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RJR: Recommended Bibliography 18 Sep 2026 at 01:53 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-09-17
CmpDate: 2026-09-17
Differential Metabolite Production Underlies Disruption of the Cystic Fibrosis Airway Microbiota by Pathogens.
bioRxiv : the preprint server for biology.
Cystic fibrosis (CF) is a multisystem disease characterized by the accumulation of mucus in the airways that promotes pathogen colonization, leading to respiratory exacerbations, lung failure, and death. Culture-independent approaches have revealed that the CF airway harbors a complex microbiota, including opportunistic pathogens and bacteria that colonize the oropharynx. Here, we reanalyzed 5,260 16S rRNA gene microbiota datasets to infer ecological associations between members of the CF microbiota. We determined that pathogens are more likely to proliferate and dominate when present, while oropharyngeal bacteria are more likely to form persistent communities. Further, we found higher diversity and increasing numbers of inferred interactions were positively associated with lung function. In contrast, pathogens were negatively associated both with each other and with oropharyngeal bacteria, suggesting that they may disrupt the microbiota. To validate these predictions, we cultured 1,597 bacterial isolates from 96 people with CF and performed 12,542 coculture assays against eight representative CF pathogenic and oropharyngeal bacteria. 23% of these interactions resulted in growth inhibition. While Pseudomonas isolates were, on average, the most inhibitory, we observed variable activity among isolates. We then confirmed that Pseudomonas aeruginosa isolates, even those from the same donor and timepoint, exhibited significant differences in their metabolome and bioactivity profiles that correlated with acquisition of mutations. Together, our results suggest that pathogens may disrupt the CF microbiota and bloom in part through differential metabolite production. Furthermore, these data highlight that characterizing multiple isolates is necessary to capture the full landscape of chemically mediated interactions within microbial communities.
Additional Links: PMID-42523320
PubMed:
Citation:
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@article {pmid42523320,
year = {2026},
author = {Morabbi, SM and Bhowmik, N and Sutherland, S and Wylie, EA and Decker, RS and Daerwish, AA and Pérez, MP and Pascual, E and Lutter, EI and Philmus, B and Stubbendieck, RM},
title = {Differential Metabolite Production Underlies Disruption of the Cystic Fibrosis Airway Microbiota by Pathogens.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42523320},
issn = {2692-8205},
abstract = {Cystic fibrosis (CF) is a multisystem disease characterized by the accumulation of mucus in the airways that promotes pathogen colonization, leading to respiratory exacerbations, lung failure, and death. Culture-independent approaches have revealed that the CF airway harbors a complex microbiota, including opportunistic pathogens and bacteria that colonize the oropharynx. Here, we reanalyzed 5,260 16S rRNA gene microbiota datasets to infer ecological associations between members of the CF microbiota. We determined that pathogens are more likely to proliferate and dominate when present, while oropharyngeal bacteria are more likely to form persistent communities. Further, we found higher diversity and increasing numbers of inferred interactions were positively associated with lung function. In contrast, pathogens were negatively associated both with each other and with oropharyngeal bacteria, suggesting that they may disrupt the microbiota. To validate these predictions, we cultured 1,597 bacterial isolates from 96 people with CF and performed 12,542 coculture assays against eight representative CF pathogenic and oropharyngeal bacteria. 23% of these interactions resulted in growth inhibition. While Pseudomonas isolates were, on average, the most inhibitory, we observed variable activity among isolates. We then confirmed that Pseudomonas aeruginosa isolates, even those from the same donor and timepoint, exhibited significant differences in their metabolome and bioactivity profiles that correlated with acquisition of mutations. Together, our results suggest that pathogens may disrupt the CF microbiota and bloom in part through differential metabolite production. Furthermore, these data highlight that characterizing multiple isolates is necessary to capture the full landscape of chemically mediated interactions within microbial communities.},
}
RevDate: 2026-09-17
Timescale mismatch: redefining ecological opportunity for evolution in the Anthropocene.
The EMBO journal, 45(18):6359-6366.
The Anthropocene is defined by unprecedented biodiversity loss, but also by a profound mismatch of timescales: environmental change unfolds orders of magnitude faster than response times for most ecological and evolutionary processes. Rapid perturbations create transient ecological opportunities, yet these windows are often too brief for diversification to manifest. The central challenge to understanding biodiversity change in the Anthropocene is not whether ecological opportunity—the availability of novel resources or niches that relax competition—arises, but whether it persists long enough for evolution to act. Microbiome-mediated as well as behavioral and physiological plasticity can buffer organisms against short-term instability and enable swift niche shifts, but such flexibility is reversible, typically non-heritable, and fragile under sustained disturbance. Without enduring selection or sufficient genetic variation, flexibility cannot substitute for evolution. The classical framework of ecological opportunity—conceived for stable environments and gradual change—is therefore inadequate. Diversification, i.e., the rebuilding of biodiversity in the Anthropocene, demands a time-scale integrated framework that unites evolutionary, ecological, and microbiome dynamics to pinpoint when fleeting opportunities can be stabilized for lasting diversification.
Additional Links: PMID-42538473
PubMed:
Citation:
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@article {pmid42538473,
year = {2026},
author = {Voolstra, CR and Hermann, RJ and Stibor, H and Keller, A and Becks, L},
title = {Timescale mismatch: redefining ecological opportunity for evolution in the Anthropocene.},
journal = {The EMBO journal},
volume = {45},
number = {18},
pages = {6359-6366},
pmid = {42538473},
issn = {1460-2075},
support = {9196//Gordon and Betty Moore Foundation (GBMF)/ ; CAP-2024-1692//CORDAP/ ; },
abstract = {The Anthropocene is defined by unprecedented biodiversity loss, but also by a profound mismatch of timescales: environmental change unfolds orders of magnitude faster than response times for most ecological and evolutionary processes. Rapid perturbations create transient ecological opportunities, yet these windows are often too brief for diversification to manifest. The central challenge to understanding biodiversity change in the Anthropocene is not whether ecological opportunity—the availability of novel resources or niches that relax competition—arises, but whether it persists long enough for evolution to act. Microbiome-mediated as well as behavioral and physiological plasticity can buffer organisms against short-term instability and enable swift niche shifts, but such flexibility is reversible, typically non-heritable, and fragile under sustained disturbance. Without enduring selection or sufficient genetic variation, flexibility cannot substitute for evolution. The classical framework of ecological opportunity—conceived for stable environments and gradual change—is therefore inadequate. Diversification, i.e., the rebuilding of biodiversity in the Anthropocene, demands a time-scale integrated framework that unites evolutionary, ecological, and microbiome dynamics to pinpoint when fleeting opportunities can be stabilized for lasting diversification.},
}
RevDate: 2026-09-16
Molecular mimicry and functional convergence of bacterial proteins in host-microbe interactions.
Cell reports, 45(9):117983 pii:S2211-1247(26)01061-2 [Epub ahead of print].
Bacterial proteins modulate host immunity through diverse molecular strategies that are often broadly described as molecular mimicry. However, inconsistent terminology has obscured distinctions between genuine host-like interactions and other forms of host-directed immune modulation. We propose an operational framework that classifies bacterial proteins into four mechanistic categories: molecular mimicry, mimic-like behavior, functional convergence, and pathway interference. The framework prioritizes explicit criteria, including host-target engagement, interaction-interface similarity, functional equivalence, predominant molecular mechanism, and strength of supporting evidence, rather than immune outcome alone. Representative bacterial effectors are discussed alongside their evolutionary origins, computational prediction, experimental validation, and emerging technologies for mechanistic investigation. By separating evolutionary processes from molecular action and applying evidence-based classification criteria, this review clarifies ambiguous terminology and provides a consistent conceptual foundation for interpreting bacterial immune modulation. The framework may also guide future mechanistic studies, comparative analyses, and translational research across diverse pathogenic and commensal host-microbe interaction systems.
Additional Links: PMID-42747964
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PubMed:
Citation:
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@article {pmid42747964,
year = {2026},
author = {Chudhary, A and Wang, X},
title = {Molecular mimicry and functional convergence of bacterial proteins in host-microbe interactions.},
journal = {Cell reports},
volume = {45},
number = {9},
pages = {117983},
doi = {10.1016/j.celrep.2026.117983},
pmid = {42747964},
issn = {2211-1247},
abstract = {Bacterial proteins modulate host immunity through diverse molecular strategies that are often broadly described as molecular mimicry. However, inconsistent terminology has obscured distinctions between genuine host-like interactions and other forms of host-directed immune modulation. We propose an operational framework that classifies bacterial proteins into four mechanistic categories: molecular mimicry, mimic-like behavior, functional convergence, and pathway interference. The framework prioritizes explicit criteria, including host-target engagement, interaction-interface similarity, functional equivalence, predominant molecular mechanism, and strength of supporting evidence, rather than immune outcome alone. Representative bacterial effectors are discussed alongside their evolutionary origins, computational prediction, experimental validation, and emerging technologies for mechanistic investigation. By separating evolutionary processes from molecular action and applying evidence-based classification criteria, this review clarifies ambiguous terminology and provides a consistent conceptual foundation for interpreting bacterial immune modulation. The framework may also guide future mechanistic studies, comparative analyses, and translational research across diverse pathogenic and commensal host-microbe interaction systems.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Early-life exposures in infants born during and after the COVID-19 pandemic: A comparative prospective observational study of the CORAL and FLORAL birth cohorts.
Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology, 37(9):e70471.
BACKGROUND: The CORAL 2020 birth cohort examined health outcomes and feeding practises in infants born during the COVID-19 pandemic, a period of reduced social mixing and altered healthcare utilization during a critical period of immune development. The 2025 FLORAL (FoLlow-on from CORAL) cohort was established to determine whether findings from the CORAL cohort were specific to the pandemic period or reflected broader evolving trends.
METHODS: FLORAL is a prospective observational birth cohort study recruiting term infants born between March and May 2025 across three Dublin maternity hospitals using almost identical methodology to the CORAL cohort. Assessments included parent-completed questionnaires and in-patient study visits. Outcomes at 6 months were compared between FLORAL and CORAL cohorts to examine differences in early-life exposures.
RESULTS: Of 574 infants whose parents provided consent, 485 completed the enrolment questionnaire. At 6 months, 442 participants completed the six-month follow-up questionnaire and 440 attended the in-person study visit. Demographic characteristics were broadly comparable between cohorts. FLORAL infants had numerically higher rates of reported infections (33.3% vs. 28%, p = .12), hospitalization (13.1% vs. 5.1%, p < .001), and antibiotic exposure (13.1% vs. 6.2%, p = .002) compared with CORAL infants. However, the introduction of allergenic foods occurred significantly more frequently in FLORAL, with peanut introduced in 44% of infants compared with 13.6% in CORAL (p < .0001).
CONCLUSION: Compared with pandemic-born infants, post-pandemic infants experienced increased infection-related healthcare utilization and increased antibiotic exposure, alongside sustained high breastfeeding rates and substantially earlier allergen introduction. These may influence microbiome development and later atopic outcomes.
Additional Links: PMID-42747972
PubMed:
Citation:
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@article {pmid42747972,
year = {2026},
author = {Sokay, A and Burke, S and Iatan, M and Byrne, S and Verdon, S and Crupper, J and Hanoudi, J and Miramontes, IM and Bout, N and Dimakos, M and Halpenny, L and White, M and McCallion, N and Curley, A and Byrne, S and O'Mahony, L and Hourihane, J},
title = {Early-life exposures in infants born during and after the COVID-19 pandemic: A comparative prospective observational study of the CORAL and FLORAL birth cohorts.},
journal = {Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology},
volume = {37},
number = {9},
pages = {e70471},
pmid = {42747972},
issn = {1399-3038},
support = {23/FFP-A/12076//Research Ireland Frontiers for the Future Programme/ ; },
mesh = {Humans ; Female ; *COVID-19/epidemiology ; Infant ; Prospective Studies ; Male ; *SARS-CoV-2 ; Infant, Newborn ; Birth Cohort ; Surveys and Questionnaires ; Pandemics ; },
abstract = {BACKGROUND: The CORAL 2020 birth cohort examined health outcomes and feeding practises in infants born during the COVID-19 pandemic, a period of reduced social mixing and altered healthcare utilization during a critical period of immune development. The 2025 FLORAL (FoLlow-on from CORAL) cohort was established to determine whether findings from the CORAL cohort were specific to the pandemic period or reflected broader evolving trends.
METHODS: FLORAL is a prospective observational birth cohort study recruiting term infants born between March and May 2025 across three Dublin maternity hospitals using almost identical methodology to the CORAL cohort. Assessments included parent-completed questionnaires and in-patient study visits. Outcomes at 6 months were compared between FLORAL and CORAL cohorts to examine differences in early-life exposures.
RESULTS: Of 574 infants whose parents provided consent, 485 completed the enrolment questionnaire. At 6 months, 442 participants completed the six-month follow-up questionnaire and 440 attended the in-person study visit. Demographic characteristics were broadly comparable between cohorts. FLORAL infants had numerically higher rates of reported infections (33.3% vs. 28%, p = .12), hospitalization (13.1% vs. 5.1%, p < .001), and antibiotic exposure (13.1% vs. 6.2%, p = .002) compared with CORAL infants. However, the introduction of allergenic foods occurred significantly more frequently in FLORAL, with peanut introduced in 44% of infants compared with 13.6% in CORAL (p < .0001).
CONCLUSION: Compared with pandemic-born infants, post-pandemic infants experienced increased infection-related healthcare utilization and increased antibiotic exposure, alongside sustained high breastfeeding rates and substantially earlier allergen introduction. These may influence microbiome development and later atopic outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*COVID-19/epidemiology
Infant
Prospective Studies
Male
*SARS-CoV-2
Infant, Newborn
Birth Cohort
Surveys and Questionnaires
Pandemics
RevDate: 2026-09-16
The Skin and Gut Microbiome in Hidradenitis Suppurativa.
Dermatology (Basel, Switzerland) pii:000554298 [Epub ahead of print].
Recent evidence indicates that both the bacterial composition of the skin and gut microbiota may contribute to the pathogenesis and progression of hidradenitis suppurativa (HS). Several studies have identified alterations in the skin bacterial microbiota, including an increased abundance of anaerobic taxa such as Prevotella spp. and Porphyromonas spp., alongside a reduction in commensal species like Cutibacterium spp., changes that may promote chronic inflammation and biofilm formation. Comparative analyses of lesional versus non-lesional skin have also revealed enrichment of bacterial pathways related to cell growth, DNA replication, and mismatch repair, suggesting enhanced microbial proliferation within HS lesions. Emerging evidence further suggests the presence of bacterial gut dysbiosis in HS, with some studies reporting reduced microbial diversity and lower abundance of protective genera Ruminococcaceae, and Lachnospiraceae families. Efforts to modulate the skin and gut microbiota in HS are underway, exploring approaches such as dietary modification, antibiotic usage, and probiotic supplementation. Moreover, comorbid conditions frequently associated with HS appear to influence disease severity and may mediate the relationship between microbial imbalance and systemic inflammation. Despite these insights, current research remains fragmented, characterized by small sample sizes, heterogeneous study designs, and a scarcity of robust interventional data.
Additional Links: PMID-42748030
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PubMed:
Citation:
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@article {pmid42748030,
year = {2026},
author = {Gupta, AK and Liddy, A and Saunte, DML and Piguet, V and Jemec, G},
title = {The Skin and Gut Microbiome in Hidradenitis Suppurativa.},
journal = {Dermatology (Basel, Switzerland)},
volume = {},
number = {},
pages = {1},
doi = {10.1159/drm/ackag018},
pmid = {42748030},
issn = {1421-9832},
abstract = {Recent evidence indicates that both the bacterial composition of the skin and gut microbiota may contribute to the pathogenesis and progression of hidradenitis suppurativa (HS). Several studies have identified alterations in the skin bacterial microbiota, including an increased abundance of anaerobic taxa such as Prevotella spp. and Porphyromonas spp., alongside a reduction in commensal species like Cutibacterium spp., changes that may promote chronic inflammation and biofilm formation. Comparative analyses of lesional versus non-lesional skin have also revealed enrichment of bacterial pathways related to cell growth, DNA replication, and mismatch repair, suggesting enhanced microbial proliferation within HS lesions. Emerging evidence further suggests the presence of bacterial gut dysbiosis in HS, with some studies reporting reduced microbial diversity and lower abundance of protective genera Ruminococcaceae, and Lachnospiraceae families. Efforts to modulate the skin and gut microbiota in HS are underway, exploring approaches such as dietary modification, antibiotic usage, and probiotic supplementation. Moreover, comorbid conditions frequently associated with HS appear to influence disease severity and may mediate the relationship between microbial imbalance and systemic inflammation. Despite these insights, current research remains fragmented, characterized by small sample sizes, heterogeneous study designs, and a scarcity of robust interventional data.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
The analysis of cervicovaginal microbiota and immune mediators in patients with adenomyosis.
Wiadomosci lekarskie (Warsaw, Poland : 1960), 79(7):1493-1499.
OBJECTIVE: Aim: To determine and characterise changes associated with microbial, inflammatory and immune factors in patients with adenomyosis.
PATIENTS AND METHODS: Materials and Methods: 115 female patients were enrolled in the study, including 85 patients with adenomyosis and 30 healthy individuals. Vaginal cleanliness was assessed by collecting vaginal samples and plating on solid bacterial agar. Urogenital infections were determined by the PCR analysis of the cervicovaginal samples. The immunological characterisation was performed using enzyme immunoassay to analyse cervicovaginal lavage for β-defensin-2 and a defined set of cytokines. Antibody titers were quantified in patients' serum using nephelometry.
RESULTS: Results: Patients with adenomyosis displayed disrupted cervicovaginal microflora that was characterised by elevated levels of pro-inflammatory cytokines and antimicrobial peptide β-defensin-2. Serum analysis of patients with adenomyosis revealed higher concentration of IgG, IgM and IgA antibodies compared to healthy control groups.
CONCLUSION: Conclusions: Analysis of inflammatory and immunological parameters in patients with adenomyosis revealed distinct features of the pathophysiology of adenomyosis. Specifically, patients with adenomyosis had disrupted cervicovaginal microflora with higher prevalence of anaerobic species. Furthermore, patients with adenomyosis had elevated levels of pro-inflammatory cytokines and interleukins in cervicovaginal lavage, and higher levels of IgG, IgM and IgA antibody serum titres. The analysis presented in the paper represents an important step towards determining precise diagnostic parameters and effective therapies to treat adenomyosis.
Additional Links: PMID-42748297
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PubMed:
Citation:
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@article {pmid42748297,
year = {2026},
author = {Shcherbina, M and Potapova, L and Lipko, O and Shcherbina, L and Chekhunova, A and Mertsalova, O},
title = {The analysis of cervicovaginal microbiota and immune mediators in patients with adenomyosis.},
journal = {Wiadomosci lekarskie (Warsaw, Poland : 1960)},
volume = {79},
number = {7},
pages = {1493-1499},
doi = {10.36740/WLek/218754},
pmid = {42748297},
issn = {0043-5147},
mesh = {Humans ; Female ; *Adenomyosis/microbiology/immunology ; *Vagina/microbiology/immunology ; Adult ; *Microbiota ; *Cervix Uteri/microbiology ; beta-Defensins ; Cytokines ; Middle Aged ; },
abstract = {OBJECTIVE: Aim: To determine and characterise changes associated with microbial, inflammatory and immune factors in patients with adenomyosis.
PATIENTS AND METHODS: Materials and Methods: 115 female patients were enrolled in the study, including 85 patients with adenomyosis and 30 healthy individuals. Vaginal cleanliness was assessed by collecting vaginal samples and plating on solid bacterial agar. Urogenital infections were determined by the PCR analysis of the cervicovaginal samples. The immunological characterisation was performed using enzyme immunoassay to analyse cervicovaginal lavage for β-defensin-2 and a defined set of cytokines. Antibody titers were quantified in patients' serum using nephelometry.
RESULTS: Results: Patients with adenomyosis displayed disrupted cervicovaginal microflora that was characterised by elevated levels of pro-inflammatory cytokines and antimicrobial peptide β-defensin-2. Serum analysis of patients with adenomyosis revealed higher concentration of IgG, IgM and IgA antibodies compared to healthy control groups.
CONCLUSION: Conclusions: Analysis of inflammatory and immunological parameters in patients with adenomyosis revealed distinct features of the pathophysiology of adenomyosis. Specifically, patients with adenomyosis had disrupted cervicovaginal microflora with higher prevalence of anaerobic species. Furthermore, patients with adenomyosis had elevated levels of pro-inflammatory cytokines and interleukins in cervicovaginal lavage, and higher levels of IgG, IgM and IgA antibody serum titres. The analysis presented in the paper represents an important step towards determining precise diagnostic parameters and effective therapies to treat adenomyosis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Adenomyosis/microbiology/immunology
*Vagina/microbiology/immunology
Adult
*Microbiota
*Cervix Uteri/microbiology
beta-Defensins
Cytokines
Middle Aged
RevDate: 2026-09-16
Gut microbial community assembly exhibits compartment-specific responses to selection for high body weight in female chickens.
Poultry science, 105(12):107712 pii:S0032-5791(26)01346-5 [Epub ahead of print].
Conventional poultry breeding primarily targets host growth traits, yet breeding may also reshape the gut microbiota through host-microbe interactions. Given the spatial heterogeneity of the chicken gastrointestinal tract, whether divergent selection for body weight is associated with compartment-specific microbial assembly and differences in the digestive ecosystem remains unclear. Here, using female primitive line and a high body weight (HBW) selected line, we systematically characterized differences in host gastrointestinal traits and gut microbial ecology associated with divergent selection history. Significant differences in gut morphology and local environmental conditions were observed between the two lines, together with region-specific shifts in microbial community assembly. Specifically, crop weight was greater and microbial assembly exhibited greater stochasticity in the HBW line, potentially reflecting differences in feeding-related gastrointestinal dynamics. In contrast, the small intestine displayed improved villus morphology and altered microbial assembly patterns, accompanied by enrichment of potentially beneficial taxa associated with nutrient utilization, including Monoglobus in the duodenum and Blautia in the ileum, indicating coordinated changes in host intestinal development and microbial ecological adaptation. The cecal community showed relatively stable assembly patterns but was enriched in metabolically relevant taxa such as Lachnospiraceae and Faecalibacterium, together with differences in predicted functional potential related to nutrient metabolism. Overall, this study shows that the HBW line is associated with distinct, compartment-specific patterns of gut microbial assembly, providing a conceptual framework for considering the gut microbiota in poultry breeding strategies.
Additional Links: PMID-42748564
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PubMed:
Citation:
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@article {pmid42748564,
year = {2026},
author = {Zhang, F and Wang, Y and Qian, J and Li, S and Deng, X and Lu, M and Liu, Y and Yang, X and Zhang, J and Ren, Z and Yang, X},
title = {Gut microbial community assembly exhibits compartment-specific responses to selection for high body weight in female chickens.},
journal = {Poultry science},
volume = {105},
number = {12},
pages = {107712},
doi = {10.1016/j.psj.2026.107712},
pmid = {42748564},
issn = {1525-3171},
abstract = {Conventional poultry breeding primarily targets host growth traits, yet breeding may also reshape the gut microbiota through host-microbe interactions. Given the spatial heterogeneity of the chicken gastrointestinal tract, whether divergent selection for body weight is associated with compartment-specific microbial assembly and differences in the digestive ecosystem remains unclear. Here, using female primitive line and a high body weight (HBW) selected line, we systematically characterized differences in host gastrointestinal traits and gut microbial ecology associated with divergent selection history. Significant differences in gut morphology and local environmental conditions were observed between the two lines, together with region-specific shifts in microbial community assembly. Specifically, crop weight was greater and microbial assembly exhibited greater stochasticity in the HBW line, potentially reflecting differences in feeding-related gastrointestinal dynamics. In contrast, the small intestine displayed improved villus morphology and altered microbial assembly patterns, accompanied by enrichment of potentially beneficial taxa associated with nutrient utilization, including Monoglobus in the duodenum and Blautia in the ileum, indicating coordinated changes in host intestinal development and microbial ecological adaptation. The cecal community showed relatively stable assembly patterns but was enriched in metabolically relevant taxa such as Lachnospiraceae and Faecalibacterium, together with differences in predicted functional potential related to nutrient metabolism. Overall, this study shows that the HBW line is associated with distinct, compartment-specific patterns of gut microbial assembly, providing a conceptual framework for considering the gut microbiota in poultry breeding strategies.},
}
RevDate: 2026-09-16
Probiotic cells-encapsulated electrospun scaffolds accelerate diabetic wound healingviasynergistic anti-infection activity and skin microbiome modulation.
Colloids and surfaces. B, Biointerfaces, 269:116188 pii:S0927-7765(26)00776-9 [Epub ahead of print].
Diabetic wound healing is often hindered by persistent pathogenic infections and associated skin microbiome dysbiosis. The efficacy of conventional antibiotic drugs is significantly compromised by increasing drug resistance and further disruption of commensal microbiota. In this study, a probiotic-loaded, dry-state electrospun scaffold, Gel@LRNF@PLA, is developed for dual-functional diabetic wound healing. By maintaining probiotic viability while enabling localized antibacterial and microbiome-regulatory effects, the dressing exhibits potent activity against both planktonic Pseudomonas aeruginosa and its biofilms. Moreover, it restores the balance of skin microbiota by suppressing opportunistic pathogens and enriching beneficial commensal bacteria, which synergistically promotes the healing of diabetic infected wounds. This approach not only offers a new structure for living cell-based wound dressings but also provides mechanistic insight into the therapeutic efficacy of living probiotics in treating diabetic wound infections.
Additional Links: PMID-42748616
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PubMed:
Citation:
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@article {pmid42748616,
year = {2026},
author = {Hu, L and Mu, X and Guo, Q and Tong, J and Jiang, J and Liu, Y},
title = {Probiotic cells-encapsulated electrospun scaffolds accelerate diabetic wound healingviasynergistic anti-infection activity and skin microbiome modulation.},
journal = {Colloids and surfaces. B, Biointerfaces},
volume = {269},
number = {},
pages = {116188},
doi = {10.1016/j.colsurfb.2026.116188},
pmid = {42748616},
issn = {1873-4367},
abstract = {Diabetic wound healing is often hindered by persistent pathogenic infections and associated skin microbiome dysbiosis. The efficacy of conventional antibiotic drugs is significantly compromised by increasing drug resistance and further disruption of commensal microbiota. In this study, a probiotic-loaded, dry-state electrospun scaffold, Gel@LRNF@PLA, is developed for dual-functional diabetic wound healing. By maintaining probiotic viability while enabling localized antibacterial and microbiome-regulatory effects, the dressing exhibits potent activity against both planktonic Pseudomonas aeruginosa and its biofilms. Moreover, it restores the balance of skin microbiota by suppressing opportunistic pathogens and enriching beneficial commensal bacteria, which synergistically promotes the healing of diabetic infected wounds. This approach not only offers a new structure for living cell-based wound dressings but also provides mechanistic insight into the therapeutic efficacy of living probiotics in treating diabetic wound infections.},
}
RevDate: 2026-09-16
Urban land use and management drive soil pollution across urban and nearby natural ecosystems in the Iberian Peninsula.
Journal of hazardous materials, 517:143215 pii:S0304-3894(26)02195-3 [Epub ahead of print].
Cities concentrate most of the world's population and human activities, generating pollution that threatens ecosystem functioning and human well-being. Yet, the relative importance of different drivers shaping urban pollution and the spatial distribution of multiple contaminants across cities remain poorly understood. Here, we conducted a standardized survey in 250 plots across 51 cities in the Iberian Peninsula to quantify heavy metals, pesticides, macrolitter and microplastics. We sampled four urban greenspace types (parks, golf courses, urban farms, roundabouts) and nearby natural areas to link contaminants with soil microbiome structure and functioning. Urban parks, roundabouts and urban farms accumulated the highest metal levels, with several sites exceeding regulatory thresholds for Zn, Pb, Ni, and As, whereas golf courses showed lower contamination levels. Pesticides were detected across both urban and natural soils, with no significant differences in concentrations among land use types. In contrast, microplastic concentrations peaked in natural areas, indicating that regional transport and deposition processes can decouple their accumulation from local urban sources. Macrolitter was most abundant in parks and roundabouts, while golf courses exhibited the lowest densities, highlighting the influence of local management and access control. The level of soil contamination, as quantified by contamination indices, was correlated with microbial richness, community composition, and key soil functions. Pesticides were negatively associated with bacterial richness and redox activity, whereas macrolitter was negatively associated with phosphatase activity. Heavy metal contamination was associated with shifts in bacterial and fungal richness and with changes in soil respiration and phosphatase activity, reflecting a potential influence of heavy metals on microbial communities. This study highlights that land use and management shape soil contamination, soil biodiversity, and ecosystem functioning, emphasizing the need for mitigation actions to support the implementation of the EU Soil Strategy in cities.
