as free-text lab notebooks, non-standardized spreadsheets, or data repositories. This lack of structure challenges interoperability, making data integration, validation, and reuse difficult.
FINDINGS: LinkML (Linked Data Modeling Language) is an open framework that simplifies the process of authoring, validating, and sharing data. LinkML can describe a range of data structures, from flat, list-based models to complex, interrelated, and normalized models that utilize polymorphism and compound inheritance. It offers an approachable syntax that is not tied to any one technical architecture and can be integrated seamlessly with many existing frameworks. The LinkML syntax provides a standard way to describe schemas, classes, and relationships, allowing modelers to build well-defined, stable, and optionally ontology-aligned data structures. Once defined, LinkML schemas may be imported into other LinkML schemas. These key features make LinkML an accessible platform for interdisciplinary collaboration and a reliable way to define and share data semantics.
CONCLUSIONS: LinkML helps reduce heterogeneity, complexity, and the proliferation of single-use data models while simultaneously enabling compliance with FAIR data standards. LinkML has seen increasing adoption in various fields, including biology, chemistry, biomedicine, microbiome research, finance, electrical engineering, transportation, and commercial software development. In short, LinkML makes implicit models explicitly computable and allows data to be standardized at its origin. LinkML documentation and code are available at linkml.io.
Additional Links: PMID-41384800
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PubMed:
Citation:
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@article {pmid41384800,
year = {2025},
author = {Moxon, SAT and Solbrig, H and Harris, NL and Kalita, P and Miller, MA and Patil, S and Schaper, K and Bizon, C and Caufield, JH and Cuesta, SC and Cox, C and Dekervel, F and Dooley, DM and Duncan, WD and Fliss, T and Gehrke, S and Graefe, ASL and Hegde, H and Ireland, AJ and Jacobsen, JOB and Krishnamurthy, M and Kroll, C and Linke, D and Ly, R and Matentzoglu, N and Overton, JA and Saunders, JL and Unni, DR and Vaidya, G and Vierdag, WAM and Ruebel, O and Chute, CG and Brush, MH and Haendel, MA and Mungall, CJ},
title = {LinkML: An Open Data Modeling Framework.},
journal = {GigaScience},
volume = {},
number = {},
pages = {},
doi = {10.1093/gigascience/giaf152},
pmid = {41384800},
issn = {2047-217X},
abstract = {BACKGROUND: Scientific research relies on well-structured, standardized data; however, much of it is stored in formats such as free-text lab notebooks, non-standardized spreadsheets, or data repositories. This lack of structure challenges interoperability, making data integration, validation, and reuse difficult.
FINDINGS: LinkML (Linked Data Modeling Language) is an open framework that simplifies the process of authoring, validating, and sharing data. LinkML can describe a range of data structures, from flat, list-based models to complex, interrelated, and normalized models that utilize polymorphism and compound inheritance. It offers an approachable syntax that is not tied to any one technical architecture and can be integrated seamlessly with many existing frameworks. The LinkML syntax provides a standard way to describe schemas, classes, and relationships, allowing modelers to build well-defined, stable, and optionally ontology-aligned data structures. Once defined, LinkML schemas may be imported into other LinkML schemas. These key features make LinkML an accessible platform for interdisciplinary collaboration and a reliable way to define and share data semantics.
CONCLUSIONS: LinkML helps reduce heterogeneity, complexity, and the proliferation of single-use data models while simultaneously enabling compliance with FAIR data standards. LinkML has seen increasing adoption in various fields, including biology, chemistry, biomedicine, microbiome research, finance, electrical engineering, transportation, and commercial software development. In short, LinkML makes implicit models explicitly computable and allows data to be standardized at its origin. LinkML documentation and code are available at linkml.io.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
[Biomarkers of aging mechanisms].
Voprosy kurortologii, fizioterapii, i lechebnoi fizicheskoi kultury, 102(5. Vyp. 2):108-119.
OBJECTIVE: To systematize current knowledge on biomarkers of fundamental aging mechanisms, their reference and target values for practical application in longevity medicine.
MATERIAL AND METHODS: Analysis of scientific literature on 14 key aging mechanisms according to the modern gerontological concept, including genomic instability, telomere shortening, epigenetic alterations, loss of proteostasis, impaired macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, microbiome dysbiosis, extracellular matrix stiffness and barrier dysfunction, as well as circadian rhythm disruption.
RESULTS: A comprehensive system of 30+biomarkers with detailed reference and target values is presented. Key biomarkers include: urinary 8-OHdG (target values<5.0 ng/mg creatinine), leukocyte telomere length (target >6000 base pairs), N7-methylguanine (<6-7 μg/g creatinine), dityrosine (≤10-12 μmol/mol creatinine), p62 and Beclin-1 for autophagy assessment, HOMA-IR (<1.5), IGF-1 (100-150 ng/ml), mitochondrial markers, senescence-associated β-galactosidase (<3% positive cells), inflammatory cytokines, microbiome-associated markers, and circadian biomarkers.
CONCLUSION: The developed biomarker panel provides a scientifically grounded foundation for personalized assessment of aging rate and correction of age-associated changes, requiring regular monitoring every 3-6 months for effective interpretation of biomarker dynamics.
Additional Links: PMID-41384525
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@article {pmid41384525,
year = {2025},
author = {Amirova, TO and Moskalev, AA},
title = {[Biomarkers of aging mechanisms].},
journal = {Voprosy kurortologii, fizioterapii, i lechebnoi fizicheskoi kultury},
volume = {102},
number = {5. Vyp. 2},
pages = {108-119},
doi = {10.17116/kurort2025102052108},
pmid = {41384525},
issn = {0042-8787},
mesh = {Humans ; *Biomarkers/urine/metabolism ; *Aging/metabolism ; Cellular Senescence ; },
abstract = {OBJECTIVE: To systematize current knowledge on biomarkers of fundamental aging mechanisms, their reference and target values for practical application in longevity medicine.
MATERIAL AND METHODS: Analysis of scientific literature on 14 key aging mechanisms according to the modern gerontological concept, including genomic instability, telomere shortening, epigenetic alterations, loss of proteostasis, impaired macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, microbiome dysbiosis, extracellular matrix stiffness and barrier dysfunction, as well as circadian rhythm disruption.
RESULTS: A comprehensive system of 30+biomarkers with detailed reference and target values is presented. Key biomarkers include: urinary 8-OHdG (target values<5.0 ng/mg creatinine), leukocyte telomere length (target >6000 base pairs), N7-methylguanine (<6-7 μg/g creatinine), dityrosine (≤10-12 μmol/mol creatinine), p62 and Beclin-1 for autophagy assessment, HOMA-IR (<1.5), IGF-1 (100-150 ng/ml), mitochondrial markers, senescence-associated β-galactosidase (<3% positive cells), inflammatory cytokines, microbiome-associated markers, and circadian biomarkers.
CONCLUSION: The developed biomarker panel provides a scientifically grounded foundation for personalized assessment of aging rate and correction of age-associated changes, requiring regular monitoring every 3-6 months for effective interpretation of biomarker dynamics.},
}
MeSH Terms:
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Humans
*Biomarkers/urine/metabolism
*Aging/metabolism
Cellular Senescence
RevDate: 2025-12-12
CmpDate: 2025-12-12
Indole-Acetic Acid Impairs Pseudomonas aeruginosa Virulence and Alters Lung Infection in Mice.
MicrobiologyOpen, 14(6):e70185.
Patients in intensive care units, especially those immunocompromised, are prone to opportunistic infections, such as respiratory and urinary tract infections. Extended antibiotic use disrupts the production of microbiome-derived metabolites, including those involved in colonization resistance to Pseudomonas aeruginosa, which is known for its multidrug resistance. Hence, prior antibiotic treatment has been shown to increase susceptibility to P. aeruginosa infection, but the role of microbiota-derived metabolic cues in this context is still elusive. This study investigates how tryptophan metabolites from the indigenous microbiota affect P. aeruginosa virulence. In vitro tests on motility, biofilm production, and pigment quantification (pyocyanin and pyoverdine) were performed on P. aeruginosa strains (PAO1, PA103, PA14) and clinical isolates. Additionally, gene expression related to virulence was analyzed, and the effects of tryptophan metabolites on experimental lung infection in mice were evaluated. Indole, indoleacetic acid (IAA), and indoleacrylic acid (IA) reduced motility and pigment production. IAA and indole promoted biofilm formation, with indole having a stronger effect. Clinical isolates showed significant phenotypic diversity, and IAA was more effective at inhibiting virulence traits than indole or IA. Mice infected with bacteria grown in the presence of IAA had lower lethality and fewer polymorphonuclear leukocyte influx compared to the control group. This suggests that tryptophan metabolites, especially IAA, can modulate P. aeruginosa virulence and may help control infection progression.
Additional Links: PMID-41384457
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PubMed:
Citation:
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@article {pmid41384457,
year = {2025},
author = {Igídio, CED and Brito, CB and Bezerra, RO and Oliveira, SN and Teixeira, CF and Amorim-Santos, BM and Andrade, ACO and Rios, DL and Pedroso, SHSP and Santos, SGD and Teixeira, MM and Souza, DDG and Mata, CPSMD and Fagundes, CT},
title = {Indole-Acetic Acid Impairs Pseudomonas aeruginosa Virulence and Alters Lung Infection in Mice.},
journal = {MicrobiologyOpen},
volume = {14},
number = {6},
pages = {e70185},
doi = {10.1002/mbo3.70185},
pmid = {41384457},
issn = {2045-8827},
support = {//Instituto Nacional de Ciencia e Tecnologia em Dengue-INCT Dengue (408527/2024-2), Fundação do Amparo a pesquisa de Minas Gerais (FAPEMIG) (APQ-00897-22), Pró-reitoria de Pesquisa da UFMG (edital01/2024), and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (88882.348380/2010-1)./ ; },
mesh = {Animals ; *Pseudomonas aeruginosa/drug effects/pathogenicity/genetics ; *Indoleacetic Acids/pharmacology/metabolism ; Virulence/drug effects ; Biofilms/drug effects/growth & development ; Mice ; *Pseudomonas Infections/microbiology/drug therapy ; Disease Models, Animal ; Humans ; Indoles/pharmacology/metabolism ; Lung/microbiology ; Female ; Tryptophan/metabolism ; Pyocyanine/metabolism ; },
abstract = {Patients in intensive care units, especially those immunocompromised, are prone to opportunistic infections, such as respiratory and urinary tract infections. Extended antibiotic use disrupts the production of microbiome-derived metabolites, including those involved in colonization resistance to Pseudomonas aeruginosa, which is known for its multidrug resistance. Hence, prior antibiotic treatment has been shown to increase susceptibility to P. aeruginosa infection, but the role of microbiota-derived metabolic cues in this context is still elusive. This study investigates how tryptophan metabolites from the indigenous microbiota affect P. aeruginosa virulence. In vitro tests on motility, biofilm production, and pigment quantification (pyocyanin and pyoverdine) were performed on P. aeruginosa strains (PAO1, PA103, PA14) and clinical isolates. Additionally, gene expression related to virulence was analyzed, and the effects of tryptophan metabolites on experimental lung infection in mice were evaluated. Indole, indoleacetic acid (IAA), and indoleacrylic acid (IA) reduced motility and pigment production. IAA and indole promoted biofilm formation, with indole having a stronger effect. Clinical isolates showed significant phenotypic diversity, and IAA was more effective at inhibiting virulence traits than indole or IA. Mice infected with bacteria grown in the presence of IAA had lower lethality and fewer polymorphonuclear leukocyte influx compared to the control group. This suggests that tryptophan metabolites, especially IAA, can modulate P. aeruginosa virulence and may help control infection progression.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Pseudomonas aeruginosa/drug effects/pathogenicity/genetics
*Indoleacetic Acids/pharmacology/metabolism
Virulence/drug effects
Biofilms/drug effects/growth & development
Mice
*Pseudomonas Infections/microbiology/drug therapy
Disease Models, Animal
Humans
Indoles/pharmacology/metabolism
Lung/microbiology
Female
Tryptophan/metabolism
Pyocyanine/metabolism
RevDate: 2025-12-12
CmpDate: 2025-12-12
Association study between intestinal microbiota dysbiosis in inflammatory bowel disease and the global disease burden growth trend.
Frontiers in medicine, 12:1635242.
BACKGROUND: Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a group of chronic intestinal inflammatory diseases. Its incidence and prevalence have been on the rise globally, imposing a heavy burden on patients' health and social medical resources. Intestinal microbiota dysbiosis is believed to play a crucial role in the occurrence and development of IBD, but the association between them and the global disease burden growth trend remains unclear.
METHODS: By searching the Global Burden of Disease (GBD) study database, we collected IBD disease burden data from 180 countries and regions between 1990 and 2023, including key indicators such as incidence, prevalence, mortality, and disability-adjusted life years (DALYs). Intestinal microbiota data were sourced from two parts: (1) Independent collection: A total of 20,000 healthy individuals and IBD patients were selected as research subjects from 180 countries and regions using a stratified random sampling method. Fecal samples (2-5 grams per person) were collected and immediately stored in a -80 °C ultra-low temperature refrigerator to avoid changes in the microbial community structure; (2) Supplementary data from public databases: Published intestinal microbiota sequencing data of corresponding regions from 1990 to 2023 were extracted from the MGnify (https://www.ebi.ac.uk/metagenomics/), Human Microbiome Project (HMP), and GMrepo (https://gmrepo.humangut.info/) databases. The sample size for each country and region was no less than 500 to cover populations of different ages (18-70 years), genders (male/female ratio approximately 1:1), and dietary habits (high-fiber diet, high-sugar and high-fat diet). Technologies like metagenomic sequencing and 16S rRNA gene sequencing were used to obtain data on the composition, abundance, and diversity of the intestinal microbiota of the corresponding regional populations. For metagenomic sequencing, the Illumina HiSeq or NovaSeq platform was used. Linear regression models, time-series analysis, and causal inference methods were applied to evaluate the correlation between intestinal microbiota dysbiosis and the growth trends of various disease burden indicators, and to explore the potential impact mechanisms.
RESULTS: The global incidence of IBD increased from 12.3 per 100,000 in 1990 to 25.6 per 100,000 in 2023, the prevalence rose from 396 per 100,000 to 523 per 100,000, and the DALY value also increased significantly (from 230 per 100,000 in 1990 to 380 per 100,000 in 2023). The average annual growth rates of the above indicators were 2.8% (95% CI: 2.5-3.1%, p < 0.001), 1.0% (95% CI: 0.8-1.2%, p < 0.001), and 1.5% (95% CI: 1.3-1.7%, p < 0.001), respectively. Further analysis showed that intestinal microbiota dysbiosis was closely related to the growth of the disease burden. In regions with severe microbiota dysbiosis, the annual growth rate of the IBD incidence was 3.2 times higher than that in balanced regions (β = 3.2, 95% CI: 2.8-3.6, p < 0.001); when the average abundance of beneficial bacteria such as Bifidobacterium and Lactobacillus in the intestine decreased by 40% (relative to the average abundance of healthy populations) and the abundance of harmful bacteria such as Escherichia coli increased by 60%, the annual growth rate of IBD incidence in this region was as high as 8.5% (95% CI: 7.9-9.1%, p < 0.001); in regions where the Shannon index decreased by 10%, the incidence of IBD increased by an average of 15% (β = 0.15, 95% CI: 0.12-0.18, p < 0.001). A positive correlation was observed between the degree of intestinal microbiota dysbiosis and disease severity (measured by DALYs): in regions where the intestinal F/B ratio deviated from the normal range by more than 30%, DALYs were 40% higher than those in regions with a normal ratio (β = 0.40, 95% CI: 0.35-0.45, p < 0.001); in regions where the content of short-chain fatty acids (SCFAs) decreased by 20%, DALYs increased by approximately 25% (β = 0.25, 95% CI: 0.21-0.29, p < 0.001). Among IBD patients with different severity levels in the Asian region, the abundance of specific bacterial genera related to inflammation regulation (e.g., Faecalibacterium) in the intestines of severe patients decreased by more than 50% compared with healthy populations, and their DALY values were 60% higher than those of mild patients (95% CI: 55-65%, p < 0.001). Additionally, the SCFA levels of severe patients were significantly lower than those of mild patients and healthy populations (median SCFA level: 2.1 mmol/L in severe patients; 4.5 mmol/L in mild patients; 6.8 mmol/L in healthy populations, p < 0.001).
CONCLUSION: This study confirms a close association between intestinal microbiota dysbiosis in inflammatory bowel disease and the global disease burden growth trend. Intestinal microbiota dysbiosis can be used as a key indicator to predict the growth of the IBD disease burden, providing an important theoretical basis for formulating targeted prevention, control strategies, and treatment methods.
Additional Links: PMID-41384120
PubMed:
Citation:
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@article {pmid41384120,
year = {2025},
author = {Li, X and Guo, G and Shi, Q and Chen, Q and Li, L},
title = {Association study between intestinal microbiota dysbiosis in inflammatory bowel disease and the global disease burden growth trend.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1635242},
pmid = {41384120},
issn = {2296-858X},
abstract = {BACKGROUND: Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a group of chronic intestinal inflammatory diseases. Its incidence and prevalence have been on the rise globally, imposing a heavy burden on patients' health and social medical resources. Intestinal microbiota dysbiosis is believed to play a crucial role in the occurrence and development of IBD, but the association between them and the global disease burden growth trend remains unclear.
METHODS: By searching the Global Burden of Disease (GBD) study database, we collected IBD disease burden data from 180 countries and regions between 1990 and 2023, including key indicators such as incidence, prevalence, mortality, and disability-adjusted life years (DALYs). Intestinal microbiota data were sourced from two parts: (1) Independent collection: A total of 20,000 healthy individuals and IBD patients were selected as research subjects from 180 countries and regions using a stratified random sampling method. Fecal samples (2-5 grams per person) were collected and immediately stored in a -80 °C ultra-low temperature refrigerator to avoid changes in the microbial community structure; (2) Supplementary data from public databases: Published intestinal microbiota sequencing data of corresponding regions from 1990 to 2023 were extracted from the MGnify (https://www.ebi.ac.uk/metagenomics/), Human Microbiome Project (HMP), and GMrepo (https://gmrepo.humangut.info/) databases. The sample size for each country and region was no less than 500 to cover populations of different ages (18-70 years), genders (male/female ratio approximately 1:1), and dietary habits (high-fiber diet, high-sugar and high-fat diet). Technologies like metagenomic sequencing and 16S rRNA gene sequencing were used to obtain data on the composition, abundance, and diversity of the intestinal microbiota of the corresponding regional populations. For metagenomic sequencing, the Illumina HiSeq or NovaSeq platform was used. Linear regression models, time-series analysis, and causal inference methods were applied to evaluate the correlation between intestinal microbiota dysbiosis and the growth trends of various disease burden indicators, and to explore the potential impact mechanisms.
RESULTS: The global incidence of IBD increased from 12.3 per 100,000 in 1990 to 25.6 per 100,000 in 2023, the prevalence rose from 396 per 100,000 to 523 per 100,000, and the DALY value also increased significantly (from 230 per 100,000 in 1990 to 380 per 100,000 in 2023). The average annual growth rates of the above indicators were 2.8% (95% CI: 2.5-3.1%, p < 0.001), 1.0% (95% CI: 0.8-1.2%, p < 0.001), and 1.5% (95% CI: 1.3-1.7%, p < 0.001), respectively. Further analysis showed that intestinal microbiota dysbiosis was closely related to the growth of the disease burden. In regions with severe microbiota dysbiosis, the annual growth rate of the IBD incidence was 3.2 times higher than that in balanced regions (β = 3.2, 95% CI: 2.8-3.6, p < 0.001); when the average abundance of beneficial bacteria such as Bifidobacterium and Lactobacillus in the intestine decreased by 40% (relative to the average abundance of healthy populations) and the abundance of harmful bacteria such as Escherichia coli increased by 60%, the annual growth rate of IBD incidence in this region was as high as 8.5% (95% CI: 7.9-9.1%, p < 0.001); in regions where the Shannon index decreased by 10%, the incidence of IBD increased by an average of 15% (β = 0.15, 95% CI: 0.12-0.18, p < 0.001). A positive correlation was observed between the degree of intestinal microbiota dysbiosis and disease severity (measured by DALYs): in regions where the intestinal F/B ratio deviated from the normal range by more than 30%, DALYs were 40% higher than those in regions with a normal ratio (β = 0.40, 95% CI: 0.35-0.45, p < 0.001); in regions where the content of short-chain fatty acids (SCFAs) decreased by 20%, DALYs increased by approximately 25% (β = 0.25, 95% CI: 0.21-0.29, p < 0.001). Among IBD patients with different severity levels in the Asian region, the abundance of specific bacterial genera related to inflammation regulation (e.g., Faecalibacterium) in the intestines of severe patients decreased by more than 50% compared with healthy populations, and their DALY values were 60% higher than those of mild patients (95% CI: 55-65%, p < 0.001). Additionally, the SCFA levels of severe patients were significantly lower than those of mild patients and healthy populations (median SCFA level: 2.1 mmol/L in severe patients; 4.5 mmol/L in mild patients; 6.8 mmol/L in healthy populations, p < 0.001).