Additional Links: PMID-42748815
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PubMed:
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@article {pmid42748815,
year = {2026},
author = {Sala-Navarro, AC and Casado-Coy, N and Campos-Castro, A and Algora, C and Aguilar-Santana, E and Zhai, K and Alday, JG and Armas, C and Bueno, CG and Calvo, L and Carmona-Yáñez, MD and Centenaro, G and Dashevskaya, S and Humia, JD and Pereiras, AR and de Guevara, ML and Felipe-Lucia, MR and Fernández-Alonso, MJ and García-Palacios, P and Chamizo, S and de la Riva, EG and Jiménez-Prieto, B and Jiménez, JJ and Leo, M and López-Velasco, A and Lorenzo, C and Lucas-Borja, ME and Pérez-López, J and Plaza-Álvarez, PA and Prieto, I and Terrones, A and Torres, A and Martos-Maestre, AL and Melián, JAH and Ferraz, UÁ and García, MJS and Costa, J and García, E and Figueira, D and Bastida, F and Delgado-Baquerizo, M and Soliveres, S and Beltrán-Sanahuja, A and Sanz-Lazaro, C},
title = {Urban land use and management drive soil pollution across urban and nearby natural ecosystems in the Iberian Peninsula.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143215},
doi = {10.1016/j.jhazmat.2026.143215},
pmid = {42748815},
issn = {1873-3336},
abstract = {Cities concentrate most of the world's population and human activities, generating pollution that threatens ecosystem functioning and human well-being. Yet, the relative importance of different drivers shaping urban pollution and the spatial distribution of multiple contaminants across cities remain poorly understood. Here, we conducted a standardized survey in 250 plots across 51 cities in the Iberian Peninsula to quantify heavy metals, pesticides, macrolitter and microplastics. We sampled four urban greenspace types (parks, golf courses, urban farms, roundabouts) and nearby natural areas to link contaminants with soil microbiome structure and functioning. Urban parks, roundabouts and urban farms accumulated the highest metal levels, with several sites exceeding regulatory thresholds for Zn, Pb, Ni, and As, whereas golf courses showed lower contamination levels. Pesticides were detected across both urban and natural soils, with no significant differences in concentrations among land use types. In contrast, microplastic concentrations peaked in natural areas, indicating that regional transport and deposition processes can decouple their accumulation from local urban sources. Macrolitter was most abundant in parks and roundabouts, while golf courses exhibited the lowest densities, highlighting the influence of local management and access control. The level of soil contamination, as quantified by contamination indices, was correlated with microbial richness, community composition, and key soil functions. Pesticides were negatively associated with bacterial richness and redox activity, whereas macrolitter was negatively associated with phosphatase activity. Heavy metal contamination was associated with shifts in bacterial and fungal richness and with changes in soil respiration and phosphatase activity, reflecting a potential influence of heavy metals on microbial communities. This study highlights that land use and management shape soil contamination, soil biodiversity, and ecosystem functioning, emphasizing the need for mitigation actions to support the implementation of the EU Soil Strategy in cities.},
}
RevDate: 2026-09-16
From dysbiosis to resilience: Microbiome engineering for sustainable shrimp aquaculture.
Comparative biochemistry and physiology. Part D, Genomics & proteomics, 61:102024 pii:S1744-117X(26)00283-2 [Epub ahead of print].
The intensification of shrimp aquaculture has increased exposure to disease, environmental perturbations, and antimicrobial pressure, making microbial stability increasingly relevant to sustainable production. Microbiome stability-encompassing resistance to disturbance and resilience of functional recovery-provides an ecological framework for understanding how shrimp and culture-environment microbial communities respond to intensive farming. This review examines the transition from microbial homeostasis to dysbiosis and evaluates how microbiome engineering could redirect disrupted communities towards resilient states. Evidence is integrated across the intestine, hepatopancreas, rearing water, sediment and biofloc to assess how host genetics, ontogeny, diet, culture conditions, antibiotics and pollutants shape microbiome assembly and destabilization. Disease-associated changes in acute hepatopancreatic necrosis disease, white faeces syndrome, Enterocytozoon hepatopenaei infection, and white spot syndrome virus infection are critically evaluated, with explicit separation of associations, pathogen-induced dysbiosis, and community-level causality. Established and emerging interventions-including probiotics, prebiotics, synbiotics, functional diets, biofloc management, phages, postbiotics, microbiota transplantation and synthetic microbial communities-are assessed according to their capacity to modify microbial function, persistence and recovery rather than taxonomic change alone. We further examine how multi-omics, microbiome-informed breeding, and environmental monitoring could support biomarker development, predictive decision support and context-specific intervention. We argue that progress requires a shift from taxonomic description to function-guided engineering, from endpoint comparisons to direct measurement of resilience, and from laboratory efficacy to reproducible farm-scale validation. Overall, microbiome management may contribute to more disease-resilient and sustainable shrimp production, provided that its effectiveness can be validated under commercial farming conditions.
Additional Links: PMID-42748875
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PubMed:
Citation:
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@article {pmid42748875,
year = {2026},
author = {Imran, S and Junejo, Y and Ahmad, HI and Ozaslan, M and Safdar, M},
title = {From dysbiosis to resilience: Microbiome engineering for sustainable shrimp aquaculture.},
journal = {Comparative biochemistry and physiology. Part D, Genomics & proteomics},
volume = {61},
number = {},
pages = {102024},
doi = {10.1016/j.cbd.2026.102024},
pmid = {42748875},
issn = {1878-0407},
abstract = {The intensification of shrimp aquaculture has increased exposure to disease, environmental perturbations, and antimicrobial pressure, making microbial stability increasingly relevant to sustainable production. Microbiome stability-encompassing resistance to disturbance and resilience of functional recovery-provides an ecological framework for understanding how shrimp and culture-environment microbial communities respond to intensive farming. This review examines the transition from microbial homeostasis to dysbiosis and evaluates how microbiome engineering could redirect disrupted communities towards resilient states. Evidence is integrated across the intestine, hepatopancreas, rearing water, sediment and biofloc to assess how host genetics, ontogeny, diet, culture conditions, antibiotics and pollutants shape microbiome assembly and destabilization. Disease-associated changes in acute hepatopancreatic necrosis disease, white faeces syndrome, Enterocytozoon hepatopenaei infection, and white spot syndrome virus infection are critically evaluated, with explicit separation of associations, pathogen-induced dysbiosis, and community-level causality. Established and emerging interventions-including probiotics, prebiotics, synbiotics, functional diets, biofloc management, phages, postbiotics, microbiota transplantation and synthetic microbial communities-are assessed according to their capacity to modify microbial function, persistence and recovery rather than taxonomic change alone. We further examine how multi-omics, microbiome-informed breeding, and environmental monitoring could support biomarker development, predictive decision support and context-specific intervention. We argue that progress requires a shift from taxonomic description to function-guided engineering, from endpoint comparisons to direct measurement of resilience, and from laboratory efficacy to reproducible farm-scale validation. Overall, microbiome management may contribute to more disease-resilient and sustainable shrimp production, provided that its effectiveness can be validated under commercial farming conditions.},
}
RevDate: 2026-09-16
Temporal Immune Surveillance in Cancer: A Circadian Framework from Mechanisms to Chronotherapeutic Integration.
Critical reviews in oncology/hematology pii:S1040-8428(26)00486-5 [Epub ahead of print].
From a traditional perspective, "immune surveillance" has long been regarded as a static process. However, recent studies have shown that the immune system's ability to detect and combat tumors is dynamically regulated by circadian rhythms; we define this concept as "temporal immune surveillance". Disruption of circadian rhythms leads to impaired immune surveillance, thereby creating an immunosuppressive microenvironment that favors the development and progression of cancer. We describe a multi-tiered regulatory network encompassing the intrinsic circadian clocks of immune cells, clock-mediated regulation of immune gene networks, and finally, systemic regulation via the neuro-immune and microbiota-immune axes. These findings pave the way for chrono-immunotherapy, a strategy built on three integrated pillars: optimizing the timing of existing therapies (e.g., immune checkpoint inhibitors), pharmacologically reprogramming disrupted circadian clocks, and pre-synchronizing host physiology through lifestyle interventions such as time-restricted eating. Developing circadian biomarkers and personalized chronotherapy regimens is crucial for advancing precision oncology.
Additional Links: PMID-42749094
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PubMed:
Citation:
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@article {pmid42749094,
year = {2026},
author = {Wang, J and Qi, DY and Jin, WL},
title = {Temporal Immune Surveillance in Cancer: A Circadian Framework from Mechanisms to Chronotherapeutic Integration.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {105599},
doi = {10.1016/j.critrevonc.2026.105599},
pmid = {42749094},
issn = {1879-0461},
abstract = {From a traditional perspective, "immune surveillance" has long been regarded as a static process. However, recent studies have shown that the immune system's ability to detect and combat tumors is dynamically regulated by circadian rhythms; we define this concept as "temporal immune surveillance". Disruption of circadian rhythms leads to impaired immune surveillance, thereby creating an immunosuppressive microenvironment that favors the development and progression of cancer. We describe a multi-tiered regulatory network encompassing the intrinsic circadian clocks of immune cells, clock-mediated regulation of immune gene networks, and finally, systemic regulation via the neuro-immune and microbiota-immune axes. These findings pave the way for chrono-immunotherapy, a strategy built on three integrated pillars: optimizing the timing of existing therapies (e.g., immune checkpoint inhibitors), pharmacologically reprogramming disrupted circadian clocks, and pre-synchronizing host physiology through lifestyle interventions such as time-restricted eating. Developing circadian biomarkers and personalized chronotherapy regimens is crucial for advancing precision oncology.},
}
RevDate: 2026-09-16
Divergent microbial preludes to necrotising enterocolitis defined by gut phages and bacterial resistomes.
Gut pii:gutjnl-2026-338976 [Epub ahead of print].
BACKGROUND: Translating microbiome correlations into robust predictive features for complex gut disorders remains elusive, partly due to oversimplified models of pathogenesis and neglect of the virome, a key player in microbial ecosystems. Necrotising enterocolitis (NEC), a devastating disease of preterm infants with no reliable clinical predictors, exemplifies this challenge.
OBJECTIVE: To determine the predictive potential of the gut prophageome and polymicrobial aetiologies for NEC.
DESIGN: We applied integrated metagenomic and metatranscriptomic analyses and machine learning to 1825 longitudinal stool samples from 43 preterm infants who later developed NEC and 86 gestational age-matched and birthweight-matched controls across three US hospitals. We characterised gut prophageome acquisitions and their association with clinical exposures, including antibiotics, diet and pharmacotherapies. To predict NEC risk, we integrated pre-onset prophageome, antibacterial resistome and bacteriome profiles with neonatal pathology, stratifying the cohort by disease onset timing (early: ≤40 days; late: >40 days) for separate analysis.
RESULTS: NEC cases exhibited distinct viral diversity trajectories before disease onset. Early-onset NEC was best predicted by phage-bacterial interaction signatures (75% accuracy, 81% sensitivity). Metatranscriptomics revealed increased phage DNA abundance with low gene expression, suggesting a lysogenic lifestyle that may stabilise pathobionts. These phages encode metabolic genes potentially enhancing pathobiont resilience. Late-onset NEC was best predicted by antibacterial resistome profiles (83% accuracy).
CONCLUSION: The gut prophageome serves as both a source of pre-symptomatic predictive signals and an active modulator of NEC pathogenesis, with distinct microbial mechanisms driving early-onset and late-onset disease. These polymicrobial etiologies inform strategies for early detection, risk stratification and the development of microbiome-targeted preventive and therapeutic interventions.
Additional Links: PMID-42749360
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PubMed:
Citation:
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@article {pmid42749360,
year = {2026},
author = {Zhang, K and Gorelik, MG and Sullivan, JE and Radmacher, P and Escobedo, M and Warner, BB and Tarr, PI and Dantas, G},
title = {Divergent microbial preludes to necrotising enterocolitis defined by gut phages and bacterial resistomes.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2026-338976},
pmid = {42749360},
issn = {1468-3288},
abstract = {BACKGROUND: Translating microbiome correlations into robust predictive features for complex gut disorders remains elusive, partly due to oversimplified models of pathogenesis and neglect of the virome, a key player in microbial ecosystems. Necrotising enterocolitis (NEC), a devastating disease of preterm infants with no reliable clinical predictors, exemplifies this challenge.
OBJECTIVE: To determine the predictive potential of the gut prophageome and polymicrobial aetiologies for NEC.
DESIGN: We applied integrated metagenomic and metatranscriptomic analyses and machine learning to 1825 longitudinal stool samples from 43 preterm infants who later developed NEC and 86 gestational age-matched and birthweight-matched controls across three US hospitals. We characterised gut prophageome acquisitions and their association with clinical exposures, including antibiotics, diet and pharmacotherapies. To predict NEC risk, we integrated pre-onset prophageome, antibacterial resistome and bacteriome profiles with neonatal pathology, stratifying the cohort by disease onset timing (early: ≤40 days; late: >40 days) for separate analysis.
RESULTS: NEC cases exhibited distinct viral diversity trajectories before disease onset. Early-onset NEC was best predicted by phage-bacterial interaction signatures (75% accuracy, 81% sensitivity). Metatranscriptomics revealed increased phage DNA abundance with low gene expression, suggesting a lysogenic lifestyle that may stabilise pathobionts. These phages encode metabolic genes potentially enhancing pathobiont resilience. Late-onset NEC was best predicted by antibacterial resistome profiles (83% accuracy).
CONCLUSION: The gut prophageome serves as both a source of pre-symptomatic predictive signals and an active modulator of NEC pathogenesis, with distinct microbial mechanisms driving early-onset and late-onset disease. These polymicrobial etiologies inform strategies for early detection, risk stratification and the development of microbiome-targeted preventive and therapeutic interventions.},
}
RevDate: 2026-09-16
Longitudinal gut microbiome dynamics during immunotherapy identify microbial features of clinical benefit in advanced primary liver cancer.
Gut pii:gutjnl-2026-339115 [Epub ahead of print].
BACKGROUND: The gut microbiome has been linked to immune checkpoint inhibitor (ICI) outcomes, but the temporal dynamics of microbial communities during treatment remain poorly characterised.
OBJECTIVE: To characterise gut microbiome trajectories during ICI therapy and evaluate whether on-treatment microbial states improve the identification and generalisability of pretreatment biomarker signatures.
DESIGN: We performed a large prospective longitudinal shotgun metagenomic study of 315 patients with advanced primary liver cancer receiving ICI-based therapy, profiling 777 serial stool metagenomes collected at baseline and at approximately 3-month intervals on treatment. Responders (durable clinical benefit ≥6 months) contributed extended follow-up beyond 18 months. On-treatment windows were used for feature discovery; baseline-trained models were evaluated across all nine public ICI cohorts (n=1204).
RESULTS: Responders showed higher baseline alpha diversity and distinct community structure. Longitudinal profiling revealed marked ecological remodelling during therapy in both response groups, characterised by reduced network connectivity, increased modularity and strong time point specificity of discriminatory species. Using the on-treatment contrast at ~6 months (T2) as a discovery window, we identified a 16-species panel. A baseline model built from this panel outperformed models based on baseline-only feature discovery and generalised across nine public ICI studies. The resulting gut microbiome-derived immunotherapy outcome score stratified overall and progression-free survival in the discovery cohort (HRs 0.49 and 0.44) and across multiple external datasets, including stable-disease subsets.
CONCLUSION: The gut microbiome undergoes structured ecological remodelling during ICI therapy; on-treatment longitudinal windows improve pretreatment signature portability and support microbiome-guided stratification in immuno-oncology.
Additional Links: PMID-42749361
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PubMed:
Citation:
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@article {pmid42749361,
year = {2026},
author = {Qian, Z and Han, J and Lyu, B and Ainiwaer, A and Zhao, Q and Wang, S and Cheng, J and Li, Y and Sun, Y and Zhang, X and Lu, Y},
title = {Longitudinal gut microbiome dynamics during immunotherapy identify microbial features of clinical benefit in advanced primary liver cancer.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2026-339115},
pmid = {42749361},
issn = {1468-3288},
abstract = {BACKGROUND: The gut microbiome has been linked to immune checkpoint inhibitor (ICI) outcomes, but the temporal dynamics of microbial communities during treatment remain poorly characterised.
OBJECTIVE: To characterise gut microbiome trajectories during ICI therapy and evaluate whether on-treatment microbial states improve the identification and generalisability of pretreatment biomarker signatures.
DESIGN: We performed a large prospective longitudinal shotgun metagenomic study of 315 patients with advanced primary liver cancer receiving ICI-based therapy, profiling 777 serial stool metagenomes collected at baseline and at approximately 3-month intervals on treatment. Responders (durable clinical benefit ≥6 months) contributed extended follow-up beyond 18 months. On-treatment windows were used for feature discovery; baseline-trained models were evaluated across all nine public ICI cohorts (n=1204).
RESULTS: Responders showed higher baseline alpha diversity and distinct community structure. Longitudinal profiling revealed marked ecological remodelling during therapy in both response groups, characterised by reduced network connectivity, increased modularity and strong time point specificity of discriminatory species. Using the on-treatment contrast at ~6 months (T2) as a discovery window, we identified a 16-species panel. A baseline model built from this panel outperformed models based on baseline-only feature discovery and generalised across nine public ICI studies. The resulting gut microbiome-derived immunotherapy outcome score stratified overall and progression-free survival in the discovery cohort (HRs 0.49 and 0.44) and across multiple external datasets, including stable-disease subsets.
CONCLUSION: The gut microbiome undergoes structured ecological remodelling during ICI therapy; on-treatment longitudinal windows improve pretreatment signature portability and support microbiome-guided stratification in immuno-oncology.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Integrated immunoinformatics for the design of novel multi-epitope vaccine and identification of new drug targets against Stenotrophomonas maltophilia, a multidrug-resistant superbug.
Journal, genetic engineering & biotechnology, 24(3):100772.
BACKGROUND: Stenotrophomonas maltophilia is a multidrug-resistant opportunistic pathogen causing severe hospital-acquired infections, especially in immunocompromised patients. The absence of an effective vaccine and rising antibiotic resistance underscore the need for novel interventions. This study employed an integrated reverse vaccinology and computational analyses to identify new immunogenic targets, design a multi-epitope vaccine (MEV), and propose potential drug targets.
METHODS: A comprehensive immunoinformatics pipeline was employed to assess antigenicity, allergenicity, human similarity, and physicochemical properties of S. maltophilia proteins. Both B- and T-cell epitopes were screened; however, only the top B-cell epitopes were selected for MEV construction, given the extracellular nature of S. maltophilia. MEV-TLR interactions were analyzed through molecular docking and dynamics simulations. In parallel, cytoplasmic proteins were screened via a subtractive genomics approach to identify essential, non-human homologous, and non-microbiome-similar proteins, which were further evaluated for druggability and interaction networks to propose novel therapeutic targets.
RESULTS: From a total of 4111 proteins, seven potential immunogenic targets were identified: GspD (WP_108270537.1), FhuE (WP_049451370.1), fimbrial protein (WP_012479122.1), TonB-dependent receptor (WP_169448402.1), TolC family protein (WP_108270106.1), autotransporter beta-barrel OMP (WP_169448945.1), and a hypothetical protein (WP_005407892.1). Subsequently, an MEV was designed using five immunogenic epitopes derived from four of these targets: WP_005407892.1 (ADQDSSNM), WP_049451370.1 (SGKAEQ and GEESKTPS), WP_108270537.1 (GVTSTQSDSERT), and WP_169448945.1 (RELGGDRNE). Molecular docking and molecular dynamics simulations demonstrated strong, stable, and feasible interactions between the MEV and TLR-2 and TLR-4 receptors. Moreover, nine novel drug targets were predicted for S. maltophilia, providing new therapeutic insights.
CONCLUSION: The designed MEV and identified immunogenic targets represent promising vaccine candidates against S. maltophilia. Further in vitro and in vivo studies are essential to confirm their safety, immunogenicity, and protective efficacy. Additionally, subtractive genomics analysis revealed nine novel, non-homologous drug targets, offering safer and more specific therapeutic avenues.
Additional Links: PMID-42749442
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PubMed:
Citation:
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@article {pmid42749442,
year = {2026},
author = {Moradkasani, S and Noori Goodarzi, N and Beig, M and Sholeh, M and Fereshteh, S and Khazani Asforooshani, M and Shahbazi, B and Shahbazi, S and Badmasti, F},
title = {Integrated immunoinformatics for the design of novel multi-epitope vaccine and identification of new drug targets against Stenotrophomonas maltophilia, a multidrug-resistant superbug.},
journal = {Journal, genetic engineering & biotechnology},
volume = {24},
number = {3},
pages = {100772},
doi = {10.1016/j.jgeb.2026.100772},
pmid = {42749442},
issn = {2090-5920},
abstract = {BACKGROUND: Stenotrophomonas maltophilia is a multidrug-resistant opportunistic pathogen causing severe hospital-acquired infections, especially in immunocompromised patients. The absence of an effective vaccine and rising antibiotic resistance underscore the need for novel interventions. This study employed an integrated reverse vaccinology and computational analyses to identify new immunogenic targets, design a multi-epitope vaccine (MEV), and propose potential drug targets.
METHODS: A comprehensive immunoinformatics pipeline was employed to assess antigenicity, allergenicity, human similarity, and physicochemical properties of S. maltophilia proteins. Both B- and T-cell epitopes were screened; however, only the top B-cell epitopes were selected for MEV construction, given the extracellular nature of S. maltophilia. MEV-TLR interactions were analyzed through molecular docking and dynamics simulations. In parallel, cytoplasmic proteins were screened via a subtractive genomics approach to identify essential, non-human homologous, and non-microbiome-similar proteins, which were further evaluated for druggability and interaction networks to propose novel therapeutic targets.
RESULTS: From a total of 4111 proteins, seven potential immunogenic targets were identified: GspD (WP_108270537.1), FhuE (WP_049451370.1), fimbrial protein (WP_012479122.1), TonB-dependent receptor (WP_169448402.1), TolC family protein (WP_108270106.1), autotransporter beta-barrel OMP (WP_169448945.1), and a hypothetical protein (WP_005407892.1). Subsequently, an MEV was designed using five immunogenic epitopes derived from four of these targets: WP_005407892.1 (ADQDSSNM), WP_049451370.1 (SGKAEQ and GEESKTPS), WP_108270537.1 (GVTSTQSDSERT), and WP_169448945.1 (RELGGDRNE). Molecular docking and molecular dynamics simulations demonstrated strong, stable, and feasible interactions between the MEV and TLR-2 and TLR-4 receptors. Moreover, nine novel drug targets were predicted for S. maltophilia, providing new therapeutic insights.
CONCLUSION: The designed MEV and identified immunogenic targets represent promising vaccine candidates against S. maltophilia. Further in vitro and in vivo studies are essential to confirm their safety, immunogenicity, and protective efficacy. Additionally, subtractive genomics analysis revealed nine novel, non-homologous drug targets, offering safer and more specific therapeutic avenues.},
}
RevDate: 2026-09-16
Gut-brain-heart axis in congenital heart disease: emerging roles of the microbiome in cardiac physiology and neurodevelopment.
Heart (British Cardiac Society) pii:heartjnl-2026-328544 [Epub ahead of print].
Congenital heart disease (CHD) is increasingly recognised as a multisystem condition extending beyond structural cardiac abnormalities to include gastrointestinal, immunological and neurodevelopmental consequences. Although advances in surgical and intensive care have significantly improved survival, children with CHD remain at heightened risk for adverse neurodevelopmental outcomes, systemic inflammation and gastrointestinal morbidity. The gut microbiome plays a central role in immune regulation, metabolic homeostasis and brain development particularly during early life. Perturbations of the microbiome are common in infants with CHD due to altered gut perfusion, antibiotic exposure, feeding disruption and cardiopulmonary bypass (CPB). These changes may influence both cardiac recovery and neurodevelopment through interconnected gut-heart-brain signalling pathways. This review synthesises current evidence linking the gut microbiome to cardiac physiology and brain development in children with CHD, with particular emphasis on early-life vulnerability, perioperative factors and emerging translational insights. Understanding these interactions may inform future strategies to optimise long-term outcomes in this high-risk population.
Additional Links: PMID-42749475
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PubMed:
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@article {pmid42749475,
year = {2026},
author = {Kelleher, ST and Patangia, D and Ross, RP and James, A and Stanton, C and McMahon, CJ},
title = {Gut-brain-heart axis in congenital heart disease: emerging roles of the microbiome in cardiac physiology and neurodevelopment.},
journal = {Heart (British Cardiac Society)},
volume = {},
number = {},
pages = {},
doi = {10.1136/heartjnl-2026-328544},
pmid = {42749475},
issn = {1468-201X},
abstract = {Congenital heart disease (CHD) is increasingly recognised as a multisystem condition extending beyond structural cardiac abnormalities to include gastrointestinal, immunological and neurodevelopmental consequences. Although advances in surgical and intensive care have significantly improved survival, children with CHD remain at heightened risk for adverse neurodevelopmental outcomes, systemic inflammation and gastrointestinal morbidity. The gut microbiome plays a central role in immune regulation, metabolic homeostasis and brain development particularly during early life. Perturbations of the microbiome are common in infants with CHD due to altered gut perfusion, antibiotic exposure, feeding disruption and cardiopulmonary bypass (CPB). These changes may influence both cardiac recovery and neurodevelopment through interconnected gut-heart-brain signalling pathways. This review synthesises current evidence linking the gut microbiome to cardiac physiology and brain development in children with CHD, with particular emphasis on early-life vulnerability, perioperative factors and emerging translational insights. Understanding these interactions may inform future strategies to optimise long-term outcomes in this high-risk population.},
}
RevDate: 2026-09-16
The textile web as a probiotic interface.
Trends in microbiology pii:S0966-842X(26)00223-4 [Epub ahead of print].
Microbiome of the Built Environment research exhibits a marked 'hard-surface bias', overlooking the dynamic soft materials that dominate human-microbial exchange. We propose a theoretical reorientation: the home as a textile web of dynamic, porous microbial reactors. Grounded in immunology's Danger Theory and the principle of 'tissue-based class control', these soft interfaces function as an external tissue analog. By treating textiles as designable interfaces (ranging from airway exchange nodes to laundry bioreactors), architecture becomes a site for proactive probiotic rituals. This framework leverages competitive exclusion to support externalized mucosal 'guard duty', transitioning from prophylactic sterility to a choreography of domestic care. Notably, this reframing recognizes that hygiene encompasses more than infection prevention: domestic cleaning rituals also shape the microbial ecology that educates the immune system. Ultimately, we frame the living home as a tolerogenic exoskeleton, biologically calibrated to protect and prime the human holobiont.
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PubMed:
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@article {pmid42749571,
year = {2026},
author = {Armstrong, R and Timmis, KN},
title = {The textile web as a probiotic interface.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.08.007},
pmid = {42749571},
issn = {1878-4380},
abstract = {Microbiome of the Built Environment research exhibits a marked 'hard-surface bias', overlooking the dynamic soft materials that dominate human-microbial exchange. We propose a theoretical reorientation: the home as a textile web of dynamic, porous microbial reactors. Grounded in immunology's Danger Theory and the principle of 'tissue-based class control', these soft interfaces function as an external tissue analog. By treating textiles as designable interfaces (ranging from airway exchange nodes to laundry bioreactors), architecture becomes a site for proactive probiotic rituals. This framework leverages competitive exclusion to support externalized mucosal 'guard duty', transitioning from prophylactic sterility to a choreography of domestic care. Notably, this reframing recognizes that hygiene encompasses more than infection prevention: domestic cleaning rituals also shape the microbial ecology that educates the immune system. Ultimately, we frame the living home as a tolerogenic exoskeleton, biologically calibrated to protect and prime the human holobiont.},
}
RevDate: 2026-09-16
Characterization of the oral microbiota and antimicrobial resistance genes in shelter dogs in Japan.
The Journal of veterinary medical science [Epub ahead of print].