CONCLUSION: This study confirms a close association between intestinal microbiota dysbiosis in inflammatory bowel disease and the global disease burden growth trend. Intestinal microbiota dysbiosis can be used as a key indicator to predict the growth of the IBD disease burden, providing an important theoretical basis for formulating targeted prevention, control strategies, and treatment methods.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Reprogramming prostate cancer through the microbiome.
Frontiers in medicine, 12:1690498.
Prostate cancer (PCa) is a major global public health challenge, driven by a multifactorial interplay of genetic, epigenetic, hormonal and environmental determinants. In recent years, the human microbiome has emerged as a critical and previously underappreciated contributor to PCa initiation, progression, and therapeutic response. Emerging high-resolution multi-omics studies have demonstrated that microbial communities across the gut, urinary tract and prostate form a functional axis that shapes immune surveillance, hormonal metabolism, inflammatory tone and epigenetic regulation. Dysbiosis in these compartments promotes chronic inflammation, modulates androgen receptor signaling, and produces bioactive metabolites, including short-chain fatty acids, that activate oncogenic IGF-1/MAPK/PI3K and NF-κB/JAK/STAT pathways. Cross-compartmental trafficking of bacterial taxa and metabolites reinforces tumor-promoting circuits, while specific commensals such as Akkermansia muciniphila enhance antitumor immunity and improve responses to androgen deprivation therapy. Importantly, microbiota-derived factors also modulate microRNA (miRNAs) expression and epigenetic signatures, thereby affecting tumor plasticity and resistance to therapy. These mechanistic insights have catalyzed interest in microbiome-based therapeutic approaches, including probiotics, prebiotics, fecal microbiota transplantation, dietary modulation and bacteriophage therapy, which hold promise for restoring eubiosis and enhancing treatment efficacy. Nevertheless, clinical translation remains limited by inter-individual variability and the need for well-designed, longitudinal studies integrating shotgun metagenomics, metabolomics and host-microbe interactomics. Overall, the prostate, urinary and gut microbiomes represent interconnected targets that may inform precision diagnostics and novel therapeutic strategies in PCa.
Additional Links: PMID-41384118
PubMed:
Citation:
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@article {pmid41384118,
year = {2025},
author = {Bautista, J and Cardona-Maya, WD and Gancino-Guevara, K and López-Cortés, A},
title = {Reprogramming prostate cancer through the microbiome.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1690498},
pmid = {41384118},
issn = {2296-858X},
abstract = {Prostate cancer (PCa) is a major global public health challenge, driven by a multifactorial interplay of genetic, epigenetic, hormonal and environmental determinants. In recent years, the human microbiome has emerged as a critical and previously underappreciated contributor to PCa initiation, progression, and therapeutic response. Emerging high-resolution multi-omics studies have demonstrated that microbial communities across the gut, urinary tract and prostate form a functional axis that shapes immune surveillance, hormonal metabolism, inflammatory tone and epigenetic regulation. Dysbiosis in these compartments promotes chronic inflammation, modulates androgen receptor signaling, and produces bioactive metabolites, including short-chain fatty acids, that activate oncogenic IGF-1/MAPK/PI3K and NF-κB/JAK/STAT pathways. Cross-compartmental trafficking of bacterial taxa and metabolites reinforces tumor-promoting circuits, while specific commensals such as Akkermansia muciniphila enhance antitumor immunity and improve responses to androgen deprivation therapy. Importantly, microbiota-derived factors also modulate microRNA (miRNAs) expression and epigenetic signatures, thereby affecting tumor plasticity and resistance to therapy. These mechanistic insights have catalyzed interest in microbiome-based therapeutic approaches, including probiotics, prebiotics, fecal microbiota transplantation, dietary modulation and bacteriophage therapy, which hold promise for restoring eubiosis and enhancing treatment efficacy. Nevertheless, clinical translation remains limited by inter-individual variability and the need for well-designed, longitudinal studies integrating shotgun metagenomics, metabolomics and host-microbe interactomics. Overall, the prostate, urinary and gut microbiomes represent interconnected targets that may inform precision diagnostics and novel therapeutic strategies in PCa.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Combination metformin and liraglutide in PCOS: clinical efficacy in women and preclinical insights from gut microbiome modulation in rats.
Frontiers in endocrinology, 16:1599879.
BACKGROUND: Metformin and liraglutide have been gradually used in the treatment of polycystic ovary syndrome (PCOS) due to their metabolic benefits, but also with some adverse reactions. Evidence suggests that gut microbiota imbalance plays an important role in the pathogenesis of PCOS. This study comprised a clinical trial to evaluate the efficacy of metformin, liraglutide, and their combination in PCOS women, and a parallel animal experiment to explore the potential involvement of gut microbiota.
METHODS: In an open-label randomized controlled trial, sixty overweight/obese women with PCOS were randomized to: the MET group received oral metformin (0.85 g twice daily; n=20), the LIRA group received subcutaneous liraglutide (1.2 mg once daily; n=20), and the COM group received both treatments (n=20) for 12 weeks. In a separate animal study, female Sprague-Dawley rats were divided into five groups: (1) PCOS model group (letrozole 1 mg/kg orally); (2) MET group (letrozole + metformin 200 mg/kg orally); (3) LIRA group (letrozole + liraglutide 0.2 mg/kg subcutaneously); (4) COM group (letrozole + metformin + liraglutide at above doses); and (5) healthy controls (no treatment). All treatments lasted 4 weeks.
RESULTS: In the clinical trial, women in MET, LIRA, and COM groups showed significant reductions in body weight, blood glucose, blood lipid, and the LH/FSH ratio. Notably, body weight, BMI, visceral fat area, and body fat percentage decreased more significantly in the COM group than in the MET group (P<0.05). Compared with the MET group, the COM group was more effective in reducing free testosterone (P=0.01). In the animal experiment, the body weight, estrus cycle, and ovarian morphology of rats in the COM group were significantly improved. Letrozole-induced PCOS rats showed intestinal flora disorder, which was improved by metformin, liraglutide, and their combination by altering the alpha and beta diversity and relative abundance of the gut microbiota.
CONCLUSION: Metformin combined with liraglutide significantly improved metabolic and endocrine characteristics in PCOS women. The associated amelioration of gut microbiota dysbiosis in PCOS rats suggests a potential mechanistic link, which warrants verification in future clinical studies.
Additional Links: PMID-41384017
PubMed:
Citation:
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@article {pmid41384017,
year = {2025},
author = {Long, XF and Fang, YQ and Li, YH and Li, JY and Wang, XP and Wang, XL and Zhang, L and Liu, Y},
title = {Combination metformin and liraglutide in PCOS: clinical efficacy in women and preclinical insights from gut microbiome modulation in rats.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1599879},
pmid = {41384017},
issn = {1664-2392},
mesh = {Animals ; Female ; *Metformin/therapeutic use/administration & dosage/pharmacology ; *Polycystic Ovary Syndrome/drug therapy/microbiology/pathology ; *Liraglutide/therapeutic use/administration & dosage/pharmacology ; Rats ; *Gastrointestinal Microbiome/drug effects ; Humans ; Rats, Sprague-Dawley ; Adult ; *Hypoglycemic Agents/therapeutic use/administration & dosage/pharmacology ; Drug Therapy, Combination ; Young Adult ; Treatment Outcome ; },
abstract = {BACKGROUND: Metformin and liraglutide have been gradually used in the treatment of polycystic ovary syndrome (PCOS) due to their metabolic benefits, but also with some adverse reactions. Evidence suggests that gut microbiota imbalance plays an important role in the pathogenesis of PCOS. This study comprised a clinical trial to evaluate the efficacy of metformin, liraglutide, and their combination in PCOS women, and a parallel animal experiment to explore the potential involvement of gut microbiota.
METHODS: In an open-label randomized controlled trial, sixty overweight/obese women with PCOS were randomized to: the MET group received oral metformin (0.85 g twice daily; n=20), the LIRA group received subcutaneous liraglutide (1.2 mg once daily; n=20), and the COM group received both treatments (n=20) for 12 weeks. In a separate animal study, female Sprague-Dawley rats were divided into five groups: (1) PCOS model group (letrozole 1 mg/kg orally); (2) MET group (letrozole + metformin 200 mg/kg orally); (3) LIRA group (letrozole + liraglutide 0.2 mg/kg subcutaneously); (4) COM group (letrozole + metformin + liraglutide at above doses); and (5) healthy controls (no treatment). All treatments lasted 4 weeks.
RESULTS: In the clinical trial, women in MET, LIRA, and COM groups showed significant reductions in body weight, blood glucose, blood lipid, and the LH/FSH ratio. Notably, body weight, BMI, visceral fat area, and body fat percentage decreased more significantly in the COM group than in the MET group (P<0.05). Compared with the MET group, the COM group was more effective in reducing free testosterone (P=0.01). In the animal experiment, the body weight, estrus cycle, and ovarian morphology of rats in the COM group were significantly improved. Letrozole-induced PCOS rats showed intestinal flora disorder, which was improved by metformin, liraglutide, and their combination by altering the alpha and beta diversity and relative abundance of the gut microbiota.
CONCLUSION: Metformin combined with liraglutide significantly improved metabolic and endocrine characteristics in PCOS women. The associated amelioration of gut microbiota dysbiosis in PCOS rats suggests a potential mechanistic link, which warrants verification in future clinical studies.},
}
MeSH Terms:
show MeSH Terms
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Animals
Female
*Metformin/therapeutic use/administration & dosage/pharmacology
*Polycystic Ovary Syndrome/drug therapy/microbiology/pathology
*Liraglutide/therapeutic use/administration & dosage/pharmacology
Rats
*Gastrointestinal Microbiome/drug effects
Humans
Rats, Sprague-Dawley
Adult
*Hypoglycemic Agents/therapeutic use/administration & dosage/pharmacology
Drug Therapy, Combination
Young Adult
Treatment Outcome
RevDate: 2025-12-12
CmpDate: 2025-12-12
A generalizable cross-continent prediction of esophageal squamous cell carcinoma using the oral microbiome.
bioRxiv : the preprint server for biology pii:2025.11.23.690048.
Esophageal squamous cell carcinoma (ESCC) is a disease with limited tools for early screening and a poor prognosis. Symptoms typically appear late, and early cancer is hard to detect without endoscopic screening, which is inaccessible in most high-risk areas. Saliva is easily accessible, and its microbiome composition can serve as a marker for upper gastrointestinal tract disease. We studied the potential utility of an oral microbiome signature for ESCC in South Africa, a region with a high incidence of the disease. In a cohort of 48 ESCC patients and 110 controls, we found marked alterations in the oral microbiome in patients with ESCC, including significantly reduced alpha diversity and increased Fusobacterium nucleatum . We devised machine learning models that classify ESCC using microbiome data, finding good performance on held-out samples (area under receiver operating characteristic curve of 0.96), and demonstrated generalization to data across independent studies conducted in different geographic regions (0.64-0.81). Overall, our results demonstrate the potential of the oral microbiome to serve as a non-invasive screening tool for ESCC.
Additional Links: PMID-41383770
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@article {pmid41383770,
year = {2025},
author = {ElNaggar, S and Chen, WC and Prodehl, LM and Marumo, TK and Khan, MU and Mathew, CG and Ruff, P and Jin, Z and Neugut, AI and Rustgi, AK and Uhlemann, AC and Korem, T and Abrams, JA},
title = {A generalizable cross-continent prediction of esophageal squamous cell carcinoma using the oral microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.23.690048},
pmid = {41383770},
issn = {2692-8205},
abstract = {Esophageal squamous cell carcinoma (ESCC) is a disease with limited tools for early screening and a poor prognosis. Symptoms typically appear late, and early cancer is hard to detect without endoscopic screening, which is inaccessible in most high-risk areas. Saliva is easily accessible, and its microbiome composition can serve as a marker for upper gastrointestinal tract disease. We studied the potential utility of an oral microbiome signature for ESCC in South Africa, a region with a high incidence of the disease. In a cohort of 48 ESCC patients and 110 controls, we found marked alterations in the oral microbiome in patients with ESCC, including significantly reduced alpha diversity and increased Fusobacterium nucleatum . We devised machine learning models that classify ESCC using microbiome data, finding good performance on held-out samples (area under receiver operating characteristic curve of 0.96), and demonstrated generalization to data across independent studies conducted in different geographic regions (0.64-0.81). Overall, our results demonstrate the potential of the oral microbiome to serve as a non-invasive screening tool for ESCC.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
The type VI secretion system governs strain maintenance in a wild mammalian gut microbiome.
bioRxiv : the preprint server for biology pii:2025.11.29.690828.
Bacteria inhabiting the mammalian gut coexist in dense communities where contact-dependent antagonism mechanisms are widespread. The type VI secretion system (T6SS) is an interbacterial toxin delivery pathway prevalent among gut Bacteroidales, yet its function in naturally evolved microbiomes remains poorly defined. Here, we examine the physiological role of the T6SS in Bacteroides within a gut community derived from wild mice (the WildR microbiome). Using newly developed genetic tools and a strategy for functional replacement of strains within the WildR community, we demonstrate that the WildR isolate B. acidifaciens employs a T6SS to antagonize co-resident Bacteroidales. We also show that loss of T6SS function compromises the long-term maintenance of B. acidifaciens in the community but not its initial colonization, establishing the system as a determinant of strain persistence. The T6SS we identified resides on an integrative and conjugative element (ICE). ICE-seq, a targeted sequencing approach, reveals that the T6SS-ICE is distributed among select Bacteroidales and Muribaculaceae species in the WildR microbiome, between which it appears to be recently exchanged. We also show that transfer of the T6SS-ICE to WildR isolate Phocaeicola vulgatus confers transient colonization benefits in mice, but an eventual fitness cost. Our findings demonstrate that the T6SS can stabilize the presence of specific strains within a complex, co-evolved gut microbiome, yet its value is context dependent and constrained by the ecological and physiological landscape of the host community.
Additional Links: PMID-41383769
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@article {pmid41383769,
year = {2025},
author = {Shen, BA and Asfahl, KL and Lim, B and Bertolli, SK and Minot, SS and Radey, MC and Penewit, K and Ngo, B and Salipante, SJ and Johnston, CD and Peterson, SB and Goodman, AL and Mougous, JD},
title = {The type VI secretion system governs strain maintenance in a wild mammalian gut microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.29.690828},
pmid = {41383769},
issn = {2692-8205},
abstract = {Bacteria inhabiting the mammalian gut coexist in dense communities where contact-dependent antagonism mechanisms are widespread. The type VI secretion system (T6SS) is an interbacterial toxin delivery pathway prevalent among gut Bacteroidales, yet its function in naturally evolved microbiomes remains poorly defined. Here, we examine the physiological role of the T6SS in Bacteroides within a gut community derived from wild mice (the WildR microbiome). Using newly developed genetic tools and a strategy for functional replacement of strains within the WildR community, we demonstrate that the WildR isolate B. acidifaciens employs a T6SS to antagonize co-resident Bacteroidales. We also show that loss of T6SS function compromises the long-term maintenance of B. acidifaciens in the community but not its initial colonization, establishing the system as a determinant of strain persistence. The T6SS we identified resides on an integrative and conjugative element (ICE). ICE-seq, a targeted sequencing approach, reveals that the T6SS-ICE is distributed among select Bacteroidales and Muribaculaceae species in the WildR microbiome, between which it appears to be recently exchanged. We also show that transfer of the T6SS-ICE to WildR isolate Phocaeicola vulgatus confers transient colonization benefits in mice, but an eventual fitness cost. Our findings demonstrate that the T6SS can stabilize the presence of specific strains within a complex, co-evolved gut microbiome, yet its value is context dependent and constrained by the ecological and physiological landscape of the host community.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
CAFT: A Compositional Log-Linear Model for Microbiome Data with Zero Cells.
bioRxiv : the preprint server for biology pii:2025.11.26.690468.
BACKGROUND: Differential abundance analysis is fundamental to microbiome research and provides valuable insights into host-microbe interactions. However, microbiome data are compositional, highly sparse (with many zero counts), and influenced by differential experimental biases across taxa. Standard statistical methods often overlook these features. Many approaches analyze relative abundances without accounting for compositionality or rely on pseudocounts, potentially leading to spurious associations and inadequate false discovery rate (FDR) control.
METHODS: We introduce a novel framework for differential abundance analysis of microbiome data: the Compositional Accelerated Failure Time (CAFT) model. CAFT addresses zero read counts by treating them as censored observations that are below a detection limit. This approach is inherently resistant to multiplicative technical bias, eliminates the need for pseudocounts, and addresses compositional bias through the establishment of appropriate score test procedures.
RESULTS: Extensive simulations show that CAFT outperforms competing compositional differential abundance methods, including LOCOM, LinDA, ANCOM-BC2, its robust variant, and LDM-clr by offering more robust type I error and FDR control with or without technical bias. Additionally, we applied CAFT to microbiome data on inflammatory bowel disease (IBD) and the upper respiratory tract (URT) to identify differentially abundant gut microbial taxa between IBD patients and healthy controls, as well as URT taxa distinguishing smokers from non-smokers.
CONCLUSION: We present CAFT, a powerful, robust, and efficient approach for compositional differential abundance analysis. CAFT effectively controls Type I error and maintains FDR control, while demonstrating enhanced power in statistical testing. These capabilities render CAFT a useful tool for compositional microbiome data analysis.
Additional Links: PMID-41383765
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@article {pmid41383765,
year = {2025},
author = {Satten, GA and Li, M and Zhao, N},
title = {CAFT: A Compositional Log-Linear Model for Microbiome Data with Zero Cells.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.26.690468},
pmid = {41383765},
issn = {2692-8205},
abstract = {BACKGROUND: Differential abundance analysis is fundamental to microbiome research and provides valuable insights into host-microbe interactions. However, microbiome data are compositional, highly sparse (with many zero counts), and influenced by differential experimental biases across taxa. Standard statistical methods often overlook these features. Many approaches analyze relative abundances without accounting for compositionality or rely on pseudocounts, potentially leading to spurious associations and inadequate false discovery rate (FDR) control.
METHODS: We introduce a novel framework for differential abundance analysis of microbiome data: the Compositional Accelerated Failure Time (CAFT) model. CAFT addresses zero read counts by treating them as censored observations that are below a detection limit. This approach is inherently resistant to multiplicative technical bias, eliminates the need for pseudocounts, and addresses compositional bias through the establishment of appropriate score test procedures.
RESULTS: Extensive simulations show that CAFT outperforms competing compositional differential abundance methods, including LOCOM, LinDA, ANCOM-BC2, its robust variant, and LDM-clr by offering more robust type I error and FDR control with or without technical bias. Additionally, we applied CAFT to microbiome data on inflammatory bowel disease (IBD) and the upper respiratory tract (URT) to identify differentially abundant gut microbial taxa between IBD patients and healthy controls, as well as URT taxa distinguishing smokers from non-smokers.
CONCLUSION: We present CAFT, a powerful, robust, and efficient approach for compositional differential abundance analysis. CAFT effectively controls Type I error and maintains FDR control, while demonstrating enhanced power in statistical testing. These capabilities render CAFT a useful tool for compositional microbiome data analysis.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Integrated multi-omics reveals distinct maternal and neonatal gut microbial and metabolic signatures associated with small for gestational age status.
Frontiers in microbiology, 16:1668148.
INTRODUCTION: Children born small for gestational age (SGA) have an elevated risk of developing metabolic disorders in later life. However, the underlying gut microbiota and metabolomic alterations in SGA mother-infant dyads remain poorly understood.
METHODS: We performed an integrated analysis of fecal metagenomics, metabolomics, and short-chain fatty acids (SCFAs) profiling in 10 SGA and 10 appropriate for gestational age (AGA) mother-infant dyads at term. Taxonomic composition, microbial functional pathways, carbohydrate-active enzyme (CAZyme) profiles, differential metabolites, and metabolite pathway enrichment were systematically evaluated.
RESULTS AND DISCUSSION: SGA neonates exhibited reduced microbial richness (Chao1 index), distinct beta-diversity, and differential abundance of key bacterial species including increased Enterococcus faecalis and Escherichia coli. Functionally, SGA maternal subjects showed divergent profiles in CAZyme genes, with lower abundance of glycoside hydrolase family 13 subfamily 16, glycosyl transferase family 66, and carbohydrate-binding module family 6, and altered structural polysaccharide degradation capacity. Metabolomic profiling revealed significant perturbations in tryptophan metabolism pathways, notably enriched in kynurenine and taurine derivatives in SGA mother and neonates. Notably, SCFA profiles were disrupted, with increased butyrate in SGA mother and reduced propionate and isobutyrate in SGA neonates. Microbe-metabolite correlation networks revealed strong associations between SGA-specific bacterial taxa and fecal metabolites. In conclusion, our analysis identifies distinct features of the early fecal microbiome and metabolome within 48 h of birth in SGA neonates compared with AGA peers, reflecting differences in initial colonization and metabolism that warrant longitudinal follow-up.