Companion animals can serve as reservoirs of antimicrobial resistance genes and zoonotic microorganisms, yet information on shelter dogs remains limited. This study characterized the oral microbiota and screened for antimicrobial resistance genes in shelter dogs in Japan. Oral swabs were collected from 81 dogs, microbial genomic DNA was extracted, bacterial communities were profiled by 16S rRNA gene amplicon sequencing, and antimicrobial resistance genes were screened by PCR. We detected genes conferring resistance to several antimicrobial classes, including β-lactams, tetracyclines, macrolide-lincosamide-streptogramin B, phenicols, and sulfonamides. cfxA was detected in all 81 samples, followed by sul1 (66/81), tet(M) and sul2 (65/81), floR (39/81), mecA (17/81), and erm(B) (15/81). We identified potentially pathogenic genera including Capnocytophaga, Pasteurella, Fusobacterium, Campylobacter and Corynebacterium. Microbiome analysis revealed that at the phylum level, Pseudomonadota and Bacteroidota were the most dominant, while Porphyromonas, Frederiksenia and Moraxella were the most prevalent genera. Our findings highlight that (i) the oral microbiota of shelter dogs broadly resembles that reported in companion dogs and (ii) shelter dogs represent an overlooked reservoir of clinically relevant antimicrobial resistance genes and potentially zoonotic bacteria. Therefore, it is necessary to include shelter animals in antimicrobial resistance surveillance programs to capture any potential gaps in the antimicrobial resistance prevalence in companion animals and prevent dissemination of resistant bacteria to humans following adoption of shelter dogs and cats.
Additional Links: PMID-42749632
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PubMed:
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@article {pmid42749632,
year = {2026},
author = {Makau, RM and Chepkirui, BE and Perera, IU and Kiuno, K and Ushine, N and Shimizu, T and Hashino, M and Ishii, Y and Watanabe, K and Watarai, M},
title = {Characterization of the oral microbiota and antimicrobial resistance genes in shelter dogs in Japan.},
journal = {The Journal of veterinary medical science},
volume = {},
number = {},
pages = {},
doi = {10.1292/jvms.26-0387},
pmid = {42749632},
issn = {1347-7439},
abstract = {Companion animals can serve as reservoirs of antimicrobial resistance genes and zoonotic microorganisms, yet information on shelter dogs remains limited. This study characterized the oral microbiota and screened for antimicrobial resistance genes in shelter dogs in Japan. Oral swabs were collected from 81 dogs, microbial genomic DNA was extracted, bacterial communities were profiled by 16S rRNA gene amplicon sequencing, and antimicrobial resistance genes were screened by PCR. We detected genes conferring resistance to several antimicrobial classes, including β-lactams, tetracyclines, macrolide-lincosamide-streptogramin B, phenicols, and sulfonamides. cfxA was detected in all 81 samples, followed by sul1 (66/81), tet(M) and sul2 (65/81), floR (39/81), mecA (17/81), and erm(B) (15/81). We identified potentially pathogenic genera including Capnocytophaga, Pasteurella, Fusobacterium, Campylobacter and Corynebacterium. Microbiome analysis revealed that at the phylum level, Pseudomonadota and Bacteroidota were the most dominant, while Porphyromonas, Frederiksenia and Moraxella were the most prevalent genera. Our findings highlight that (i) the oral microbiota of shelter dogs broadly resembles that reported in companion dogs and (ii) shelter dogs represent an overlooked reservoir of clinically relevant antimicrobial resistance genes and potentially zoonotic bacteria. Therefore, it is necessary to include shelter animals in antimicrobial resistance surveillance programs to capture any potential gaps in the antimicrobial resistance prevalence in companion animals and prevent dissemination of resistant bacteria to humans following adoption of shelter dogs and cats.},
}
RevDate: 2026-09-16
Early-Onset Colorectal Cancer: Clinical and Molecular Features with Emerging Insights from Comprehensive Genomic Profiling.
Oncology and therapy [Epub ahead of print].
Early‑onset colorectal cancer (EOCRC), defined as colorectal cancer (CRC) diagnosed before 50 years of age, is increasing globally. Colorectal cancer is currently the third most commonly diagnosed cancer and the second leading cause of cancer-related death worldwide, with GLOBOCAN 2024 estimating approximately 2.04 million new cases and 917,895 deaths in 2024. Recent studies indicate a sustained rise in EOCRC incidence across multiple regions and birth cohorts, with the greatest increases observed among younger adults. Although hereditary cancer syndromes account for 20-25% of EOCRC cases, most occur in the absence of known genetic predispositions or established risk factors. Emerging evidence implicates the gut microbiome as a potential contributor to EOCRC, with distinct microbial signatures differentiating it from late‑onset colorectal cancer (LOCRC) diagnosed after 50 years of age. This review synthesizes current evidence on clinical, molecular, and diagnostic features distinguishing EOCRC from LOCRC, including differences in anatomical distribution, histopathology, genomic and epigenetic alterations, microbiome composition, and immune landscape, and discusses their implications for personalised screening and therapeutic strategies. We performed a retrospective secondary analysis of comprehensive genomic and immune profiling data from 1737 patients with colorectal cancer tested between June 2021 and June 2023. The analysis showed that tumours arising in patients with EOCRC had lower tumour mutational burden than tumours diagnosed as LOCRC, whereas other immune-related biomarkers, including tumour immunogenicity score, did not remain significantly different after correction for multiple testing. Despite these emerging biological differences, current screening strategies remain largely dependent on an age threshold of 50 years, and EOCRC is not addressed by age‑specific treatment approaches. We therefore review the translational potential of emerging biomarkers, including microbial signatures and liquid biopsy approaches, and propose a framework for integrating molecular profiling into clinical practice. Finally, we highlight the unmet need for coordinated efforts to improve screening in younger populations, address fertility preservation considerations, and ensure adequate psychosocial support for patients with EOCRC.
Additional Links: PMID-42749910
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@article {pmid42749910,
year = {2026},
author = {Nogueira, A and Brondon, J and Haradinov, K and Gopalakrishnan, S and Huang, K and Mukherjee, D and Agarwal, S and Strickland, KC and Vidal, L and Joshi, C and Brookes, R and Prasad, R and Das, S and Mankan, AK and Munje, A and de Las Heras, B and Singh, BP and Gandia, D and Ramkissoon, S and Raza, FS and Chico, I and Prasad, SK and Perez, J and Prasad, A and Sarker, D and Taieb, J and Saini, KS},
title = {Early-Onset Colorectal Cancer: Clinical and Molecular Features with Emerging Insights from Comprehensive Genomic Profiling.},
journal = {Oncology and therapy},
volume = {},
number = {},
pages = {},
pmid = {42749910},
issn = {2366-1089},
abstract = {Early‑onset colorectal cancer (EOCRC), defined as colorectal cancer (CRC) diagnosed before 50 years of age, is increasing globally. Colorectal cancer is currently the third most commonly diagnosed cancer and the second leading cause of cancer-related death worldwide, with GLOBOCAN 2024 estimating approximately 2.04 million new cases and 917,895 deaths in 2024. Recent studies indicate a sustained rise in EOCRC incidence across multiple regions and birth cohorts, with the greatest increases observed among younger adults. Although hereditary cancer syndromes account for 20-25% of EOCRC cases, most occur in the absence of known genetic predispositions or established risk factors. Emerging evidence implicates the gut microbiome as a potential contributor to EOCRC, with distinct microbial signatures differentiating it from late‑onset colorectal cancer (LOCRC) diagnosed after 50 years of age. This review synthesizes current evidence on clinical, molecular, and diagnostic features distinguishing EOCRC from LOCRC, including differences in anatomical distribution, histopathology, genomic and epigenetic alterations, microbiome composition, and immune landscape, and discusses their implications for personalised screening and therapeutic strategies. We performed a retrospective secondary analysis of comprehensive genomic and immune profiling data from 1737 patients with colorectal cancer tested between June 2021 and June 2023. The analysis showed that tumours arising in patients with EOCRC had lower tumour mutational burden than tumours diagnosed as LOCRC, whereas other immune-related biomarkers, including tumour immunogenicity score, did not remain significantly different after correction for multiple testing. Despite these emerging biological differences, current screening strategies remain largely dependent on an age threshold of 50 years, and EOCRC is not addressed by age‑specific treatment approaches. We therefore review the translational potential of emerging biomarkers, including microbial signatures and liquid biopsy approaches, and propose a framework for integrating molecular profiling into clinical practice. Finally, we highlight the unmet need for coordinated efforts to improve screening in younger populations, address fertility preservation considerations, and ensure adequate psychosocial support for patients with EOCRC.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-17
Differential Responses of Tree Phyllosphere and Rhizosphere Microbiomes to Mycorrhizal Types and Planting Patterns in a Young Subtropical Forest Plantation.
Environmental microbiology, 28(9):e70425.
Arbuscular mycorrhizal (AM) and ectomycorrhizal (EM) tree species are ubiquitous in subtropical forests and have distinctive root colonisation characteristics and leaf traits, resulting in differences in nutrient acquisition strategies and ecological functions. Here, we investigated the responses of bacteria, fungi and protists inhabiting tree phyllosphere and rhizosphere to tree mycorrhizal types (AM vs. EM) and planting patterns (single or double tree species planting with the same or different mycorrhizal type) in two seasons. Both leaf- and root-associated fungal richness and community composition were strongly structured by tree mycorrhizal type, whereas the bacterial community was primarily influenced by leaf habit. Protistan communities, however, exhibited weak host specificity and were dominated by stochastic processes, with seasonal variation acting as the main influencing factor. Overall, the phyllosphere microbiomes were jointly shaped by leaf traits and seasonal effects, but rhizosphere fungal communities were directly and indirectly regulated by tree mycorrhizal type via root nutrient and colonisation statuses. Altogether, tree phyllosphere and rhizosphere microbiomes differ from the interaction of mycorrhizal symbiosis, planting pattern and seasonality, with distinct ecological processes manipulating across bacteria, fungi and protists. This study highlights the necessity of integrating tree mycorrhizal types and above- and belowground habitats perspectives to better understand forest microbiomes.
Additional Links: PMID-42749996
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@article {pmid42749996,
year = {2026},
author = {Yang, H and Shi, J and Wang, J and Jin, S and Lin, Y and Zheng, Y},
title = {Differential Responses of Tree Phyllosphere and Rhizosphere Microbiomes to Mycorrhizal Types and Planting Patterns in a Young Subtropical Forest Plantation.},
journal = {Environmental microbiology},
volume = {28},
number = {9},
pages = {e70425},
doi = {10.1111/1462-2920.70425},
pmid = {42749996},
issn = {1462-2920},
support = {32371595//National Natural Science Foundation of China/ ; 2022J02025//Natural Science Foundation of Fujian Province/ ; },
mesh = {*Mycorrhizae/physiology/classification ; *Rhizosphere ; *Microbiota ; *Trees/microbiology/growth & development ; Forests ; Plant Leaves/microbiology ; Soil Microbiology ; Plant Roots/microbiology ; Bacteria/classification/isolation & purification/genetics ; Fungi/classification/isolation & purification ; Symbiosis ; Seasons ; },
abstract = {Arbuscular mycorrhizal (AM) and ectomycorrhizal (EM) tree species are ubiquitous in subtropical forests and have distinctive root colonisation characteristics and leaf traits, resulting in differences in nutrient acquisition strategies and ecological functions. Here, we investigated the responses of bacteria, fungi and protists inhabiting tree phyllosphere and rhizosphere to tree mycorrhizal types (AM vs. EM) and planting patterns (single or double tree species planting with the same or different mycorrhizal type) in two seasons. Both leaf- and root-associated fungal richness and community composition were strongly structured by tree mycorrhizal type, whereas the bacterial community was primarily influenced by leaf habit. Protistan communities, however, exhibited weak host specificity and were dominated by stochastic processes, with seasonal variation acting as the main influencing factor. Overall, the phyllosphere microbiomes were jointly shaped by leaf traits and seasonal effects, but rhizosphere fungal communities were directly and indirectly regulated by tree mycorrhizal type via root nutrient and colonisation statuses. Altogether, tree phyllosphere and rhizosphere microbiomes differ from the interaction of mycorrhizal symbiosis, planting pattern and seasonality, with distinct ecological processes manipulating across bacteria, fungi and protists. This study highlights the necessity of integrating tree mycorrhizal types and above- and belowground habitats perspectives to better understand forest microbiomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Mycorrhizae/physiology/classification
*Rhizosphere
*Microbiota
*Trees/microbiology/growth & development
Forests
Plant Leaves/microbiology
Soil Microbiology
Plant Roots/microbiology
Bacteria/classification/isolation & purification/genetics
Fungi/classification/isolation & purification
Symbiosis
Seasons
RevDate: 2026-09-17
CmpDate: 2026-09-17
Decoding the cancer microbiome: multi-omics, AI, and translational opportunities.
Genome biology, 27(1):.
Multi-omics technologies, coupled with AI technologies, have the potential to enable the systematic investigation of complex cancer microbiome biology by uncovering informative patterns and associations across complementary datasets. Here, we review existing and emerging cancer microbiome data, discuss the development, interpretation, and validation of AI models as key considerations for their integration and analysis, and provide practical suggestions for improving the reliability and biological relevance of AI-driven discoveries. We further highlight the opportunities and challenges of translating these discoveries into clinical practice, emphasizing strategies to bridge the gap between research-oriented models and clinical implementations.
Additional Links: PMID-42750046
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@article {pmid42750046,
year = {2026},
author = {Sun, Y and Cheng, OJ and Ma, A and Shabnaz, S and Huang, X and Zhao, J and Tan, AC and Ma, Q},
title = {Decoding the cancer microbiome: multi-omics, AI, and translational opportunities.},
journal = {Genome biology},
volume = {27},
number = {1},
pages = {},
pmid = {42750046},
issn = {1474-760X},
support = {R01GM152585/NH/NIH HHS/United States ; },
mesh = {Humans ; Multiomics ; *Neoplasms/microbiology/genetics ; *Microbiota ; *Artificial Intelligence ; Translational Research, Biomedical ; },
abstract = {Multi-omics technologies, coupled with AI technologies, have the potential to enable the systematic investigation of complex cancer microbiome biology by uncovering informative patterns and associations across complementary datasets. Here, we review existing and emerging cancer microbiome data, discuss the development, interpretation, and validation of AI models as key considerations for their integration and analysis, and provide practical suggestions for improving the reliability and biological relevance of AI-driven discoveries. We further highlight the opportunities and challenges of translating these discoveries into clinical practice, emphasizing strategies to bridge the gap between research-oriented models and clinical implementations.},
}
MeSH Terms:
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Humans
Multiomics
*Neoplasms/microbiology/genetics
*Microbiota
*Artificial Intelligence
Translational Research, Biomedical
RevDate: 2026-09-17
CmpDate: 2026-09-17
Not All Children Are the Same: Differences in the Microbiome Assembly During Early Development of Seaweeds.
Environmental microbiology, 28(9):e70418.
Microbial symbionts play key roles in macroalgal development, yet the processes structuring early-life microbiomes remain poorly understood. Using laboratory outgrowth experiments and 16S rRNA gene amplicon sequencing we compared microbiome acquisition and assembly during the early development of three distinct macroalgae: Ulva australis (Chlorophyta), Hormosira banksii (Phaeophyceae) and Delisea pulchra (Rhodophyta). All species established distinct bacterial communities within the first week of outgrowth, with significant shifts in community composition and structure associated with major developmental stages. Stage-enriched taxa included Phaeobacter, Roseobacter and Maribacter, which include members reported to influence algal growth or morphogenesis. Vertical inheritance contributed unevenly to the microbiome assembly across hosts. U. australis recruited low-abundance environmental bacteria, possibly via strong host filtering. H. banksii selectively retained a small, consistent subset of adult-derived bacteria, whereas D. pulchra retained fewer of its inherited bacteria. These results suggest that macroalgae can employ diverse transmission and recruitment strategies to assemble early microbiomes, combining selective inheritance with stage-specific retention and/or environmental acquisition.
Additional Links: PMID-42750157
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@article {pmid42750157,
year = {2026},
author = {Syukur, S and Nappi, J and Majzoub, ME and Thomas, T and Egan, S},
title = {Not All Children Are the Same: Differences in the Microbiome Assembly During Early Development of Seaweeds.},
journal = {Environmental microbiology},
volume = {28},
number = {9},
pages = {e70418},
doi = {10.1111/1462-2920.70418},
pmid = {42750157},
issn = {1462-2920},
support = {//Australian Department of Foreign Affairs and Trade/ ; },
mesh = {*Microbiota ; *Seaweed/microbiology/growth & development ; RNA, Ribosomal, 16S/genetics ; *Bacteria/classification/genetics/isolation & purification ; Symbiosis ; *Rhodophyta/microbiology/growth & development ; *Phaeophyceae/microbiology/growth & development ; *Ulva/microbiology/growth & development ; Chlorophyta/microbiology/growth & development ; },
abstract = {Microbial symbionts play key roles in macroalgal development, yet the processes structuring early-life microbiomes remain poorly understood. Using laboratory outgrowth experiments and 16S rRNA gene amplicon sequencing we compared microbiome acquisition and assembly during the early development of three distinct macroalgae: Ulva australis (Chlorophyta), Hormosira banksii (Phaeophyceae) and Delisea pulchra (Rhodophyta). All species established distinct bacterial communities within the first week of outgrowth, with significant shifts in community composition and structure associated with major developmental stages. Stage-enriched taxa included Phaeobacter, Roseobacter and Maribacter, which include members reported to influence algal growth or morphogenesis. Vertical inheritance contributed unevenly to the microbiome assembly across hosts. U. australis recruited low-abundance environmental bacteria, possibly via strong host filtering. H. banksii selectively retained a small, consistent subset of adult-derived bacteria, whereas D. pulchra retained fewer of its inherited bacteria. These results suggest that macroalgae can employ diverse transmission and recruitment strategies to assemble early microbiomes, combining selective inheritance with stage-specific retention and/or environmental acquisition.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Microbiota
*Seaweed/microbiology/growth & development
RNA, Ribosomal, 16S/genetics
*Bacteria/classification/genetics/isolation & purification
Symbiosis
*Rhodophyta/microbiology/growth & development
*Phaeophyceae/microbiology/growth & development
*Ulva/microbiology/growth & development
Chlorophyta/microbiology/growth & development
RevDate: 2026-09-17
CmpDate: 2026-09-17
Inclusion of Multi-Omic Biomarkers Improves Prediction Accuracy of Response, Relapse, and Overall Survival in Acute Myeloid Leukemia Patients Receiving High-Intensity Induction Chemotherapy.
Cancer medicine, 15(9):e72281.
BACKGROUND: Despite advancements in genetic markers for acute myeloid leukemia (AML) risk stratification, outcome prediction remains challenging due to disease heterogeneity and dynamic genetic changes, highlighting the need for reliable biomarkers to improve AML treatment strategies and patient outcomes. To refine outcome predictions, we investigated the use of microbial-derived biomarkers to predict composite complete remission (CRc), relapse, and survival for patients on high- and low-intensity regimens, and to integrate those variables into the widely clinically utilized European Leukemia Network (ELN-2022) genetic risk classification model for high-intensity-treated patients.
METHODS: We first developed machine learning models that integrate baseline fecal metabolomics, 16S rRNA-based stool microbiome features, and clinical metadata (sex, antibiotic administration, AML somatic mutations, and cytogenetics) from two cohorts of AML patients (n = 83) undergoing remission induction chemotherapy. Univariate tests and sparse canonical correlation analysis were employed for variable selection and to explore fecal metabolite-microbe relationships. A robust machine learning approach using XGBoost was employed, with 100 stratified data splits (80% training, 20% testing) and coarse-to-fine hyperparameter optimization. Variable importance was aggregated across all models to select key predictors.
RESULTS: For high-intensity-treated patients, XGBoost models achieved aggregated AUROC scores of 0.719, 0.729, and 0.65 for CRc, relapse, and overall survival, respectively. For low-intensity-treated patients, these models achieved aggregate AUROC scores of 0.945, 0.724, and 0.768 for these same outcomes, respectively. Integrating the biomarkers identified in the high-intensity machine-learning models with the current ELN-2022 AML risk stratification system effectively stratified patients into risk categories, which obtained higher concordance indices and likelihood ratios, demonstrating improved prognostic accuracy for each outcome compared to ELN-2022 alone.
CONCLUSIONS: The inclusion of microbial-derived biomarkers serves as a robust prognostic tool to improve outcome prediction in AML patients, highlighting the potential of its integration into AML risk assessment and paving the way for personalized treatment strategies and improved patient outcomes.
Additional Links: PMID-42750261
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PubMed:
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@article {pmid42750261,
year = {2026},
author = {Franklin, S and Sahasrabhojane, P and Ivanov, I and Hayase, T and Hayase, E and Chang, CC and Senapati, J and Desikan, SP and Kadia, T and Lorenzi, P and Jenq, RR and Shelburne, S and Galloway-Peña, J},
title = {Inclusion of Multi-Omic Biomarkers Improves Prediction Accuracy of Response, Relapse, and Overall Survival in Acute Myeloid Leukemia Patients Receiving High-Intensity Induction Chemotherapy.},
journal = {Cancer medicine},
volume = {15},
number = {9},
pages = {e72281},
doi = {10.1002/cam4.72281},
pmid = {42750261},
issn = {2045-7634},
support = {K01AI143881//Division of Intramural Research, National Institute of Allergy and Infectious Diseases/ ; },
mesh = {Humans ; *Leukemia, Myeloid, Acute/drug therapy/mortality/genetics/microbiology ; Multiomics ; Female ; *Biomarkers, Tumor ; *Induction Chemotherapy/methods ; Male ; Neoplasm Recurrence, Local ; Middle Aged ; Prognosis ; Machine Learning ; Feces/microbiology ; Predictive Learning Models ; Adult ; Boosting Machine Learning Algorithms ; *Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Recurrence ; Aged ; Risk Assessment ; },
abstract = {BACKGROUND: Despite advancements in genetic markers for acute myeloid leukemia (AML) risk stratification, outcome prediction remains challenging due to disease heterogeneity and dynamic genetic changes, highlighting the need for reliable biomarkers to improve AML treatment strategies and patient outcomes. To refine outcome predictions, we investigated the use of microbial-derived biomarkers to predict composite complete remission (CRc), relapse, and survival for patients on high- and low-intensity regimens, and to integrate those variables into the widely clinically utilized European Leukemia Network (ELN-2022) genetic risk classification model for high-intensity-treated patients.
METHODS: We first developed machine learning models that integrate baseline fecal metabolomics, 16S rRNA-based stool microbiome features, and clinical metadata (sex, antibiotic administration, AML somatic mutations, and cytogenetics) from two cohorts of AML patients (n = 83) undergoing remission induction chemotherapy. Univariate tests and sparse canonical correlation analysis were employed for variable selection and to explore fecal metabolite-microbe relationships. A robust machine learning approach using XGBoost was employed, with 100 stratified data splits (80% training, 20% testing) and coarse-to-fine hyperparameter optimization. Variable importance was aggregated across all models to select key predictors.
RESULTS: For high-intensity-treated patients, XGBoost models achieved aggregated AUROC scores of 0.719, 0.729, and 0.65 for CRc, relapse, and overall survival, respectively. For low-intensity-treated patients, these models achieved aggregate AUROC scores of 0.945, 0.724, and 0.768 for these same outcomes, respectively. Integrating the biomarkers identified in the high-intensity machine-learning models with the current ELN-2022 AML risk stratification system effectively stratified patients into risk categories, which obtained higher concordance indices and likelihood ratios, demonstrating improved prognostic accuracy for each outcome compared to ELN-2022 alone.
CONCLUSIONS: The inclusion of microbial-derived biomarkers serves as a robust prognostic tool to improve outcome prediction in AML patients, highlighting the potential of its integration into AML risk assessment and paving the way for personalized treatment strategies and improved patient outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Leukemia, Myeloid, Acute/drug therapy/mortality/genetics/microbiology
Multiomics
Female
*Biomarkers, Tumor
*Induction Chemotherapy/methods
Male
Neoplasm Recurrence, Local
Middle Aged
Prognosis
Machine Learning
Feces/microbiology
Predictive Learning Models
Adult
Boosting Machine Learning Algorithms
*Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Recurrence
Aged
Risk Assessment
RevDate: 2026-09-17
Alamandine/MrgD pathway modulates gut-bone marrow axis in ageing.
British journal of pharmacology [Epub ahead of print].
BACKGROUND AND PURPOSE: Ageing is associated with colon epithelial barrier disruption and up-regulation of myelopoiesis in the bone marrow (BM). Alamandine (Ala) and MrgD are novel members of the renin angiotensin system (RAS). This study tested the hypothesis that Ala restores the colon epithelial barrier integrity in ageing via modulating gut-BM axis.
EXPERIMENTAL APPROACH: Mice, 2-3 (Young) or 22-24 months (Old), were treated with saline or Ala by using Osmotic pumps. The intestinal permeability was evaluated using FITC-dextran. Lgr5[+]Olfm4[+] intestinal stem cells (ISCs), Wnt3a and β-catenin were evaluated by immunohistochemistry or western blotting. Faecal microbiome was analysed by 16S rRNA sequencing. Monocyte-macrophages were characterized by flow cytometry. Caecal or serum bacterial metabolites were analysed and the caecal supernatants (CS) were tested for myelopoietic potential.
KEY RESULTS: MrgD was expressed in ISCs, which was decreased in the Old. Increased intestinal permeability in ageing was reversed by Ala. In the colon organoids, Ala increased Wnt3a levels and this was antagonized by NF449, SQ22536 or 666-15. Ala restored phospho-CREB and active β-catenin levels that were decreased in the Old colon-organoids. Ala increased the richness and β-diversity of the microbiota with decreased Bacillota/Bacteroidota in ageing. Ala decreased the CD80[+] and increased CX3CR[+] macrophages in the Old colons. Old-CS induced myelopoiesis in BM cells with higher number of pro-inflammatory macrophages, which was prevented by Ala treatment.
CONCLUSIONS AND IMPLICATIONS: Targeting Ala/MrgD pathway is a promising approach for ameliorating the inflammatory stress in ageing by restoring homeostasis in the gut-BM inter-organ communication.
Additional Links: PMID-42750336
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PubMed:
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@article {pmid42750336,
year = {2026},
author = {Chittimalli, K and Rozario, HE and Martinez, V and McAdams, ZL and Adkins, SA and Ericsson, AC and Jarajapu, YPR},
title = {Alamandine/MrgD pathway modulates gut-bone marrow axis in ageing.},
journal = {British journal of pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bph.70656},
pmid = {42750336},
issn = {1476-5381},
support = {AG056881/NH/NIH HHS/United States ; P20GM103442/NH/NIH HHS/United States ; U42 OD010918/NH/NIH HHS/United States ; },
abstract = {BACKGROUND AND PURPOSE: Ageing is associated with colon epithelial barrier disruption and up-regulation of myelopoiesis in the bone marrow (BM). Alamandine (Ala) and MrgD are novel members of the renin angiotensin system (RAS). This study tested the hypothesis that Ala restores the colon epithelial barrier integrity in ageing via modulating gut-BM axis.
EXPERIMENTAL APPROACH: Mice, 2-3 (Young) or 22-24 months (Old), were treated with saline or Ala by using Osmotic pumps. The intestinal permeability was evaluated using FITC-dextran. Lgr5[+]Olfm4[+] intestinal stem cells (ISCs), Wnt3a and β-catenin were evaluated by immunohistochemistry or western blotting. Faecal microbiome was analysed by 16S rRNA sequencing. Monocyte-macrophages were characterized by flow cytometry. Caecal or serum bacterial metabolites were analysed and the caecal supernatants (CS) were tested for myelopoietic potential.
KEY RESULTS: MrgD was expressed in ISCs, which was decreased in the Old. Increased intestinal permeability in ageing was reversed by Ala. In the colon organoids, Ala increased Wnt3a levels and this was antagonized by NF449, SQ22536 or 666-15. Ala restored phospho-CREB and active β-catenin levels that were decreased in the Old colon-organoids. Ala increased the richness and β-diversity of the microbiota with decreased Bacillota/Bacteroidota in ageing. Ala decreased the CD80[+] and increased CX3CR[+] macrophages in the Old colons. Old-CS induced myelopoiesis in BM cells with higher number of pro-inflammatory macrophages, which was prevented by Ala treatment.
CONCLUSIONS AND IMPLICATIONS: Targeting Ala/MrgD pathway is a promising approach for ameliorating the inflammatory stress in ageing by restoring homeostasis in the gut-BM inter-organ communication.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Artificial Intelligence-Driven Multidimensional Phenotyping of Gut Metabolic States for Personalized Prebiotic, Probiotic, and Postbiotic Strategies.
Molecular nutrition & food research, 70(18):e70607.