Additional Links: PMID-41383742
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Citation:
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@article {pmid41383742,
year = {2025},
author = {Bian, X and Xu, H and Li, J and Kuang, J and Shi, F and Li, X and Li, J},
title = {Integrated multi-omics reveals distinct maternal and neonatal gut microbial and metabolic signatures associated with small for gestational age status.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1668148},
pmid = {41383742},
issn = {1664-302X},
abstract = {INTRODUCTION: Children born small for gestational age (SGA) have an elevated risk of developing metabolic disorders in later life. However, the underlying gut microbiota and metabolomic alterations in SGA mother-infant dyads remain poorly understood.
METHODS: We performed an integrated analysis of fecal metagenomics, metabolomics, and short-chain fatty acids (SCFAs) profiling in 10 SGA and 10 appropriate for gestational age (AGA) mother-infant dyads at term. Taxonomic composition, microbial functional pathways, carbohydrate-active enzyme (CAZyme) profiles, differential metabolites, and metabolite pathway enrichment were systematically evaluated.
RESULTS AND DISCUSSION: SGA neonates exhibited reduced microbial richness (Chao1 index), distinct beta-diversity, and differential abundance of key bacterial species including increased Enterococcus faecalis and Escherichia coli. Functionally, SGA maternal subjects showed divergent profiles in CAZyme genes, with lower abundance of glycoside hydrolase family 13 subfamily 16, glycosyl transferase family 66, and carbohydrate-binding module family 6, and altered structural polysaccharide degradation capacity. Metabolomic profiling revealed significant perturbations in tryptophan metabolism pathways, notably enriched in kynurenine and taurine derivatives in SGA mother and neonates. Notably, SCFA profiles were disrupted, with increased butyrate in SGA mother and reduced propionate and isobutyrate in SGA neonates. Microbe-metabolite correlation networks revealed strong associations between SGA-specific bacterial taxa and fecal metabolites. In conclusion, our analysis identifies distinct features of the early fecal microbiome and metabolome within 48 h of birth in SGA neonates compared with AGA peers, reflecting differences in initial colonization and metabolism that warrant longitudinal follow-up.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Comparative metagenomic analysis on COPD and health control samples reveals taxonomic and functional motifs.
Frontiers in microbiology, 16:1636322.
Chronic obstructive pulmonary disease (COPD) is a progressive lung condition marked by persistent respiratory symptoms and airflow limitation and significantly affects global health. The intricate relationship between COPD and the lung microbiome has garnered attention, with metagenomic analyses revealing critical insights into microbial community dynamics and their functional roles. In this study, we conducted a comprehensive metagenomic analysis comparing throat samples from COPD patients (n = 26) and healthy controls (n = 32) derived from a large cohort analyzed at the Saarland University Hospital. Taxonomic profiling and differential abundance analysis indicated a significant reduction of the microbial diversity in COPD patients, with notable overrepresentation of pathogenic bacteria, such as Veillonella parvula (NCBI:txid29466), Streptococcus gordonii (NCBI:txid1302), Scardovia wiggsiae (NCBI:txid230143), as well as a less stable microbiome composition than in healthy individuals. Functional profiling identified alterations in metabolic pathways implicating microbial dysbiosis in disease progression. The study also highlighted enrichment of inflammation-related pathways in COPD samples, emphasizing the microbiome's role in inflammatory processes. Comparative analysis of bronchoalveolar lavage (BAL) and throat samples collected from the same 11 individuals further underscored distinct microbial compositions across respiratory tract regions, suggesting spatial variability in microbial communities. Metagenomic approaches including analysis of metabolic pathways showed significant alteration of the microbiome of the lung in COPD.
Additional Links: PMID-41383738
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Citation:
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@article {pmid41383738,
year = {2025},
author = {Chen, G and Wiegand, C and Willett, A and Herr, C and Müller, R and Bals, R and Kalinina, OV},
title = {Comparative metagenomic analysis on COPD and health control samples reveals taxonomic and functional motifs.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1636322},
pmid = {41383738},
issn = {1664-302X},
abstract = {Chronic obstructive pulmonary disease (COPD) is a progressive lung condition marked by persistent respiratory symptoms and airflow limitation and significantly affects global health. The intricate relationship between COPD and the lung microbiome has garnered attention, with metagenomic analyses revealing critical insights into microbial community dynamics and their functional roles. In this study, we conducted a comprehensive metagenomic analysis comparing throat samples from COPD patients (n = 26) and healthy controls (n = 32) derived from a large cohort analyzed at the Saarland University Hospital. Taxonomic profiling and differential abundance analysis indicated a significant reduction of the microbial diversity in COPD patients, with notable overrepresentation of pathogenic bacteria, such as Veillonella parvula (NCBI:txid29466), Streptococcus gordonii (NCBI:txid1302), Scardovia wiggsiae (NCBI:txid230143), as well as a less stable microbiome composition than in healthy individuals. Functional profiling identified alterations in metabolic pathways implicating microbial dysbiosis in disease progression. The study also highlighted enrichment of inflammation-related pathways in COPD samples, emphasizing the microbiome's role in inflammatory processes. Comparative analysis of bronchoalveolar lavage (BAL) and throat samples collected from the same 11 individuals further underscored distinct microbial compositions across respiratory tract regions, suggesting spatial variability in microbial communities. Metagenomic approaches including analysis of metabolic pathways showed significant alteration of the microbiome of the lung in COPD.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Dexmedetomidine modulates gut microbiota and improves long-term survival in sepsis patients with pre-existing malignancies: a propensity-matched analysis.
Frontiers in microbiology, 16:1720867.
BACKGROUND: The interplay between sedative agents and the gut microbiome may influence long-term outcomes in sepsis, but data are scarce. This study compared the effects of dexmedetomidine vs. propofol sedation on long-term survival in mechanically ventilated sepsis adults, with an exploratory focus on the gut microbiome and pre-existing malignancies.
METHODS: In this multicenter, retrospective cohort study, 1,295 mechanically ventilated adults with sepsis (2013-2020) were analyzed. Propensity score matching (1:1) balanced 27 baseline covariates, producing 177 matched pairs. Primary outcomes were 30-day, 90-day, and 5-year mortality. Secondary outcomes included delirium/coma-free days, cardiovascular safety, and 6-month functional status. Subgroup analyses assessed pre-existing malignancies and high antibiotic exposure (≥7 days before enrollment) as proxies for microbiome disruption. Gut microbiota composition was characterized via 16S rRNA sequencing in a pre-specified subcohort (n = 89).
RESULTS: After matching, dexmedetomidine was associated with significantly lower 5-year mortality (34.5% vs. 45.2%; HR 0.64, 95% CI 0.52-0.79; p = 0.039). Survival curves progressively diverged beyond 180 days. No differences were observed in short-term neurological outcomes or cardiovascular safety. Subgroup analyses showed enhanced survival benefits with dexmedetomidine in patients aged >65, females, those with pulmonary-source sepsis, SOFA >10, baseline delirium, pre-existing malignancies (OR 2.10, 95% CI 1.15-3.85; p = 0.015), and high antibiotic exposure as a proxy for gut dysbiosis (OR 1.95, 95% CI 1.08-3.52; p = 0.028). Exploratory 16S rRNA analysis in a subset (n = 89) revealed that dexmedetomidine was associated with enriched beneficial genera such as Faecalibacterium and Bifidobacterium, while propofol correlated with increased Enterococcusand Escherichia/Shigella.
CONCLUSIONS: Dexmedetomidine sedation is associated with a significant 5-year survival benefit in mechanically ventilated sepsis patients, particularly among those with malignancies or factors predisposing to gut dysbiosis. The observed modulation of the gut microbiome toward a more symbiotic state provides a plausible mechanistic insight into these clinical findings, highlighting a potential role for microbiota-centric strategies in critical care.
Additional Links: PMID-41383725
PubMed:
Citation:
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@article {pmid41383725,
year = {2025},
author = {Zeng, Y and Wu, H and Zhang, H and Ye, X and Chen, L and Ye, Y},
title = {Dexmedetomidine modulates gut microbiota and improves long-term survival in sepsis patients with pre-existing malignancies: a propensity-matched analysis.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1720867},
pmid = {41383725},
issn = {1664-302X},
abstract = {BACKGROUND: The interplay between sedative agents and the gut microbiome may influence long-term outcomes in sepsis, but data are scarce. This study compared the effects of dexmedetomidine vs. propofol sedation on long-term survival in mechanically ventilated sepsis adults, with an exploratory focus on the gut microbiome and pre-existing malignancies.
METHODS: In this multicenter, retrospective cohort study, 1,295 mechanically ventilated adults with sepsis (2013-2020) were analyzed. Propensity score matching (1:1) balanced 27 baseline covariates, producing 177 matched pairs. Primary outcomes were 30-day, 90-day, and 5-year mortality. Secondary outcomes included delirium/coma-free days, cardiovascular safety, and 6-month functional status. Subgroup analyses assessed pre-existing malignancies and high antibiotic exposure (≥7 days before enrollment) as proxies for microbiome disruption. Gut microbiota composition was characterized via 16S rRNA sequencing in a pre-specified subcohort (n = 89).
RESULTS: After matching, dexmedetomidine was associated with significantly lower 5-year mortality (34.5% vs. 45.2%; HR 0.64, 95% CI 0.52-0.79; p = 0.039). Survival curves progressively diverged beyond 180 days. No differences were observed in short-term neurological outcomes or cardiovascular safety. Subgroup analyses showed enhanced survival benefits with dexmedetomidine in patients aged >65, females, those with pulmonary-source sepsis, SOFA >10, baseline delirium, pre-existing malignancies (OR 2.10, 95% CI 1.15-3.85; p = 0.015), and high antibiotic exposure as a proxy for gut dysbiosis (OR 1.95, 95% CI 1.08-3.52; p = 0.028). Exploratory 16S rRNA analysis in a subset (n = 89) revealed that dexmedetomidine was associated with enriched beneficial genera such as Faecalibacterium and Bifidobacterium, while propofol correlated with increased Enterococcusand Escherichia/Shigella.
CONCLUSIONS: Dexmedetomidine sedation is associated with a significant 5-year survival benefit in mechanically ventilated sepsis patients, particularly among those with malignancies or factors predisposing to gut dysbiosis. The observed modulation of the gut microbiome toward a more symbiotic state provides a plausible mechanistic insight into these clinical findings, highlighting a potential role for microbiota-centric strategies in critical care.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
In-situ diet-microbiota associations across taxonomic scales in desert-dwelling amphibians and reptiles.
ISME communications, 5(1):ycaf213.
Understanding how host and environmental factors shape gut microbiota is central to microbial ecology and evolution. However, the extent to which gut microbes covary with diet and how such variation reflects host phylogeny, remains unclear under natural conditions. Here, we used DNA metabarcoding of gut contents to analyze the dietary arthropod composition and gut microbiota of four amphibian and three reptile species from the Tarim Desert, Xinjiang, China. These species showed pronounced differences in both diet and microbial profiles. Dominant dietary arthropod families exhibited generally low overlap among species, and dietary variation did not align with host phylogeny. Interestingly, Bufotes pewzowi (amphibian) and Teratoscincus przewalskii (reptile)-the most common species in their respective groups-both primarily consumed ants (Formicidae). Conversely, gut microbial composition more closely reflected host phylogeny than diet, with a clear separation between amphibians and reptiles, particularly in the relative abundances of Bacteroidetes and the genera Bacteroides and Blautia. These findings suggest that the previously reported phylosymbiosis in these species is not primarily driven by dietary overlap. Significant diet-microbiota correlations were observed across all species and within each taxonomic class but were largely absent within species. This highlights taxonomic-level differences in the diet-microbiota relationship, indicating that diet-microbiota covariation is more pronounced over evolutionary timescales than in response to real-time dietary variation. Taken together, our results show that gut microbiota and diet exhibit distinct phylogenetic patterns, with microbiota showing both associations with diet and resilience to short-term dietary changes, underscoring the importance of considering timescales in diet-microbiota studies.
Additional Links: PMID-41383635
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Citation:
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@article {pmid41383635,
year = {2025},
author = {Zhu, W and Ni, R and Cai, B and Ma, S and Jiang, J and Wang, B},
title = {In-situ diet-microbiota associations across taxonomic scales in desert-dwelling amphibians and reptiles.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf213},
pmid = {41383635},
issn = {2730-6151},
abstract = {Understanding how host and environmental factors shape gut microbiota is central to microbial ecology and evolution. However, the extent to which gut microbes covary with diet and how such variation reflects host phylogeny, remains unclear under natural conditions. Here, we used DNA metabarcoding of gut contents to analyze the dietary arthropod composition and gut microbiota of four amphibian and three reptile species from the Tarim Desert, Xinjiang, China. These species showed pronounced differences in both diet and microbial profiles. Dominant dietary arthropod families exhibited generally low overlap among species, and dietary variation did not align with host phylogeny. Interestingly, Bufotes pewzowi (amphibian) and Teratoscincus przewalskii (reptile)-the most common species in their respective groups-both primarily consumed ants (Formicidae). Conversely, gut microbial composition more closely reflected host phylogeny than diet, with a clear separation between amphibians and reptiles, particularly in the relative abundances of Bacteroidetes and the genera Bacteroides and Blautia. These findings suggest that the previously reported phylosymbiosis in these species is not primarily driven by dietary overlap. Significant diet-microbiota correlations were observed across all species and within each taxonomic class but were largely absent within species. This highlights taxonomic-level differences in the diet-microbiota relationship, indicating that diet-microbiota covariation is more pronounced over evolutionary timescales than in response to real-time dietary variation. Taken together, our results show that gut microbiota and diet exhibit distinct phylogenetic patterns, with microbiota showing both associations with diet and resilience to short-term dietary changes, underscoring the importance of considering timescales in diet-microbiota studies.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
The molecular interplay among gut dysbiosis, adipose tissue, and metabolite-derived damage-associated molecular patterns in metainflammation and atherogenesis.
Frontiers in immunology, 16:1694061.
Metainflammation is a low-grade systemic inflammatory response that can persist for months or even years, during which monocytes, macrophages, and other immune cells become hyperactivated, contributing to metabolic disease and atherogenesis. Although we now better understand the role of metainflammation in atherosclerosis, uncertainty persists about how gut dysbiosis, adipose tissue expansion, and metabolite-derived damage-associated molecular patterns (Md-DAMPs) can trigger metainflammation and promote atherogenesis. In this comprehensive review, we summarize the role of gut dysbiosis in lipopolysaccharide (LPS) production, a component of gram-negative bacteria that can trigger metainflammation by stimulating circulating monocytes and tissue-resident macrophages. We also outline adipose tissue expansion as an additional igniter of metainflammation by driving the expression of hypoxia-inducible factor 1α (HIF-1α), a master transcription factor that leads to nuclear factor kappa B (NFκB)-dependent proinflammatory cytokine production. Furthermore, we thoroughly explored the precise nature of Md-DAMPs, including glutamate, bile acids, lipoproteins, short-chain fatty acids (SCFAs), uric acid, and excess glucose, with emphasis on the molecular mechanisms that mediate their roles in metainflammation and atherosclerosis. Finally, we integrate the molecular interplay among gut dysbiosis, adipose tissue expansion, and Md-DAMPs to a scenario in which circulating monocytes, macrophages, and foam cells contribute to atherosclerotic plaque formation, instability, and rupture. In conclusion, the information examined here may help refresh our conceptual understanding of atherogenesis, incorporating novel actors as gut dysbiosis, adipose tissue expansion, and Md-DAMPs in the complex network that leads to metainflammation and cardiovascular disease.
Additional Links: PMID-41383632
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Citation:
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@article {pmid41383632,
year = {2025},
author = {González-Hermosillo, LM and Ávila-Soto, KI and Méndez-García, LA and Cérbulo-Vázquez, A and Esquivel-Velázquez, M and Bueno-Hernández, N and Fonseca-Sánchez, MÁ and Escobedo, G},
title = {The molecular interplay among gut dysbiosis, adipose tissue, and metabolite-derived damage-associated molecular patterns in metainflammation and atherogenesis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1694061},
pmid = {41383632},
issn = {1664-3224},
mesh = {Humans ; *Dysbiosis/immunology/metabolism ; *Atherosclerosis/metabolism/immunology/etiology/pathology ; *Gastrointestinal Microbiome/immunology ; Animals ; *Adipose Tissue/metabolism/immunology/pathology ; *Inflammation/immunology/metabolism ; Macrophages/immunology ; },
abstract = {Metainflammation is a low-grade systemic inflammatory response that can persist for months or even years, during which monocytes, macrophages, and other immune cells become hyperactivated, contributing to metabolic disease and atherogenesis. Although we now better understand the role of metainflammation in atherosclerosis, uncertainty persists about how gut dysbiosis, adipose tissue expansion, and metabolite-derived damage-associated molecular patterns (Md-DAMPs) can trigger metainflammation and promote atherogenesis. In this comprehensive review, we summarize the role of gut dysbiosis in lipopolysaccharide (LPS) production, a component of gram-negative bacteria that can trigger metainflammation by stimulating circulating monocytes and tissue-resident macrophages. We also outline adipose tissue expansion as an additional igniter of metainflammation by driving the expression of hypoxia-inducible factor 1α (HIF-1α), a master transcription factor that leads to nuclear factor kappa B (NFκB)-dependent proinflammatory cytokine production. Furthermore, we thoroughly explored the precise nature of Md-DAMPs, including glutamate, bile acids, lipoproteins, short-chain fatty acids (SCFAs), uric acid, and excess glucose, with emphasis on the molecular mechanisms that mediate their roles in metainflammation and atherosclerosis. Finally, we integrate the molecular interplay among gut dysbiosis, adipose tissue expansion, and Md-DAMPs to a scenario in which circulating monocytes, macrophages, and foam cells contribute to atherosclerotic plaque formation, instability, and rupture. In conclusion, the information examined here may help refresh our conceptual understanding of atherogenesis, incorporating novel actors as gut dysbiosis, adipose tissue expansion, and Md-DAMPs in the complex network that leads to metainflammation and cardiovascular disease.},
}
MeSH Terms:
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Humans
*Dysbiosis/immunology/metabolism
*Atherosclerosis/metabolism/immunology/etiology/pathology
*Gastrointestinal Microbiome/immunology
Animals
*Adipose Tissue/metabolism/immunology/pathology
*Inflammation/immunology/metabolism
Macrophages/immunology
RevDate: 2025-12-12
CmpDate: 2025-12-12
Oral microbiota and central nervous system diseases: A review.
Neuroprotection (Chichester, England), 3(1):79-94.
Oral microbiota is the second largest microbial colony in the body and forms a complex ecological community that influences oral and brain health. Impaired homeostasis of the oral microbiota can lead to pathological changes, resulting in central nervous system (CNS) diseases. However, the mechanisms and clinical value of how the oral microbiome influences the brain remain unclear. This review summarizes recent clinical findings on the role of the oral microbiota in CNS diseases and proposes potential approaches to understand the way the oral microbiota and brain communicate. We propose three underlying patterns involving neuroinflammation, neuroendocrine regulation, and CNS signaling between oral microbiota and CNS diseases. We also summarize the clinical characteristics and potential utilization of the oral microbiota in ischemic stroke, Alzheimer's and Parkinson's disease, intracranial aneurysms, and mental disorders. Although the current findings are preliminary and clinical evidence is incomplete, oral microbiota is a potential biomarker for the clinical diagnosis and treatment of CNS diseases.
Additional Links: PMID-41383524
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@article {pmid41383524,
year = {2025},
author = {Zhang, X and Zhong, M and Li, Y and Wang, H and Xi, G and Wang, F and Cheng, C and Shi, Y},
title = {Oral microbiota and central nervous system diseases: A review.},
journal = {Neuroprotection (Chichester, England)},
volume = {3},
number = {1},
pages = {79-94},
pmid = {41383524},
issn = {2770-730X},
abstract = {Oral microbiota is the second largest microbial colony in the body and forms a complex ecological community that influences oral and brain health. Impaired homeostasis of the oral microbiota can lead to pathological changes, resulting in central nervous system (CNS) diseases. However, the mechanisms and clinical value of how the oral microbiome influences the brain remain unclear. This review summarizes recent clinical findings on the role of the oral microbiota in CNS diseases and proposes potential approaches to understand the way the oral microbiota and brain communicate. We propose three underlying patterns involving neuroinflammation, neuroendocrine regulation, and CNS signaling between oral microbiota and CNS diseases. We also summarize the clinical characteristics and potential utilization of the oral microbiota in ischemic stroke, Alzheimer's and Parkinson's disease, intracranial aneurysms, and mental disorders. Although the current findings are preliminary and clinical evidence is incomplete, oral microbiota is a potential biomarker for the clinical diagnosis and treatment of CNS diseases.},
}
RevDate: 2025-12-12
Widespread antimicrobial use in laboratory rodent vivaria in North America revealed by a cross-sectional survey of American College of Laboratory Animal Medicine certified veterinarians.