This study presents multidimensional physicochemical phenotyping of human gut metabolic states using integrated multimodal profiling and machine learning. A total of 680 stool samples were analyzed using time-resolved optical, electrochemical, acoustic, magnetic, and spectral measurements implemented in a compact 3D-printed screening platform. Multivariate analysis explained 78.4% of structured variance, and cluster optimization identified seven primary clusters and 26 structurally retained subclusters representing proteolytic, saccharolytic, bile/lipid-rich, oxidative, diarrheal, pigment-linked, and normobiotic-like profiles. Clinical categories were linked to 21 subclusters after descriptor-based structure definition. A separate supervised layer assessed out-of-fold reproduction of fixed primary CL1-CL7 assignments, achieving 81.7% accuracy and a 0.799 macro F1-score in repeated cross-validation. Separately, cohort-internal diagonal category-to-subcluster distribution reached 84.1% (572/680 diagonal assignments, Wilson 95% CI: 81.2%-86.7%). 16S rRNA/laboratory-marker profiling supported the physicochemical structure, showing high diversity and low dysbiosis in the normobiotic-like phenotype, acidic high-diversity behavior in the saccharolytic phenotype, alkaline proteolytic behavior with elevated phenols and ammonia, bile-associated functional enrichment, and high dysbiosis with reduced diversity in the pigment-rich phenotype. SHAP and LIME attributed CL1-CL7 assignment to coordinated multimodal contributions. The method represents standardized extractable stool matrix profiling associated with microbiome-supported functional states, not a stand-alone diagnostic test.
Additional Links: PMID-42750414
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@article {pmid42750414,
year = {2026},
author = {Tóth, A and Furka, S and Vengríni, J and Neogrády, P and Bandura, A and Dueñas Casas, S and Petrovič, R and Tomka, M and Slopovský, J and Furka, D},
title = {Artificial Intelligence-Driven Multidimensional Phenotyping of Gut Metabolic States for Personalized Prebiotic, Probiotic, and Postbiotic Strategies.},
journal = {Molecular nutrition & food research},
volume = {70},
number = {18},
pages = {e70607},
pmid = {42750414},
issn = {1613-4133},
mesh = {Humans ; Feces/microbiology/chemistry ; Phenotype ; *Probiotics ; *Prebiotics ; *Artificial Intelligence ; *Gastrointestinal Microbiome/physiology ; RNA, Ribosomal, 16S/genetics ; Machine Learning ; Dysbiosis ; },
abstract = {This study presents multidimensional physicochemical phenotyping of human gut metabolic states using integrated multimodal profiling and machine learning. A total of 680 stool samples were analyzed using time-resolved optical, electrochemical, acoustic, magnetic, and spectral measurements implemented in a compact 3D-printed screening platform. Multivariate analysis explained 78.4% of structured variance, and cluster optimization identified seven primary clusters and 26 structurally retained subclusters representing proteolytic, saccharolytic, bile/lipid-rich, oxidative, diarrheal, pigment-linked, and normobiotic-like profiles. Clinical categories were linked to 21 subclusters after descriptor-based structure definition. A separate supervised layer assessed out-of-fold reproduction of fixed primary CL1-CL7 assignments, achieving 81.7% accuracy and a 0.799 macro F1-score in repeated cross-validation. Separately, cohort-internal diagonal category-to-subcluster distribution reached 84.1% (572/680 diagonal assignments, Wilson 95% CI: 81.2%-86.7%). 16S rRNA/laboratory-marker profiling supported the physicochemical structure, showing high diversity and low dysbiosis in the normobiotic-like phenotype, acidic high-diversity behavior in the saccharolytic phenotype, alkaline proteolytic behavior with elevated phenols and ammonia, bile-associated functional enrichment, and high dysbiosis with reduced diversity in the pigment-rich phenotype. SHAP and LIME attributed CL1-CL7 assignment to coordinated multimodal contributions. The method represents standardized extractable stool matrix profiling associated with microbiome-supported functional states, not a stand-alone diagnostic test.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Feces/microbiology/chemistry
Phenotype
*Probiotics
*Prebiotics
*Artificial Intelligence
*Gastrointestinal Microbiome/physiology
RNA, Ribosomal, 16S/genetics
Machine Learning
Dysbiosis
RevDate: 2026-09-17
CmpDate: 2026-09-17
Effects of Wilac D001 (Weissella confusa WIKIM51) Supplementation on Metabolic Parameters and Central Adiposity in Overweight Adults: A 12-Week Randomized, Double-Blind, Placebo-Controlled Trial.
Journal of microbiology and biotechnology, 36:e2606054 pii:jmb.2606.06054.
Recent research has emphasized the importance of gut microbiota in regulating energy and lipid metabolism as well as gut hormone secretion, indicating that probiotics could contribute to improving metabolic parameters associated with excess adiposity. This study evaluated the metabolic effects of Weissella confusa WIKIM51 (Wilac D001) and explored the potential involvement of glucagon-like peptide-1 (GLP-1)-related mechanisms. First, GLP-1 secretory activity following Wilac D001 treatment was evaluated in vitro using STC-1 enteroendocrine cells. Male C57BL/6 mice were fed a high-fat diet to induce obesity-associated metabolic dysregulation, and Wilac D001 was orally administered for 10 weeks. Glucose tolerance was subsequently examined using an oral glucose tolerance test (OGTT). Finally, in a 12-week randomized, double-blind, placebo-controlled clinical trial, overweight adults aged 19-64 years received either Wilac D001 (1.0 × 10[10] colony-forming units/day) or a placebo. Blood lipid parameters, glycated hemoglobin, abdominal fat distribution, body composition, body weight, regional anthropometric measures, and lifestyle factors were evaluated. Wilac D001 significantly increased GLP-1 secretion in STC-1 cells versus the control (p < 0.01). High-fat diet-fed mice administered Wilac D001 exhibited lower fasting blood glucose levels and more rapid glucose recovery during the OGTT (p < 0.01). In the clinical trial, Wilac D001 supplementation led to reductions in several markers, including a significant reduction in triglyceride levels, alongside improvements in total abdominal fat area, visceral fat area, and subcutaneous fat area. No serious adverse events were reported. These findings support the potential of Wilac D001 as a functional probiotic for promoting microbiome-based metabolic health management.
Additional Links: PMID-42750456
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@article {pmid42750456,
year = {2026},
author = {Park, S and Lee, B and Sun, H and Shin, W and Mok, JY and Seo, J and Choi, HJ and Choi, GH and Son, JY and Yoo, B},
title = {Effects of Wilac D001 (Weissella confusa WIKIM51) Supplementation on Metabolic Parameters and Central Adiposity in Overweight Adults: A 12-Week Randomized, Double-Blind, Placebo-Controlled Trial.},
journal = {Journal of microbiology and biotechnology},
volume = {36},
number = {},
pages = {e2606054},
doi = {10.4014/jmb.2606.06054},
pmid = {42750456},
issn = {1738-8872},
mesh = {Animals ; Male ; Mice, Inbred C57BL ; Glucagon-Like Peptide 1/metabolism ; Mice ; Humans ; Adult ; *Probiotics/administration & dosage ; Double-Blind Method ; Middle Aged ; *Weissella ; *Overweight/metabolism/therapy ; Diet, High-Fat ; Dietary Supplements ; *Adiposity/drug effects ; Young Adult ; Glucose Tolerance Test ; Blood Glucose ; Gastrointestinal Microbiome ; },
abstract = {Recent research has emphasized the importance of gut microbiota in regulating energy and lipid metabolism as well as gut hormone secretion, indicating that probiotics could contribute to improving metabolic parameters associated with excess adiposity. This study evaluated the metabolic effects of Weissella confusa WIKIM51 (Wilac D001) and explored the potential involvement of glucagon-like peptide-1 (GLP-1)-related mechanisms. First, GLP-1 secretory activity following Wilac D001 treatment was evaluated in vitro using STC-1 enteroendocrine cells. Male C57BL/6 mice were fed a high-fat diet to induce obesity-associated metabolic dysregulation, and Wilac D001 was orally administered for 10 weeks. Glucose tolerance was subsequently examined using an oral glucose tolerance test (OGTT). Finally, in a 12-week randomized, double-blind, placebo-controlled clinical trial, overweight adults aged 19-64 years received either Wilac D001 (1.0 × 10[10] colony-forming units/day) or a placebo. Blood lipid parameters, glycated hemoglobin, abdominal fat distribution, body composition, body weight, regional anthropometric measures, and lifestyle factors were evaluated. Wilac D001 significantly increased GLP-1 secretion in STC-1 cells versus the control (p < 0.01). High-fat diet-fed mice administered Wilac D001 exhibited lower fasting blood glucose levels and more rapid glucose recovery during the OGTT (p < 0.01). In the clinical trial, Wilac D001 supplementation led to reductions in several markers, including a significant reduction in triglyceride levels, alongside improvements in total abdominal fat area, visceral fat area, and subcutaneous fat area. No serious adverse events were reported. These findings support the potential of Wilac D001 as a functional probiotic for promoting microbiome-based metabolic health management.},
}
MeSH Terms:
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Animals
Male
Mice, Inbred C57BL
Glucagon-Like Peptide 1/metabolism
Mice
Humans
Adult
*Probiotics/administration & dosage
Double-Blind Method
Middle Aged
*Weissella
*Overweight/metabolism/therapy
Diet, High-Fat
Dietary Supplements
*Adiposity/drug effects
Young Adult
Glucose Tolerance Test
Blood Glucose
Gastrointestinal Microbiome
RevDate: 2026-09-17
CmpDate: 2026-09-17
Probiotics in Cardiometabolic Diseases: Current Evidence, Postbiotic Perspectives, and Future Directions.
Journal of microbiology and biotechnology, 36:e2605001 pii:jmb.2605.05001.
The rise in urbanization and sedentary lifestyles, along with the aging of the global population, is contributing to an increasing burden of life-threatening diseases. The cardiometabolic disease (CMD) spectrum, which includes heart failure, hypertension, coronary heart disease, and diabetes, is closely associated with metabolic syndrome components such as obesity and elevated hepatic lipid accumulation. The gut microbiome mediates these disorders through multiple signaling axes. Imbalance of the intestinal microbiota is closely linked to the pathogenesis of atherosclerosis and hypertensive vascular remodeling. Supplementation with probiotics - and, more recently, their derived postbiotic products - can alter the composition and functional metabolic outputs of the gut ecosystem, offering a mechanistically informed approach for CMD management. This review delineates the mechanisms of action of six well-studied probiotics (Akkermansia muciniphila, Bifidobacterium, Lactobacillus, Bacillus, Enterococcus, and Lactococcus lactis), with selected discussion of their postbiotic derivatives where evidence is available. We further examine how antimicrobial and metabolic interventions integrated through the gut-heart-liver axis may improve clinical outcomes and attenuate disease progression. The advancement of precision cardiometabolic medicine through the combined effects of these therapies may facilitate the development of personalized treatment strategies.
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@article {pmid42750461,
year = {2026},
author = {Yang, F and Qin, W and Zhang, G and Li, X and Yang, X and Zhou, L and Xing, Y},
title = {Probiotics in Cardiometabolic Diseases: Current Evidence, Postbiotic Perspectives, and Future Directions.},
journal = {Journal of microbiology and biotechnology},
volume = {36},
number = {},
pages = {e2605001},
doi = {10.4014/jmb.2605.05001},
pmid = {42750461},
issn = {1738-8872},
mesh = {*Probiotics/therapeutic use ; Humans ; *Cardiovascular Diseases/therapy/microbiology ; Gastrointestinal Microbiome/drug effects ; Animals ; *Metabolic Syndrome/therapy ; Precision Medicine ; *Metabolic Diseases/therapy ; },
abstract = {The rise in urbanization and sedentary lifestyles, along with the aging of the global population, is contributing to an increasing burden of life-threatening diseases. The cardiometabolic disease (CMD) spectrum, which includes heart failure, hypertension, coronary heart disease, and diabetes, is closely associated with metabolic syndrome components such as obesity and elevated hepatic lipid accumulation. The gut microbiome mediates these disorders through multiple signaling axes. Imbalance of the intestinal microbiota is closely linked to the pathogenesis of atherosclerosis and hypertensive vascular remodeling. Supplementation with probiotics - and, more recently, their derived postbiotic products - can alter the composition and functional metabolic outputs of the gut ecosystem, offering a mechanistically informed approach for CMD management. This review delineates the mechanisms of action of six well-studied probiotics (Akkermansia muciniphila, Bifidobacterium, Lactobacillus, Bacillus, Enterococcus, and Lactococcus lactis), with selected discussion of their postbiotic derivatives where evidence is available. We further examine how antimicrobial and metabolic interventions integrated through the gut-heart-liver axis may improve clinical outcomes and attenuate disease progression. The advancement of precision cardiometabolic medicine through the combined effects of these therapies may facilitate the development of personalized treatment strategies.},
}
MeSH Terms:
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*Probiotics/therapeutic use
Humans
*Cardiovascular Diseases/therapy/microbiology
Gastrointestinal Microbiome/drug effects
Animals
*Metabolic Syndrome/therapy
Precision Medicine
*Metabolic Diseases/therapy
RevDate: 2026-09-17
Molecular biomarker profiling in noninfectious uveitis: a chronological review of discovery.
Current opinion in ophthalmology [Epub ahead of print].
PURPOSE OR REVIEW: Noninfectious uveitis (NIU) encompasses a heterogeneous group of immune-mediated intraocular inflammatory diseases whose complexity has driven systematic molecular biomarker discovery. This review presents NIU molecular biomarkers organized by biological category; autoantigens, human leukocyte antigens (HLA) and genetic markers, cellular immune subsets, cytokines, chemokines, and multiomics platforms including proteomics, microbiome metagenomics, metabolomics, and single-cell transcriptomics with each category presented in strict chronological order of landmark discovery.
RECENT FINDINGS: We present a review organized along two nested timelines. Categories are presented in the order they historically emerged in the field, and within each category, landmark discoveries appear in chronological sequence. This allows the reader to trace how each biomarker category evolved: from foundational autoantigen identification in experimental uveitis models, through the genomic revolution of HLA association studies, into cellular immunophenotyping, cytokine profiling of aqueous humor, chemokine mapping of intraocular trafficking, and finally the emerging omics platforms that may potentially anchor precision medicine in NIU. Each biomarker is paired in line with its linked targeted therapeutic.
SUMMARY: Biomarker research has transformed the understanding of NIU from a clinically defined syndrome into a group of molecularly distinct immune disorders. Advances spanning autoantigens, genetics, immune-cell profiling, cytokines, chemokines, and multiomics have revealed novel pathogenic mechanisms and therapeutic targets. Integration of these biomarkers with targeted therapies may accelerate the transition toward precision medicine in uveitis care.
Additional Links: PMID-42750565
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@article {pmid42750565,
year = {2026},
author = {Pothikamjorn, TL and Gonzales, JA},
title = {Molecular biomarker profiling in noninfectious uveitis: a chronological review of discovery.},
journal = {Current opinion in ophthalmology},
volume = {},
number = {},
pages = {},
pmid = {42750565},
issn = {1531-7021},
abstract = {PURPOSE OR REVIEW: Noninfectious uveitis (NIU) encompasses a heterogeneous group of immune-mediated intraocular inflammatory diseases whose complexity has driven systematic molecular biomarker discovery. This review presents NIU molecular biomarkers organized by biological category; autoantigens, human leukocyte antigens (HLA) and genetic markers, cellular immune subsets, cytokines, chemokines, and multiomics platforms including proteomics, microbiome metagenomics, metabolomics, and single-cell transcriptomics with each category presented in strict chronological order of landmark discovery.
RECENT FINDINGS: We present a review organized along two nested timelines. Categories are presented in the order they historically emerged in the field, and within each category, landmark discoveries appear in chronological sequence. This allows the reader to trace how each biomarker category evolved: from foundational autoantigen identification in experimental uveitis models, through the genomic revolution of HLA association studies, into cellular immunophenotyping, cytokine profiling of aqueous humor, chemokine mapping of intraocular trafficking, and finally the emerging omics platforms that may potentially anchor precision medicine in NIU. Each biomarker is paired in line with its linked targeted therapeutic.
SUMMARY: Biomarker research has transformed the understanding of NIU from a clinically defined syndrome into a group of molecularly distinct immune disorders. Advances spanning autoantigens, genetics, immune-cell profiling, cytokines, chemokines, and multiomics have revealed novel pathogenic mechanisms and therapeutic targets. Integration of these biomarkers with targeted therapies may accelerate the transition toward precision medicine in uveitis care.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Therapeutic modulation of the gut-brain axis in alcohol use disorder: A systematic review.
Metabolism open, 32:100495.
BACKGROUND: Alcohol Use Disorder (AUD) involves gut-brain axis dysfunction. Modulating microbiota offers a promising therapeutic strategy.
METHODS: Clinical trials on fecal microbiota transplant (FMT), prebiotics (inulin), probiotics, and neurohormonal agents like glucagon-like peptide-1 (GLP-1) and ghrelin receptor antagonists) were identified through PubMed, Google Scholar, Scopus, and ClinicalTrials.gov (until 07/31/2026). Of the eleven included studies, five identified gut dysbiosis as a common feature in individuals with AUD.
RESULTS: Gut dysbiosis-directed interventions were associated with benefits on behavioral (alcohol craving, consumption, relapse), psychological (anxiety, sociability), and physiological (MELD score, AST/ALT ratio, systemic inflammation) outcomes. However, the magnitude and consistency of these effects varied among studies. Three studies specifically involved AUD patients with alcohol-associated liver disease (ALD), while the others focused on AUD. In another study, Ghrelin, which was investigated as a neurohormonal target, emerged as a potential anti-inflammatory agent. However, ghrelin receptor antagonism in the presence of alcohol did not alter systemic inflammation. Of five trials using GLP-1 receptor agonists, three showed a reduction in alcohol use, but the other two, although directionally consistent, did not reach statistically significant effects. The current evidence supports the gut-brain axis as a dual therapeutic target, offering potential benefits for both AUD and ALD. Microbial therapies (FMT, probiotics, prebiotics) show some benefits in AUD, albeit studies are small. Hormonal targets such as ghrelin and GLP-1 receptors are mechanistically relevant. Data on ghrelin are limited. Data on GLP-1 receptor agonists are directionally consistent but not statistically robust. Large-scale, controlled trials are needed to validate and optimize the integration of this approach into AUD treatment strategies.
Additional Links: PMID-42750798
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@article {pmid42750798,
year = {2026},
author = {Bhandari, P and Sideeg, A and Elfeki, M and Xie, C and Singal, AK},
title = {Therapeutic modulation of the gut-brain axis in alcohol use disorder: A systematic review.},
journal = {Metabolism open},
volume = {32},
number = {},
pages = {100495},
pmid = {42750798},
issn = {2589-9368},
abstract = {BACKGROUND: Alcohol Use Disorder (AUD) involves gut-brain axis dysfunction. Modulating microbiota offers a promising therapeutic strategy.
METHODS: Clinical trials on fecal microbiota transplant (FMT), prebiotics (inulin), probiotics, and neurohormonal agents like glucagon-like peptide-1 (GLP-1) and ghrelin receptor antagonists) were identified through PubMed, Google Scholar, Scopus, and ClinicalTrials.gov (until 07/31/2026). Of the eleven included studies, five identified gut dysbiosis as a common feature in individuals with AUD.
RESULTS: Gut dysbiosis-directed interventions were associated with benefits on behavioral (alcohol craving, consumption, relapse), psychological (anxiety, sociability), and physiological (MELD score, AST/ALT ratio, systemic inflammation) outcomes. However, the magnitude and consistency of these effects varied among studies. Three studies specifically involved AUD patients with alcohol-associated liver disease (ALD), while the others focused on AUD. In another study, Ghrelin, which was investigated as a neurohormonal target, emerged as a potential anti-inflammatory agent. However, ghrelin receptor antagonism in the presence of alcohol did not alter systemic inflammation. Of five trials using GLP-1 receptor agonists, three showed a reduction in alcohol use, but the other two, although directionally consistent, did not reach statistically significant effects. The current evidence supports the gut-brain axis as a dual therapeutic target, offering potential benefits for both AUD and ALD. Microbial therapies (FMT, probiotics, prebiotics) show some benefits in AUD, albeit studies are small. Hormonal targets such as ghrelin and GLP-1 receptors are mechanistically relevant. Data on ghrelin are limited. Data on GLP-1 receptor agonists are directionally consistent but not statistically robust. Large-scale, controlled trials are needed to validate and optimize the integration of this approach into AUD treatment strategies.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Gut microbiota dysbiosis and the gut-lung axis in COPD: mechanisms, clinical relevance, and microbiota-targeted interventions.
Frontiers in cell and developmental biology, 14:1915007.
Chronic obstructive pulmonary disease (COPD), which is characterised by persistent inflammation and airflow limitation, has increasingly been linked to the gut-lung axis. Patients with COPD commonly exhibit reduced diversity of gut microbiota, decreased levels of bacteria that produce short-chain fatty acids (SCFAs), increased levels of opportunistic pathogens, and compromised intestinal barrier function. These alterations are driven by factors such as smoking, hypoxia, oxidative stress, medication use and ageing, and promote bacterial translocation and systemic inflammation, thereby exacerbating lung injury. Gut microbiota metabolites, including SCFAs, bile acids, tryptophan metabolites and trimetlylamine N-oxide (TMAO), further modulate immune responses and metabolic pathways, thereby influencing disease progression. Intervention strategies targeting the microbiome, including dietary fibre, probiotics, prebiotics, faecal microbiota transplantation (FMT) and phage therapy, have demonstrated potential therapeutic value, though clinical evidence remains limited. Elucidating the mechanisms linking gut dysbiosis and COPD will provide novel targets for precision interventions and disease management.
Additional Links: PMID-42750861
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@article {pmid42750861,
year = {2026},
author = {Chai, Y and Lan, J and Li, K and Mei, X and Chen, Y and Zhou, N and Liu, X and Gong, W and Lei, H},
title = {Gut microbiota dysbiosis and the gut-lung axis in COPD: mechanisms, clinical relevance, and microbiota-targeted interventions.},
journal = {Frontiers in cell and developmental biology},
volume = {14},
number = {},
pages = {1915007},
pmid = {42750861},
issn = {2296-634X},
abstract = {Chronic obstructive pulmonary disease (COPD), which is characterised by persistent inflammation and airflow limitation, has increasingly been linked to the gut-lung axis. Patients with COPD commonly exhibit reduced diversity of gut microbiota, decreased levels of bacteria that produce short-chain fatty acids (SCFAs), increased levels of opportunistic pathogens, and compromised intestinal barrier function. These alterations are driven by factors such as smoking, hypoxia, oxidative stress, medication use and ageing, and promote bacterial translocation and systemic inflammation, thereby exacerbating lung injury. Gut microbiota metabolites, including SCFAs, bile acids, tryptophan metabolites and trimetlylamine N-oxide (TMAO), further modulate immune responses and metabolic pathways, thereby influencing disease progression. Intervention strategies targeting the microbiome, including dietary fibre, probiotics, prebiotics, faecal microbiota transplantation (FMT) and phage therapy, have demonstrated potential therapeutic value, though clinical evidence remains limited. Elucidating the mechanisms linking gut dysbiosis and COPD will provide novel targets for precision interventions and disease management.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
More than an infection: the ecological puzzle of recurrent urinary tract infections.
Frontiers in cellular and infection microbiology, 16:1927507.
Recurrent urinary tract infections (rUTIs) represent one of the most common infectious conditions worldwide, yet their pathophysiology extends far beyond repeated episodes of acute bacterial cystitis. Increasing evidence indicates that recurrence may arise through overlapping mechanisms including reinfection from intestinal or periurethral reservoirs, intracellular bacterial persistence, microbial dysbiosis, impaired mucosal immunity and chronic inflammatory remodelling of the bladder microenvironment. Current diagnostic frameworks remain largely based on symptom-based definitions and standard urine culture, approaches that incompletely capture the biological complexity of recurrent disease. This limitation is evident even at the definitional level, where clinically pragmatic categories often fail to reflect the heterogeneous mechanisms underlying recurrence. Advances in expanded urine culture techniques, metagenomics and metabolomics have reshaped the understanding of the urinary tract as a dynamic ecological system interconnected with vaginal, intestinal and prostatic microbial compartments. These approaches have identified diverse microbial communities, virulence-associated functional profiles and host-microbe interactions linked to recurrence-prone phenotypes. Significant challenges continue to persist in elucidating the biological mechanisms driving recurrence. Addressing these gaps is essential to improve disease characterization and support the development of more effective diagnostic and therapeutic approaches.
Additional Links: PMID-42750901
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@article {pmid42750901,
year = {2026},
author = {Musleh, L and Montilli, M and Ammendolia, MG and Sciarra, A and Riccioli, A and Maurizi, L and Longhi, C},
title = {More than an infection: the ecological puzzle of recurrent urinary tract infections.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1927507},
pmid = {42750901},
issn = {2235-2988},
mesh = {Humans ; *Urinary Tract Infections/microbiology/diagnosis/drug therapy/immunology ; Recurrence ; Microbiota ; Reinfection/microbiology ; Host Microbial Interactions ; Dysbiosis ; Urinary Tract/microbiology ; },
abstract = {Recurrent urinary tract infections (rUTIs) represent one of the most common infectious conditions worldwide, yet their pathophysiology extends far beyond repeated episodes of acute bacterial cystitis. Increasing evidence indicates that recurrence may arise through overlapping mechanisms including reinfection from intestinal or periurethral reservoirs, intracellular bacterial persistence, microbial dysbiosis, impaired mucosal immunity and chronic inflammatory remodelling of the bladder microenvironment. Current diagnostic frameworks remain largely based on symptom-based definitions and standard urine culture, approaches that incompletely capture the biological complexity of recurrent disease. This limitation is evident even at the definitional level, where clinically pragmatic categories often fail to reflect the heterogeneous mechanisms underlying recurrence. Advances in expanded urine culture techniques, metagenomics and metabolomics have reshaped the understanding of the urinary tract as a dynamic ecological system interconnected with vaginal, intestinal and prostatic microbial compartments. These approaches have identified diverse microbial communities, virulence-associated functional profiles and host-microbe interactions linked to recurrence-prone phenotypes. Significant challenges continue to persist in elucidating the biological mechanisms driving recurrence. Addressing these gaps is essential to improve disease characterization and support the development of more effective diagnostic and therapeutic approaches.},
}
MeSH Terms:
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Humans
*Urinary Tract Infections/microbiology/diagnosis/drug therapy/immunology
Recurrence
Microbiota
Reinfection/microbiology
Host Microbial Interactions
Dysbiosis
Urinary Tract/microbiology
RevDate: 2026-09-17
CmpDate: 2026-09-17
Maternal methionine supplementation in low-protein diets during late gestation and lactation increases performance and alters fecal microbiota of sows and their offspring.
Animal nutrition (Zhongguo xu mu shou yi xue hui), 27:206-217.
Methionine (Met) is known to enhance antioxidant defense and reproductive efficiency in sows, but its role under low-protein feeding conditions is unclear. This study evaluated the effects of Met supplementation on lactation performance, antioxidant status, and gut microbiota of sows and their offspring. Sixty-six multiparous sows with two parity and similar body weight (244.1 ± 1.73 kg) were assigned to a normal protein diet (18% crude protein [CP]) or low-protein diets (15% CP) containing graded standardized ileal digestible (SID) Met levels (0.23%, 0.30%, 0.37%, 0.44%, and 0.51%, respectively) from d 107 of gestation to d 21 of lactation, with 11 replicates in each group and one sow per replicate. The results showed that sows fed low-protein diets supplemented with 0.30% Met achieved milk yields and piglet growth comparable to those of the normal protein group (P > 0.05). In addition, 0.30% Met supplementation reduced serum urea nitrogen content, enhanced the concentrations of milk immunoglobulin M, glutathione, and taurine, and increased the activities of serum total superoxide dismutase in sows and glutathione peroxidase in piglets when compared with the normal protein diet (P < 0.05). Microbiome analysis indicated higher relative abundance of Christensenellaceae _R-7_group in piglets from the 0.30% Met group, and this relative abundance was positively correlated with growth traits. These findings suggest that supplementation with 0.30% Met within the 15% CP diet supports sow performance and piglet development comparable to normal protein feeding, via enhanced antioxidant capacity and favorable modulation of gut microbiota.