Laboratory animals [Epub ahead of print].
Antimicrobial resistance (AMR) is a major global threat to human health, animal welfare and sustainable development. Whilst resistance can arise naturally, inappropriate antimicrobial exposure accelerates its emergence. Recognizing this risk, international One Health initiatives emphasize reducing antimicrobial use, especially of drugs considered critical for human medicine. Much of the evidence guiding these efforts comes from food-producing and companion animals, but antimicrobial use in laboratory animals, particularly rodents, remains poorly described. To address this gap, we surveyed all veterinarians certified by the American College of Laboratory Animal Medicine in the United States (921) and Canada (10). A total of 157 veterinarians completed the survey, resulting in a 16.9% overall response rate. The response rate was 16.6% for participants in the United States and 40.0% for those in Canada. Despite a strong response, the small number of eligible veterinarians restricts data extrapolation in the Canadian context. Survey results showed that antimicrobial use is common and routine in rodent vivaria. Overall, 91.7% of respondents reported regular antimicrobial use. Applications included both clinical treatment and research purposes such as induction of microbiome dysbiosis, prophylaxis in immunocompromised rodents and gene induction. Reported drug classes included fluoroquinolones and third-generation cephalosporins, with some use of glycopeptides and carbapenems, all considered critically important to human health. Disposal practices often involved release into sewerage or landfill without inactivation, raising environmental concerns. These findings suggest that antimicrobial use in laboratory rodents may represent an underrecognized contributor to AMR and highlight the importance of targeted stewardship.
Additional Links: PMID-41383079
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PubMed:
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@article {pmid41383079,
year = {2025},
author = {Wilcox, RS and Marenda, MS and Devlin, JM and Pritchett-Corning, KR and Wilks, CR},
title = {Widespread antimicrobial use in laboratory rodent vivaria in North America revealed by a cross-sectional survey of American College of Laboratory Animal Medicine certified veterinarians.},
journal = {Laboratory animals},
volume = {},
number = {},
pages = {236772251385020},
doi = {10.1177/00236772251385020},
pmid = {41383079},
issn = {1758-1117},
abstract = {Antimicrobial resistance (AMR) is a major global threat to human health, animal welfare and sustainable development. Whilst resistance can arise naturally, inappropriate antimicrobial exposure accelerates its emergence. Recognizing this risk, international One Health initiatives emphasize reducing antimicrobial use, especially of drugs considered critical for human medicine. Much of the evidence guiding these efforts comes from food-producing and companion animals, but antimicrobial use in laboratory animals, particularly rodents, remains poorly described. To address this gap, we surveyed all veterinarians certified by the American College of Laboratory Animal Medicine in the United States (921) and Canada (10). A total of 157 veterinarians completed the survey, resulting in a 16.9% overall response rate. The response rate was 16.6% for participants in the United States and 40.0% for those in Canada. Despite a strong response, the small number of eligible veterinarians restricts data extrapolation in the Canadian context. Survey results showed that antimicrobial use is common and routine in rodent vivaria. Overall, 91.7% of respondents reported regular antimicrobial use. Applications included both clinical treatment and research purposes such as induction of microbiome dysbiosis, prophylaxis in immunocompromised rodents and gene induction. Reported drug classes included fluoroquinolones and third-generation cephalosporins, with some use of glycopeptides and carbapenems, all considered critically important to human health. Disposal practices often involved release into sewerage or landfill without inactivation, raising environmental concerns. These findings suggest that antimicrobial use in laboratory rodents may represent an underrecognized contributor to AMR and highlight the importance of targeted stewardship.},
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
[Mechanisms and protective strategies for astronaut skin injury in deep space environments].
Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 50(8):1346-1354.
With the continuous advancement of deep space exploration missions, maintaining astronaut skin health has become a critical medical issue affecting the safety and effectiveness of long-duration missions. Deep space environmental stressors, including microgravity, ionizing radiation, lunar dust exposure, and microbiome dysbiosis, can synergistically disrupt the skin barrier structure, leading to immune homeostasis imbalance and impaired wound healing. In recent years, research on skin protection in deep space has gradually evolved into a systematic "multi-dimensional integrated protective" framework. From the engineering protection perspective, optimization of multi-layer composite spacesuit structures, the use of hydrogen-rich and boron-containing shielding materials, as well as cabin temperature-humidity regulation and debris-resistant technologies, have greatly enhanced environmental defense capacity. From the biomedical protection perspective, functional hydrogels, antimicrobial dressings, and active compounds derived from traditional Chinese medicine have demonstrated remarkable potential in repairing the skin barrier, modulating immunity, and providing antioxidant defense. Meanwhile, the development of skin microecological interventions and wearable physiological monitoring systems has fostered a trend toward personalized health management. Future research should focus on elucidating the interactive mechanisms among the space environment, skin, and immune barrier, while exploring intelligent monitoring and nanotechnology-based protection strategies. Establishing a predictive and preventive skin health safeguarding system will provide comprehensive medical support for future deep space missions.
Additional Links: PMID-41382996
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@article {pmid41382996,
year = {2025},
author = {Xie, Y and Zeng, J},
title = {[Mechanisms and protective strategies for astronaut skin injury in deep space environments].},
journal = {Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences},
volume = {50},
number = {8},
pages = {1346-1354},
doi = {10.11817/j.issn.1672-7347.2025.250443},
pmid = {41382996},
issn = {1672-7347},
support = {2024RC3064//the Science and Technology Innovation Program of Hunan Province/ ; },
mesh = {Humans ; *Astronauts ; *Skin/injuries/radiation effects ; *Space Flight ; *Weightlessness/adverse effects ; Wound Healing ; Extraterrestrial Environment ; },
abstract = {With the continuous advancement of deep space exploration missions, maintaining astronaut skin health has become a critical medical issue affecting the safety and effectiveness of long-duration missions. Deep space environmental stressors, including microgravity, ionizing radiation, lunar dust exposure, and microbiome dysbiosis, can synergistically disrupt the skin barrier structure, leading to immune homeostasis imbalance and impaired wound healing. In recent years, research on skin protection in deep space has gradually evolved into a systematic "multi-dimensional integrated protective" framework. From the engineering protection perspective, optimization of multi-layer composite spacesuit structures, the use of hydrogen-rich and boron-containing shielding materials, as well as cabin temperature-humidity regulation and debris-resistant technologies, have greatly enhanced environmental defense capacity. From the biomedical protection perspective, functional hydrogels, antimicrobial dressings, and active compounds derived from traditional Chinese medicine have demonstrated remarkable potential in repairing the skin barrier, modulating immunity, and providing antioxidant defense. Meanwhile, the development of skin microecological interventions and wearable physiological monitoring systems has fostered a trend toward personalized health management. Future research should focus on elucidating the interactive mechanisms among the space environment, skin, and immune barrier, while exploring intelligent monitoring and nanotechnology-based protection strategies. Establishing a predictive and preventive skin health safeguarding system will provide comprehensive medical support for future deep space missions.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Astronauts
*Skin/injuries/radiation effects
*Space Flight
*Weightlessness/adverse effects
Wound Healing
Extraterrestrial Environment
RevDate: 2025-12-11
A duo of fungi and complex and dynamic bacterial community networks contribute to shape the Ascophyllum nodosum holobiont.
Environmental microbiome pii:10.1186/s40793-025-00825-z [Epub ahead of print].
BACKGROUND: The brown alga Ascophyllum nodosum and its microbiota form a dynamic functional entity named holobiont. Some microbial partners may play a role in seaweed health through bioactive compounds crucial for normal morphology, development, and physiological acclimation. However, the full spectrum of the microbial diversity and its variations according to algal life stage, season, and location have not been comprehensively studied. This study uses 208 short-read metabarcoding samples to characterize the bacterial, archaeal, and microeukaryotic communities of A. nodosum across three nearby sites, four thallus parts, and a monthly survey, aiming to explore the dynamics of ecological interactions within the holobiont.
RESULTS: Our results revealed that A. nodosum harbors a predominantly bacterial microbiota, varying significantly across all covariables, while archaea were virtually absent. An innovative normalization using the co-amplified host reads provided an estimation of bacterial abundance, revealing a drastic decline in May, potentially linked to epidermal shedding. In contrast, fungal communities were stable, dominated by Mycophycias ascophylli and Moheitospora sp., which remained closely associated with the host year-round. We identified a core microbiome of 22 ASVs, consistently found in all samples, including Granulosicoccus, a genus consistently abundant in other brown algal microbiota. Sequence clustering revealed multiple species which vary according seasons, even in the overall stable Granulosicoccus genus. Co-occurrence network analysis revealed putative interactions between microbial groups in response to ecological niches.
CONCLUSIONS: Overall, these findings highlight the dynamic of bacterial interactions and stable fungal associations within the A. nodosum holobiont, providing new insights into the ecology of its microbiota.
Additional Links: PMID-41382286
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PubMed:
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@article {pmid41382286,
year = {2025},
author = {Rousseau, C and Tanguy, G and Legeay, E and Blanquart, S and Belcour, A and Rousvoal, S and Potin, P and Leblanc, C and Dittami, SM},
title = {A duo of fungi and complex and dynamic bacterial community networks contribute to shape the Ascophyllum nodosum holobiont.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-025-00825-z},
pmid = {41382286},
issn = {2524-6372},
support = {AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; },
abstract = {BACKGROUND: The brown alga Ascophyllum nodosum and its microbiota form a dynamic functional entity named holobiont. Some microbial partners may play a role in seaweed health through bioactive compounds crucial for normal morphology, development, and physiological acclimation. However, the full spectrum of the microbial diversity and its variations according to algal life stage, season, and location have not been comprehensively studied. This study uses 208 short-read metabarcoding samples to characterize the bacterial, archaeal, and microeukaryotic communities of A. nodosum across three nearby sites, four thallus parts, and a monthly survey, aiming to explore the dynamics of ecological interactions within the holobiont.
RESULTS: Our results revealed that A. nodosum harbors a predominantly bacterial microbiota, varying significantly across all covariables, while archaea were virtually absent. An innovative normalization using the co-amplified host reads provided an estimation of bacterial abundance, revealing a drastic decline in May, potentially linked to epidermal shedding. In contrast, fungal communities were stable, dominated by Mycophycias ascophylli and Moheitospora sp., which remained closely associated with the host year-round. We identified a core microbiome of 22 ASVs, consistently found in all samples, including Granulosicoccus, a genus consistently abundant in other brown algal microbiota. Sequence clustering revealed multiple species which vary according seasons, even in the overall stable Granulosicoccus genus. Co-occurrence network analysis revealed putative interactions between microbial groups in response to ecological niches.
CONCLUSIONS: Overall, these findings highlight the dynamic of bacterial interactions and stable fungal associations within the A. nodosum holobiont, providing new insights into the ecology of its microbiota.},
}
RevDate: 2025-12-11
Investigating the core microbiome concept: Daphnia as a case study.
Environmental microbiome pii:10.1186/s40793-025-00834-y [Epub ahead of print].
BACKGROUND: Host-associated microbiomes play an important role in the ecology and fitness of organisms. Given their significance, it is much debated to what extent these associations are widespread and even obligatory. Such frequent associations are captured by the concept of the core microbiome. The cladoceran Daphnia is a pivotal genus in freshwater ecosystems occupying a central position in the food webs of standing waters. With its unique standing in pelagic waters, Daphnia serves as a key grazer, regulating algal populations and nutrient cycling, making its microbiome essential to understanding ecosystem function and stability. In recent years, Daphnia has become an increasingly popular study system for exploring host‒microbiota interactions. There is, however, limited knowledge on the baseline taxa that consistently inhabit this host and potentially contribute to its fitness. Identifying whether such a host-associated "core microbiome" exists for Daphnia and, if so, which microbial taxa it comprises is important both for enhancing our ecological understanding of this genus and its ecosystem function and for interpreting future experiments.
RESULTS: We compiled a dataset on Daphnia magna microbiome based on 12 published studies, comprising gut and whole microbiome samples of both laboratory-cultured and field-grown animals across five countries spanning three continents. To identify core taxa, we employ quantification metrics based on prevalence and a combination of prevalence and relative abundance. Our analysis demonstrates that the D. magna microbiome is highly variable, yet, a consistent association with specific taxa, notably Limnohabitans planktonicus, is observed especially under laboratory conditions. However, this pattern is tempered by the observation that field-grown animals exhibit a more diverse microbiome with a weaker presence of L. planktonicus, challenging its status as a core member.
CONCLUSIONS: Our analysis suggests that the D. magna microbiome is defined by its high variability and few conserved associations, with L. planktonicus being the most stable taxon in laboratory settings but not necessarily a core member in natural environments. These findings underscore the need for caution when using laboratory results to interpret natural microbiome compositions and emphasize the need for further research on field-grown animals to better understand the structuring of microbial communities under natural settings.
Additional Links: PMID-41382248
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PubMed:
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@article {pmid41382248,
year = {2025},
author = {Gurung, A and Callens, M and Massol, F and Souffreau, C and Mukherjee, S and Houwenhuyse, S and Stoks, R and De Meester, L and Decaestecker, E},
title = {Investigating the core microbiome concept: Daphnia as a case study.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-025-00834-y},
pmid = {41382248},
issn = {2524-6372},
support = {C16/23/003//Onderzoeksraad, KU Leuven , Belgium/ ; G092619N, G014423N and G061824N//Fonds Wetenschappelijk Onderzoek/ ; },
abstract = {BACKGROUND: Host-associated microbiomes play an important role in the ecology and fitness of organisms. Given their significance, it is much debated to what extent these associations are widespread and even obligatory. Such frequent associations are captured by the concept of the core microbiome. The cladoceran Daphnia is a pivotal genus in freshwater ecosystems occupying a central position in the food webs of standing waters. With its unique standing in pelagic waters, Daphnia serves as a key grazer, regulating algal populations and nutrient cycling, making its microbiome essential to understanding ecosystem function and stability. In recent years, Daphnia has become an increasingly popular study system for exploring host‒microbiota interactions. There is, however, limited knowledge on the baseline taxa that consistently inhabit this host and potentially contribute to its fitness. Identifying whether such a host-associated "core microbiome" exists for Daphnia and, if so, which microbial taxa it comprises is important both for enhancing our ecological understanding of this genus and its ecosystem function and for interpreting future experiments.
RESULTS: We compiled a dataset on Daphnia magna microbiome based on 12 published studies, comprising gut and whole microbiome samples of both laboratory-cultured and field-grown animals across five countries spanning three continents. To identify core taxa, we employ quantification metrics based on prevalence and a combination of prevalence and relative abundance. Our analysis demonstrates that the D. magna microbiome is highly variable, yet, a consistent association with specific taxa, notably Limnohabitans planktonicus, is observed especially under laboratory conditions. However, this pattern is tempered by the observation that field-grown animals exhibit a more diverse microbiome with a weaker presence of L. planktonicus, challenging its status as a core member.
CONCLUSIONS: Our analysis suggests that the D. magna microbiome is defined by its high variability and few conserved associations, with L. planktonicus being the most stable taxon in laboratory settings but not necessarily a core member in natural environments. These findings underscore the need for caution when using laboratory results to interpret natural microbiome compositions and emphasize the need for further research on field-grown animals to better understand the structuring of microbial communities under natural settings.},
}
RevDate: 2025-12-11
Multi-meta-omics reveal unique symbiotic synchronization between ectomycorrhizal fungus and soil microbiome in Tricholoma matsutake habitat.
Microbiome pii:10.1186/s40168-025-02292-7 [Epub ahead of print].
BACKGROUND: Ectomycorrhizal (ECM) fungi establish symbiotic relationships with plant roots, enhancing nutrient uptake, improving plant health, and boosting ecosystem resilience. Although previous studies reported molecular interactions among plant-ECM fungi-surrounding microbes near plant roots, microbiome-wide metabolic shifts and associations with the fungi remain unclear.
RESULTS: Using Tricholoma matsutake as a model, we initially found that T. matsutake induced remarkable microbial community turnover linked to altered soil moisture, nitrogen, and phosphorus levels. Parallel with the compositional alteration, microbiome-wide metabolic capacities, including glutamate metabolism, oligopeptide transport, and siderophore activity, were enriched in the T. matsutake-colonizing soil compared to the soils where the fungus was not colonized. From metatranscriptome data, we found that T. matsutake induced functional remodeling in nitrogen metabolism. Notably, the fungus and soil microbiome were metabolically synchronized with the upregulation of nitrate reduction, glutamate biosynthesis, tryptophan biosynthesis, and indole-3-acetic acid (IAA) biosynthesis. Metabarcoding and metatranscriptome-guided microbial associations revealed potential T. matsutake helper bacteria consisting of Conexibacter and Paraburkholderia. Phage community analyses further showed that the colonization of the ECM fungus influenced phage distributions along with the increase in temperate phage populations. The differential expression of auxiliary metabolic genes also demonstrated that phages could influence bacterial fitness in response to T. matsutake colonization.
CONCLUSION: Our multi-meta-omics-based approaches revealed unique environmental changes by T. matsutake compared to other mycorrhizal systems, as well as metabolic synchronization between the ECM fungus and surrounding microbiomes. These findings will expand our understanding of ECM symbiotic frameworks by highlighting integrated microbial and viral metabolic dynamics. Video Abstract.
Additional Links: PMID-41382244
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PubMed:
Citation:
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@article {pmid41382244,
year = {2025},
author = {Bae, IH and Kim, H and Kim, SM and Lee, YH},
title = {Multi-meta-omics reveal unique symbiotic synchronization between ectomycorrhizal fungus and soil microbiome in Tricholoma matsutake habitat.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02292-7},
pmid = {41382244},
issn = {2049-2618},
support = {RS-2022-NR072199//National Research Foundation of Korea/ ; RS-2025-00512558//National Research Foundation of Korea/ ; },
abstract = {BACKGROUND: Ectomycorrhizal (ECM) fungi establish symbiotic relationships with plant roots, enhancing nutrient uptake, improving plant health, and boosting ecosystem resilience. Although previous studies reported molecular interactions among plant-ECM fungi-surrounding microbes near plant roots, microbiome-wide metabolic shifts and associations with the fungi remain unclear.
RESULTS: Using Tricholoma matsutake as a model, we initially found that T. matsutake induced remarkable microbial community turnover linked to altered soil moisture, nitrogen, and phosphorus levels. Parallel with the compositional alteration, microbiome-wide metabolic capacities, including glutamate metabolism, oligopeptide transport, and siderophore activity, were enriched in the T. matsutake-colonizing soil compared to the soils where the fungus was not colonized. From metatranscriptome data, we found that T. matsutake induced functional remodeling in nitrogen metabolism. Notably, the fungus and soil microbiome were metabolically synchronized with the upregulation of nitrate reduction, glutamate biosynthesis, tryptophan biosynthesis, and indole-3-acetic acid (IAA) biosynthesis. Metabarcoding and metatranscriptome-guided microbial associations revealed potential T. matsutake helper bacteria consisting of Conexibacter and Paraburkholderia. Phage community analyses further showed that the colonization of the ECM fungus influenced phage distributions along with the increase in temperate phage populations. The differential expression of auxiliary metabolic genes also demonstrated that phages could influence bacterial fitness in response to T. matsutake colonization.
CONCLUSION: Our multi-meta-omics-based approaches revealed unique environmental changes by T. matsutake compared to other mycorrhizal systems, as well as metabolic synchronization between the ECM fungus and surrounding microbiomes. These findings will expand our understanding of ECM symbiotic frameworks by highlighting integrated microbial and viral metabolic dynamics. Video Abstract.},
}
RevDate: 2025-12-11
Harnessing haloarchaea from halophyte Atriplex nummularia rhizosphere to enhance salt stress tolerance in maize seedlings.
Environmental microbiome pii:10.1186/s40793-025-00698-2 [Epub ahead of print].
Soil salinization is a critical global issue threatening agricultural productivity and significantly reducing the availability of arable land. Effective mitigation and recovery strategies are vital for sustaining food production, especially in the context of climate change. Halophytic plants, such as Atriplex nummularia, have shown potential for remediating saline soils, though their large-scale application remains limited. An alternative approach involves leveraging microorganisms adapted to saline environments to enhance plant stress tolerance. In this study, we investigated the microbiome of A. nummularia under saline and non-saline irrigation conditions to identify extremophilic microorganisms that promote salt stress tolerance. Through 16S rRNA analysis, we identified members of the genus Haladaptatus exclusively in the rhizosphere of salt-irrigated plants. These microorganisms were isolated and inoculated into maize crop systems to evaluate their ability to confer salt tolerance. Our results demonstrate that Haladaptatus strains significantly enhance salinity tolerance in maize, with a marked increase in the relative abundance of archaeal 16S rRNA in soils as NaCl irrigation levels rise. This study provides the first evidence that Haladaptatus, an archaeon isolated from the rhizosphere of a halophyte, can significantly enhance salt tolerance in an agriculturally important crop. These findings suggest a promising biotechnological application for improving crop resilience in saline environments, offering a sustainable strategy for addressing soil salinization and securing food production in the context of global climate challenges.