Additional Links: PMID-42751010
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@article {pmid42751010,
year = {2026},
author = {Wan, M and Kong, Z and Gao, Y and Yin, Y and Li, F and Duan, Y},
title = {Maternal methionine supplementation in low-protein diets during late gestation and lactation increases performance and alters fecal microbiota of sows and their offspring.},
journal = {Animal nutrition (Zhongguo xu mu shou yi xue hui)},
volume = {27},
number = {},
pages = {206-217},
pmid = {42751010},
issn = {2405-6383},
abstract = {Methionine (Met) is known to enhance antioxidant defense and reproductive efficiency in sows, but its role under low-protein feeding conditions is unclear. This study evaluated the effects of Met supplementation on lactation performance, antioxidant status, and gut microbiota of sows and their offspring. Sixty-six multiparous sows with two parity and similar body weight (244.1 ± 1.73 kg) were assigned to a normal protein diet (18% crude protein [CP]) or low-protein diets (15% CP) containing graded standardized ileal digestible (SID) Met levels (0.23%, 0.30%, 0.37%, 0.44%, and 0.51%, respectively) from d 107 of gestation to d 21 of lactation, with 11 replicates in each group and one sow per replicate. The results showed that sows fed low-protein diets supplemented with 0.30% Met achieved milk yields and piglet growth comparable to those of the normal protein group (P > 0.05). In addition, 0.30% Met supplementation reduced serum urea nitrogen content, enhanced the concentrations of milk immunoglobulin M, glutathione, and taurine, and increased the activities of serum total superoxide dismutase in sows and glutathione peroxidase in piglets when compared with the normal protein diet (P < 0.05). Microbiome analysis indicated higher relative abundance of Christensenellaceae _R-7_group in piglets from the 0.30% Met group, and this relative abundance was positively correlated with growth traits. These findings suggest that supplementation with 0.30% Met within the 15% CP diet supports sow performance and piglet development comparable to normal protein feeding, via enhanced antioxidant capacity and favorable modulation of gut microbiota.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Mangrove microbiomes: diversity, ecological functions, and applications.
Frontiers in microbiology, 17:1908615.
Mangrove ecosystems are dynamic coastal environments that offer essential ecological services, socioeconomic benefits, and resilience against climate change. Central to their functionality there are complex microbial communities-primarily bacteria and fungi-that drive key biogeochemical processes such as organic matter decomposition, nitrogen fixation, carbon sequestration, and sulfur cycling. This review aims to synthesize current knowledge on mangrove microbiomes, focusing on microbial taxonomic diversity, ecological roles, and environmental responsiveness. The effect of abiotic factors such as salinity, tidal regimes, vegetation type, and anthropogenic pressures on microbial community structure and function is also assessed. Key findings highlight the presence of both conserved microbial taxa across biogeographic regions and functional adaptations to local conditions, underscoring the global ecological significance of these microbial assemblages. Particular attention is given to microbe-mediated nutrient cycling, symbiotic plant-microbe interactions, and microbial contributions to pollutant degradation, including microplastics and heavy metals. Additionally, recent advances in omics-based approaches have expanded our understanding of microbial functionality and unveiled promising avenues for biotechnological applications, such as enzyme production and bioactive compound discovery. The review also identifies critical knowledge gaps, including the need for long-term monitoring, methodological standardization, and integrated multi-omics frameworks. Overall, recognizing microbial communities as foundational components of mangrove health is essential for effective conservation, ecosystem restoration, and sustainable resource management in the face of accelerating global environmental change.
Additional Links: PMID-42751019
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Citation:
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@article {pmid42751019,
year = {2026},
author = {Muñoz Puebla, D and Mindiola-Reyes, K and Nieto-Wigby, J and Cevallos-Cevallos, JM},
title = {Mangrove microbiomes: diversity, ecological functions, and applications.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1908615},
pmid = {42751019},
issn = {1664-302X},
abstract = {Mangrove ecosystems are dynamic coastal environments that offer essential ecological services, socioeconomic benefits, and resilience against climate change. Central to their functionality there are complex microbial communities-primarily bacteria and fungi-that drive key biogeochemical processes such as organic matter decomposition, nitrogen fixation, carbon sequestration, and sulfur cycling. This review aims to synthesize current knowledge on mangrove microbiomes, focusing on microbial taxonomic diversity, ecological roles, and environmental responsiveness. The effect of abiotic factors such as salinity, tidal regimes, vegetation type, and anthropogenic pressures on microbial community structure and function is also assessed. Key findings highlight the presence of both conserved microbial taxa across biogeographic regions and functional adaptations to local conditions, underscoring the global ecological significance of these microbial assemblages. Particular attention is given to microbe-mediated nutrient cycling, symbiotic plant-microbe interactions, and microbial contributions to pollutant degradation, including microplastics and heavy metals. Additionally, recent advances in omics-based approaches have expanded our understanding of microbial functionality and unveiled promising avenues for biotechnological applications, such as enzyme production and bioactive compound discovery. The review also identifies critical knowledge gaps, including the need for long-term monitoring, methodological standardization, and integrated multi-omics frameworks. Overall, recognizing microbial communities as foundational components of mangrove health is essential for effective conservation, ecosystem restoration, and sustainable resource management in the face of accelerating global environmental change.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Childhood asthma and the microbiome: from gut-lung axis mechanisms to precision prevention strategies.
Frontiers in immunology, 17:1902053.
Childhood asthma is a highly heterogeneous chronic respiratory disease, and its onset and progression are intricately linked to genetic susceptibility, environmental exposure, immune development, and the establishment of the early-life microbiome. In recent years, studies on the gut and respiratory microbiomes have suggested that the composition, metabolic functions, and interactions of microbial communities with the host immune system may be involved in the formation of asthma susceptibility, shaping of inflammatory phenotypes, and disease progression in children. The gut-lung axis, as an important pathway connecting gut microbiome, respiratory immunity, and systemic inflammatory responses, provides a new perspective for understanding the early mechanisms of childhood asthma. This article reviews the characteristics of the respiratory and gut microbiomes associated with childhood asthma, with a focus on the roles of the gut-lung axis, microbial metabolites, mucosal immune regulation, and environmental exposure. It also evaluates the research progress of probiotics, prebiotics, nutritional interventions, and novel microecological therapies. Additionally, the potential of microbial maturity, microbial metabolites, and immunophenotypes as biomarkers for risk prediction, phenotype stratification, and treatment response is analyzed. Furthermore, the role of multi-omics integration in supporting the identification of responsive populations, matching of intervention strategies, and dynamic monitoring of efficacy is discussed. Current evidence suggests that the microbiome offers promising targets for risk assessment and precision prevention of childhood asthma. However, relevant research still faces challenges such as ambiguous causality, high cohort heterogeneity, limited reproducibility of candidate biomarkers, inconsistent intervention outcomes, and insufficient evidence of long-term safety. At present, most biomarkers and multi-omics models remain in the stage of association discovery, lacking unified thresholds, cross-cohort validation, and biomarker-guided randomized controlled trials in children. Therefore, they cannot be routinely used for patient stratification or intervention selection. Future efforts should rely on standardized longitudinal birth cohorts, multi-omics integration, external validation, and high-quality clinical trials to clarify the incremental value of microbiome biomarkers over traditional clinical indicators and their clinical utility in the individualized management of childhood asthma.
Additional Links: PMID-42751182
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@article {pmid42751182,
year = {2026},
author = {Liang, X and Chen, D and Hu, J and Guo, L and Yang, H and Guo, Q and Zhang, R},
title = {Childhood asthma and the microbiome: from gut-lung axis mechanisms to precision prevention strategies.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1902053},
pmid = {42751182},
issn = {1664-3224},
mesh = {Humans ; *Asthma/prevention & control/microbiology/immunology/etiology ; *Gastrointestinal Microbiome/immunology ; Child ; *Lung/immunology/microbiology ; Animals ; Precision Medicine ; *Microbiota ; Biomarkers ; Probiotics/therapeutic use ; Environmental Exposure/adverse effects ; Disease Susceptibility ; },
abstract = {Childhood asthma is a highly heterogeneous chronic respiratory disease, and its onset and progression are intricately linked to genetic susceptibility, environmental exposure, immune development, and the establishment of the early-life microbiome. In recent years, studies on the gut and respiratory microbiomes have suggested that the composition, metabolic functions, and interactions of microbial communities with the host immune system may be involved in the formation of asthma susceptibility, shaping of inflammatory phenotypes, and disease progression in children. The gut-lung axis, as an important pathway connecting gut microbiome, respiratory immunity, and systemic inflammatory responses, provides a new perspective for understanding the early mechanisms of childhood asthma. This article reviews the characteristics of the respiratory and gut microbiomes associated with childhood asthma, with a focus on the roles of the gut-lung axis, microbial metabolites, mucosal immune regulation, and environmental exposure. It also evaluates the research progress of probiotics, prebiotics, nutritional interventions, and novel microecological therapies. Additionally, the potential of microbial maturity, microbial metabolites, and immunophenotypes as biomarkers for risk prediction, phenotype stratification, and treatment response is analyzed. Furthermore, the role of multi-omics integration in supporting the identification of responsive populations, matching of intervention strategies, and dynamic monitoring of efficacy is discussed. Current evidence suggests that the microbiome offers promising targets for risk assessment and precision prevention of childhood asthma. However, relevant research still faces challenges such as ambiguous causality, high cohort heterogeneity, limited reproducibility of candidate biomarkers, inconsistent intervention outcomes, and insufficient evidence of long-term safety. At present, most biomarkers and multi-omics models remain in the stage of association discovery, lacking unified thresholds, cross-cohort validation, and biomarker-guided randomized controlled trials in children. Therefore, they cannot be routinely used for patient stratification or intervention selection. Future efforts should rely on standardized longitudinal birth cohorts, multi-omics integration, external validation, and high-quality clinical trials to clarify the incremental value of microbiome biomarkers over traditional clinical indicators and their clinical utility in the individualized management of childhood asthma.},
}
MeSH Terms:
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Humans
*Asthma/prevention & control/microbiology/immunology/etiology
*Gastrointestinal Microbiome/immunology
Child
*Lung/immunology/microbiology
Animals
Precision Medicine
*Microbiota
Biomarkers
Probiotics/therapeutic use
Environmental Exposure/adverse effects
Disease Susceptibility
RevDate: 2026-09-17
CmpDate: 2026-09-17
Advancing the study of microbial symbionts of amphibians and reptiles.
Frontiers in amphibian and reptile science, 4:.
Amphibian and reptile microbiomes are important contributors to host health and ecosystem dynamics but understudied compared to microbiomes of other vertebrates. Through study of amphibian and reptile microbiomes, investigators can advance theory and practice in animal health, ecosystem function, conservation, and more. This special issue of Frontiers of Amphibian and Reptile Science features six publications in the field of amphibian and reptile microbiome research, and here, we highlight the contributions of these and other recent publications to four main areas of recent advancement in the field: 1) expanding "microbiome" beyond bacteria, 2) expanding study of host life-history stages and anatomical microbial habitats, 3) characterizing whole microbial communities, particularly in disease ecology studies, and 4) developing and implementing databases and bioinformatics tools. We also discuss several avenues for future research that would bring amphibians and reptiles to the forefront of microbiome research. With the continued implementation of classic culture-based and sequencing approaches paired with cutting-edge tools in vivo, in vitro, and in silico, herpetofauna microbiome research is poised for exciting growth in the near future.
Additional Links: PMID-42751268
PubMed:
Citation:
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@article {pmid42751268,
year = {2026},
author = {Doolin, ML and Woodhams, DC},
title = {Advancing the study of microbial symbionts of amphibians and reptiles.},
journal = {Frontiers in amphibian and reptile science},
volume = {4},
number = {},
pages = {},
pmid = {42751268},
issn = {2813-6780},
abstract = {Amphibian and reptile microbiomes are important contributors to host health and ecosystem dynamics but understudied compared to microbiomes of other vertebrates. Through study of amphibian and reptile microbiomes, investigators can advance theory and practice in animal health, ecosystem function, conservation, and more. This special issue of Frontiers of Amphibian and Reptile Science features six publications in the field of amphibian and reptile microbiome research, and here, we highlight the contributions of these and other recent publications to four main areas of recent advancement in the field: 1) expanding "microbiome" beyond bacteria, 2) expanding study of host life-history stages and anatomical microbial habitats, 3) characterizing whole microbial communities, particularly in disease ecology studies, and 4) developing and implementing databases and bioinformatics tools. We also discuss several avenues for future research that would bring amphibians and reptiles to the forefront of microbiome research. With the continued implementation of classic culture-based and sequencing approaches paired with cutting-edge tools in vivo, in vitro, and in silico, herpetofauna microbiome research is poised for exciting growth in the near future.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
New Insights into the Role of Mitochondrial Dysfunction in Diabetic Kidney Disease in the Omics Era.
Diabetes, metabolic syndrome and obesity : targets and therapy, 19:622389.
Diabetic kidney disease (DKD) is a major microvascular complication of diabetes and the leading cause of end-stage renal disease worldwide. Accumulating evidence identifies mitochondrial dysfunction as a central driver of DKD progression by linking metabolic reprogramming, oxidative stress, and inflammatory responses. Recent advances in spatial omics, genomics, transcriptomics, proteomics, metabolomics, and microbiome analyses have enabled the characterization of cell-specific and dynamic alterations in mitochondrial function and their interactions with the renal microenvironment. Integrative analyses across these molecular layers have revealed key mechanisms involving mitochondrial quality control, metabolic reprogramming, and inflammatory signaling, while identifying potential biomarkers and therapeutic targets. Furthermore, these approaches have provided mechanistic insights into the renoprotective effects of conventional therapies and bioactive compounds from traditional Chinese medicine. This integrative review synthesizes current evidence to clarify the role of mitochondrial dysfunction in DKD pathogenesis and discusses emerging opportunities for biomarker discovery and precision therapeutics.
Additional Links: PMID-42751271
PubMed:
Citation:
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@article {pmid42751271,
year = {2026},
author = {Liu, XK and Zhou, XL and Xia, WR},
title = {New Insights into the Role of Mitochondrial Dysfunction in Diabetic Kidney Disease in the Omics Era.},
journal = {Diabetes, metabolic syndrome and obesity : targets and therapy},
volume = {19},
number = {},
pages = {622389},
pmid = {42751271},
issn = {1178-7007},
abstract = {Diabetic kidney disease (DKD) is a major microvascular complication of diabetes and the leading cause of end-stage renal disease worldwide. Accumulating evidence identifies mitochondrial dysfunction as a central driver of DKD progression by linking metabolic reprogramming, oxidative stress, and inflammatory responses. Recent advances in spatial omics, genomics, transcriptomics, proteomics, metabolomics, and microbiome analyses have enabled the characterization of cell-specific and dynamic alterations in mitochondrial function and their interactions with the renal microenvironment. Integrative analyses across these molecular layers have revealed key mechanisms involving mitochondrial quality control, metabolic reprogramming, and inflammatory signaling, while identifying potential biomarkers and therapeutic targets. Furthermore, these approaches have provided mechanistic insights into the renoprotective effects of conventional therapies and bioactive compounds from traditional Chinese medicine. This integrative review synthesizes current evidence to clarify the role of mitochondrial dysfunction in DKD pathogenesis and discusses emerging opportunities for biomarker discovery and precision therapeutics.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Anaerobic stress index to predict microbial ecological shifts in clear aligners.
Journal of oral microbiology, 18(1):2701561.
OBJECTIVES: Clear aligners are clinically perceived as periodontally 'friendlier' than fixed appliances (FA), yet localized gingivitis persists. Salivary diagnostics often mask site-specific dysbiosis through a 'dilution effect'. This study aimed to characterize distinct ecological pressures and propose a novel anaerobic stress index (ASI) to quantify localized microbial burden.
METHODS: A computational meta-analysis was conducted using longitudinal 16S rRNA sequencing datasets (n = 976 samples from 10 distinct studies). Data was processed through a standardized Kraken2/Bracken pipeline. The ASI was calculated as the ratio of key anaerobic pathobionts (Fusobacterium, Prevotella) to facultative commensals (Streptococcus, Rothia).
RESULTS: Saliva acts as a 'dilution filter,' failing to capture sessile biofilm dynamics (AUC = 0.51 in FA). Fixed appliances exhibited mechanical dysbiosis with a 2.64-fold increase in Actinomyces (p < 0.0001) within the first month. Clear aligners induced a 'silent hypoxia'. The supragingival biofilm showed a progressive shift toward anaerobiosis. The ASI in aligner patients quadrupled by month 6 (from 0.58 to 2.52; p = 0.002), a shift not detectable in matched saliva samples.
CONCLUSIONS: Physical entrapment in fixed appliances versus micro-environmental hypoxia under clear aligners drives divergent dysbiotic pathways. The ASI serves as a robust biomarker for subclinical dysbiosis, suggesting periodic re-oxygenation therapeutics are necessary to restore host-microbe homeostasis.
Additional Links: PMID-42751289
PubMed:
Citation:
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@article {pmid42751289,
year = {2026},
author = {Demirci, M and Unlu, O and Kantarci, A},
title = {Anaerobic stress index to predict microbial ecological shifts in clear aligners.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2701561},
pmid = {42751289},
issn = {2000-2297},
abstract = {OBJECTIVES: Clear aligners are clinically perceived as periodontally 'friendlier' than fixed appliances (FA), yet localized gingivitis persists. Salivary diagnostics often mask site-specific dysbiosis through a 'dilution effect'. This study aimed to characterize distinct ecological pressures and propose a novel anaerobic stress index (ASI) to quantify localized microbial burden.
METHODS: A computational meta-analysis was conducted using longitudinal 16S rRNA sequencing datasets (n = 976 samples from 10 distinct studies). Data was processed through a standardized Kraken2/Bracken pipeline. The ASI was calculated as the ratio of key anaerobic pathobionts (Fusobacterium, Prevotella) to facultative commensals (Streptococcus, Rothia).
RESULTS: Saliva acts as a 'dilution filter,' failing to capture sessile biofilm dynamics (AUC = 0.51 in FA). Fixed appliances exhibited mechanical dysbiosis with a 2.64-fold increase in Actinomyces (p < 0.0001) within the first month. Clear aligners induced a 'silent hypoxia'. The supragingival biofilm showed a progressive shift toward anaerobiosis. The ASI in aligner patients quadrupled by month 6 (from 0.58 to 2.52; p = 0.002), a shift not detectable in matched saliva samples.
CONCLUSIONS: Physical entrapment in fixed appliances versus micro-environmental hypoxia under clear aligners drives divergent dysbiotic pathways. The ASI serves as a robust biomarker for subclinical dysbiosis, suggesting periodic re-oxygenation therapeutics are necessary to restore host-microbe homeostasis.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Toward nursing-integrated biomarker surveillance for immune-related adverse events during immune checkpoint inhibitor therapy.
Frontiers in medicine, 13:1943642.
Immune checkpoint inhibitors (ICIs) have transformed cancer care but can cause immune-related adverse events (irAEs) involving almost any organ system. Delayed recognition may permit reversible inflammation to progress to organ dysfunction, treatment interruption, prolonged immunosuppression, or death. Biomarker surveillance offers an objective complement to symptom assessment, yet no single marker is sufficiently accurate for universal prediction. This Mini Review examines the mechanistic basis and clinical evidence for nursing-led biomarker monitoring during ICI therapy. Targeted autoantibody, cytokine, or immune-cell assays may support selected clinical evaluations, whereas germline, T-cell receptor, and microbiome signatures remain investigational. Dynamic changes are generally more informative than isolated values, but interpretation is complicated by cancer burden, infection, concomitant treatment, and pre-existing disease. Nurses are positioned to connect serial laboratory trends with patient-reported symptoms, vital signs, treatment timing, and escalation pathways. Prospective studies are needed to validate multimarker panels and determine whether biomarker-informed nursing pathways reduce severe irAEs without unnecessary testing or interruption of effective immunotherapy.
Additional Links: PMID-42751376
PubMed:
Citation:
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@article {pmid42751376,
year = {2026},
author = {Jin, J and Zheng, L and Tian, Y and Chu, M and Cao, B},
title = {Toward nursing-integrated biomarker surveillance for immune-related adverse events during immune checkpoint inhibitor therapy.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1943642},
pmid = {42751376},
issn = {2296-858X},
abstract = {Immune checkpoint inhibitors (ICIs) have transformed cancer care but can cause immune-related adverse events (irAEs) involving almost any organ system. Delayed recognition may permit reversible inflammation to progress to organ dysfunction, treatment interruption, prolonged immunosuppression, or death. Biomarker surveillance offers an objective complement to symptom assessment, yet no single marker is sufficiently accurate for universal prediction. This Mini Review examines the mechanistic basis and clinical evidence for nursing-led biomarker monitoring during ICI therapy. Targeted autoantibody, cytokine, or immune-cell assays may support selected clinical evaluations, whereas germline, T-cell receptor, and microbiome signatures remain investigational. Dynamic changes are generally more informative than isolated values, but interpretation is complicated by cancer burden, infection, concomitant treatment, and pre-existing disease. Nurses are positioned to connect serial laboratory trends with patient-reported symptoms, vital signs, treatment timing, and escalation pathways. Prospective studies are needed to validate multimarker panels and determine whether biomarker-informed nursing pathways reduce severe irAEs without unnecessary testing or interruption of effective immunotherapy.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
metadeconfoundR: Covariate analysis of high-dimensional cross-sectional omics data.
Bioinformatics advances, 6(1):vbag242.
MOTIVATION: Identifying disease biomarkers from large molecular datasets is complicated by correlated and confounded signals like comorbidities and treatment regimens, batch effects, and cohort biases. These effects bias statistical inference and clinical conclusions. Robust methodologies are fundamental for reliable biomarker discovery.
RESULTS: metadeconfoundR is an R package for conservative biomarker discovery in (multi-)omics case-control datasets. It has a scalable two-step confounder-aware statistical framework for retaining only associations with independent support. It identifies covariate-naive univariate associations between omics features and metadata, then re-evaluates these associations using parallel post-hoc nested linear model testing to account for potential confounders. Confounded associations are flagged if they fully reduce to at least one other variable. metadeconfoundR supports parallel computation for large-scale datasets, offers visualization and tools for interpreting results and secondary analyses. We benchmark metadeconfoundR against state-of-the-art methods for identifying biomarkers using simulated ground truth derived from microbiome data, and demonstrate its ability to disentangle confounding effects while preserving statistical power, offering particular advantage when multiple covariates are present. metadeconfoundR functions for any -omics data type with continuous or categorical metadata/covariates.
AVAILABILITY: metadeconfoundR is available on CRAN (https://cran.r-project.org/web/packages/metadeconfoundR/) and GitHub (https://github.com/TillBirkner/metadeconfoundR).
Additional Links: PMID-42751396
PubMed:
Citation:
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@article {pmid42751396,
year = {2026},
author = {Birkner, T and Chen, CY and Essex, M and Dahm, K and Löber, U and Ulas, T and Jarquín-Díaz, VH and Forslund-Startceva, SK},
title = {metadeconfoundR: Covariate analysis of high-dimensional cross-sectional omics data.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag242},
pmid = {42751396},
issn = {2635-0041},
abstract = {MOTIVATION: Identifying disease biomarkers from large molecular datasets is complicated by correlated and confounded signals like comorbidities and treatment regimens, batch effects, and cohort biases. These effects bias statistical inference and clinical conclusions. Robust methodologies are fundamental for reliable biomarker discovery.
RESULTS: metadeconfoundR is an R package for conservative biomarker discovery in (multi-)omics case-control datasets. It has a scalable two-step confounder-aware statistical framework for retaining only associations with independent support. It identifies covariate-naive univariate associations between omics features and metadata, then re-evaluates these associations using parallel post-hoc nested linear model testing to account for potential confounders. Confounded associations are flagged if they fully reduce to at least one other variable. metadeconfoundR supports parallel computation for large-scale datasets, offers visualization and tools for interpreting results and secondary analyses. We benchmark metadeconfoundR against state-of-the-art methods for identifying biomarkers using simulated ground truth derived from microbiome data, and demonstrate its ability to disentangle confounding effects while preserving statistical power, offering particular advantage when multiple covariates are present. metadeconfoundR functions for any -omics data type with continuous or categorical metadata/covariates.
AVAILABILITY: metadeconfoundR is available on CRAN (https://cran.r-project.org/web/packages/metadeconfoundR/) and GitHub (https://github.com/TillBirkner/metadeconfoundR).},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Polyphenol-rich sugarcane extract reduces circulating trans fatty acids, VLDL cholesterol, and triglycerides in healthy adults.
Frontiers in nutrition, 13:1923420.
BACKGROUND: Polyphenol-rich sugarcane extracts (PRSEs) are food-derived sources of naturally occurring bioactive polyphenols with increasing relevance to metabolic regulation, gut microbiome function, and overall well-being.
OBJECTIVE: This fully remote trial investigated the effects of PRSE supplementation on cardiometabolic biomarkers and gut microbiota.
METHODS: Healthy adults aged 18-55 years (n = 47, female = 36 and male = 11) residing in Australia were recruited to a remote quadruple-blinded, randomised, placebo-controlled cross-over trial, with each intervention arm lasting 90 days. Participants received PRSE oral capsules at 500 mg/day (two 250 mg doses) or maltodextrin placebo capsules. Blood and faecal samples were collected for subsequent blood biomarkers and microbiome analyses, respectively. Self-reported qualitative surveys were conducted to assess overall wellbeing over the 6-month period.
RESULTS: Significant treatment × time effects were observed for circulating trans-fatty acids (%), triglycerides and VLDL cholesterol, as well as several microbial metabolic pathways, including glycerol degradation III, pyruvate dehydrogenase, and p-cresol degradation. No significant effects were detected for body weight, inflammatory, or glycaemic markers following correction for multiple comparisons.
CONCLUSION: PRSE supplementation was associated with a lower circulating proportion of trans-fatty acids, and lower triglyceride and VLDL cholesterol concentrations compared with placebo. PRSE supplementation also modulated selected microbial functional pathways without affecting overall microbiome diversity or community composition. These findings support the biological activity of PRSE and suggest potential interactions between host metabolic and microbiome-related mechanisms.
CLINICAL TRIAL REGISTRATION: https://anzctr.org.au/Trial/Registration/TrialReview.aspx?id=386733&isReview=true, identifier, ANZCTR; ACTRN12624000055505.
Additional Links: PMID-42751563
PubMed:
Citation:
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@article {pmid42751563,
year = {2026},
author = {Lewin, S and Hartley, C and Llalla Vidal, TM and Rose, JJA and Costanzo, A and Jadhav, SR and Bromfield, J and Keast, RSJ and Mitchell, S and Flavel, M and Dias, DA},
title = {Polyphenol-rich sugarcane extract reduces circulating trans fatty acids, VLDL cholesterol, and triglycerides in healthy adults.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1923420},
pmid = {42751563},
issn = {2296-861X},
abstract = {BACKGROUND: Polyphenol-rich sugarcane extracts (PRSEs) are food-derived sources of naturally occurring bioactive polyphenols with increasing relevance to metabolic regulation, gut microbiome function, and overall well-being.
OBJECTIVE: This fully remote trial investigated the effects of PRSE supplementation on cardiometabolic biomarkers and gut microbiota.
METHODS: Healthy adults aged 18-55 years (n = 47, female = 36 and male = 11) residing in Australia were recruited to a remote quadruple-blinded, randomised, placebo-controlled cross-over trial, with each intervention arm lasting 90 days. Participants received PRSE oral capsules at 500 mg/day (two 250 mg doses) or maltodextrin placebo capsules. Blood and faecal samples were collected for subsequent blood biomarkers and microbiome analyses, respectively. Self-reported qualitative surveys were conducted to assess overall wellbeing over the 6-month period.
RESULTS: Significant treatment × time effects were observed for circulating trans-fatty acids (%), triglycerides and VLDL cholesterol, as well as several microbial metabolic pathways, including glycerol degradation III, pyruvate dehydrogenase, and p-cresol degradation. No significant effects were detected for body weight, inflammatory, or glycaemic markers following correction for multiple comparisons.
CONCLUSION: PRSE supplementation was associated with a lower circulating proportion of trans-fatty acids, and lower triglyceride and VLDL cholesterol concentrations compared with placebo. PRSE supplementation also modulated selected microbial functional pathways without affecting overall microbiome diversity or community composition. These findings support the biological activity of PRSE and suggest potential interactions between host metabolic and microbiome-related mechanisms.
CLINICAL TRIAL REGISTRATION: https://anzctr.org.au/Trial/Registration/TrialReview.aspx?id=386733&isReview=true, identifier, ANZCTR; ACTRN12624000055505.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Estrobolome dysbiosis in canine mammary gland tumors: Eggerthella lenta as a candidate microbial marker for hormone-dependent mammary tumorigenesis.
Frontiers in microbiology, 17:1923235.
Canine mammary gland tumors (MGTs) are the most prevalent neoplasms in intact female dogs, yet the role of the gut microbiome in their pathogenesis remains largely unexplored. This pilot study investigated the gut microbiota composition of 40 female dogs classified into MGT (n = 11), Non-MGT (n = 20), and under 2 years (U2Y, n = 9) groups using 16S rRNA gene sequencing. Alpha diversity indices showed no significant differences between the MGT and Non-MGT groups, whereas beta diversity analysis revealed significant overall community-level differences across all three groups (PERMANOVA, p = 0.0001), with the U2Y group compositionally distinct from both adult groups. In contrast, MGT and Non-MGT groups showed substantial overlap in community structure after correction for multiple comparisons. Differential abundance analysis identified Eggerthella as a candidate MGT-associated taxon, and species-specific quantitative PCR (qPCR) demonstrated a significantly higher normalized abundance of Eggerthella lenta in MGT samples than in Non-MGT controls (Mann-Whitney U test, p = 0.0159). Conversely, potentially beneficial short-chain fatty acid (SCFA)-producing bacteria, including Clostridium and Megamonas, showed reduced relative abundance in tumor-bearing dogs (Clostridium, ANCOM-BC; Megamonas, exploratory post hoc Mann-Whitney test). PICRUSt2 analysis suggested a trend toward enrichment of polyamine biosynthesis pathways in the MGT group, although no pathway remained significant after multiple-testing correction in the MGT vs. Non-MGT comparison. To our knowledge, this study provides the first evidence linking the estrobolome-associated bacterium Eggerthella lenta with canine MGTs. Together with the depletion of beneficial SCFA-producing bacteria, these findings suggest a pattern of gut microbial dysbiosis that may influence hormone-dependent mammary tumorigenesis through microbiome-associated alterations in estrogen metabolism. Although E. lenta was detected in both MGT and Non-MGT dogs, its significantly higher normalized abundance in MGT samples supports its potential as an abundance-based candidate microbial marker that warrants validation in large, independent prospective cohorts before clinical application. Collectively, these findings provide new insights into the gut-mammary axis and support future investigations into microbiome-based diagnostic and therapeutic strategies for canine mammary gland tumors.
Additional Links: PMID-42751581
PubMed:
Citation:
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@article {pmid42751581,
year = {2026},
author = {Kim, KW and Farooq, M and Jin, DY and Kim, W and Shin, J and Park, S and Ko, G and Park, S and Kim, G and Na, S and Kim, M and Kim, YJ and Kim, C and Lee, HJ and Choi, S and Ahn, HJ and Jang, HJ and Choi, HS and Yoon, KY and Kang, KK and Jung, SC and Song, WJ and Kim, JS and Jung, YH},
title = {Estrobolome dysbiosis in canine mammary gland tumors: Eggerthella lenta as a candidate microbial marker for hormone-dependent mammary tumorigenesis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1923235},
pmid = {42751581},
issn = {1664-302X},
abstract = {Canine mammary gland tumors (MGTs) are the most prevalent neoplasms in intact female dogs, yet the role of the gut microbiome in their pathogenesis remains largely unexplored. This pilot study investigated the gut microbiota composition of 40 female dogs classified into MGT (n = 11), Non-MGT (n = 20), and under 2 years (U2Y, n = 9) groups using 16S rRNA gene sequencing. Alpha diversity indices showed no significant differences between the MGT and Non-MGT groups, whereas beta diversity analysis revealed significant overall community-level differences across all three groups (PERMANOVA, p = 0.0001), with the U2Y group compositionally distinct from both adult groups. In contrast, MGT and Non-MGT groups showed substantial overlap in community structure after correction for multiple comparisons. Differential abundance analysis identified Eggerthella as a candidate MGT-associated taxon, and species-specific quantitative PCR (qPCR) demonstrated a significantly higher normalized abundance of Eggerthella lenta in MGT samples than in Non-MGT controls (Mann-Whitney U test, p = 0.0159). Conversely, potentially beneficial short-chain fatty acid (SCFA)-producing bacteria, including Clostridium and Megamonas, showed reduced relative abundance in tumor-bearing dogs (Clostridium, ANCOM-BC; Megamonas, exploratory post hoc Mann-Whitney test). PICRUSt2 analysis suggested a trend toward enrichment of polyamine biosynthesis pathways in the MGT group, although no pathway remained significant after multiple-testing correction in the MGT vs. Non-MGT comparison. To our knowledge, this study provides the first evidence linking the estrobolome-associated bacterium Eggerthella lenta with canine MGTs. Together with the depletion of beneficial SCFA-producing bacteria, these findings suggest a pattern of gut microbial dysbiosis that may influence hormone-dependent mammary tumorigenesis through microbiome-associated alterations in estrogen metabolism. Although E. lenta was detected in both MGT and Non-MGT dogs, its significantly higher normalized abundance in MGT samples supports its potential as an abundance-based candidate microbial marker that warrants validation in large, independent prospective cohorts before clinical application. Collectively, these findings provide new insights into the gut-mammary axis and support future investigations into microbiome-based diagnostic and therapeutic strategies for canine mammary gland tumors.},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
The impact of microbiome diversity and composition on host health and susceptibility to disease across amphibian life stages.
Frontiers in amphibian and reptile science, 3:1666714.
Germ-free (i.e., absence of all microbes) and gnotobiotic (i.e., specific known microbial communities) study systems have classically been used to investigate the critical role the microbiome plays in the development of the host immune system. To date, most systems that have been used to experimentally manipulate the microbiome have been developed in model organisms, such as mice and pigs. However, amphibians are rapidly emerging as a valuable model for studying host-microbiome interactions and their effects on health and immunity, especially in the context of infectious disease. Amphibians are a particularly compelling system because, unlike many current systems, they include many species that do not need direct parental care during development, and they undergo a complete reorganization of their immune system during metamorphosis. Amphibians are a group of particular conservation importance as they are currently affected by the infectious disease chytridiomycosis, caused by the fungal pathogen Batrachochytrium dendrobatidis. Here, we review current research aimed at manipulating the amphibian microbiome through the use of antimicrobial treatments, with a focus on how a depletion of the microbiome diversity influences host development, immunity, and susceptibility to infectious disease. We structure our review in three parts: (1) how microbiome depletion affects chytridiomycosis disease dynamics, (2) how microbiome bioaugmentation through the use of probiotics influences susceptibility to chytridiomycosis, and (3) how microbiome depletion affects amphibian health across different life stages. Overall, research on this topic is important for the conservation of wild amphibian populations because it adds to understanding of the amphibian immune system and susceptibility to disease, both of which are important to inform management strategies and optimize potential therapeutics to aid susceptible populations.
Additional Links: PMID-42751604
PubMed:
Citation:
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@article {pmid42751604,
year = {2025},
author = {Miller, AJ and Voyles, J},
title = {The impact of microbiome diversity and composition on host health and susceptibility to disease across amphibian life stages.},
journal = {Frontiers in amphibian and reptile science},
volume = {3},
number = {},
pages = {1666714},
pmid = {42751604},
issn = {2813-6780},
abstract = {Germ-free (i.e., absence of all microbes) and gnotobiotic (i.e., specific known microbial communities) study systems have classically been used to investigate the critical role the microbiome plays in the development of the host immune system. To date, most systems that have been used to experimentally manipulate the microbiome have been developed in model organisms, such as mice and pigs. However, amphibians are rapidly emerging as a valuable model for studying host-microbiome interactions and their effects on health and immunity, especially in the context of infectious disease. Amphibians are a particularly compelling system because, unlike many current systems, they include many species that do not need direct parental care during development, and they undergo a complete reorganization of their immune system during metamorphosis. Amphibians are a group of particular conservation importance as they are currently affected by the infectious disease chytridiomycosis, caused by the fungal pathogen Batrachochytrium dendrobatidis. Here, we review current research aimed at manipulating the amphibian microbiome through the use of antimicrobial treatments, with a focus on how a depletion of the microbiome diversity influences host development, immunity, and susceptibility to infectious disease. We structure our review in three parts: (1) how microbiome depletion affects chytridiomycosis disease dynamics, (2) how microbiome bioaugmentation through the use of probiotics influences susceptibility to chytridiomycosis, and (3) how microbiome depletion affects amphibian health across different life stages. Overall, research on this topic is important for the conservation of wild amphibian populations because it adds to understanding of the amphibian immune system and susceptibility to disease, both of which are important to inform management strategies and optimize potential therapeutics to aid susceptible populations.},
}
RevDate: 2026-09-17
Transmembrane MUC1 assists oral microbial colonization in oral mucosa of potentially malignant disorders and oral squamous carcinoma.
European journal of oral sciences [Epub ahead of print].
Transmembrane mucin 1 (tMUC1) provides oral mucosal barrier against pathogens. The invasion of oncopathogenic microbes can promote cancerous proliferation of cells via inflammatory responses, abnormal cellular signaling, angiogenesis, anti-adhesion, and tumorigenesis. Oral potentially malignant disorders (OPMDs), such as oral lichen planus (OLP) and oral leukoplakia (OLK), include lesions with often dysplastic features and a risk of malignant transformation to oral squamous cell carcinoma (OSCC). This study examined the expression of tMUC1 and oral microbial colonization in these conditions using scanning electron microscopy (SEM). Forty-one formalin-fixed, paraffin-embedded biopsies were distinguished into controls, OLP, OLK, and OSCC groups. They were immunohistochemically stained for tMUC1 and were evaluated on light microscopy and SEM. Immunohistochemical expression of tMUC1 was limited to superficial layers in controls. OSCC presented considerable staining in all epithelial layers, whereas OLP and OLK samples showed no to minimal staining in the intermediate and superficial layers of epithelium. SEM displayed increased oral microbial colonization on the superficial surface of OLP and OLK when compared to controls. The altered expression of tMUC1 in OLP, OLK, and OSCC may enhance oral microbial colonization. OPMDs' transformation to OSCC could be due to influence of inflammatory response to microbial colonization.
Additional Links: PMID-42751960
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@article {pmid42751960,
year = {2026},
author = {Soiniemi, L and Kanniainen, M and Ramsay, S and Kullaa, A and Kashyap, B},
title = {Transmembrane MUC1 assists oral microbial colonization in oral mucosa of potentially malignant disorders and oral squamous carcinoma.},
journal = {European journal of oral sciences},
volume = {},
number = {},
pages = {e70144},
doi = {10.1111/eos.70144},
pmid = {42751960},
issn = {1600-0722},
support = {//by Finnish Dental Foundation, Finnish Cultural Foundation, and University of Eastern Finland/ ; //Itä-Suomen Yliopisto/ ; //Suomen Kulttuurirahasto/ ; //Suomen Hammaslääkäriseura Apollonia/ ; },
abstract = {Transmembrane mucin 1 (tMUC1) provides oral mucosal barrier against pathogens. The invasion of oncopathogenic microbes can promote cancerous proliferation of cells via inflammatory responses, abnormal cellular signaling, angiogenesis, anti-adhesion, and tumorigenesis. Oral potentially malignant disorders (OPMDs), such as oral lichen planus (OLP) and oral leukoplakia (OLK), include lesions with often dysplastic features and a risk of malignant transformation to oral squamous cell carcinoma (OSCC). This study examined the expression of tMUC1 and oral microbial colonization in these conditions using scanning electron microscopy (SEM). Forty-one formalin-fixed, paraffin-embedded biopsies were distinguished into controls, OLP, OLK, and OSCC groups. They were immunohistochemically stained for tMUC1 and were evaluated on light microscopy and SEM. Immunohistochemical expression of tMUC1 was limited to superficial layers in controls. OSCC presented considerable staining in all epithelial layers, whereas OLP and OLK samples showed no to minimal staining in the intermediate and superficial layers of epithelium. SEM displayed increased oral microbial colonization on the superficial surface of OLP and OLK when compared to controls. The altered expression of tMUC1 in OLP, OLK, and OSCC may enhance oral microbial colonization. OPMDs' transformation to OSCC could be due to influence of inflammatory response to microbial colonization.},
}
RevDate: 2026-09-17
Examining the multidimensional implications of oral health in chronic kidney disease: A systematic review.
Journal of the American Dental Association (1939) pii:S0002-8177(26)00400-9 [Epub ahead of print].
BACKGROUND: The authors of this systematic review aimed to synthesize the evidence on the multidimensional oral health outcomes associated with chronic kidney disease (CKD), including oral health status, oral manifestations, oral health-related quality of life, underlying biological mechanisms, and access to oral health care.
TYPES OF STUDIES REVIEWED: A total of 46 English-language studies published over the past decade were included, comprising randomized controlled trials, nonrandomized interventional studies, and observational designs (eg, cohort, case-control, and cross-sectional studies). Studies were selected according to predefined population, exposure, comparator, and outcomes criteria. Risk of bias and methodological quality were assessed independently, and findings were synthesized qualitatively due to heterogeneity. The certainty of evidence was evaluated using the Grading of Recommendations Assessment, Development and Evaluation approach.
RESULTS: Patients with CKD exhibited poorer oral health outcomes than healthy controls across multiple domains. These included reduced oral health-related quality of life (standardized mean difference, 0.45), high prevalence of oral mucosal lesions (81.8%), higher salivary pH (standardized mean difference, 1.74), and substantial tooth loss (mean, 15 teeth). Proposed mechanisms include systemic inflammation, altered mineral metabolism, kidney osteodystrophy, salivary changes, and oral microbiome dysbiosis.
Routine use of the 14-item Oral Health Impact Profile can help clinicians identify oral health-related quality of life issues in patients with CKD, guide early detection and prevention of oral complications, and support integration of oral health care with overall medical management, including monitoring kidney function tests to identify patients at higher risk. In the future, researchers should focus on underrepresented groups, particularly patients with mild to moderate CKD, and use robust study designs to clarify longitudinal outcomes and the complex interactions between CKD and oral health. The protocol used in this systematic review was registered in the International Prospective Register of Systematic Reviews database (registration CRD42024618866).
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@article {pmid42752066,
year = {2026},
author = {Ventura, SMR and Mesquita, PMV},
title = {Examining the multidimensional implications of oral health in chronic kidney disease: A systematic review.},
journal = {Journal of the American Dental Association (1939)},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.adaj.2026.06.004},
pmid = {42752066},
issn = {1943-4723},
abstract = {BACKGROUND: The authors of this systematic review aimed to synthesize the evidence on the multidimensional oral health outcomes associated with chronic kidney disease (CKD), including oral health status, oral manifestations, oral health-related quality of life, underlying biological mechanisms, and access to oral health care.
TYPES OF STUDIES REVIEWED: A total of 46 English-language studies published over the past decade were included, comprising randomized controlled trials, nonrandomized interventional studies, and observational designs (eg, cohort, case-control, and cross-sectional studies). Studies were selected according to predefined population, exposure, comparator, and outcomes criteria. Risk of bias and methodological quality were assessed independently, and findings were synthesized qualitatively due to heterogeneity. The certainty of evidence was evaluated using the Grading of Recommendations Assessment, Development and Evaluation approach.
RESULTS: Patients with CKD exhibited poorer oral health outcomes than healthy controls across multiple domains. These included reduced oral health-related quality of life (standardized mean difference, 0.45), high prevalence of oral mucosal lesions (81.8%), higher salivary pH (standardized mean difference, 1.74), and substantial tooth loss (mean, 15 teeth). Proposed mechanisms include systemic inflammation, altered mineral metabolism, kidney osteodystrophy, salivary changes, and oral microbiome dysbiosis.
Routine use of the 14-item Oral Health Impact Profile can help clinicians identify oral health-related quality of life issues in patients with CKD, guide early detection and prevention of oral complications, and support integration of oral health care with overall medical management, including monitoring kidney function tests to identify patients at higher risk. In the future, researchers should focus on underrepresented groups, particularly patients with mild to moderate CKD, and use robust study designs to clarify longitudinal outcomes and the complex interactions between CKD and oral health. The protocol used in this systematic review was registered in the International Prospective Register of Systematic Reviews database (registration CRD42024618866).},
}
RevDate: 2026-09-17
CmpDate: 2026-09-17
Promotion of long-term health in early life.
Proceedings of the National Academy of Sciences of the United States of America, 123(39):e2601943123.
Noncommunicable chronic diseases (NCDs) are on the rise in high-income countries, leading to substantial morbidity and mortality and contributing to increased resource demands and healthcare costs. Early-life exposures can initiate trajectories that culminate in NCDs later in life. Examples include the metabolic-endocrine pathway to obesity, diabetes, and cardiovascular diseases; the immune-mediated pathway to asthma and allergies; or the neurodevelopmental-psychological pathway to mental health problems. The interconnected trajectories involving microbiome composition, epigenetic signatures, nutrition, and psychological factors in early life can establish a basis for long-term health. While universal vaccination programs are in place to prevent infectious diseases, a coordinated effort to mitigate the rise of NCDs is missing. Examples of how to balance short- and long-term effects in early life include the use of appropriate medications, balanced healthcare interventions, optimized nutrition, and a nurturing care in early life. While these examples will not provide simple answers, they may stimulate important discussions and research into the overarching question: How can we deliver care in early life that achieves optimal short-term outcomes while promoting long-term health trajectories and well-being? While it is imperative to underscore the significance of subsequent periods to circumvent a deterministic conceptualization of a singular period as the primary catalyst for the development of physical and mental health, early life remains an underexploited window of opportunity fostering long-term health and mitigating the growing resource challenges faced by healthcare systems.
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@article {pmid42752199,
year = {2026},
author = {Stocker, M and Klingenberg, C and Rogers, JA and Patel, N and Morgillo, D and Peitler, A and Christmann, M and von Meyenn, F and Domellöf, M and Xu, S and McDonald, S and Brodin, P and van Rossum, EFC and van Rossum, A and Bogaert, D and Boucoiran, I and Ronzoni, S and Boes, S and Lannen, P and Pilgrim, T and El Helou, S},
title = {Promotion of long-term health in early life.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {39},
pages = {e2601943123},
doi = {10.1073/pnas.2601943123},
pmid = {42752199},
issn = {1091-6490},
mesh = {Humans ; *Health Promotion/methods ; *Noncommunicable Diseases/prevention & control ; Chronic Disease/prevention & control ; },
abstract = {Noncommunicable chronic diseases (NCDs) are on the rise in high-income countries, leading to substantial morbidity and mortality and contributing to increased resource demands and healthcare costs. Early-life exposures can initiate trajectories that culminate in NCDs later in life. Examples include the metabolic-endocrine pathway to obesity, diabetes, and cardiovascular diseases; the immune-mediated pathway to asthma and allergies; or the neurodevelopmental-psychological pathway to mental health problems. The interconnected trajectories involving microbiome composition, epigenetic signatures, nutrition, and psychological factors in early life can establish a basis for long-term health. While universal vaccination programs are in place to prevent infectious diseases, a coordinated effort to mitigate the rise of NCDs is missing. Examples of how to balance short- and long-term effects in early life include the use of appropriate medications, balanced healthcare interventions, optimized nutrition, and a nurturing care in early life. While these examples will not provide simple answers, they may stimulate important discussions and research into the overarching question: How can we deliver care in early life that achieves optimal short-term outcomes while promoting long-term health trajectories and well-being? While it is imperative to underscore the significance of subsequent periods to circumvent a deterministic conceptualization of a singular period as the primary catalyst for the development of physical and mental health, early life remains an underexploited window of opportunity fostering long-term health and mitigating the growing resource challenges faced by healthcare systems.},
}
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Humans
*Health Promotion/methods
*Noncommunicable Diseases/prevention & control
Chronic Disease/prevention & control
RevDate: 2026-09-17
Deletion of interleukin-22 binding protein increases gut permeability, dysbiosis, and mortality in sepsis.
Shock (Augusta, Ga.) pii:00024382-990000000-00950 [Epub ahead of print].
The gut is hypothesized to play a pivotal role in sepsis progression through increased intestinal permeability, dysbiosis, and immune dysregulation. Interleukin (IL)-22 maintains intestinal homeostasis and is negatively regulated by IL-22 binding protein (IL-22BP), yet the roles of IL-22 and IL-22BP in sepsis remain undetermined. Using a cecal ligation and puncture (CLP) model with a sham control, we measured IL-22 and IL-22BP at 24 h and compared IL-22-deficient (Il22-/-) and IL-22BP-deficient (Il22ra2-/-) mice with wild-type (WT) mice. Gut permeability, tight junction protein expression, histology, and cytokines were assessed at 24 and 48 h, and the microbiome at baseline and 24 h. Survival was monitored for 168 h; co-housed mice were also evaluated. Plasma and jejunal IL-22, along with plasma IL-22BP levels, were significantly higher in CLP than in sham mice. In Il22-/- mice, mortality and gut permeability showed no significant difference from those in WT mice. By contrast, Il22ra2-/- mice exhibited significantly higher mortality (85% vs. 40%) and increased gut permeability. These changes were associated with elevated claudin-4 and reduced claudin-15 expression, localized cytokine upregulation, and no histological differences. Fecal bacterial loads were comparable between WT and Il22ra2-/- mice, but microbiome composition differed at baseline and 24 h after CLP. Co-housing eliminated the survival difference between groups. In conclusion, whereas IL-22 deficiency had no impact on gut permeability or mortality, IL-22BP deficiency increased gut permeability and mortality with altered cytokine expression and gut dysbiosis, suggesting that IL-22BP plays a protective role in maintaining gut homeostasis in sepsis.
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@article {pmid42752565,
year = {2026},
author = {Miyauchi, S and Oami, T and Satoh-Takayama, N and Shimazui, T and Kondo, K and Fujimura, L and Sakamoto, A and Nakada, TA},
title = {Deletion of interleukin-22 binding protein increases gut permeability, dysbiosis, and mortality in sepsis.},
journal = {Shock (Augusta, Ga.)},
volume = {},
number = {},
pages = {},
doi = {10.1097/SHK.0000000000002942},
pmid = {42752565},
issn = {1540-0514},
abstract = {The gut is hypothesized to play a pivotal role in sepsis progression through increased intestinal permeability, dysbiosis, and immune dysregulation. Interleukin (IL)-22 maintains intestinal homeostasis and is negatively regulated by IL-22 binding protein (IL-22BP), yet the roles of IL-22 and IL-22BP in sepsis remain undetermined. Using a cecal ligation and puncture (CLP) model with a sham control, we measured IL-22 and IL-22BP at 24 h and compared IL-22-deficient (Il22-/-) and IL-22BP-deficient (Il22ra2-/-) mice with wild-type (WT) mice. Gut permeability, tight junction protein expression, histology, and cytokines were assessed at 24 and 48 h, and the microbiome at baseline and 24 h. Survival was monitored for 168 h; co-housed mice were also evaluated. Plasma and jejunal IL-22, along with plasma IL-22BP levels, were significantly higher in CLP than in sham mice. In Il22-/- mice, mortality and gut permeability showed no significant difference from those in WT mice. By contrast, Il22ra2-/- mice exhibited significantly higher mortality (85% vs. 40%) and increased gut permeability. These changes were associated with elevated claudin-4 and reduced claudin-15 expression, localized cytokine upregulation, and no histological differences. Fecal bacterial loads were comparable between WT and Il22ra2-/- mice, but microbiome composition differed at baseline and 24 h after CLP. Co-housing eliminated the survival difference between groups. In conclusion, whereas IL-22 deficiency had no impact on gut permeability or mortality, IL-22BP deficiency increased gut permeability and mortality with altered cytokine expression and gut dysbiosis, suggesting that IL-22BP plays a protective role in maintaining gut homeostasis in sepsis.},
}
RevDate: 2026-09-17
Retraction Note: Phage therapy and the microbiome in hematologic malignancies: opportunities, mechanisms, and early evidence.
Journal of cancer research and clinical oncology, 152(9): pii:10.1007/s00432-026-06623-5.
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@article {pmid42752689,
year = {2026},
author = {Zhang, J and Liu, J and Bayani, A},
title = {Retraction Note: Phage therapy and the microbiome in hematologic malignancies: opportunities, mechanisms, and early evidence.},
journal = {Journal of cancer research and clinical oncology},
volume = {152},
number = {9},
pages = {},
doi = {10.1007/s00432-026-06623-5},
pmid = {42752689},
issn = {1432-1335},
}
RevDate: 2026-09-15
Isoquinoline alkaloids enhance growth performance through multifaceted modulation of the bacterial-fungal microbiome, CAZyme profiles, gut health, and neuroendocrine function in broilers.
Poultry science, 105(12):107663 pii:S0032-5791(26)01297-6 [Epub ahead of print].
The bacterial-fungal microbiome and its carbohydrate-active enzyme (CAZyme) capacity play critical roles in regulating gut health and growth performance in broiler chickens. This study evaluated the effects of dietary isoquinoline alkaloids (IQ) on growth performance, gut microbiome composition, CAZyme profiles, and the microbiome-gut-neuroendocrine axis in broilers. A total of 400 Ross 308 (1-day-old) chicks were randomly assigned to either a Basal diet (CON) or IQ supplemented diet (IQ). Dietary IQ supplementation significantly increased final body weight and cumulative body weight gain (P < 0.0001) and improved feed conversion ratio (P < 0.05). Intestinal permeability was reduced (lower FITC-dextran; P < 0.05), accompanied by increased serotonin and serotonin-to-corticosterone ratio and decreased corticosterone (P < 0.05). Expression of inflammatory genes (TNF-α, NF-κB, IL-4, and TLR-1) was downregulated (P < 0.05). Microbiome analysis showed increased α-diversity (P < 0.05) and clear β-diversity separation (PERMANOVA, P < 0.001), with enrichment of beneficial bacteria (Akkermansia muciniphila, Lactobacillus salivarius, Turicibacter sanguinis, Bacillus subtilis) and suppression of fungal taxa (Aspergillus, Penicillium). CAZyme-related pathways involved in lignin and carbohydrate degradation were increased (P < 0.05). Microbial diversity was negatively correlated with inflammation and gut permeability, whereas network analysis identified 164 significant associations (|ρ| ≥ 0.50), revealing strong negative correlations between beneficial bacteria and inflammatory markers (ρ = -0.65 to -0.78) and positive associations for fungal taxa (ρ = 0.62-0.81). Serotonin was positively associated with microbial diversity (ρ = 0.63-0.70). In conclusion, IQ supplementation promotes a bacteria-dominant and metabolically active microbiome, reduces inflammation and intestinal permeability, and improves neuroendocrine balance, collectively enhancing gut health and growth performance in broiler chickens.
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@article {pmid42743728,
year = {2026},
author = {Saikhwan, N and Thodsapol, A and Rueangpotjanapruek, S and Faroongsarng, D and Nopparat, J and Kraitavin, W and Theapparat, Y},
title = {Isoquinoline alkaloids enhance growth performance through multifaceted modulation of the bacterial-fungal microbiome, CAZyme profiles, gut health, and neuroendocrine function in broilers.},
journal = {Poultry science},
volume = {105},
number = {12},
pages = {107663},
doi = {10.1016/j.psj.2026.107663},
pmid = {42743728},
issn = {1525-3171},
abstract = {The bacterial-fungal microbiome and its carbohydrate-active enzyme (CAZyme) capacity play critical roles in regulating gut health and growth performance in broiler chickens. This study evaluated the effects of dietary isoquinoline alkaloids (IQ) on growth performance, gut microbiome composition, CAZyme profiles, and the microbiome-gut-neuroendocrine axis in broilers. A total of 400 Ross 308 (1-day-old) chicks were randomly assigned to either a Basal diet (CON) or IQ supplemented diet (IQ). Dietary IQ supplementation significantly increased final body weight and cumulative body weight gain (P < 0.0001) and improved feed conversion ratio (P < 0.05). Intestinal permeability was reduced (lower FITC-dextran; P < 0.05), accompanied by increased serotonin and serotonin-to-corticosterone ratio and decreased corticosterone (P < 0.05). Expression of inflammatory genes (TNF-α, NF-κB, IL-4, and TLR-1) was downregulated (P < 0.05). Microbiome analysis showed increased α-diversity (P < 0.05) and clear β-diversity separation (PERMANOVA, P < 0.001), with enrichment of beneficial bacteria (Akkermansia muciniphila, Lactobacillus salivarius, Turicibacter sanguinis, Bacillus subtilis) and suppression of fungal taxa (Aspergillus, Penicillium). CAZyme-related pathways involved in lignin and carbohydrate degradation were increased (P < 0.05). Microbial diversity was negatively correlated with inflammation and gut permeability, whereas network analysis identified 164 significant associations (|ρ| ≥ 0.50), revealing strong negative correlations between beneficial bacteria and inflammatory markers (ρ = -0.65 to -0.78) and positive associations for fungal taxa (ρ = 0.62-0.81). Serotonin was positively associated with microbial diversity (ρ = 0.63-0.70). In conclusion, IQ supplementation promotes a bacteria-dominant and metabolically active microbiome, reduces inflammation and intestinal permeability, and improves neuroendocrine balance, collectively enhancing gut health and growth performance in broiler chickens.},
}
RevDate: 2026-09-15
Curcumin ameliorates fatty liver hemorrhagic syndrome in broiler breeders by regulating lipid metabolism via the gut-liver axis.