Additional Links: PMID-41382235
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@article {pmid41382235,
year = {2025},
author = {Ventura, JP and Lacerda-Júnior, GV and Rados, T and Bisson, A and Fernandes-Júnior, PI and Melo, IS},
title = {Harnessing haloarchaea from halophyte Atriplex nummularia rhizosphere to enhance salt stress tolerance in maize seedlings.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-025-00698-2},
pmid = {41382235},
issn = {2524-6372},
abstract = {Soil salinization is a critical global issue threatening agricultural productivity and significantly reducing the availability of arable land. Effective mitigation and recovery strategies are vital for sustaining food production, especially in the context of climate change. Halophytic plants, such as Atriplex nummularia, have shown potential for remediating saline soils, though their large-scale application remains limited. An alternative approach involves leveraging microorganisms adapted to saline environments to enhance plant stress tolerance. In this study, we investigated the microbiome of A. nummularia under saline and non-saline irrigation conditions to identify extremophilic microorganisms that promote salt stress tolerance. Through 16S rRNA analysis, we identified members of the genus Haladaptatus exclusively in the rhizosphere of salt-irrigated plants. These microorganisms were isolated and inoculated into maize crop systems to evaluate their ability to confer salt tolerance. Our results demonstrate that Haladaptatus strains significantly enhance salinity tolerance in maize, with a marked increase in the relative abundance of archaeal 16S rRNA in soils as NaCl irrigation levels rise. This study provides the first evidence that Haladaptatus, an archaeon isolated from the rhizosphere of a halophyte, can significantly enhance salt tolerance in an agriculturally important crop. These findings suggest a promising biotechnological application for improving crop resilience in saline environments, offering a sustainable strategy for addressing soil salinization and securing food production in the context of global climate challenges.},
}
RevDate: 2025-12-11
Intestinal congestion-driven gut dysbiosis: a cross-disease hemodynamic mechanism in liver cirrhosis and heart failure.
Journal of translational medicine pii:10.1186/s12967-025-07547-3 [Epub ahead of print].
Additional Links: PMID-41382117
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PubMed:
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@article {pmid41382117,
year = {2025},
author = {Wang, Y and Bai, Z and Sun, J and Gong, Q and Miao, W and Niu, Z and Li, X and Xu, J and Lai, Z},
title = {Intestinal congestion-driven gut dysbiosis: a cross-disease hemodynamic mechanism in liver cirrhosis and heart failure.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-025-07547-3},
pmid = {41382117},
issn = {1479-5876},
support = {SYYYRC-2022006//First Hospital of Shanxi Medical University/ ; 202103021224408//Natural Science Foundation of Shanxi Province/ ; 202203021221248//Natural Science Foundation of Shanxi Province/ ; 202204010931008//Shanxi Provincial Science and Technology Department/ ; YDZJSX2021B012//Shanxi Provincial Science and Technology Department/ ; 82470693//Innovative Research Group Project of the National Natural Science Foundation of China/ ; 2023065//Health Commission of Shanxi Province/ ; },
}
RevDate: 2025-12-12
CmpDate: 2025-12-12
Myco- and microbiological profiling of a human cadaver reveals drug-resistant strains and new fungal records.
Applied microbiology and biotechnology, 109(1):268.
In this study, the composition of the postmortem mycobiome and microbiome of a cadaver in an advanced stage of decomposition, had been deposited outdoors and showed extensive mycelial growth, was characterized using culture methods. This approach allowed for the identification of a total of 26 fungal and 16 bacterial species. The dominant fungal species were Penicillium polonicum, Debaryomyces hansenii, and Penicillium commune. Sensitivity tests for voriconazole and amphotericin B were also performed, to which several isolates were resistant. In the case of bacteria, the distribution of dominant species differed between samples taken from outside the body and samples taken from inside the body. Sensitivity tests for 16 antibiotics showed that 23.08% of isolates were resistant to the tested drugs. Importantly, to the best of our knowledge, we detected several species that have not been previously associated with cadavers: Botryotrichum domesticum, Chaetomium subaffine, Penicillium allii, Scopulariopsis crassa, Scopulariopsis fusca and Yarrowia deformans. These results not only expand our understanding of the ecological roles of fungi in cadaver decomposition but also highlight their potential forensic value. First and foremost, it broadens our understanding of local fungal communities associated with human remains, which in the future may provide valuable information about the location or environmental conditions of body deposition, while specific taxa could assist in estimating the postmortem interval. Moreover, the identification of drug-resistant strains underscores the importance of biosafety in forensic practice and raises awareness of the potential for pathogen dissemination from decomposing remains. KEY POINTS: • Twenty-six fungi and sixteen bacterial species were identified from the cadaver • New fungal records isolated from human remains, expanding forensic mycology knowledge • Antimicrobial susceptibility testing revealed the presence of drug-resistant fungal and bacterial isolates.
Additional Links: PMID-41381939
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@article {pmid41381939,
year = {2025},
author = {Spychała, K and Piecuch, A and Korzekwa, K and Szleszkowski, Ł and Thannhäuser, A and Siuta, J and Kadej, M and Ogórek, R},
title = {Myco- and microbiological profiling of a human cadaver reveals drug-resistant strains and new fungal records.},
journal = {Applied microbiology and biotechnology},
volume = {109},
number = {1},
pages = {268},
pmid = {41381939},
issn = {1432-0614},
mesh = {Humans ; Cadaver ; *Fungi/drug effects/isolation & purification/classification/genetics ; Microbial Sensitivity Tests ; *Bacteria/drug effects/isolation & purification/classification/genetics ; Antifungal Agents/pharmacology ; *Drug Resistance, Fungal ; *Mycobiome ; Anti-Bacterial Agents/pharmacology ; Microbiota ; },
abstract = {In this study, the composition of the postmortem mycobiome and microbiome of a cadaver in an advanced stage of decomposition, had been deposited outdoors and showed extensive mycelial growth, was characterized using culture methods. This approach allowed for the identification of a total of 26 fungal and 16 bacterial species. The dominant fungal species were Penicillium polonicum, Debaryomyces hansenii, and Penicillium commune. Sensitivity tests for voriconazole and amphotericin B were also performed, to which several isolates were resistant. In the case of bacteria, the distribution of dominant species differed between samples taken from outside the body and samples taken from inside the body. Sensitivity tests for 16 antibiotics showed that 23.08% of isolates were resistant to the tested drugs. Importantly, to the best of our knowledge, we detected several species that have not been previously associated with cadavers: Botryotrichum domesticum, Chaetomium subaffine, Penicillium allii, Scopulariopsis crassa, Scopulariopsis fusca and Yarrowia deformans. These results not only expand our understanding of the ecological roles of fungi in cadaver decomposition but also highlight their potential forensic value. First and foremost, it broadens our understanding of local fungal communities associated with human remains, which in the future may provide valuable information about the location or environmental conditions of body deposition, while specific taxa could assist in estimating the postmortem interval. Moreover, the identification of drug-resistant strains underscores the importance of biosafety in forensic practice and raises awareness of the potential for pathogen dissemination from decomposing remains. KEY POINTS: • Twenty-six fungi and sixteen bacterial species were identified from the cadaver • New fungal records isolated from human remains, expanding forensic mycology knowledge • Antimicrobial susceptibility testing revealed the presence of drug-resistant fungal and bacterial isolates.},
}
MeSH Terms:
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Humans
Cadaver
*Fungi/drug effects/isolation & purification/classification/genetics
Microbial Sensitivity Tests
*Bacteria/drug effects/isolation & purification/classification/genetics
Antifungal Agents/pharmacology
*Drug Resistance, Fungal
*Mycobiome
Anti-Bacterial Agents/pharmacology
Microbiota
RevDate: 2025-12-11
Declining FXR expression coordinates neonatal beta cell mass development with microbial bile acid metabolism maturation in mice.
Diabetologia [Epub ahead of print].
AIMS/HYPOTHESIS: Diet switch during weaning induces gut microbiome maturation, accompanied by the formation of adequate functional beta cell mass. Bile acid (BA), an essential microbial metabolite, regulates host glucose homeostasis by binding to its main receptor, farnesoid X receptor (FXR, encoded by NR1H4). However, the precise roles of microbial BA metabolism and FXR signalling in neonatal beta cell development are still unclear.
METHODS: Islet FXR levels were determined at different perinatal stages. Postnatal changes in gut microbiome and BA profiles were examined in mice, with changes in germ-free mouse BAs serving as the control. We genetically modified beta cells to sustain FXR expression after birth (using Nr1h4-knockin [βFxrKI] mice) and performed morphological and functional analysis on murine islets. Single-cell RNA-seq and single-cell assay for transposase-accessible chromatin sequencing of islet cells were used to study FXR-mediated downstream regulation in islets. Lineage tracing was performed to evaluate beta cell fate transition. Mendelian randomisation (MR) and human islet proteomics data analysis were applied to study the pathological relevance in human diabetes.
RESULTS: FXR expression in beta cells declined after birth (positive cell proportion, 29.1 ± 3.1% at embryonic day 18.5 vs 4.2 ± 2.4% at 3 weeks postnatal in mice, p<0.001). This physiological change paralleled the ascending of FXR-agonistic BAs derived from gut microbiome maturation (unconjugated BA proportion, 0.9 ± 0.6% at 1 week vs 14.0 ± 5.6% at 3 weeks, p<0.05). βFxrKI mice had limited beta cell mass growth (approximately 70% of the control level at 1 week of age and only 15% of the control level at 8 weeks of age) and developed high blood glucose levels by weaning (random blood glucose, 15.2 ± 1.7 mmol/l in βFxrKI vs 7.7 ± 0.5 mmol/l in control, p<0.001), mainly resulting from elevated cell apoptosis (1.95-, 1.79-, and 3.27-fold increase vs control at 1, 2 and 3 weeks, respectively) and altered beta cell identity. Casp6 was identified as a key downstream target in beta cell FXR. Intervention with antibiotics or a specific caspase-6 (CASP6) inhibitor partially recovered the phenotypes of βFxrKI mice. Further validation in humans showed that islet FXR/CASP6 levels were elevated in individuals with type 2 diabetes (FXR, -0.039 ± 1.257 a.u. in donors without diabetes vs 0.646 ± 1.140 a.u. in donors with diabetes, p=0.0371; CASP6, -1.575 ± 0.307 a.u. in donors without diabetes vs -1.325 ± 0.381 a.u. in donors with diabetes, p=0.011). MR analysis further supported the effect of human islet FXR expression in elevating HbA1c (β=0.006, p<0.001) with lowering fasting insulin level (β=-0.009, p=0.02) and the effect of CASP6 expression in enhancing 2 h glucose (β=0.039, p=0.01).
CONCLUSIONS/INTERPRETATION: The declining FXR-CASP6 signals in neonatal beta cells could serve as a programmed host response to the maturing gut microbial BA metabolism to maintain normal postnatal beta cell mass development and ensure glycaemic homeostasis in adults.
DATA AVAILABILITY: Raw data of scRNA-seq and scATAC-seq are deposited in the Gene Expression Omnibus (GEO) database under the accession number GSE241408. The code used in this Mendelian randomisation study is publicly available at https://github.com/Angela-linyt/Gene_Glu_MR.git .
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@article {pmid41381886,
year = {2025},
author = {Fu, C and Li, T and Hao, Y and Lin, Y and Qiu, Y and Jia, Y and Yang, J and Liu, B and Hua, D and Wang, C and Chen, T and Piron, A and Cnop, M and Ni, Q and Zheng, J and Ning, G and Gu, Y},
title = {Declining FXR expression coordinates neonatal beta cell mass development with microbial bile acid metabolism maturation in mice.},
journal = {Diabetologia},
volume = {},
number = {},
pages = {},
pmid = {41381886},
issn = {1432-0428},
support = {82100835//National Natural Science Foundation of China/ ; 92157112//National Natural Science Foundation of China/ ; },
abstract = {AIMS/HYPOTHESIS: Diet switch during weaning induces gut microbiome maturation, accompanied by the formation of adequate functional beta cell mass. Bile acid (BA), an essential microbial metabolite, regulates host glucose homeostasis by binding to its main receptor, farnesoid X receptor (FXR, encoded by NR1H4). However, the precise roles of microbial BA metabolism and FXR signalling in neonatal beta cell development are still unclear.
METHODS: Islet FXR levels were determined at different perinatal stages. Postnatal changes in gut microbiome and BA profiles were examined in mice, with changes in germ-free mouse BAs serving as the control. We genetically modified beta cells to sustain FXR expression after birth (using Nr1h4-knockin [βFxrKI] mice) and performed morphological and functional analysis on murine islets. Single-cell RNA-seq and single-cell assay for transposase-accessible chromatin sequencing of islet cells were used to study FXR-mediated downstream regulation in islets. Lineage tracing was performed to evaluate beta cell fate transition. Mendelian randomisation (MR) and human islet proteomics data analysis were applied to study the pathological relevance in human diabetes.
RESULTS: FXR expression in beta cells declined after birth (positive cell proportion, 29.1 ± 3.1% at embryonic day 18.5 vs 4.2 ± 2.4% at 3 weeks postnatal in mice, p<0.001). This physiological change paralleled the ascending of FXR-agonistic BAs derived from gut microbiome maturation (unconjugated BA proportion, 0.9 ± 0.6% at 1 week vs 14.0 ± 5.6% at 3 weeks, p<0.05). βFxrKI mice had limited beta cell mass growth (approximately 70% of the control level at 1 week of age and only 15% of the control level at 8 weeks of age) and developed high blood glucose levels by weaning (random blood glucose, 15.2 ± 1.7 mmol/l in βFxrKI vs 7.7 ± 0.5 mmol/l in control, p<0.001), mainly resulting from elevated cell apoptosis (1.95-, 1.79-, and 3.27-fold increase vs control at 1, 2 and 3 weeks, respectively) and altered beta cell identity. Casp6 was identified as a key downstream target in beta cell FXR. Intervention with antibiotics or a specific caspase-6 (CASP6) inhibitor partially recovered the phenotypes of βFxrKI mice. Further validation in humans showed that islet FXR/CASP6 levels were elevated in individuals with type 2 diabetes (FXR, -0.039 ± 1.257 a.u. in donors without diabetes vs 0.646 ± 1.140 a.u. in donors with diabetes, p=0.0371; CASP6, -1.575 ± 0.307 a.u. in donors without diabetes vs -1.325 ± 0.381 a.u. in donors with diabetes, p=0.011). MR analysis further supported the effect of human islet FXR expression in elevating HbA1c (β=0.006, p<0.001) with lowering fasting insulin level (β=-0.009, p=0.02) and the effect of CASP6 expression in enhancing 2 h glucose (β=0.039, p=0.01).
CONCLUSIONS/INTERPRETATION: The declining FXR-CASP6 signals in neonatal beta cells could serve as a programmed host response to the maturing gut microbial BA metabolism to maintain normal postnatal beta cell mass development and ensure glycaemic homeostasis in adults.
DATA AVAILABILITY: Raw data of scRNA-seq and scATAC-seq are deposited in the Gene Expression Omnibus (GEO) database under the accession number GSE241408. The code used in this Mendelian randomisation study is publicly available at https://github.com/Angela-linyt/Gene_Glu_MR.git .},
}
RevDate: 2025-12-11
Endoscopic swab sampling as a novel method for gastric Microbiome profiling: A pilot study compared with tissue biopsy.
Scientific reports pii:10.1038/s41598-025-32028-4 [Epub ahead of print].
Additional Links: PMID-41381881
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@article {pmid41381881,
year = {2025},
author = {Park, G and Chung, H},
title = {Endoscopic swab sampling as a novel method for gastric Microbiome profiling: A pilot study compared with tissue biopsy.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-025-32028-4},
pmid = {41381881},
issn = {2045-2322},
}
RevDate: 2025-12-11
Bacterial Carbonic Anhydrase Inhibitor CAI0019 Demonstrates Efficacy in Enterococcus faecium Septicemic Peritonitis Mouse Model While Sparing the Microbiome.
ACS infectious diseases [Epub ahead of print].
Vancomycin-resistant enterococci are multidrug-resistant bacteria that as of 2021 continue to pervade the U.S. healthcare system as the second-most prevalent source of healthcare-acquired infections behind Escherichia coli. Given the limited treatment options for vancomycin-resistant enterococci and growing concerns about antibiotic-induced gut microbiome dysbiosis, there is an urgent need for narrow-spectrum antibiotics that can selectively target vancomycin-resistant enterococci while preserving the integrity of the gut microbiome. Previous studies have demonstrated the in vivo potential of orally dosed acetazolamide-based compounds to reduce vancomycin-resistant enterococci bioburden in the gastrointestinal tract and internal organs of mice. However, while it is hypothesized that these molecules inhibit bacterial carbonic anhydrases, the exact target of the acetazolamide scaffold in vancomycin-resistant enterococci has remained unconfirmed. Additionally, the impact of the scaffold on in vivo gut microbiome diversity remains uncharacterized. The work herein reports the chemoproteomic identification of α-carbonic anhydrase as the primary target of the acetazolamide scaffold in E. faecium and presents its uniqueness as a narrow-spectrum antibiotic target that can be exploited by CAI0019, a lead acetazolamide derivative with in vivo efficacy, while sparing gut microbiome diversity in mice. This work presents compelling data that not only confirm α-carbonic anhydrase as an antibiotic target in Enterococcus but also demonstrate that narrow-spectrum in vivo antienterococcal efficacy can be achieved through targeting α-carbonic anhydrase such that gut commensal microbiota remain unimpacted.
Additional Links: PMID-41381410
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@article {pmid41381410,
year = {2025},
author = {Abutaleb, NS and Holly, KJ and Metcalfe, CK and Abouelkhair, AA and Tharra, PR and Shrinidhi, A and Abdelsattar, AS and Burgo, V and Melotte, G and Akin-Olabiyi, T and Knoblauch, S and Ramaswamy, R and Woodson, C and Thirumalaikumar, VP and Rodriguez, JA and Yeo, FJ and Snell, OC and Nocentini, A and Sundararajan, A and Olson, MR and Supuran, CT and Seleem, MN and Flaherty, DP},
title = {Bacterial Carbonic Anhydrase Inhibitor CAI0019 Demonstrates Efficacy in Enterococcus faecium Septicemic Peritonitis Mouse Model While Sparing the Microbiome.},
journal = {ACS infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1021/acsinfecdis.5c00736},
pmid = {41381410},
issn = {2373-8227},
abstract = {Vancomycin-resistant enterococci are multidrug-resistant bacteria that as of 2021 continue to pervade the U.S. healthcare system as the second-most prevalent source of healthcare-acquired infections behind Escherichia coli. Given the limited treatment options for vancomycin-resistant enterococci and growing concerns about antibiotic-induced gut microbiome dysbiosis, there is an urgent need for narrow-spectrum antibiotics that can selectively target vancomycin-resistant enterococci while preserving the integrity of the gut microbiome. Previous studies have demonstrated the in vivo potential of orally dosed acetazolamide-based compounds to reduce vancomycin-resistant enterococci bioburden in the gastrointestinal tract and internal organs of mice. However, while it is hypothesized that these molecules inhibit bacterial carbonic anhydrases, the exact target of the acetazolamide scaffold in vancomycin-resistant enterococci has remained unconfirmed. Additionally, the impact of the scaffold on in vivo gut microbiome diversity remains uncharacterized. The work herein reports the chemoproteomic identification of α-carbonic anhydrase as the primary target of the acetazolamide scaffold in E. faecium and presents its uniqueness as a narrow-spectrum antibiotic target that can be exploited by CAI0019, a lead acetazolamide derivative with in vivo efficacy, while sparing gut microbiome diversity in mice. This work presents compelling data that not only confirm α-carbonic anhydrase as an antibiotic target in Enterococcus but also demonstrate that narrow-spectrum in vivo antienterococcal efficacy can be achieved through targeting α-carbonic anhydrase such that gut commensal microbiota remain unimpacted.},
}
RevDate: 2025-12-11
Longitudinal analysis of gut microbiota dysbiosis and bacterial signatures predictive of postoperative enterocolitis in children with Hirschsprung disease.
Clinical and experimental pediatrics pii:cep.2025.01886 [Epub ahead of print].