Poultry science, 105(12):107650 pii:S0032-5791(26)01284-8 [Epub ahead of print].
Fatty liver syndrome (FLS) is closely linked to disruptions in lipid metabolism, imbalances in the gut microbiome, and alterations in bile acid composition. Curcumin (CUR), a bioactive compound derived from turmeric, has been reported to exert anti‑inflammatory and hepatoprotective effects. The present study aimed to evaluate the potential of dietary CUR to mitigate fatty liver‑related metabolic disturbances in broiler breeder hens fed a low‑protein high‑energy (LPHE) diet. A total of 600 Qingyuan partridge broiler breeder hens (42 weeks of age) were used in a randomized experimental design. Birds were allocated to five dietary regimens, including a control diet (CON), a low‑protein high‑energy diet (LPHE), and LPHE diets supplemented with CUR at 100, 200, or 400 mg/kg. Each group consisted of six replicates with 20 birds per replicate. The feeding trial was conducted over an eight‑week period. The results showed that dietary supplementation with CUR at 100 and 200 mg/kg improved productive performance by reducing feed-to-egg ratio, abnormal egg rate, fat pad mass and lipid droplet in hepatic tissue versus hens fed the LPHE diet. In addition, CUR supplementation reduced plasma and hepatic levels of TG, TCHO, and LDL, as well as ALT activity and concentrations of TGF-β and TNF-α, while elevating IL-10 and IL-22 levels (P<0.05). Bile acid profiling demonstrated that DCA levels were increased in the LPHE_CUR200 group, while GCDCA, GDCA, and TLCA were reduced relative to LPHE group. Moreover, CUR corrected LPHE-induced disruptions in lipid metabolism and bile acid regulatory genes, including FXR, BSEP, PPARα, CPT1α and CYP7A1. Metabolomics demonstrated that LPHE altered hepatic metabolism, and it was partially restored in that of LPHE_CUR100 group. Dietary supplementation with 100 to 200 mg/kg CUR enriched Lactobacillus and Peptococcus populations in cecum. In summary, dietary inclusion of CUR at 100 to 200 mg/kg improved hepatic function, lipid metabolism in broiler breeder hens subjected to the LPHE diet, which may be regulated through the gut microbiota-Bile acid axis.
Additional Links: PMID-42743732
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@article {pmid42743732,
year = {2026},
author = {Ye, J and Huang, Y and Fouad, AM and Zhang, S and El-Senousey, HAK and Gou, Z and Zhang, C and Jiang, Z and Jiang, S and Ruan, D},
title = {Curcumin ameliorates fatty liver hemorrhagic syndrome in broiler breeders by regulating lipid metabolism via the gut-liver axis.},
journal = {Poultry science},
volume = {105},
number = {12},
pages = {107650},
doi = {10.1016/j.psj.2026.107650},
pmid = {42743732},
issn = {1525-3171},
abstract = {Fatty liver syndrome (FLS) is closely linked to disruptions in lipid metabolism, imbalances in the gut microbiome, and alterations in bile acid composition. Curcumin (CUR), a bioactive compound derived from turmeric, has been reported to exert anti‑inflammatory and hepatoprotective effects. The present study aimed to evaluate the potential of dietary CUR to mitigate fatty liver‑related metabolic disturbances in broiler breeder hens fed a low‑protein high‑energy (LPHE) diet. A total of 600 Qingyuan partridge broiler breeder hens (42 weeks of age) were used in a randomized experimental design. Birds were allocated to five dietary regimens, including a control diet (CON), a low‑protein high‑energy diet (LPHE), and LPHE diets supplemented with CUR at 100, 200, or 400 mg/kg. Each group consisted of six replicates with 20 birds per replicate. The feeding trial was conducted over an eight‑week period. The results showed that dietary supplementation with CUR at 100 and 200 mg/kg improved productive performance by reducing feed-to-egg ratio, abnormal egg rate, fat pad mass and lipid droplet in hepatic tissue versus hens fed the LPHE diet. In addition, CUR supplementation reduced plasma and hepatic levels of TG, TCHO, and LDL, as well as ALT activity and concentrations of TGF-β and TNF-α, while elevating IL-10 and IL-22 levels (P<0.05). Bile acid profiling demonstrated that DCA levels were increased in the LPHE_CUR200 group, while GCDCA, GDCA, and TLCA were reduced relative to LPHE group. Moreover, CUR corrected LPHE-induced disruptions in lipid metabolism and bile acid regulatory genes, including FXR, BSEP, PPARα, CPT1α and CYP7A1. Metabolomics demonstrated that LPHE altered hepatic metabolism, and it was partially restored in that of LPHE_CUR100 group. Dietary supplementation with 100 to 200 mg/kg CUR enriched Lactobacillus and Peptococcus populations in cecum. In summary, dietary inclusion of CUR at 100 to 200 mg/kg improved hepatic function, lipid metabolism in broiler breeder hens subjected to the LPHE diet, which may be regulated through the gut microbiota-Bile acid axis.},
}
RevDate: 2026-09-15
Impact of electron-beam dose on microbial diversity and succession dynamics of refrigerated poultry meat during extended storage.
Poultry science, 105(12):107685 pii:S0032-5791(26)01319-2 [Epub ahead of print].
Electron-beam (E-beam) irradiation is used as a post-harvest intervention to reduce microbial contamination in poultry products, yet less is known about how irradiation doses influence microbial succession during extended refrigerated storage. This study evaluated the effects of E-beam dose on the bacterial community structure of tray-packed chicken tenderloins stored under refrigeration for 27 days. Chicken tenderloins were treated with 0, 1.0, 1.5, 2.5, or 3.5 kGy and sampled on Days 3, 7, 24, and 27. Bacterial communities were characterized using 16S rRNA amplicon sequencing, and alpha diversity, beta diversity, and differential abundance analyses were used to assess dose-response and storage-associated changes. E-beam treatment and storage time interacted to significantly influence microbial community composition, as measured by Weighted UniFrac and Bray-Curtis distances (P = 0.038 and P = 0.05, respectively). Storage time was a major driver of succession, with significant differences in Shannon entropy (P = 0.03) and Faith's phylogenetic diversity (P = 0.0001), along with changes in abundance-based community structure by Bray-Curtis dissimilarity (Q = 0.002). Weighted UniFrac analysis further showed significant differences across storage days, including Day 3 compared with Days 7, 24, and 27 (Q < 0.0061) and Day 7 compared with Days 24 and 27 (Q < 0.05). Taxonomic analysis displayed Pseudomonas increased throughout storage and approached approximately 80% relative abundance by the final sampling day (ANCOM, P < 0.05). Sequential ANCOM-BC comparisons further exhibited the enrichment of Pseudomonas from Day 3 to Day 7 (LFC = +3.52) and from Day 7 to Day 24 (LFC = +2.71). In contrast, several early-storage or competing taxa, including Bacillus, Fabibacter, Yersinia, Carnobacterium, Aeromonas, declined across later comparisons. E-beam dose also influenced community structure, with the highest dose (3.5 kGy) producing the most pronounced early shifts in microbial community composition. Overall, these findings suggest that E-beam irradiation shapes the initial poultry meat microbiome, while refrigerated storage remains a dominant factor influencing late-stage convergence toward a lower-diversity, Pseudomonas-dominated community.
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@article {pmid42743741,
year = {2026},
author = {McDonald, B and Olson, EG and Collie, P and Hawkins, O and Betancourt-Barszcz, GK and Bodie, AR},
title = {Impact of electron-beam dose on microbial diversity and succession dynamics of refrigerated poultry meat during extended storage.},
journal = {Poultry science},
volume = {105},
number = {12},
pages = {107685},
doi = {10.1016/j.psj.2026.107685},
pmid = {42743741},
issn = {1525-3171},
abstract = {Electron-beam (E-beam) irradiation is used as a post-harvest intervention to reduce microbial contamination in poultry products, yet less is known about how irradiation doses influence microbial succession during extended refrigerated storage. This study evaluated the effects of E-beam dose on the bacterial community structure of tray-packed chicken tenderloins stored under refrigeration for 27 days. Chicken tenderloins were treated with 0, 1.0, 1.5, 2.5, or 3.5 kGy and sampled on Days 3, 7, 24, and 27. Bacterial communities were characterized using 16S rRNA amplicon sequencing, and alpha diversity, beta diversity, and differential abundance analyses were used to assess dose-response and storage-associated changes. E-beam treatment and storage time interacted to significantly influence microbial community composition, as measured by Weighted UniFrac and Bray-Curtis distances (P = 0.038 and P = 0.05, respectively). Storage time was a major driver of succession, with significant differences in Shannon entropy (P = 0.03) and Faith's phylogenetic diversity (P = 0.0001), along with changes in abundance-based community structure by Bray-Curtis dissimilarity (Q = 0.002). Weighted UniFrac analysis further showed significant differences across storage days, including Day 3 compared with Days 7, 24, and 27 (Q < 0.0061) and Day 7 compared with Days 24 and 27 (Q < 0.05). Taxonomic analysis displayed Pseudomonas increased throughout storage and approached approximately 80% relative abundance by the final sampling day (ANCOM, P < 0.05). Sequential ANCOM-BC comparisons further exhibited the enrichment of Pseudomonas from Day 3 to Day 7 (LFC = +3.52) and from Day 7 to Day 24 (LFC = +2.71). In contrast, several early-storage or competing taxa, including Bacillus, Fabibacter, Yersinia, Carnobacterium, Aeromonas, declined across later comparisons. E-beam dose also influenced community structure, with the highest dose (3.5 kGy) producing the most pronounced early shifts in microbial community composition. Overall, these findings suggest that E-beam irradiation shapes the initial poultry meat microbiome, while refrigerated storage remains a dominant factor influencing late-stage convergence toward a lower-diversity, Pseudomonas-dominated community.},
}
RevDate: 2026-09-15
Gut microbiota composition across clinical subtype and antibody burden in myasthenia gravis.
Journal of neuroimmunology, 421:579098 pii:S0165-5728(26)00247-X [Epub ahead of print].
BACKGROUND: Myasthenia gravis (MG) exhibits clinical heterogeneity ranging from ocular to generalized forms. Although gut microbiota has been implicated in autoimmune diseases, its relationship with clinical subtype and antibody burden in MG remains unclear.
METHODS: We conducted a cross-sectional study of fecal microbiota in 14 patients with MG (3 ocular and 11 generalized) and 10 healthy controls using 16S rRNA sequencing. Patients with MG were stratified according to acetylcholine receptor antibody (AChR-Ab) titers into low (n = 5), moderate (n = 5), and high (n = 4) groups.
RESULTS: Alpha and beta diversity did not differ significantly between clinical subtypes or antibody-defined groups. Exploratory genus-level analyses identified nominal differences in the relative abundance of several bacterial genera across both clinical subtype and antibody-defined groups. SCFA-associated taxa, including Anaerostipes, Blautia, and Faecalibacterium, appeared relatively more abundant in ocular MG and lower antibody groups, whereas Streptococcus and Bacteroides appeared relatively more abundant in generalized MG and higher antibody groups. PICRUSt2-based analyses were used to explore variation in predicted metabolic pathways between groups; however, no pathway remained significant after correction for multiple testing.
CONCLUSIONS: Descriptive genus-level microbiome patterns were observed across both clinical subtype and antibody-defined groups despite similar global diversity measures. These exploratory findings suggest that microbiome variation within MG may be associated with multiple aspects of disease heterogeneity. However, given the small sample size, particularly within the ocular MG subgroup, these observations should be considered hypothesis-generating and require validation in larger independent cohorts.
Additional Links: PMID-42743755
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@article {pmid42743755,
year = {2026},
author = {Park, SH and Jin, DY and Yoo, S and Lee, JW and Kim, JS and Kim, NH},
title = {Gut microbiota composition across clinical subtype and antibody burden in myasthenia gravis.},
journal = {Journal of neuroimmunology},
volume = {421},
number = {},
pages = {579098},
doi = {10.1016/j.jneuroim.2026.579098},
pmid = {42743755},
issn = {1872-8421},
abstract = {BACKGROUND: Myasthenia gravis (MG) exhibits clinical heterogeneity ranging from ocular to generalized forms. Although gut microbiota has been implicated in autoimmune diseases, its relationship with clinical subtype and antibody burden in MG remains unclear.
METHODS: We conducted a cross-sectional study of fecal microbiota in 14 patients with MG (3 ocular and 11 generalized) and 10 healthy controls using 16S rRNA sequencing. Patients with MG were stratified according to acetylcholine receptor antibody (AChR-Ab) titers into low (n = 5), moderate (n = 5), and high (n = 4) groups.
RESULTS: Alpha and beta diversity did not differ significantly between clinical subtypes or antibody-defined groups. Exploratory genus-level analyses identified nominal differences in the relative abundance of several bacterial genera across both clinical subtype and antibody-defined groups. SCFA-associated taxa, including Anaerostipes, Blautia, and Faecalibacterium, appeared relatively more abundant in ocular MG and lower antibody groups, whereas Streptococcus and Bacteroides appeared relatively more abundant in generalized MG and higher antibody groups. PICRUSt2-based analyses were used to explore variation in predicted metabolic pathways between groups; however, no pathway remained significant after correction for multiple testing.
CONCLUSIONS: Descriptive genus-level microbiome patterns were observed across both clinical subtype and antibody-defined groups despite similar global diversity measures. These exploratory findings suggest that microbiome variation within MG may be associated with multiple aspects of disease heterogeneity. However, given the small sample size, particularly within the ocular MG subgroup, these observations should be considered hypothesis-generating and require validation in larger independent cohorts.},
}
RevDate: 2026-09-15
Lung microbiome alterations in idiopathic pulmonary fibrosis and hypersensitivity pneumonitis: A systematic review with insights into microbiome-host interactions and the gut-lung axis.
Respiratory investigation, 64(6):101515 pii:S2212-5345(26)00149-8 [Epub ahead of print].
The lung microbiome is increasingly recognized as an important factor in idiopathic pulmonary fibrosis (IPF) and hypersensitivity pneumonitis (HP), two interstitial lung diseases with overlapping clinical features but distinct underlying mechanisms and management. This systematic review, conducted in accordance with PRISMA guidelines, evaluated the current evidence regarding lung microbiome alterations in IPF and HP. A literature search was performed using PubMed as the primary database and supplemented by Google Scholar searches. The review protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD420261415180). Fourteen unique studies met the inclusion criteria, comprising 13 studies involving IPF and 2 studies involving HP, with one study overlapping between the two disease groups. Current evidence suggests that IPF is associated with increased bacterial burden, reduced microbial diversity, and enrichment of specific taxa, including Streptococcus and Staphylococcus, which have been linked to immune activation and fibrotic progression. In contrast, limited available evidence suggests that HP may exhibit a lower bacterial burden, with microbial patterns influenced predominantly by environmental exposures, including bacterial and fungal antigens from occupational and domestic sources. Emerging studies highlight host-microbiome and environment-microbiome interactions in disease progression. Overall, the current evidence supports a role for microbial dysbiosis in IPF, whereas microbiome alterations in HP appear to be more closely associated with environmental microbial exposures. However, conclusions regarding HP should be interpreted cautiously due to the limited number of studies. Further longitudinal and multi-omics studies are needed to clarify causality and identify robust microbial biomarkers for diagnosis and therapy.
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@article {pmid42743786,
year = {2026},
author = {Dasgupta, S and Roychowdhury, S and Chaudhury, K},
title = {Lung microbiome alterations in idiopathic pulmonary fibrosis and hypersensitivity pneumonitis: A systematic review with insights into microbiome-host interactions and the gut-lung axis.},
journal = {Respiratory investigation},
volume = {64},
number = {6},
pages = {101515},
doi = {10.1016/j.resinv.2026.101515},
pmid = {42743786},
issn = {2212-5353},
abstract = {The lung microbiome is increasingly recognized as an important factor in idiopathic pulmonary fibrosis (IPF) and hypersensitivity pneumonitis (HP), two interstitial lung diseases with overlapping clinical features but distinct underlying mechanisms and management. This systematic review, conducted in accordance with PRISMA guidelines, evaluated the current evidence regarding lung microbiome alterations in IPF and HP. A literature search was performed using PubMed as the primary database and supplemented by Google Scholar searches. The review protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD420261415180). Fourteen unique studies met the inclusion criteria, comprising 13 studies involving IPF and 2 studies involving HP, with one study overlapping between the two disease groups. Current evidence suggests that IPF is associated with increased bacterial burden, reduced microbial diversity, and enrichment of specific taxa, including Streptococcus and Staphylococcus, which have been linked to immune activation and fibrotic progression. In contrast, limited available evidence suggests that HP may exhibit a lower bacterial burden, with microbial patterns influenced predominantly by environmental exposures, including bacterial and fungal antigens from occupational and domestic sources. Emerging studies highlight host-microbiome and environment-microbiome interactions in disease progression. Overall, the current evidence supports a role for microbial dysbiosis in IPF, whereas microbiome alterations in HP appear to be more closely associated with environmental microbial exposures. However, conclusions regarding HP should be interpreted cautiously due to the limited number of studies. Further longitudinal and multi-omics studies are needed to clarify causality and identify robust microbial biomarkers for diagnosis and therapy.},
}
RevDate: 2026-09-15
Decoding the rhizosphere immune signaling network: Microbiome-driven modulation of plant immunity and disease resistance.
Microbiological research, 314:128726 pii:S0944-5013(26)00290-9 [Epub ahead of print].
Classical plant immunity models rely on pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), yet these frameworks largely overlook the rhizosphere microbiome as a functional determinant of disease resistance. Plants act as holobionts, their root exudates comprising flavonoids, coumarins, benzoxazinoids, strigolactones, and primary metabolites selectively recruit microbial communities whose composition is shaped by host genotype and dynamically reprogrammed under biotic and abiotic stress. Recruited microorganisms return a diverse signal range including flagellin, siderophores, lipopeptides, lactones, mycorrhizal lipochitooligosaccharides, and volatile organic compounds, which are perceived by LRR (leucine rich repeats) and LysM (lysin motif) domain receptors. This in turn engages the salicylic acid, jasmonic acid, and ethylene signaling pathways. The beneficial rhizosphere members predominantly trigger the JA/ET-dependent induced systemic resistance (ISR) through epigenetic mechanisms, including the H3K4me3 deposition at defense loci that establish heritable primed states that enhance the immune response when pathogens attack. This review synthesizes these interactions within the rhizosphere immune signaling network (RIsN) framework. This reconceptualizes the rhizosphere as multi-kingdom signaling systems whose emergent properties including the signal cooperation, competitive interference, and feedback stabilization, collectively determine disease suppression capacity. Climate change threatens the RIsN stability through microbiome dysbiosis while advances in syncoms, spatial metabolomics, and AI-driven network modeling provide new opportunities for predictive and targeted rhizosphere engineering for durable crop protection.
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@article {pmid42743795,
year = {2026},
author = {Sun, S and Li, J and Liu, L and Li, Z and Wang, Y and Li, H and Ullah, MW},
title = {Decoding the rhizosphere immune signaling network: Microbiome-driven modulation of plant immunity and disease resistance.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128726},
doi = {10.1016/j.micres.2026.128726},
pmid = {42743795},
issn = {1618-0623},
abstract = {Classical plant immunity models rely on pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), yet these frameworks largely overlook the rhizosphere microbiome as a functional determinant of disease resistance. Plants act as holobionts, their root exudates comprising flavonoids, coumarins, benzoxazinoids, strigolactones, and primary metabolites selectively recruit microbial communities whose composition is shaped by host genotype and dynamically reprogrammed under biotic and abiotic stress. Recruited microorganisms return a diverse signal range including flagellin, siderophores, lipopeptides, lactones, mycorrhizal lipochitooligosaccharides, and volatile organic compounds, which are perceived by LRR (leucine rich repeats) and LysM (lysin motif) domain receptors. This in turn engages the salicylic acid, jasmonic acid, and ethylene signaling pathways. The beneficial rhizosphere members predominantly trigger the JA/ET-dependent induced systemic resistance (ISR) through epigenetic mechanisms, including the H3K4me3 deposition at defense loci that establish heritable primed states that enhance the immune response when pathogens attack. This review synthesizes these interactions within the rhizosphere immune signaling network (RIsN) framework. This reconceptualizes the rhizosphere as multi-kingdom signaling systems whose emergent properties including the signal cooperation, competitive interference, and feedback stabilization, collectively determine disease suppression capacity. Climate change threatens the RIsN stability through microbiome dysbiosis while advances in syncoms, spatial metabolomics, and AI-driven network modeling provide new opportunities for predictive and targeted rhizosphere engineering for durable crop protection.},
}
RevDate: 2026-09-15
Multi-omics evidence reveals robust airborne-human resistome connectivity driven by high-risk ARGs and mediated by Staphylococcus.
Environment international, 216:110525 pii:S0160-4120(26)00483-6 [Epub ahead of print].
Airborne microbiomes are considered an important source of human antimicrobial resistance (AMR) exposure, yet multi-omics evidence linking airborne and human nasal resistomes remains limited. Here, we integrated metagenomic sequencing and whole-genome sequencing of antibiotic-resistant Staphylococcus isolates to investigate the connectivity between air and human nasal resistomes in dairy farm environments. Metagenomic taxonomic profiling showed that Staphylococcus was prominent in total suspended particles (TSP) and consistently detected across all samples. Among environmental reservoirs, TSP resistomes exhibited the strongest similarity to human nasal resistomes. This connectivity was supported by multiple lines of evidence, including highly similar resistome profiles, extensive homologous antibiotic resistance gene (ARG) pairs, strain-level similarity of resistant Staphylococcus isolates, and conserved mobile ARG genetic contexts. Notably, this connectivity was primarily driven by high-risk ARGs, while Staphylococcus was frequently associated with mobile ARGs and represented the only shared pathogenic genomes carrying both ARGs and virulence factor genes between airborne and nasal samples. Although lower ARG diversity, nasal resistomes exhibited higher ARG burden, risk scores, antibiotic-resistant bacterial genome abundance, and prevalence of resistant Staphylococcus. Occupational exposure further increased total and high-risk ARG burdens among farm workers. Together, these findings indicate that TSP can serve as an important route of occupational AMR exposure, with high-risk ARGs and Staphylococcus contributing to connectivity between airborne and nasal resistomes. Incorporating the host microbiome may therefore provide a more complete assessment of human-associated AMR exposure within a One Health framework.
Additional Links: PMID-42743804
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@article {pmid42743804,
year = {2026},
author = {Chen, ZY and Gao, FZ and Li, P and Bai, H and He, LY and Liu, YS and Ying, GG},
title = {Multi-omics evidence reveals robust airborne-human resistome connectivity driven by high-risk ARGs and mediated by Staphylococcus.},
journal = {Environment international},
volume = {216},
number = {},
pages = {110525},
doi = {10.1016/j.envint.2026.110525},
pmid = {42743804},
issn = {1873-6750},
abstract = {Airborne microbiomes are considered an important source of human antimicrobial resistance (AMR) exposure, yet multi-omics evidence linking airborne and human nasal resistomes remains limited. Here, we integrated metagenomic sequencing and whole-genome sequencing of antibiotic-resistant Staphylococcus isolates to investigate the connectivity between air and human nasal resistomes in dairy farm environments. Metagenomic taxonomic profiling showed that Staphylococcus was prominent in total suspended particles (TSP) and consistently detected across all samples. Among environmental reservoirs, TSP resistomes exhibited the strongest similarity to human nasal resistomes. This connectivity was supported by multiple lines of evidence, including highly similar resistome profiles, extensive homologous antibiotic resistance gene (ARG) pairs, strain-level similarity of resistant Staphylococcus isolates, and conserved mobile ARG genetic contexts. Notably, this connectivity was primarily driven by high-risk ARGs, while Staphylococcus was frequently associated with mobile ARGs and represented the only shared pathogenic genomes carrying both ARGs and virulence factor genes between airborne and nasal samples. Although lower ARG diversity, nasal resistomes exhibited higher ARG burden, risk scores, antibiotic-resistant bacterial genome abundance, and prevalence of resistant Staphylococcus. Occupational exposure further increased total and high-risk ARG burdens among farm workers. Together, these findings indicate that TSP can serve as an important route of occupational AMR exposure, with high-risk ARGs and Staphylococcus contributing to connectivity between airborne and nasal resistomes. Incorporating the host microbiome may therefore provide a more complete assessment of human-associated AMR exposure within a One Health framework.},
}
RevDate: 2026-09-15
Circulating free bacterial DNA as a novel biomarker for monitoring therapy response in patients with advanced pancreatic cancer.
European journal of cancer (Oxford, England : 1990), 247:117040 pii:S0959-8049(26)00821-X [Epub ahead of print].
BACKGROUND: Monitoring therapy response in pancreatic cancer (PDAC) remains challenging. The microbiome affects therapy efficacy, but its role in response prediction is unclear. We assessed whether changes in circulating free bacterial DNA (cfbDNA) levels predict outcome of advanced PDAC (aPDAC) patients treated with systemic chemotherapy.
PATIENTS AND METHODS: We analyzed the prognostic impact of serum cfbDNA dynamics of 13 patients with aPDAC receiving mFOLFIRINOX (FFX) before treatment initiation and after two chemotherapy cycles. We validated the findings in the samples of 47 patients with locally advanced pancreatic cancer from the NEOLAP-AIO-PAK-0113 trial.
RESULTS: Decreased cfbDNA during FFX treatment was associated with improved PFS (14.3 vs. 2.9 months; p < 0.001) and OS (23.2 vs. 8.4 months; p = 0.006) in the exploratory cohort. Equal or increased cfbDNA was associated with inferior OS in univariate analyses (HR, 7.74; 95% CI, 1.38-43.24; p = 0.020) and a model adjusted for CA-19-9 group (HR, 11.75; 95% CI, 1.87-73.85; p = 0.009). In the NEOLAP cohort, decreased cfbDNA was associated with improved PFS (12.4 vs. 8.7 months, p = 0.003) and OS (39.8 vs. 14.7 months, p = 0.001) in FFX treated patients, whereas in patients continuing on gemcitabine plus nab-paclitaxel (GnP), decreased cfbDNA was associated with shorter PFS (6.2 vs. 11.5 months, p < 0.001) and OS (12.9 vs. 18.8 months, p = 0.013).
CONCLUSIONS: cfbDNA dynamics may serve as blood-based biomarker for monitoring therapy response in aPDAC. Its treatment-dependent predictive impact may inform clinical decisions. These findings suggest therapy-specific host-microbiome-tumor interactions and warrant prospective validation.
CLINICAL TRIAL NUMBER: NCT02125136.
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@article {pmid42743886,
year = {2026},
author = {Surendran, SA and Guenther, M and Nemati, N and Incera, ML and Zhang, D and Boeck, S and Heinemann, V and Kimmel, B and Kunzmann, V and Ormanns, S},
title = {Circulating free bacterial DNA as a novel biomarker for monitoring therapy response in patients with advanced pancreatic cancer.},
journal = {European journal of cancer (Oxford, England : 1990)},
volume = {247},
number = {},
pages = {117040},
doi = {10.1016/j.ejca.2026.117040},
pmid = {42743886},
issn = {1879-0852},
abstract = {BACKGROUND: Monitoring therapy response in pancreatic cancer (PDAC) remains challenging. The microbiome affects therapy efficacy, but its role in response prediction is unclear. We assessed whether changes in circulating free bacterial DNA (cfbDNA) levels predict outcome of advanced PDAC (aPDAC) patients treated with systemic chemotherapy.
PATIENTS AND METHODS: We analyzed the prognostic impact of serum cfbDNA dynamics of 13 patients with aPDAC receiving mFOLFIRINOX (FFX) before treatment initiation and after two chemotherapy cycles. We validated the findings in the samples of 47 patients with locally advanced pancreatic cancer from the NEOLAP-AIO-PAK-0113 trial.
RESULTS: Decreased cfbDNA during FFX treatment was associated with improved PFS (14.3 vs. 2.9 months; p < 0.001) and OS (23.2 vs. 8.4 months; p = 0.006) in the exploratory cohort. Equal or increased cfbDNA was associated with inferior OS in univariate analyses (HR, 7.74; 95% CI, 1.38-43.24; p = 0.020) and a model adjusted for CA-19-9 group (HR, 11.75; 95% CI, 1.87-73.85; p = 0.009). In the NEOLAP cohort, decreased cfbDNA was associated with improved PFS (12.4 vs. 8.7 months, p = 0.003) and OS (39.8 vs. 14.7 months, p = 0.001) in FFX treated patients, whereas in patients continuing on gemcitabine plus nab-paclitaxel (GnP), decreased cfbDNA was associated with shorter PFS (6.2 vs. 11.5 months, p < 0.001) and OS (12.9 vs. 18.8 months, p = 0.013).