BACKGROUND: We aimed to investigate differences in gut microbiota between patients with Hirschsprung disease (HSCR) and healthy children; assess longitudinal changes in the microbiota of patients with HSCR from diagnosis through postoperative period; and identify microbial markers predictive of postoperative HSCR-associated enterocolitis (HAEC).
PURPOSE: To investigate alterations in the gut microbiota of patients with HSCR by assessing longitudinal microbiome changes after surgery and identifying microbial signatures predictive of postoperative HAEC.
METHODS: A case-control study of 20 patients with HSCR and 20 controls was conducted at Maharaj Nakorn Chiang Mai Hospital. Fecal specimens were collected from patients with HSCR at initial diagnosis and from age-matched controls. Additional samples were obtained from patients intraoperatively and at 1 and 6 months postoperatively. A microbial analysis was performed using 16S rRNA gene sequencing (V3-V4 hypervariable regions).
RESULTS: Compared to controls, patients with HSCR exhibited gut dysbiosis characterized by reduced microbial diversity and altered community composition as determined by Analysis of Compositions of Microbiomes with Bias Correction. Increased relative abundances of Robinsoniella, Fusobacterium, Cutibacterium, Citrobacter, and Eubacterium fissicatena were observed in patients with HSCR, whereas NK4A214, Lachnospiraceae XPB1014 groups, Acinetobacter and Acetitomaculum were decreased (q< 0.05). Alpha diversity in patients with HSCR was significantly increased at 6 months postoperatively versus at theinitial diagnosis (P<0.05). Longitudinal changes in Eubacterium and Eubacteriales suggest their potential use as markers of treatment efficacy. In patients who developed postoperative HAEC, Olsenella was enriched in the proximal intestine, whereas Holdemanella, Corynebacterium, Collinsella, and CAG-352 were elevated in the distal intestine (q<0.05).
CONCLUSION: Patients with HSCR exhibited distinct alterations in the gut microbiota, with significant shifts observed between the pretreatment period and 6 months postoperatively. Specific bacterial taxa were identified as potential markers for HAEC development. Future microbiome- targeted.
Additional Links: PMID-41381080
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@article {pmid41381080,
year = {2025},
author = {Chantakhow, S and Kunasol, C and Khorana, J and Tepmalai, K and Chattipakorn, N and Chattipakorn, SC},
title = {Longitudinal analysis of gut microbiota dysbiosis and bacterial signatures predictive of postoperative enterocolitis in children with Hirschsprung disease.},
journal = {Clinical and experimental pediatrics},
volume = {},
number = {},
pages = {},
doi = {10.3345/cep.2025.01886},
pmid = {41381080},
issn = {2713-4148},
abstract = {BACKGROUND: We aimed to investigate differences in gut microbiota between patients with Hirschsprung disease (HSCR) and healthy children; assess longitudinal changes in the microbiota of patients with HSCR from diagnosis through postoperative period; and identify microbial markers predictive of postoperative HSCR-associated enterocolitis (HAEC).
PURPOSE: To investigate alterations in the gut microbiota of patients with HSCR by assessing longitudinal microbiome changes after surgery and identifying microbial signatures predictive of postoperative HAEC.
METHODS: A case-control study of 20 patients with HSCR and 20 controls was conducted at Maharaj Nakorn Chiang Mai Hospital. Fecal specimens were collected from patients with HSCR at initial diagnosis and from age-matched controls. Additional samples were obtained from patients intraoperatively and at 1 and 6 months postoperatively. A microbial analysis was performed using 16S rRNA gene sequencing (V3-V4 hypervariable regions).
RESULTS: Compared to controls, patients with HSCR exhibited gut dysbiosis characterized by reduced microbial diversity and altered community composition as determined by Analysis of Compositions of Microbiomes with Bias Correction. Increased relative abundances of Robinsoniella, Fusobacterium, Cutibacterium, Citrobacter, and Eubacterium fissicatena were observed in patients with HSCR, whereas NK4A214, Lachnospiraceae XPB1014 groups, Acinetobacter and Acetitomaculum were decreased (q< 0.05). Alpha diversity in patients with HSCR was significantly increased at 6 months postoperatively versus at theinitial diagnosis (P<0.05). Longitudinal changes in Eubacterium and Eubacteriales suggest their potential use as markers of treatment efficacy. In patients who developed postoperative HAEC, Olsenella was enriched in the proximal intestine, whereas Holdemanella, Corynebacterium, Collinsella, and CAG-352 were elevated in the distal intestine (q<0.05).
CONCLUSION: Patients with HSCR exhibited distinct alterations in the gut microbiota, with significant shifts observed between the pretreatment period and 6 months postoperatively. Specific bacterial taxa were identified as potential markers for HAEC development. Future microbiome- targeted.},
}
RevDate: 2025-12-11
Why Is the Current Monitoring of Rodentibacter spp. Exclusively by Molecular Methods Insufficient?.
Journal of the American Association for Laboratory Animal Science : JAALAS [Epub ahead of print].
The former [Pasteurella] pneumotropica complex has rendered until now 12 Rodentibacter species, which has implications in the monitoring of these highly prevalent laboratory rodent microorganisms. Rodentibacter spp. are known as classic opportunistic pathogens of laboratory rodents and represent noteworthy members of the oral and genital microbiome, with potential pathophysiological interferences in colonized animals. Laboratory mice and rats are predominantly colonized by host-specific Rodentibacter spp., with R. pneumotropicus and R. heylii as mouse-specific species and R. ratti, R. heidelbergensis, R. rarus, and R. trehalosifermentans as rat-specific species; however, host specificity of R. haemolyticus, currently prevalent in both species, remains to be elucidated. Nevertheless, cross contaminations with the taxa from the opposite host occurs between mice and rats. The monitoring occurs by classic culture and/or by molecular techniques, although the latter are currently available only for a few Rodentibacter taxa. Unfortunately, many current health monitoring strategies do not take into consideration the host specificities of these taxa and are often focused nearly exclusively on the molecular diagnostics of R. pneumotropicus and R. heylii, thus neglecting the remaining taxa. Until future research addresses the lack of molecular tests available for all relevant Rodentibacter spp. and a host-specific monitoring is implemented, we consider that monitoring exclusively by current molecular methods risks missing opportunistic members of this genus. Importing laboratory rodents based on health reports relying solely on molecular assays is currently associated with an increased risk of accepting Rodentibacter-positive animals.
Additional Links: PMID-41381065
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@article {pmid41381065,
year = {2025},
author = {Benga, L and Benten, WPM and Bischoff, SJ and Christensen, H},
title = {Why Is the Current Monitoring of Rodentibacter spp. Exclusively by Molecular Methods Insufficient?.},
journal = {Journal of the American Association for Laboratory Animal Science : JAALAS},
volume = {},
number = {},
pages = {1-4},
doi = {10.30802/AALAS-JAALAS-25-143},
pmid = {41381065},
issn = {2769-6677},
abstract = {The former [Pasteurella] pneumotropica complex has rendered until now 12 Rodentibacter species, which has implications in the monitoring of these highly prevalent laboratory rodent microorganisms. Rodentibacter spp. are known as classic opportunistic pathogens of laboratory rodents and represent noteworthy members of the oral and genital microbiome, with potential pathophysiological interferences in colonized animals. Laboratory mice and rats are predominantly colonized by host-specific Rodentibacter spp., with R. pneumotropicus and R. heylii as mouse-specific species and R. ratti, R. heidelbergensis, R. rarus, and R. trehalosifermentans as rat-specific species; however, host specificity of R. haemolyticus, currently prevalent in both species, remains to be elucidated. Nevertheless, cross contaminations with the taxa from the opposite host occurs between mice and rats. The monitoring occurs by classic culture and/or by molecular techniques, although the latter are currently available only for a few Rodentibacter taxa. Unfortunately, many current health monitoring strategies do not take into consideration the host specificities of these taxa and are often focused nearly exclusively on the molecular diagnostics of R. pneumotropicus and R. heylii, thus neglecting the remaining taxa. Until future research addresses the lack of molecular tests available for all relevant Rodentibacter spp. and a host-specific monitoring is implemented, we consider that monitoring exclusively by current molecular methods risks missing opportunistic members of this genus. Importing laboratory rodents based on health reports relying solely on molecular assays is currently associated with an increased risk of accepting Rodentibacter-positive animals.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Transitions in lung microbiota landscape associate with distinct patterns of pneumonia progression.
Cell host & microbe, 33(12):2148-2166.e8.
The precise microbial determinants driving clinical outcomes in severe pneumonia are unknown. Competing ecological forces produce dynamic microbiota states in health and disease, and a more thorough understanding of these states has the potential to improve pneumonia therapy. Here, we leverage a large collection of bronchoscopic samples from patients with suspected pneumonia to determine lung microbial ecosystem dynamics throughout the course of pneumonia. We combine 16S rRNA gene, metagenomic, and metatranscriptomic sequencing with bacterial-load quantification to reveal clinically relevant drivers of pneumonia progression. Microbiota states are predictive of pneumonia subtypes and exhibit differential stability and pneumonia therapy response. Disruptive forces, such as aspiration, are associated with cohesive changes in gene expression and microbial community structure. In summary, we show that host and microbiota landscapes change in unison with clinical phenotypes and that microbiota state dynamics reflect pneumonia progression. We suggest that distinct pathways of lung microbial community succession mediate pneumonia progression.
Additional Links: PMID-41380668
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@article {pmid41380668,
year = {2025},
author = {Sumner, JT and Huttelmaier, S and Pickens, CI and Moghadam, AA and Abdala-Valencia, H and Shen, J and , and Hauser, AR and Seed, PC and Wunderink, RG and Hartmann, EM},
title = {Transitions in lung microbiota landscape associate with distinct patterns of pneumonia progression.},
journal = {Cell host & microbe},
volume = {33},
number = {12},
pages = {2148-2166.e8},
doi = {10.1016/j.chom.2025.11.011},
pmid = {41380668},
issn = {1934-6069},
mesh = {Humans ; *Microbiota/genetics ; *Lung/microbiology ; Disease Progression ; RNA, Ribosomal, 16S/genetics ; *Pneumonia/microbiology/pathology ; Metagenomics ; Bacteria/classification/genetics/isolation & purification ; Male ; Female ; Bacterial Load ; Middle Aged ; Aged ; },
abstract = {The precise microbial determinants driving clinical outcomes in severe pneumonia are unknown. Competing ecological forces produce dynamic microbiota states in health and disease, and a more thorough understanding of these states has the potential to improve pneumonia therapy. Here, we leverage a large collection of bronchoscopic samples from patients with suspected pneumonia to determine lung microbial ecosystem dynamics throughout the course of pneumonia. We combine 16S rRNA gene, metagenomic, and metatranscriptomic sequencing with bacterial-load quantification to reveal clinically relevant drivers of pneumonia progression. Microbiota states are predictive of pneumonia subtypes and exhibit differential stability and pneumonia therapy response. Disruptive forces, such as aspiration, are associated with cohesive changes in gene expression and microbial community structure. In summary, we show that host and microbiota landscapes change in unison with clinical phenotypes and that microbiota state dynamics reflect pneumonia progression. We suggest that distinct pathways of lung microbial community succession mediate pneumonia progression.},
}
MeSH Terms:
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Humans
*Microbiota/genetics
*Lung/microbiology
Disease Progression
RNA, Ribosomal, 16S/genetics
*Pneumonia/microbiology/pathology
Metagenomics
Bacteria/classification/genetics/isolation & purification
Male
Female
Bacterial Load
Middle Aged
Aged
RevDate: 2025-12-11
CmpDate: 2025-12-11
Pseudomonas can make or break a happy phyllosphere microbiota.
Cell host & microbe, 33(12):2004-2007.
In this issue of Cell Host & Microbe, Xu and colleagues investigate host pH modulation as a microbiome-mediated defense mechanism. Pseudomonas strains can protect wheat against the pathogenic fungus Fusarium graminearum by counteracting alkalinization of the host environment by the fungus, although other Pseudomonas strains support the fungus by further alkalinization.
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@article {pmid41380664,
year = {2025},
author = {Ramírez-Sánchez, D and Weigel, D},
title = {Pseudomonas can make or break a happy phyllosphere microbiota.},
journal = {Cell host & microbe},
volume = {33},
number = {12},
pages = {2004-2007},
doi = {10.1016/j.chom.2025.11.006},
pmid = {41380664},
issn = {1934-6069},
mesh = {*Pseudomonas/physiology ; *Microbiota ; *Fusarium/pathogenicity/growth & development ; *Triticum/microbiology ; *Plant Diseases/microbiology ; Hydrogen-Ion Concentration ; },
abstract = {In this issue of Cell Host & Microbe, Xu and colleagues investigate host pH modulation as a microbiome-mediated defense mechanism. Pseudomonas strains can protect wheat against the pathogenic fungus Fusarium graminearum by counteracting alkalinization of the host environment by the fungus, although other Pseudomonas strains support the fungus by further alkalinization.},
}
MeSH Terms:
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*Pseudomonas/physiology
*Microbiota
*Fusarium/pathogenicity/growth & development
*Triticum/microbiology
*Plant Diseases/microbiology
Hydrogen-Ion Concentration
RevDate: 2025-12-12
Different Classes of Antibiotics Have Varying Effects on the Risk of Developing Opioid Use Disorder: A National Database Study.
Journal of substance use, 28(1):101-111.
OBJECTIVE: To examine whether different classes of antibiotics in combination with opioids differentially affect the risk of developing opioid use disorder (OUD).
METHODS: A cohort study was conducted to identify adult subjects (18-65 years old) with no previous history of OUD. Two cohorts were defined: subjects who were prescribed an opioid or an opioid in combination with antibiotics in the emergency department or inpatient unit, from the years 2015 to 2018. The diagnosis of an Opioid Related Disorder (F11.10-F11.20) 12 months following discharge from the emergency department or inpatient unit was then observed within the cohorts following the index event as identified by the ICD-10 procedural coding system.
RESULTS: Primary analysis showed that penicillin G had no statistically significant effect, while the following list of antibiotics were associated with increased risk of developing OUD in order from highest to lowest risk: cefepime > tazobactam > ertapenem > doxycycline > ceftriaxone, sulfamethoxazole > clindamycin > azithromycin > ciprofloxacin > penicillins > cefazolin > amoxicillin > penicillin V.
CONCLUSIONS: These findings suggest that the type of antibiotic prescribed in combination with opioid treatment may have important implications on the risk of developing OUD at later time points following hospital discharge.
Additional Links: PMID-41384134
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@article {pmid41384134,
year = {2023},
author = {Clegg, TJ and Kawmi, N and Graziane, NM},
title = {Different Classes of Antibiotics Have Varying Effects on the Risk of Developing Opioid Use Disorder: A National Database Study.},
journal = {Journal of substance use},
volume = {28},
number = {1},
pages = {101-111},
pmid = {41384134},
issn = {1465-9891},
abstract = {OBJECTIVE: To examine whether different classes of antibiotics in combination with opioids differentially affect the risk of developing opioid use disorder (OUD).
METHODS: A cohort study was conducted to identify adult subjects (18-65 years old) with no previous history of OUD. Two cohorts were defined: subjects who were prescribed an opioid or an opioid in combination with antibiotics in the emergency department or inpatient unit, from the years 2015 to 2018. The diagnosis of an Opioid Related Disorder (F11.10-F11.20) 12 months following discharge from the emergency department or inpatient unit was then observed within the cohorts following the index event as identified by the ICD-10 procedural coding system.
RESULTS: Primary analysis showed that penicillin G had no statistically significant effect, while the following list of antibiotics were associated with increased risk of developing OUD in order from highest to lowest risk: cefepime > tazobactam > ertapenem > doxycycline > ceftriaxone, sulfamethoxazole > clindamycin > azithromycin > ciprofloxacin > penicillins > cefazolin > amoxicillin > penicillin V.
CONCLUSIONS: These findings suggest that the type of antibiotic prescribed in combination with opioid treatment may have important implications on the risk of developing OUD at later time points following hospital discharge.},
}
RevDate: 2025-12-11
Ecological resilience of the rectal microbiome to environmental stressors in Hulunbuir grazing sheep: response to feed restriction and extreme cold challenge.
Journal of thermal biology, 134:104351 pii:S0306-4565(25)00308-0 [Epub ahead of print].
The gut microbiota is essential for helping animals to adapt to food shortages and extreme environments. In China's Hulunbuir region, local grazing sheep endure harsh winters characterized by intense cold and limited food supply. Uncovering the adaptive mechanisms that underpin their resilience is essential for improving their productivity, breeding practices, and management strategies. This research investigated the effects of feed restriction (set at 40 % of ad libitum intake) and extreme cold stress (temperature-humidity index set at 22.27) on the dynamics of gut microbiota in Hulunbuir sheep. We employed 16S rRNA gene sequencing to investigate alterations in rectal microbial diversity, community composition, and functional pathways in response to these stressors. Our findings revealed a significant reduction in bacterial diversity and microbial community structure in response to both stressors (P < 0.05), with cold stress exerting a more pronounced impact than feed restriction. Several key bacterial genera, including Akkermansia, Christensenellaceae, Monoglobus, Bacteroides, Alistipes, and Solibacillus, were identified as major contributors to the adaptive microbiota-drives responses of Hulunbuir sheep under environmental stress. A Spearman correlation analysis revealed strong associations between these genera and essential functional pathways such as fat digestion and absorption, quorum sensing, and mineral uptake, all of which were differentially regulated in response to stress (|r| > 0.6, Padj < 0.05). These findings offer novel insights into how the gut microbiota in Hulunbuir sheep supports physiological adaptation to extreme cold and nutritional stress, laying a robust foundation for creating microbiota-targeted strategies to enhance resilience, promote animal health, and improve productivity of grazing ruminants in harsh winter environments.
Additional Links: PMID-41380402
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PubMed:
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@article {pmid41380402,
year = {2025},
author = {Huang, Q and Khan, NA and Tang, S and Zhou, C and He, Z and Tan, Z and Liu, Y},
title = {Ecological resilience of the rectal microbiome to environmental stressors in Hulunbuir grazing sheep: response to feed restriction and extreme cold challenge.},
journal = {Journal of thermal biology},
volume = {134},
number = {},
pages = {104351},
doi = {10.1016/j.jtherbio.2025.104351},
pmid = {41380402},
issn = {0306-4565},
abstract = {The gut microbiota is essential for helping animals to adapt to food shortages and extreme environments. In China's Hulunbuir region, local grazing sheep endure harsh winters characterized by intense cold and limited food supply. Uncovering the adaptive mechanisms that underpin their resilience is essential for improving their productivity, breeding practices, and management strategies. This research investigated the effects of feed restriction (set at 40 % of ad libitum intake) and extreme cold stress (temperature-humidity index set at 22.27) on the dynamics of gut microbiota in Hulunbuir sheep. We employed 16S rRNA gene sequencing to investigate alterations in rectal microbial diversity, community composition, and functional pathways in response to these stressors. Our findings revealed a significant reduction in bacterial diversity and microbial community structure in response to both stressors (P < 0.05), with cold stress exerting a more pronounced impact than feed restriction. Several key bacterial genera, including Akkermansia, Christensenellaceae, Monoglobus, Bacteroides, Alistipes, and Solibacillus, were identified as major contributors to the adaptive microbiota-drives responses of Hulunbuir sheep under environmental stress. A Spearman correlation analysis revealed strong associations between these genera and essential functional pathways such as fat digestion and absorption, quorum sensing, and mineral uptake, all of which were differentially regulated in response to stress (|r| > 0.6, Padj < 0.05). These findings offer novel insights into how the gut microbiota in Hulunbuir sheep supports physiological adaptation to extreme cold and nutritional stress, laying a robust foundation for creating microbiota-targeted strategies to enhance resilience, promote animal health, and improve productivity of grazing ruminants in harsh winter environments.},
}
RevDate: 2025-12-11
The impact of embryonic thermal manipulation on the microbiome of the jejunum and cecum in response to post-hatch acute heat stress.
Poultry science, 105(1):106212 pii:S0032-5791(25)01452-X [Epub ahead of print].
Thermal manipulation (TM) during embryogenesis has been proposed as a sustainable strategy to enhance thermotolerance and resilience in broiler chickens. However, its long-term Influence on gut microbiota composition, particularly under post-hatch acute heat stress (AHS), remains unclear. This study investigated the effects of TM on the jejunal and cecal microbiota of Ross broilers following AHS. Fertile eggs (n = 182) were incubated under standard conditions (37.8°C and 56 % relative humidity), while the thermally manipulated group (n = 182) was incubated at 38.5°C and 65 % relative humidity for 18 h/day during embryonic days 10-18. On day 35 post-hatch, birds were exposed to 35°C and 60-65 % RH for three hours to induce AHS, and jejunal and cecal contents were analyzed by 16S rRNA gene sequencing (V3-V4 region, Illumina MiSeq). Alpha diversity indices (Shannon, evenness) did not differ significantly between treatments (P > 0.05), although the cecum consistently exhibited higher richness and evenness than the jejunum (P < 0.05). Beta diversity analysis revealed strong separation between intestinal segments but no treatment-driven clustering. Firmicutes and Bacteroidota dominated all groups, with regional enrichment of Lactobacillus and Ligilactobacillus in the jejunum, and Faecalibacterium in the cecum. Differential abundance analysis revealed 30 taxa that differed significantly (q < 0.05) at the family level across intestinal segments. In contrast, comparing the TM, AHS, and control groups within any single segment yielded no significant taxonomic differences after false discovery rate (FDR) correction. These results indicate that anatomical location within the intestine exerts a more substantial influence on microbial community composition than either embryonic or post-hatch heat exposure. The stability of microbial diversity under acute thermal challenge suggests that the beneficial effects of TM on thermotolerance, as reported in the literature, are likely mediated through host physiological or epigenetic mechanisms rather than microbiome remodeling.
Additional Links: PMID-41380320
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@article {pmid41380320,
year = {2025},
author = {Hundam, S and Al-Zghoul, MB and Almaasfeh, M},
title = {The impact of embryonic thermal manipulation on the microbiome of the jejunum and cecum in response to post-hatch acute heat stress.},
journal = {Poultry science},
volume = {105},
number = {1},
pages = {106212},
doi = {10.1016/j.psj.2025.106212},
pmid = {41380320},
issn = {1525-3171},
abstract = {Thermal manipulation (TM) during embryogenesis has been proposed as a sustainable strategy to enhance thermotolerance and resilience in broiler chickens. However, its long-term Influence on gut microbiota composition, particularly under post-hatch acute heat stress (AHS), remains unclear. This study investigated the effects of TM on the jejunal and cecal microbiota of Ross broilers following AHS. Fertile eggs (n = 182) were incubated under standard conditions (37.8°C and 56 % relative humidity), while the thermally manipulated group (n = 182) was incubated at 38.5°C and 65 % relative humidity for 18 h/day during embryonic days 10-18. On day 35 post-hatch, birds were exposed to 35°C and 60-65 % RH for three hours to induce AHS, and jejunal and cecal contents were analyzed by 16S rRNA gene sequencing (V3-V4 region, Illumina MiSeq). Alpha diversity indices (Shannon, evenness) did not differ significantly between treatments (P > 0.05), although the cecum consistently exhibited higher richness and evenness than the jejunum (P < 0.05). Beta diversity analysis revealed strong separation between intestinal segments but no treatment-driven clustering. Firmicutes and Bacteroidota dominated all groups, with regional enrichment of Lactobacillus and Ligilactobacillus in the jejunum, and Faecalibacterium in the cecum. Differential abundance analysis revealed 30 taxa that differed significantly (q < 0.05) at the family level across intestinal segments. In contrast, comparing the TM, AHS, and control groups within any single segment yielded no significant taxonomic differences after false discovery rate (FDR) correction. These results indicate that anatomical location within the intestine exerts a more substantial influence on microbial community composition than either embryonic or post-hatch heat exposure. The stability of microbial diversity under acute thermal challenge suggests that the beneficial effects of TM on thermotolerance, as reported in the literature, are likely mediated through host physiological or epigenetic mechanisms rather than microbiome remodeling.},
}
RevDate: 2025-12-11
Metagenomic insights into rhizosphere microbiome dynamics of Oenanthe javanica in ecological floating beds under different hydrodynamic regimes.
Journal of contaminant hydrology, 277:104795 pii:S0169-7722(25)00300-6 [Epub ahead of print].
Ecological floating beds (EFBs) are a cost-effective and sustainable technology that utilizes macrophyte to remove nutrients from aquatic ecosystems, where rhizosphere bacterial degradation and assimilation play a key role in nutrient removal. However, the current knowledge about how hydrodynamic regimes impact the rhizosphere bacterial community on EFB systems remains limited. Here, we investigated the effects of different hydrodynamic regimes (i.e., stagnant water, pulsed water, and flowing water conditions) on the rhizosphere bacterial community structure and function of Oenanthe javanica in an experimental EFB system based on metagenomic sequencing. We observed that bacterial community compositions on the roots of O. javanica were significantly differed across the three hydrodynamic regimes, with the highest bacterial biodiversity captured from the flowing water condition. Moreover, a total of 65 nitrogen functional genes (NFGs) were identified in the rhizosphere bacterial community, with nitrate reduction pathways dominating the nitrogen cycling processes. In contrast, totally 139 phosphorus functional genes (PFGs) were detected, primarily involved in purine metabolism, which drove the phosphorus cycling dynamics. We found the distinct nitrogen and phosphorus metabolic strategies of rhizosphere bacterial communities in response to hydrodynamic regime changes. Specifically, the relative abundances of NFGs like nasB, narl, and ansB were significantly increased under the pulsed water condition, whereas gdh_K00262 were relative abundant under the flowing condition. Moreover, pulsed water condition promoted the relative abundances of PFGs such asas phnC, phoD, and pgtP in rhizosphere bacterial communities, in contrast to the stagnant condition, which favored genes like ugpC, purK, phoH, and purA. Our study offers technical support for regulating plant degradation of pollutants to improve EFB's performance in engineering applications.
Additional Links: PMID-41380282
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@article {pmid41380282,
year = {2025},
author = {Xu, X and Wang, J and Deng, C and Yu, X and Nie, R and Wang, S and Huang, W},
title = {Metagenomic insights into rhizosphere microbiome dynamics of Oenanthe javanica in ecological floating beds under different hydrodynamic regimes.},
journal = {Journal of contaminant hydrology},
volume = {277},
number = {},
pages = {104795},
doi = {10.1016/j.jconhyd.2025.104795},
pmid = {41380282},
issn = {1873-6009},
abstract = {Ecological floating beds (EFBs) are a cost-effective and sustainable technology that utilizes macrophyte to remove nutrients from aquatic ecosystems, where rhizosphere bacterial degradation and assimilation play a key role in nutrient removal. However, the current knowledge about how hydrodynamic regimes impact the rhizosphere bacterial community on EFB systems remains limited. Here, we investigated the effects of different hydrodynamic regimes (i.e., stagnant water, pulsed water, and flowing water conditions) on the rhizosphere bacterial community structure and function of Oenanthe javanica in an experimental EFB system based on metagenomic sequencing. We observed that bacterial community compositions on the roots of O. javanica were significantly differed across the three hydrodynamic regimes, with the highest bacterial biodiversity captured from the flowing water condition. Moreover, a total of 65 nitrogen functional genes (NFGs) were identified in the rhizosphere bacterial community, with nitrate reduction pathways dominating the nitrogen cycling processes. In contrast, totally 139 phosphorus functional genes (PFGs) were detected, primarily involved in purine metabolism, which drove the phosphorus cycling dynamics. We found the distinct nitrogen and phosphorus metabolic strategies of rhizosphere bacterial communities in response to hydrodynamic regime changes. Specifically, the relative abundances of NFGs like nasB, narl, and ansB were significantly increased under the pulsed water condition, whereas gdh_K00262 were relative abundant under the flowing condition. Moreover, pulsed water condition promoted the relative abundances of PFGs such asas phnC, phoD, and pgtP in rhizosphere bacterial communities, in contrast to the stagnant condition, which favored genes like ugpC, purK, phoH, and purA. Our study offers technical support for regulating plant degradation of pollutants to improve EFB's performance in engineering applications.},
}
RevDate: 2025-12-11
The effect of maternal exposure to Tris(n-butyl) phosphate on the gut microbiome of SD rats and offspring.
Journal of hazardous materials, 501:140763 pii:S0304-3894(25)03683-0 [Epub ahead of print].
Tris (n-butyl) phosphate (TnBP), a heavily utilized organophosphate ester, remains poorly characterized with respect to its long-term effects on the structure and metabolic capacity of the gut microbiota. The purpose of this study is to explore how TnBP exposure affects the intestinal microbiota of maternal Sprague-Dawley (SD) rats and their corresponding progeny, as well as the impact of its metabolite, dibutyl phosphate (DBP), in the human population. A cross-sectional analysis revealed a significant positive correlation between DBP concentrations and the C-reactive protein/albumin ratio (CAR) in the United States population. Results of 16S rRNA gene sequencing revealed that maternal TnBP exposure significantly increased gut bacterial α-diversity in both dams and their F1-generation offspring (Shannon index, P < 0.05). Principal-coordinate analysis (PCoA) based on Bray-Curtis dissimilarity showed distinct clustering of the microbial communities, and PERMANOVA confirmed significant differences between the exposed and control groupsAt the phylum level, TnBP exposure elicited a proportional expansion of Proteobacteria coupled with concomitant reductions in Bacillota and Bacteroidetes in both dams and their F1 offspring. Genus-level profiling further revealed a selective enrichment of Bifidobacterium and significant perturbations in Lactobacillus, Limosilactobacillus, Muribaculum, Turicibacter, Allobaculum, and Clostridium.Furthermore, TnBP exposure significantly elevated total short-chain fatty acid (SCFA) levels in the offspring, indicating a functional shift in microbial metabolism. Correlation analysis further revealed that under TnBP treatment the relative abundances of Allobaculum and Collinsella were positively associated with the concentrations of acetate, propionate, and butyrate (P < 0.05 for each). Quantitative PCR and histopathological examination collectively demonstrated a pronounced inflammatory signature in the colons of juvenile offspring exposed to TnBP. These observations underscore the potential for persistent adverse health outcomes following developmental exposure and warrant comprehensive mechanistic and epidemiological investigations.
Additional Links: PMID-41380257
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@article {pmid41380257,
year = {2025},
author = {Zeng, C and Wu, D and Yang, J and Chen, J and Tan, C and Wang, D and Zhang, G},
title = {The effect of maternal exposure to Tris(n-butyl) phosphate on the gut microbiome of SD rats and offspring.},
journal = {Journal of hazardous materials},
volume = {501},
number = {},
pages = {140763},
doi = {10.1016/j.jhazmat.2025.140763},
pmid = {41380257},
issn = {1873-3336},
abstract = {Tris (n-butyl) phosphate (TnBP), a heavily utilized organophosphate ester, remains poorly characterized with respect to its long-term effects on the structure and metabolic capacity of the gut microbiota. The purpose of this study is to explore how TnBP exposure affects the intestinal microbiota of maternal Sprague-Dawley (SD) rats and their corresponding progeny, as well as the impact of its metabolite, dibutyl phosphate (DBP), in the human population. A cross-sectional analysis revealed a significant positive correlation between DBP concentrations and the C-reactive protein/albumin ratio (CAR) in the United States population. Results of 16S rRNA gene sequencing revealed that maternal TnBP exposure significantly increased gut bacterial α-diversity in both dams and their F1-generation offspring (Shannon index, P < 0.05). Principal-coordinate analysis (PCoA) based on Bray-Curtis dissimilarity showed distinct clustering of the microbial communities, and PERMANOVA confirmed significant differences between the exposed and control groupsAt the phylum level, TnBP exposure elicited a proportional expansion of Proteobacteria coupled with concomitant reductions in Bacillota and Bacteroidetes in both dams and their F1 offspring. Genus-level profiling further revealed a selective enrichment of Bifidobacterium and significant perturbations in Lactobacillus, Limosilactobacillus, Muribaculum, Turicibacter, Allobaculum, and Clostridium.Furthermore, TnBP exposure significantly elevated total short-chain fatty acid (SCFA) levels in the offspring, indicating a functional shift in microbial metabolism. Correlation analysis further revealed that under TnBP treatment the relative abundances of Allobaculum and Collinsella were positively associated with the concentrations of acetate, propionate, and butyrate (P < 0.05 for each). Quantitative PCR and histopathological examination collectively demonstrated a pronounced inflammatory signature in the colons of juvenile offspring exposed to TnBP. These observations underscore the potential for persistent adverse health outcomes following developmental exposure and warrant comprehensive mechanistic and epidemiological investigations.},
}
RevDate: 2025-12-11
The Gut Microbiome and Butyrate Differentiate Clostridioides difficile Colonization and Infection in Children.
The Journal of infectious diseases pii:8377423 [Epub ahead of print].
BACKGROUND AND AIMS: Symptomatic Clostridioides difficile infection (CDI) can cause significant morbidity and mortality. Conversely, patients can be colonized with toxigenic C. difficile in the absence of symptoms, termed asymptomatic colonization. We previously demonstrated that the presence and function of C. difficile toxins do not differentiate between asymptomatic colonization and CDI in children, suggesting the influence of other factors. This study aimed to interrogate the intestinal microbiome and butyrate in stool samples from children with CDI and asymptomatic colonization.
METHODS: Design: Case-control studySetting: Tertiary care children's hospitalParticipants and measures: Asymptomatic children had stool tested for C. difficile by nucleic-acid amplification-based testing (NAAT) and were considered colonized if positive (N=50). Residual stool was also obtained from symptomatic children who tested positive for C. difficile by NAAT (N=55). The microbiome was assessed via 16S rRNA sequencing and butyrate via liquid chromatography-mass spectrometry.
RESULTS: Compared to clinical co-variates and comorbidities, C. difficile symptom status (i.e., asymptomatic colonization versus symptomatic CDI) demonstrated the strongest differential abundance association on gut microbes. Symptomatic CDI was associated with increased abundance of Escherichia/Shigella (Benjamini-Hochberg adjusted q=3.94x10-5), Haemophilus (q=0.022), and Gemella (q=0.085), and depleted abundance of gut commensals such as Faecalibacterium (q=0.041), Blautia (q=0.041), and Bifidobacterium (q=0.063). We also observed depletion in the abundance of microbial butyrate producers and fecal butyrate in participants with symptomatic CDI versus asymptomatic colonization.
CONCLUSION: The gut microbiota and butyrate differ between participants with asymptomatic C. difficile colonization and symptomatic CDI, suggesting their potential role in symptom development.
Additional Links: PMID-41379981
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PubMed:
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@article {pmid41379981,
year = {2025},
author = {Nicholson, MR and Ma, S and Strickland, BA and Cecala, M and Zhang, L and Reasoner, S and Guiberson, ER and Munneke, MJ and Shilts, MH and Skaar, EP and Das, SR},
title = {The Gut Microbiome and Butyrate Differentiate Clostridioides difficile Colonization and Infection in Children.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiaf631},
pmid = {41379981},
issn = {1537-6613},
abstract = {BACKGROUND AND AIMS: Symptomatic Clostridioides difficile infection (CDI) can cause significant morbidity and mortality. Conversely, patients can be colonized with toxigenic C. difficile in the absence of symptoms, termed asymptomatic colonization. We previously demonstrated that the presence and function of C. difficile toxins do not differentiate between asymptomatic colonization and CDI in children, suggesting the influence of other factors. This study aimed to interrogate the intestinal microbiome and butyrate in stool samples from children with CDI and asymptomatic colonization.
METHODS: Design: Case-control studySetting: Tertiary care children's hospitalParticipants and measures: Asymptomatic children had stool tested for C. difficile by nucleic-acid amplification-based testing (NAAT) and were considered colonized if positive (N=50). Residual stool was also obtained from symptomatic children who tested positive for C. difficile by NAAT (N=55). The microbiome was assessed via 16S rRNA sequencing and butyrate via liquid chromatography-mass spectrometry.
RESULTS: Compared to clinical co-variates and comorbidities, C. difficile symptom status (i.e., asymptomatic colonization versus symptomatic CDI) demonstrated the strongest differential abundance association on gut microbes. Symptomatic CDI was associated with increased abundance of Escherichia/Shigella (Benjamini-Hochberg adjusted q=3.94x10-5), Haemophilus (q=0.022), and Gemella (q=0.085), and depleted abundance of gut commensals such as Faecalibacterium (q=0.041), Blautia (q=0.041), and Bifidobacterium (q=0.063). We also observed depletion in the abundance of microbial butyrate producers and fecal butyrate in participants with symptomatic CDI versus asymptomatic colonization.
CONCLUSION: The gut microbiota and butyrate differ between participants with asymptomatic C. difficile colonization and symptomatic CDI, suggesting their potential role in symptom development.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Microbial dysbiosis and host-microbe interactions in proliferative verrucous leukoplakia: insights into carcinogenic potential.
Archives of microbiology, 208(1):65.
Proliferative verrucous leukoplakia (PVL) is a rare and aggressive oral potentially malignant disorder (OPMD) characterized by multifocal keratotic plaques, progressive expansion, high recurrence, and a strong risk of malignant transformation. Although its etiology remains unclear, recent evidence emphasizes the role of the oral microbiome as a key factor in disease progression. Alterations in microbial diversity and ecological balance create a shift toward dysbiosis, supporting a chronic inflammatory microenvironment that favors epithelial transformation. Specific taxa, including Fusobacterium and Porphyromonas, have been implicated in biofilm formation, immune evasion, and modulation of epithelial signaling pathways. These interactions highlight the potential of microbial communities to drive oncogenic processes through host-microbe crosstalk. Advanced methodological approaches such as metagenomics, functional microbiome profiling, and multi-omics integration provide novel opportunities to unravel the mechanisms of dysbiosis in PVL. Beyond pathogenesis, microbiome research opens perspectives for the identification of predictive biomarkers, targeted prevention, and microbiome-based therapeutics. This review synthesizes current insights into the microbial basis of PVL and outlines future directions aimed at improving understanding of host-microbe interactions and their role in oral carcinogenesis. Relevant literature was identified through PubMed and Web of Science searches (1985-2025) using terms related to PVL, oral leukoplakia, OPMD, oral microbiome, and oral squamous cell carcinoma. In conclusion, current evidence suggests that while microbial dysbiosis is not an isolated driver, it likely synergizes with genetic, epigenetic, and immunological factors in PVL progression, offering opportunities for biomarker discovery and novel therapeutic strategies. This study also provides a potential direction for the early diagnosis of PVL and the development of microecologically targeted interventions.
Additional Links: PMID-41379255
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Citation:
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@article {pmid41379255,
year = {2025},
author = {Špiljak, B and Ozretić, P and Brailo, V and Škrinjar, I and Lončar Brzak, B and Andabak Rogulj, A and Butić, I and Tambić Andrašević, A and Vidović Juras, D},
title = {Microbial dysbiosis and host-microbe interactions in proliferative verrucous leukoplakia: insights into carcinogenic potential.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {65},
pmid = {41379255},
issn = {1432-072X},
mesh = {Humans ; *Dysbiosis/microbiology ; *Leukoplakia, Oral/microbiology/pathology ; Microbiota ; *Host Microbial Interactions ; Carcinogenesis ; Mouth Neoplasms/microbiology/pathology ; },
abstract = {Proliferative verrucous leukoplakia (PVL) is a rare and aggressive oral potentially malignant disorder (OPMD) characterized by multifocal keratotic plaques, progressive expansion, high recurrence, and a strong risk of malignant transformation. Although its etiology remains unclear, recent evidence emphasizes the role of the oral microbiome as a key factor in disease progression. Alterations in microbial diversity and ecological balance create a shift toward dysbiosis, supporting a chronic inflammatory microenvironment that favors epithelial transformation. Specific taxa, including Fusobacterium and Porphyromonas, have been implicated in biofilm formation, immune evasion, and modulation of epithelial signaling pathways. These interactions highlight the potential of microbial communities to drive oncogenic processes through host-microbe crosstalk. Advanced methodological approaches such as metagenomics, functional microbiome profiling, and multi-omics integration provide novel opportunities to unravel the mechanisms of dysbiosis in PVL. Beyond pathogenesis, microbiome research opens perspectives for the identification of predictive biomarkers, targeted prevention, and microbiome-based therapeutics. This review synthesizes current insights into the microbial basis of PVL and outlines future directions aimed at improving understanding of host-microbe interactions and their role in oral carcinogenesis. Relevant literature was identified through PubMed and Web of Science searches (1985-2025) using terms related to PVL, oral leukoplakia, OPMD, oral microbiome, and oral squamous cell carcinoma. In conclusion, current evidence suggests that while microbial dysbiosis is not an isolated driver, it likely synergizes with genetic, epigenetic, and immunological factors in PVL progression, offering opportunities for biomarker discovery and novel therapeutic strategies. This study also provides a potential direction for the early diagnosis of PVL and the development of microecologically targeted interventions.},
}
MeSH Terms:
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Humans
*Dysbiosis/microbiology
*Leukoplakia, Oral/microbiology/pathology
Microbiota
*Host Microbial Interactions
Carcinogenesis
Mouth Neoplasms/microbiology/pathology
RevDate: 2025-12-11
CmpDate: 2025-12-11
Comparative metagenomic analysis of bacterial communities associated with two mealybug species, Phenacoccus saccharifolii and Dysmicoccus carens infesting sugarcane in Tamil Nadu, India.
World journal of microbiology & biotechnology, 41(12):504.
This study presents a comparative metagenomic analysis of the gut bacterial communities of two sugarcane-infesting mealybug species, Phenacoccus saccharifolii (WR) and Dysmicoccus carens (RR), from Tamil Nadu, India. Using Oxford Nanopore sequencing of the 16s rRNA gene spanning the hypervariable regions V1 - V9 and predictive metagenomics, differences in microbial diversity, taxonomy, and functional potential were assessed to explore the ecological adaptations of the gut microbiota in mealybugs. The D. carens gut microbiome showed higher species richness than P. saccharifolii (WR) (125 vs. 45 species, p < 0.05) but lower community evenness (0.43 vs. 0.61, p < 0.05), resulting in similar overall Shannon diversity (2.08 vs. 2.30) despite markedly different community structures, which may be influenced by their different feeding niches, including the sugarcane crown region, leaf sheath tissues, and basal stem and root portions. Both mealybug species exhibited contrasting bacterial community structures. D. carens (RR) harbored high abundances of endosymbionts (43.8%), Gilliamella (22.3%), Enterobacter (18.3%), and Candidatus Tremblaya (9.3%), representing a symbiont-dominated microbiome typical of many hemipteran insects. P. saccharifolii (WR) displayed a distinct profile with Serratia as the dominant genus (43.2%), followed by Enterobacter (20.1%), Klebsiella (14.6%), and substantially reduced endosymbiont abundances (14.8%). Beta diversity analysis revealed distinct community clustering of species, highlighting the variation driven by feeding habitat and host genotype. Functional profiling indicated largely conserved metabolic capabilities dominated by amino acid and carbohydrate metabolism, which was a key to compensate the nutrient-poor phloem sap diet. The core microbiome identified several genera that form complex ecological networks, emphasizing their importance in community stability. These findings provide insights into the role of symbiotic bacteria in mealybug adaptation to different ecological niches within the sugarcane agroecosystem. Understanding these host-microbiome interactions may facilitate the development of targeted, microbiome-based biocontrol strategies for sustainable mealybug management in sugarcane cultivation.
Additional Links: PMID-41379245
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Citation:
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@article {pmid41379245,
year = {2025},
author = {Namadara, S and Pragadeesh, ARU and Uthandi, S and Rangasamy, A and Malaichamy, K and Venkatesan, M and Narayanan, MB and Murugaiyan, S},
title = {Comparative metagenomic analysis of bacterial communities associated with two mealybug species, Phenacoccus saccharifolii and Dysmicoccus carens infesting sugarcane in Tamil Nadu, India.},
journal = {World journal of microbiology & biotechnology},
volume = {41},
number = {12},
pages = {504},
pmid = {41379245},
issn = {1573-0972},
support = {DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; },
mesh = {*Saccharum/parasitology ; Animals ; India ; *Bacteria/classification/genetics/isolation & purification ; *Hemiptera/microbiology ; RNA, Ribosomal, 16S/genetics ; *Metagenomics/methods ; *Gastrointestinal Microbiome/genetics ; Phylogeny ; DNA, Bacterial/genetics ; },
abstract = {This study presents a comparative metagenomic analysis of the gut bacterial communities of two sugarcane-infesting mealybug species, Phenacoccus saccharifolii (WR) and Dysmicoccus carens (RR), from Tamil Nadu, India. Using Oxford Nanopore sequencing of the 16s rRNA gene spanning the hypervariable regions V1 - V9 and predictive metagenomics, differences in microbial diversity, taxonomy, and functional potential were assessed to explore the ecological adaptations of the gut microbiota in mealybugs. The D. carens gut microbiome showed higher species richness than P. saccharifolii (WR) (125 vs. 45 species, p < 0.05) but lower community evenness (0.43 vs. 0.61, p < 0.05), resulting in similar overall Shannon diversity (2.08 vs. 2.30) despite markedly different community structures, which may be influenced by their different feeding niches, including the sugarcane crown region, leaf sheath tissues, and basal stem and root portions. Both mealybug species exhibited contrasting bacterial community structures. D. carens (RR) harbored high abundances of endosymbionts (43.8%), Gilliamella (22.3%), Enterobacter (18.3%), and Candidatus Tremblaya (9.3%), representing a symbiont-dominated microbiome typical of many hemipteran insects. P. saccharifolii (WR) displayed a distinct profile with Serratia as the dominant genus (43.2%), followed by Enterobacter (20.1%), Klebsiella (14.6%), and substantially reduced endosymbiont abundances (14.8%). Beta diversity analysis revealed distinct community clustering of species, highlighting the variation driven by feeding habitat and host genotype. Functional profiling indicated largely conserved metabolic capabilities dominated by amino acid and carbohydrate metabolism, which was a key to compensate the nutrient-poor phloem sap diet. The core microbiome identified several genera that form complex ecological networks, emphasizing their importance in community stability. These findings provide insights into the role of symbiotic bacteria in mealybug adaptation to different ecological niches within the sugarcane agroecosystem. Understanding these host-microbiome interactions may facilitate the development of targeted, microbiome-based biocontrol strategies for sustainable mealybug management in sugarcane cultivation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Saccharum/parasitology
Animals
India
*Bacteria/classification/genetics/isolation & purification
*Hemiptera/microbiology
RNA, Ribosomal, 16S/genetics
*Metagenomics/methods
*Gastrointestinal Microbiome/genetics
Phylogeny
DNA, Bacterial/genetics
RevDate: 2025-12-11
CmpDate: 2025-12-11
EFFICACY OF PROBIOTICS IN PREVENTING CHEMOTHERAPY-INDUCED DIARRHEA IN GASTROINTESTINAL CANCER PATIENTS.
Arquivos de gastroenterologia, 62:e25020 pii:S0004-28032025000100211.
BACKGROUND: Chemotherapy-induced diarrhea is a common and distressing side effect experienced by patients undergoing cancer treatment, particularly those with gastrointestinal cancer. It can lead to significant health complications, including dehydration, electrolyte imbalances, and treatment interruptions. Recent studies have shown that the gut microbiome plays an important role in the development and severity of chemotherapy-induced diarrhea. Modulating the gut microbiome with probiotics has emerged as a potential strategy for preventing and managing chemotherapy-induced diarrhea.
OBJECTIVE: In this study we aimed to evaluate the efficacy of one probiotic containing a mixture of several strains of Lactobacillus and Bifidobacterium species in prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.
METHODS: Between April 2022 and June 2024, a total of 28 patients diagnosed with gastrointestinal cancer who were intended to receive chemotherapy based on fluoropyrimidine, oxaliplatin, and/or irinotecan were randomized in a ratio 1:1 to receive either a placebo or 20 billion colony-forming units (CFU) of a mixture containing five viable strains including 335 mg of Lactobacillus acidophilus NCFM®, Lactobacillus paracasei Lpc-37TM, Bifidobacterium lactis Bi-04TM, Bifidobacterium lactis Bi-07TM, and Bifidobacterium bifidum Bb-02TM. Patients were instructed to take the product orally once daily for 90 days and to record their bowel habits in a diary using the Bristol stool scale.
RESULTS: The use of probiotics, compared to placebo, did not result in reduction of grade 2/3 diarrhea episodes (placebo arm 55.56% vs probiotic arm 44.44%; P=1). Likewise, no statistically significant difference was observed in the overall incidence of diarrhea between the two groups (71.43% vs 64.29%; P=1). The median number of diarrhea episodes during the 90-day follow-up tended to be lower in the probiotic group (eight episodes) compared to the placebo group (9 episodes) (P=0.639) Subgroup analyses failed to identify any specific patient characteristics that associated any benefit from the probiotic use, regardless of diarrhea grade. Also, no infections related to the probiotic strains administered in this study were detected.
CONCLUSION: Probiotic in comparison to a placebo did not result in a statistically significant effect, suggesting a lack of benefit of administered probiotic for prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.
Additional Links: PMID-41379184
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PubMed:
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@article {pmid41379184,
year = {2025},
author = {DE Souza, GC and Araujo Filho, HB and DE Oliveira, CZ and Paiotti, APR and Forones, NM},
title = {EFFICACY OF PROBIOTICS IN PREVENTING CHEMOTHERAPY-INDUCED DIARRHEA IN GASTROINTESTINAL CANCER PATIENTS.},
journal = {Arquivos de gastroenterologia},
volume = {62},
number = {},
pages = {e25020},
doi = {10.1590/S0004-2803.24612025-020},
pmid = {41379184},
issn = {1678-4219},
mesh = {Humans ; *Probiotics/therapeutic use ; *Diarrhea/prevention & control/chemically induced ; Female ; Male ; Middle Aged ; *Gastrointestinal Neoplasms/drug therapy ; Aged ; Treatment Outcome ; *Antineoplastic Agents/adverse effects ; Bifidobacterium ; Lactobacillus ; Gastrointestinal Microbiome/drug effects ; Adult ; Double-Blind Method ; },
abstract = {BACKGROUND: Chemotherapy-induced diarrhea is a common and distressing side effect experienced by patients undergoing cancer treatment, particularly those with gastrointestinal cancer. It can lead to significant health complications, including dehydration, electrolyte imbalances, and treatment interruptions. Recent studies have shown that the gut microbiome plays an important role in the development and severity of chemotherapy-induced diarrhea. Modulating the gut microbiome with probiotics has emerged as a potential strategy for preventing and managing chemotherapy-induced diarrhea.
OBJECTIVE: In this study we aimed to evaluate the efficacy of one probiotic containing a mixture of several strains of Lactobacillus and Bifidobacterium species in prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.
METHODS: Between April 2022 and June 2024, a total of 28 patients diagnosed with gastrointestinal cancer who were intended to receive chemotherapy based on fluoropyrimidine, oxaliplatin, and/or irinotecan were randomized in a ratio 1:1 to receive either a placebo or 20 billion colony-forming units (CFU) of a mixture containing five viable strains including 335 mg of Lactobacillus acidophilus NCFM®, Lactobacillus paracasei Lpc-37TM, Bifidobacterium lactis Bi-04TM, Bifidobacterium lactis Bi-07TM, and Bifidobacterium bifidum Bb-02TM. Patients were instructed to take the product orally once daily for 90 days and to record their bowel habits in a diary using the Bristol stool scale.
RESULTS: The use of probiotics, compared to placebo, did not result in reduction of grade 2/3 diarrhea episodes (placebo arm 55.56% vs probiotic arm 44.44%; P=1). Likewise, no statistically significant difference was observed in the overall incidence of diarrhea between the two groups (71.43% vs 64.29%; P=1). The median number of diarrhea episodes during the 90-day follow-up tended to be lower in the probiotic group (eight episodes) compared to the placebo group (9 episodes) (P=0.639) Subgroup analyses failed to identify any specific patient characteristics that associated any benefit from the probiotic use, regardless of diarrhea grade. Also, no infections related to the probiotic strains administered in this study were detected.
CONCLUSION: Probiotic in comparison to a placebo did not result in a statistically significant effect, suggesting a lack of benefit of administered probiotic for prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/therapeutic use
*Diarrhea/prevention & control/chemically induced
Female
Male
Middle Aged
*Gastrointestinal Neoplasms/drug therapy
Aged
Treatment Outcome
*Antineoplastic Agents/adverse effects
Bifidobacterium
Lactobacillus
Gastrointestinal Microbiome/drug effects
Adult
Double-Blind Method
RevDate: 2025-12-11
CmpDate: 2025-12-11
Community Modeling Reveals Disrupted Gut Microbial Secretion in Autism Associated With Redox and Neurometabolic Alterations.
Biotechnology journal, 20(12):e70164.
Emerging evidence suggests that disruptions in the gut microbiome may influence autism spectrum disorder (ASD) through altered microbial metabolism and gut-brain communication. However, the specific metabolic impacts of these microbial changes remain unclear. Community-scale metabolic modeling was applied to shotgun metagenomics data from children with ASD and neurotypical controls to predict secretion of host-impacting metabolites. Modeled ASD-associated communities exhibited altered predicted secretion of metabolites related to redox balance and neurotransmission, including increased 2-ketobutyrate and GABA and reduced riboflavin and inositol, with microbiota transfer therapy (MTT) shifting these profiles toward NT. Empirical fecal metabolomics data showed generally consistent directional trends with model predictions. Reductions in autism severity scores following MTT were associated with increased predicted secretion potentials for inositol and arginine. Taxonomic analysis revealed a depletion of beneficial and an enrichment of pro-inflammatory species, such as Escherichia and Flavonifractor, in ASD. Associations between microbial taxa (e.g., Bacteroides, Bifidobacterium) and neuroactive metabolites highlight microbial modulation as a promising therapeutic strategy in ASD. These results emphasize microbial metabolism as a contributor to ASD traits and a target for therapeutic intervention.
Additional Links: PMID-41379027
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41379027,
year = {2025},
author = {Esvap, E and Ulgen, KO},
title = {Community Modeling Reveals Disrupted Gut Microbial Secretion in Autism Associated With Redox and Neurometabolic Alterations.},
journal = {Biotechnology journal},
volume = {20},
number = {12},
pages = {e70164},
doi = {10.1002/biot.70164},
pmid = {41379027},
issn = {1860-7314},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/genetics ; Oxidation-Reduction ; Child ; Male ; Feces/microbiology ; *Autism Spectrum Disorder/microbiology/metabolism ; Female ; Child, Preschool ; Metagenomics ; Metabolomics ; Bacteria/metabolism/classification/genetics ; *Autistic Disorder/microbiology/metabolism ; },
abstract = {Emerging evidence suggests that disruptions in the gut microbiome may influence autism spectrum disorder (ASD) through altered microbial metabolism and gut-brain communication. However, the specific metabolic impacts of these microbial changes remain unclear. Community-scale metabolic modeling was applied to shotgun metagenomics data from children with ASD and neurotypical controls to predict secretion of host-impacting metabolites. Modeled ASD-associated communities exhibited altered predicted secretion of metabolites related to redox balance and neurotransmission, including increased 2-ketobutyrate and GABA and reduced riboflavin and inositol, with microbiota transfer therapy (MTT) shifting these profiles toward NT. Empirical fecal metabolomics data showed generally consistent directional trends with model predictions. Reductions in autism severity scores following MTT were associated with increased predicted secretion potentials for inositol and arginine. Taxonomic analysis revealed a depletion of beneficial and an enrichment of pro-inflammatory species, such as Escherichia and Flavonifractor, in ASD. Associations between microbial taxa (e.g., Bacteroides, Bifidobacterium) and neuroactive metabolites highlight microbial modulation as a promising therapeutic strategy in ASD. These results emphasize microbial metabolism as a contributor to ASD traits and a target for therapeutic intervention.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology/genetics
Oxidation-Reduction
Child
Male
Feces/microbiology
*Autism Spectrum Disorder/microbiology/metabolism
Female
Child, Preschool
Metagenomics
Metabolomics
Bacteria/metabolism/classification/genetics
*Autistic Disorder/microbiology/metabolism
RevDate: 2025-12-11
Analysis of gut microbiota in Restless Legs Syndrome: searching for a metagenomic signature.
Sleep pii:8377255 [Epub ahead of print].
STUDY OBJECTIVES: We aim to analyse the microbiota composition in RLS patients and its relationship with the different RLS phenotypes.
METHODS: We recruited idiopathic RLS (RLS) and insomnia (INS) patients and healthy subjects (CTRL). Validated questionnaires (PSQI, IRLS, ISI, BDI-II) were administered in the RLS and INS. Fecal microbiota was analysed by 16S rRNA gene sequencing according to Illumina metagenomics standard procedure on MiSeq Platform. Dada2 pipeline was used to process sequencing data, while DESeq2 and Aldex2 tools were used to calculate differential abundance taxa, correcting for age, sex, Body Mass Index, sequencing run and presence of mood disorders.
RESULTS: The sample included 37 RLS (28 females, mean age 64.78 years), 31 INS (22 females, mean age 60.64 years) and 33 CTRL (24 females, mean age 62.54 years). Differential abundance analysis revealed a statistically significant decrease in the abundance of Lachnoclostridium and Flavonifractor genera in RLS compared to CTRL and INS, but not in the INS compared to CTRL. Lachnoclostridium abundance tended to decrease with long disease duration and a predominant motor phenotype. In the RLS group, several genera were identified as significantly associated with IRLS and PSQI scores.
CONCLUSIONS: Although only a few previous studies have reported the presence of small intestinal bacterial overgrowth (SIBO) in RLS, to the best of our knowledge this is the first study to highlight significant differences in the gut microbiota composition of RLS compared to both CTRL and INS, identifying a specific RLS metagenomic signature.
Additional Links: PMID-41378921
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41378921,
year = {2025},
author = {Montini, A and Pellegrini, C and Loddo, G and Ravaioli, F and Baldelli, L and Mainieri, G and Pirazzini, C and Mazzotta, E and Carano, F and Sala, C and De Fanti, S and Bacalini, MG and Provini, F},
title = {Analysis of gut microbiota in Restless Legs Syndrome: searching for a metagenomic signature.},
journal = {Sleep},
volume = {},
number = {},
pages = {},
doi = {10.1093/sleep/zsaf383},
pmid = {41378921},
issn = {1550-9109},
abstract = {STUDY OBJECTIVES: We aim to analyse the microbiota composition in RLS patients and its relationship with the different RLS phenotypes.
METHODS: We recruited idiopathic RLS (RLS) and insomnia (INS) patients and healthy subjects (CTRL). Validated questionnaires (PSQI, IRLS, ISI, BDI-II) were administered in the RLS and INS. Fecal microbiota was analysed by 16S rRNA gene sequencing according to Illumina metagenomics standard procedure on MiSeq Platform. Dada2 pipeline was used to process sequencing data, while DESeq2 and Aldex2 tools were used to calculate differential abundance taxa, correcting for age, sex, Body Mass Index, sequencing run and presence of mood disorders.
RESULTS: The sample included 37 RLS (28 females, mean age 64.78 years), 31 INS (22 females, mean age 60.64 years) and 33 CTRL (24 females, mean age 62.54 years). Differential abundance analysis revealed a statistically significant decrease in the abundance of Lachnoclostridium and Flavonifractor genera in RLS compared to CTRL and INS, but not in the INS compared to CTRL. Lachnoclostridium abundance tended to decrease with long disease duration and a predominant motor phenotype. In the RLS group, several genera were identified as significantly associated with IRLS and PSQI scores.
CONCLUSIONS: Although only a few previous studies have reported the presence of small intestinal bacterial overgrowth (SIBO) in RLS, to the best of our knowledge this is the first study to highlight significant differences in the gut microbiota composition of RLS compared to both CTRL and INS, identifying a specific RLS metagenomic signature.},
}
RevDate: 2025-12-11
Dormancy and reactivation of the seed and its microbiome: a holobiont perspective.
mSystems [Epub ahead of print].
Desiccation-tolerant seeds provide an intriguing system for studying microbial dormancy, which includes reversible inactivation and reactivation in response to stress. Focusing on bacterial responses to desiccation and rehydration, we offer a holistic interpretation of dormancy and quiescence within the seed holobiont, highlighting both parallels and distinctions between microbes and their plant host. Based on pilot evidence, we propose that microbial dormancy supports persistence throughout the life cycle of desiccation-tolerant seeds. Transcriptomic analyses of seed-transmitted bacteria have identified genes implicated in inactivation and the viable-but-nonculturable state. Our analysis of Xanthomonas citri pv. fuscans illustrates this during seed maturation. However, the signals triggering microbial reactivation and the potential reciprocal interactions between seed dormancy and quiescence, and microbial dormancy, remain unknown. Elucidating this interplay within the seed holobiont could enhance plant growth and health either by promoting seed germination through microbial inoculation or by enabling early detection of seed-transmitted phytopathogens.
Additional Links: PMID-41378889
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41378889,
year = {2025},
author = {Gerna, D and Chadelaud, T and Lamouche, F and Barret, M and Darrasse, A and Simonin, M},
title = {Dormancy and reactivation of the seed and its microbiome: a holobiont perspective.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0114025},
doi = {10.1128/msystems.01140-25},
pmid = {41378889},
issn = {2379-5077},
abstract = {Desiccation-tolerant seeds provide an intriguing system for studying microbial dormancy, which includes reversible inactivation and reactivation in response to stress. Focusing on bacterial responses to desiccation and rehydration, we offer a holistic interpretation of dormancy and quiescence within the seed holobiont, highlighting both parallels and distinctions between microbes and their plant host. Based on pilot evidence, we propose that microbial dormancy supports persistence throughout the life cycle of desiccation-tolerant seeds. Transcriptomic analyses of seed-transmitted bacteria have identified genes implicated in inactivation and the viable-but-nonculturable state. Our analysis of Xanthomonas citri pv. fuscans illustrates this during seed maturation. However, the signals triggering microbial reactivation and the potential reciprocal interactions between seed dormancy and quiescence, and microbial dormancy, remain unknown. Elucidating this interplay within the seed holobiont could enhance plant growth and health either by promoting seed germination through microbial inoculation or by enabling early detection of seed-transmitted phytopathogens.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
ESP Usage
Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
ESP Content
When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
ESP Help
Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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