CONCLUSIONS: cfbDNA dynamics may serve as blood-based biomarker for monitoring therapy response in aPDAC. Its treatment-dependent predictive impact may inform clinical decisions. These findings suggest therapy-specific host-microbiome-tumor interactions and warrant prospective validation.
CLINICAL TRIAL NUMBER: NCT02125136.},
}
RevDate: 2026-09-15
Single-cell-resolved genome atlas of prokaryoplankton inhabiting the ocean's interior.
Cell pii:S0092-8674(26)01009-3 [Epub ahead of print].
The ocean's aphotic interior harbors three-quarters of planktonic bacteria and archaea (prokaryoplankton), whose composition, ecology, and biotechnological potential remain poorly constrained. To address this knowledge gap, we created Global Oceans Reference Genomes (GORG)-Dark, a dataset of 9,698 genomes from individual prokaryoplankton cells sampled unselectively across a broad range of depths, geographic locations, and environmental conditions below the ocean's photic surface. Biogeographic analyses revealed prokaryoplankton vertical stratification extending to abyssal depths, the presence of particle-attached lineages of Pelagibacterales, and the previously overlooked abundance of Patescibacteria and Nanoarchaeota in the Baltic and Black Seas. We identified coding potential for chemolithoautotrophy, pharmacologically relevant secondary metabolisms, and a distinct type of proteorhodopsins in prokaryoplankton lineages prevalent throughout the aphotic ocean. This study offers a quantitative, global assessment of the composition and coding potential of microorganisms inhabiting the vast ocean's interior and contributes an extensive, single-cell-resolved dataset to microbial oceanography's cyberinfrastructure.
Additional Links: PMID-42743927
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PubMed:
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@article {pmid42743927,
year = {2026},
author = {Chang, T and Pachiadaki, MG and Gavelis, GS and Poulton, NJ and Thompson, B and Mascena, C and Macartney, K and Brown, JM and La Clair, JJ and Weinheimer, AR and Yokokawa, T and Ruiz-Fernández, P and Anstett, J and Berube, PM and Biller, SJ and Orcutt, BN and Baltar, F and Burkart, MD and Hallam, SJ and Jürgens, K and Ulloa, O and Nunoura, T and Sintes, E and Herndl, GJ and Stepanauskas, R},
title = {Single-cell-resolved genome atlas of prokaryoplankton inhabiting the ocean's interior.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2026.08.036},
pmid = {42743927},
issn = {1097-4172},
abstract = {The ocean's aphotic interior harbors three-quarters of planktonic bacteria and archaea (prokaryoplankton), whose composition, ecology, and biotechnological potential remain poorly constrained. To address this knowledge gap, we created Global Oceans Reference Genomes (GORG)-Dark, a dataset of 9,698 genomes from individual prokaryoplankton cells sampled unselectively across a broad range of depths, geographic locations, and environmental conditions below the ocean's photic surface. Biogeographic analyses revealed prokaryoplankton vertical stratification extending to abyssal depths, the presence of particle-attached lineages of Pelagibacterales, and the previously overlooked abundance of Patescibacteria and Nanoarchaeota in the Baltic and Black Seas. We identified coding potential for chemolithoautotrophy, pharmacologically relevant secondary metabolisms, and a distinct type of proteorhodopsins in prokaryoplankton lineages prevalent throughout the aphotic ocean. This study offers a quantitative, global assessment of the composition and coding potential of microorganisms inhabiting the vast ocean's interior and contributes an extensive, single-cell-resolved dataset to microbial oceanography's cyberinfrastructure.},
}
RevDate: 2026-09-15
Fungal-derived nanoparticles confer cadmium tolerance in maize through transcriptional reconfiguration and microbiome modulation.
Bioresource technology pii:S0960-8524(26)01944-9 [Epub ahead of print].
The application of nanotechnology presents a promising strategy for mitigating heavy metal toxicity in crops, yet the integrative mechanisms underlying nanoparticle-mediated stress alleviation across the plant-soil system remain poorly understood. Herein, we investigated the transcriptomic and rhizosphere microbial responses of maize to cadmium (Cd) stress and the responses associated with fungal-mediated iron-based nanoparticles (NPs). Characterization confirmed the synthesis of spherical, Fe-O dominant NPs with uniform distribution. Under Cd stress, transmission electron microscopy revealed severe ultrastructural damage in leaf cells, which was associated with pronounced cellular alterations, whereas NPs application was associated with preservation of leaf ultrastructure. RNA-sequencing analysis demonstrated that Cd stress triggered extensive transcriptional reprogramming, suppressing defense-related and phenylpropanoid biosynthetic genes while activating stress-signaling pathways. NPs treatment alone was associated with a distinct transcriptional response, including changes in defense and metabolism-related genes without pronounced stress-associated transcriptional signatures. In NPCd co-treated plants, NPs were associated with reversal of Cd-induced transcriptional changes, particularly in starch/sucrose and phenylpropanoid metabolism and ethylene and jasmonate related signaling pathways. Rhizosphere microbiome analysis further revealed that NPs application significantly altered bacterial diversity and community composition, with treatment-associated shifts in several bacterial genera, including Sphingomonas and Methylobacterium. Collectively, the results showed that fungal-mediated NPs application was associated with improved Cd tolerance in maize, accompanied by preservation of leaf ultrastructure, reduced Cd-associated superoxide accumulation, transcriptional reprogramming of defense and metabolism related pathways, and changes in rhizosphere bacterial communities. These findings highlight the potential of fungal-mediated NPs as a promising strategy for improving crop performance under Cd stress.
Additional Links: PMID-42744023
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PubMed:
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@article {pmid42744023,
year = {2026},
author = {Rahman, SU and Khalid, M and Rehman, A and Liaquat, F and Zhao, C and Liu, X and Wang, P and Zhang, W and Khan, R and Ahmad, N and Amaran, NB and Hui, N},
title = {Fungal-derived nanoparticles confer cadmium tolerance in maize through transcriptional reconfiguration and microbiome modulation.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {135862},
doi = {10.1016/j.biortech.2026.135862},
pmid = {42744023},
issn = {1873-2976},
abstract = {The application of nanotechnology presents a promising strategy for mitigating heavy metal toxicity in crops, yet the integrative mechanisms underlying nanoparticle-mediated stress alleviation across the plant-soil system remain poorly understood. Herein, we investigated the transcriptomic and rhizosphere microbial responses of maize to cadmium (Cd) stress and the responses associated with fungal-mediated iron-based nanoparticles (NPs). Characterization confirmed the synthesis of spherical, Fe-O dominant NPs with uniform distribution. Under Cd stress, transmission electron microscopy revealed severe ultrastructural damage in leaf cells, which was associated with pronounced cellular alterations, whereas NPs application was associated with preservation of leaf ultrastructure. RNA-sequencing analysis demonstrated that Cd stress triggered extensive transcriptional reprogramming, suppressing defense-related and phenylpropanoid biosynthetic genes while activating stress-signaling pathways. NPs treatment alone was associated with a distinct transcriptional response, including changes in defense and metabolism-related genes without pronounced stress-associated transcriptional signatures. In NPCd co-treated plants, NPs were associated with reversal of Cd-induced transcriptional changes, particularly in starch/sucrose and phenylpropanoid metabolism and ethylene and jasmonate related signaling pathways. Rhizosphere microbiome analysis further revealed that NPs application significantly altered bacterial diversity and community composition, with treatment-associated shifts in several bacterial genera, including Sphingomonas and Methylobacterium. Collectively, the results showed that fungal-mediated NPs application was associated with improved Cd tolerance in maize, accompanied by preservation of leaf ultrastructure, reduced Cd-associated superoxide accumulation, transcriptional reprogramming of defense and metabolism related pathways, and changes in rhizosphere bacterial communities. These findings highlight the potential of fungal-mediated NPs as a promising strategy for improving crop performance under Cd stress.},
}
RevDate: 2026-09-15
Psychobiotics and the microbiota-gut-brain axis: a comprehensive review of mechanisms, efficacy, and translational challenges.
Clinical nutrition ESPEN pii:S2405-4577(26)02216-3 [Epub ahead of print].
The bidirectional communication network between the gastrointestinal tract and the central nervous system, known as the microbiota-gut-brain axis, is increasingly recognized as a critical interface for neuropsychiatric health. Psychobiotics, encompassing specific live bacterial strains, prebiotics, and targeted dietary interventions, represent a novel class of microbiome-modulating therapeutics capable of influencing mental well-being. This comprehensive review synthesises current evidence regarding the neurobiological mechanisms and clinical efficacy of psychobiotics in the context of psychiatric and neurodegenerative conditions. Commensal bacteria and psychobiotic strains synthesise essential neuroactive compounds, including gamma-aminobutyric acid, serotonin precursors, and short-chain fatty acids, which communicate with the brain via vagal, neuroendocrine, and neuroimmune pathways. Current clinical and preclinical literature demonstrates that specific taxa, particularly within the Lactobacilli and Bifidobacterium genera, can attenuate stress reactivity, reduce systemic inflammation, and regulate hypothalamic-pituitary-adrenal axis hyperactivity. Furthermore, the therapeutic modulation of ecological biomarkers, such as the Firmicutes/Bacteroidetes ratio, provides valuable insights into restoring microbial homeostasis and mitigating neuroinflammation. While preliminary trials demonstrate significant anxiolytic and antidepressant potential, widespread clinical implementation remains hindered by methodological heterogeneity. This review highlights these translational challenges, emphasizing the critical need for standardized experimental protocols, robust multi-omics profiling, and strain-specific validation. Addressing these barriers is essential for the successful integration of psychobiotics into precision psychiatry as safe, evidence-based interventions for severe mental health disorders.
Additional Links: PMID-42744054
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PubMed:
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@article {pmid42744054,
year = {2026},
author = {Ahmed, AMF and Akhiljith, and Balasubramanian, S and Afeeza, M and Nair, M and George, J and Saraswathy, GR},
title = {Psychobiotics and the microbiota-gut-brain axis: a comprehensive review of mechanisms, efficacy, and translational challenges.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105119},
doi = {10.1016/j.clnesp.2026.105119},
pmid = {42744054},
issn = {2405-4577},
abstract = {The bidirectional communication network between the gastrointestinal tract and the central nervous system, known as the microbiota-gut-brain axis, is increasingly recognized as a critical interface for neuropsychiatric health. Psychobiotics, encompassing specific live bacterial strains, prebiotics, and targeted dietary interventions, represent a novel class of microbiome-modulating therapeutics capable of influencing mental well-being. This comprehensive review synthesises current evidence regarding the neurobiological mechanisms and clinical efficacy of psychobiotics in the context of psychiatric and neurodegenerative conditions. Commensal bacteria and psychobiotic strains synthesise essential neuroactive compounds, including gamma-aminobutyric acid, serotonin precursors, and short-chain fatty acids, which communicate with the brain via vagal, neuroendocrine, and neuroimmune pathways. Current clinical and preclinical literature demonstrates that specific taxa, particularly within the Lactobacilli and Bifidobacterium genera, can attenuate stress reactivity, reduce systemic inflammation, and regulate hypothalamic-pituitary-adrenal axis hyperactivity. Furthermore, the therapeutic modulation of ecological biomarkers, such as the Firmicutes/Bacteroidetes ratio, provides valuable insights into restoring microbial homeostasis and mitigating neuroinflammation. While preliminary trials demonstrate significant anxiolytic and antidepressant potential, widespread clinical implementation remains hindered by methodological heterogeneity. This review highlights these translational challenges, emphasizing the critical need for standardized experimental protocols, robust multi-omics profiling, and strain-specific validation. Addressing these barriers is essential for the successful integration of psychobiotics into precision psychiatry as safe, evidence-based interventions for severe mental health disorders.},
}
RevDate: 2026-09-15
Biomarker-Guided Treatment Selection in Metastatic Colorectal Cancer: A Critical Review of Established and Emerging Therapies.
Critical reviews in oncology/hematology pii:S1040-8428(26)00484-1 [Epub ahead of print].
Metastatic colorectal cancer (mCRC) is increasingly managed according to mismatch repair status and actionable molecular alterations. In this structured narrative review, we separately examine mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H) and microsatellite-stable/mismatch repair-proficient (MSS/pMMR) disease and distinguish established treatments from investigational strategies. In dMMR/MSI-H mCRC, immune checkpoint inhibition is the established first-line standard, with pembrolizumab and nivolumab plus ipilimumab producing durable disease control. In MSS/pMMR mCRC, tumor molecular findings guide targeted therapy. For BRAF V600E-mutant disease, encorafenib plus cetuximab with fluoropyrimidine-based chemotherapy is a first-line standard. HER2-directed therapy with tucatinib plus trastuzumab or trastuzumab deruxtecan and combined KRAS G12C and EGFR inhibition are established after prior treatment but are not approved in the first-line setting. Across MMR subgroups, rare NTRK or RET fusions can confer eligibility for tumor-agnostic TRK or RET inhibition, although CRC-specific cohorts remain small. In previously treated non-MSI-H/dMMR mCRC, STELLAR-303 was the first phase 3 trial to demonstrate a significant overall survival benefit with an immune checkpoint inhibitor-containing regimen, zanzalintinib plus atezolizumab. Other investigational strategies include additional immunotherapy combinations, EGFR-MET bispecific antibody therapy with amivantamab, T-cell-engaging bispecific antibodies, therapeutic cancer vaccines, cellular therapies, and microbiome-directed approaches. For each therapeutic class, we summarize the supporting evidence, define its place in the treatment sequence, and identify the remaining evidence gaps.
Additional Links: PMID-42744133
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PubMed:
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@article {pmid42744133,
year = {2026},
author = {Tojjari, A and Pourbahrighesmat, S and Alkhazna, S and Saeed, A},
title = {Biomarker-Guided Treatment Selection in Metastatic Colorectal Cancer: A Critical Review of Established and Emerging Therapies.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {105597},
doi = {10.1016/j.critrevonc.2026.105597},
pmid = {42744133},
issn = {1879-0461},
abstract = {Metastatic colorectal cancer (mCRC) is increasingly managed according to mismatch repair status and actionable molecular alterations. In this structured narrative review, we separately examine mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H) and microsatellite-stable/mismatch repair-proficient (MSS/pMMR) disease and distinguish established treatments from investigational strategies. In dMMR/MSI-H mCRC, immune checkpoint inhibition is the established first-line standard, with pembrolizumab and nivolumab plus ipilimumab producing durable disease control. In MSS/pMMR mCRC, tumor molecular findings guide targeted therapy. For BRAF V600E-mutant disease, encorafenib plus cetuximab with fluoropyrimidine-based chemotherapy is a first-line standard. HER2-directed therapy with tucatinib plus trastuzumab or trastuzumab deruxtecan and combined KRAS G12C and EGFR inhibition are established after prior treatment but are not approved in the first-line setting. Across MMR subgroups, rare NTRK or RET fusions can confer eligibility for tumor-agnostic TRK or RET inhibition, although CRC-specific cohorts remain small. In previously treated non-MSI-H/dMMR mCRC, STELLAR-303 was the first phase 3 trial to demonstrate a significant overall survival benefit with an immune checkpoint inhibitor-containing regimen, zanzalintinib plus atezolizumab. Other investigational strategies include additional immunotherapy combinations, EGFR-MET bispecific antibody therapy with amivantamab, T-cell-engaging bispecific antibodies, therapeutic cancer vaccines, cellular therapies, and microbiome-directed approaches. For each therapeutic class, we summarize the supporting evidence, define its place in the treatment sequence, and identify the remaining evidence gaps.},
}
RevDate: 2026-09-15
EpOMEs Compromise Colonic Homeostasis Through Microbiome Dysbiosis and Inflammatory Activation.
Prostaglandins & other lipid mediators pii:S1098-8823(26)00060-2 [Epub ahead of print].
Linoleic acid-derived epoxyoctadecenoic acids (EpOMEs) have been implicated in inflammatory and metabolic diseases, yet their direct effects on colonic homeostasis under normal physiological conditions remain unclear. In this study, we investigated whether EpOMEs exposure alters colonic crypt structure, immune activation, and gut microbiome composition in C57BL/6 mice. We found that EpOMEs administration shortened colonic crypt length and reduced the expression of antimicrobial peptide genes, including Defb1 and Reg3g, indicating impaired epithelial architecture and weakened antimicrobial defense. EpOMEs also promoted macrophage accumulation in the colon and elevated expression of pro-inflammatory cytokines. Furthermore, 16S rRNA gene sequencing revealed that EpOMEs exposure altered gut microbial composition, characterized by reduced microbial diversity, depletion of potentially beneficial taxa including Muribaculaceae and Akkermansia, and enrichment of inflammation-associated Romboutsia. Together, these findings demonstrate that EpOMEs exposure is associated with impaired epithelial structure, enhanced macrophage-associated inflammatory responses, and gut microbiome dysbiosis. This study could provide new insight into how linoleic acid-derived lipid mediators may contribute to the early stages of gut dysfunction and increase susceptibility to associated inflammatory disorders.
Additional Links: PMID-42744188
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@article {pmid42744188,
year = {2026},
author = {Woo, J and Karunathilaka, JC and Shen, G and Oleskey, TJ and Lee, KSS and Kim, KH and Wang, W},
title = {EpOMEs Compromise Colonic Homeostasis Through Microbiome Dysbiosis and Inflammatory Activation.},
journal = {Prostaglandins & other lipid mediators},
volume = {},
number = {},
pages = {107115},
doi = {10.1016/j.prostaglandins.2026.107115},
pmid = {42744188},
issn = {1098-8823},
abstract = {Linoleic acid-derived epoxyoctadecenoic acids (EpOMEs) have been implicated in inflammatory and metabolic diseases, yet their direct effects on colonic homeostasis under normal physiological conditions remain unclear. In this study, we investigated whether EpOMEs exposure alters colonic crypt structure, immune activation, and gut microbiome composition in C57BL/6 mice. We found that EpOMEs administration shortened colonic crypt length and reduced the expression of antimicrobial peptide genes, including Defb1 and Reg3g, indicating impaired epithelial architecture and weakened antimicrobial defense. EpOMEs also promoted macrophage accumulation in the colon and elevated expression of pro-inflammatory cytokines. Furthermore, 16S rRNA gene sequencing revealed that EpOMEs exposure altered gut microbial composition, characterized by reduced microbial diversity, depletion of potentially beneficial taxa including Muribaculaceae and Akkermansia, and enrichment of inflammation-associated Romboutsia. Together, these findings demonstrate that EpOMEs exposure is associated with impaired epithelial structure, enhanced macrophage-associated inflammatory responses, and gut microbiome dysbiosis. This study could provide new insight into how linoleic acid-derived lipid mediators may contribute to the early stages of gut dysfunction and increase susceptibility to associated inflammatory disorders.},
}
RevDate: 2026-09-16
Potential contribution of the microbiota-gut-brain axis to doxorubicin-associated cognitive impairment: Mechanisms, evidence, and therapeutic opportunities.
Pharmacological research, 233:108455 pii:S1043-6618(26)00370-1 [Epub ahead of print].
Chemotherapy-induced cognitive impairment (CICI), often termed chemobrain, is a clinically important complication of cancer treatment that can affect memory, attention, executive function, and processing speed during and after therapy. Doxorubicin is of particular mechanistic interest because brain parenchymal exposure is limited, yet preclinical studies consistently identify neuroinflammatory, oxidative, vascular, and synaptic abnormalities after treatment. This critical narrative review evaluates whether intestinal injury and disruption of the microbiota-gut-brain axis may contribute to these central effects. Preclinical evidence indicates that doxorubicin can alter microbial community structure, injure the intestinal barrier, modify SCFA-associated taxa or predicted functions, alter selected metabolite profiles, and promote systemic inflammatory and metabolic signaling. These peripheral changes could interact with brain endothelial cells, glia, mitochondria, hippocampal neurogenesis, and synaptic-plasticity pathways. However, the proposed doxorubicin-gut-brain pathway remains a predominantly preclinical and incompletely tested framework. No longitudinal human study has yet established, within the same patients, the temporal sequence linking doxorubicin exposure, microbiome or metabolome changes, systemic inflammation, and objective cognitive outcomes. Existing animal studies also vary in dose, regimen, tumor context, sampling time, microbiome methodology, and control of behavioral or microbiological confounders, while causal rescue experiments remain limited. Key priorities are therefore longitudinal human cohorts with pretreatment baselines and repeated multi-omics and cognitive assessments; animal studies that test temporal precedence and causal rescue or pathway blockade in the same model; mediation analyses that determine whether microbial or metabolic changes lie between treatment and cognitive dysfunction; and mechanism-informed clinical trials that demonstrate target engagement, cognitive benefit, oncology safety, and preservation of antitumor efficacy. Microbiome-directed interventions are promising but remain investigational for doxorubicin-associated CICI.
Additional Links: PMID-42744193
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@article {pmid42744193,
year = {2026},
author = {Madkoor, M and Ahmed, R and Hany, R and Abdelnaby, M and Hagar, Z and Ahmed, A and Akl, H and Elshorbagy, D and Emad, A and Elsayed, J and Abdelfatah, H and Akawi, N and George, MY},
title = {Potential contribution of the microbiota-gut-brain axis to doxorubicin-associated cognitive impairment: Mechanisms, evidence, and therapeutic opportunities.},
journal = {Pharmacological research},
volume = {233},
number = {},
pages = {108455},
doi = {10.1016/j.phrs.2026.108455},
pmid = {42744193},
issn = {1096-1186},
abstract = {Chemotherapy-induced cognitive impairment (CICI), often termed chemobrain, is a clinically important complication of cancer treatment that can affect memory, attention, executive function, and processing speed during and after therapy. Doxorubicin is of particular mechanistic interest because brain parenchymal exposure is limited, yet preclinical studies consistently identify neuroinflammatory, oxidative, vascular, and synaptic abnormalities after treatment. This critical narrative review evaluates whether intestinal injury and disruption of the microbiota-gut-brain axis may contribute to these central effects. Preclinical evidence indicates that doxorubicin can alter microbial community structure, injure the intestinal barrier, modify SCFA-associated taxa or predicted functions, alter selected metabolite profiles, and promote systemic inflammatory and metabolic signaling. These peripheral changes could interact with brain endothelial cells, glia, mitochondria, hippocampal neurogenesis, and synaptic-plasticity pathways. However, the proposed doxorubicin-gut-brain pathway remains a predominantly preclinical and incompletely tested framework. No longitudinal human study has yet established, within the same patients, the temporal sequence linking doxorubicin exposure, microbiome or metabolome changes, systemic inflammation, and objective cognitive outcomes. Existing animal studies also vary in dose, regimen, tumor context, sampling time, microbiome methodology, and control of behavioral or microbiological confounders, while causal rescue experiments remain limited. Key priorities are therefore longitudinal human cohorts with pretreatment baselines and repeated multi-omics and cognitive assessments; animal studies that test temporal precedence and causal rescue or pathway blockade in the same model; mediation analyses that determine whether microbial or metabolic changes lie between treatment and cognitive dysfunction; and mechanism-informed clinical trials that demonstrate target engagement, cognitive benefit, oncology safety, and preservation of antitumor efficacy. Microbiome-directed interventions are promising but remain investigational for doxorubicin-associated CICI.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
A prospective randomized controlled pilot study of gut microbiome modulation by Nigella sativa seed oil and thymoquinone metabolism in healthy volunteers: implications for gastrointestinal surgery.
Scientific reports, 16(1):.
Maintaining gut microbial balance may influence outcomes in gastrointestinal surgery. Dietary supplementation has the potential to selectively modify its composition. Nigella sativa seed oil (NSSO), which contains the bioactive compound thymoquinone (TQ), has antimicrobial and immunomodulatory properties, but human data on NSSO-associated gut microbiome changes and urinary TQ detectability after repeated oral exposure remain limited. In this prospective, single-center, randomized open-label pilot study, eight healthy adults were assigned to a treatment group (n = 4) receiving TQ-containing NSSO capsules (two capsules, three times daily for 20 days) or a control group (n = 4) without supplementation. Fecal samples were collected at five time points and analyzed by 16 S rRNA gene sequencing. Alpha and beta diversity, exploratory differential abundance, and machine learning analyses were performed. Food diaries were reviewed descriptively. Urine samples obtained at two time points were analyzed using Gas Chromatography Mass Spectrometry (GC-MS) to detect TQ and its metabolites. No significant differences in alpha or beta diversity were observed between groups, proving a stable microbiome composition. However, specific taxa increased or decreased, among them Mediterraneibacter lactaris (p = 9 × 10[-5]) and Terrisporobacter mayombei (p = 3 × 10[-4]), respectively. TQ and/or TQ-H2 were qualitatively detected in urine samples from the treatment group after repeated NSSO intake. This pilot study suggests that repeated NSSO intake is feasible for longitudinal microbiome and urinary metabolite sampling and provides preliminary evidence for taxon-specific changes in healthy adults. Urinary detection of TQ/TQ-H2 confirms detectability following repeated NSSO intake but does not permit pharmacokinetic conclusions. These findings may guide the design of future blinded, placebo-controlled, diet-controlled perioperative microbiome studies.Trial Registration: The trial was retrospectively registered at ClinicalTrials.gov (NCT07450807) on 4 March 2026.
Additional Links: PMID-42744850
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@article {pmid42744850,
year = {2026},
author = {El-Banna, AF and Junca, H and Steube, A and Wissenbach, DK and Settmacher, U and Schneider, C and Tekbaş, A},
title = {A prospective randomized controlled pilot study of gut microbiome modulation by Nigella sativa seed oil and thymoquinone metabolism in healthy volunteers: implications for gastrointestinal surgery.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42744850},
issn = {2045-2322},
mesh = {Humans ; *Plant Oils/pharmacology/administration & dosage ; *Benzoquinones/metabolism/urine/pharmacology/administration & dosage ; Adult ; Male ; Pilot Projects ; Female ; Prospective Studies ; *Gastrointestinal Microbiome/drug effects ; Nigella sativa/chemistry ; Healthy Volunteers ; Feces/microbiology ; Dietary Supplements ; Carum/chemistry ; Seeds/chemistry ; Young Adult ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Maintaining gut microbial balance may influence outcomes in gastrointestinal surgery. Dietary supplementation has the potential to selectively modify its composition. Nigella sativa seed oil (NSSO), which contains the bioactive compound thymoquinone (TQ), has antimicrobial and immunomodulatory properties, but human data on NSSO-associated gut microbiome changes and urinary TQ detectability after repeated oral exposure remain limited. In this prospective, single-center, randomized open-label pilot study, eight healthy adults were assigned to a treatment group (n = 4) receiving TQ-containing NSSO capsules (two capsules, three times daily for 20 days) or a control group (n = 4) without supplementation. Fecal samples were collected at five time points and analyzed by 16 S rRNA gene sequencing. Alpha and beta diversity, exploratory differential abundance, and machine learning analyses were performed. Food diaries were reviewed descriptively. Urine samples obtained at two time points were analyzed using Gas Chromatography Mass Spectrometry (GC-MS) to detect TQ and its metabolites. No significant differences in alpha or beta diversity were observed between groups, proving a stable microbiome composition. However, specific taxa increased or decreased, among them Mediterraneibacter lactaris (p = 9 × 10[-5]) and Terrisporobacter mayombei (p = 3 × 10[-4]), respectively. TQ and/or TQ-H2 were qualitatively detected in urine samples from the treatment group after repeated NSSO intake. This pilot study suggests that repeated NSSO intake is feasible for longitudinal microbiome and urinary metabolite sampling and provides preliminary evidence for taxon-specific changes in healthy adults. Urinary detection of TQ/TQ-H2 confirms detectability following repeated NSSO intake but does not permit pharmacokinetic conclusions. These findings may guide the design of future blinded, placebo-controlled, diet-controlled perioperative microbiome studies.Trial Registration: The trial was retrospectively registered at ClinicalTrials.gov (NCT07450807) on 4 March 2026.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Plant Oils/pharmacology/administration & dosage
*Benzoquinones/metabolism/urine/pharmacology/administration & dosage
Adult
Male
Pilot Projects
Female
Prospective Studies
*Gastrointestinal Microbiome/drug effects
Nigella sativa/chemistry
Healthy Volunteers
Feces/microbiology
Dietary Supplements
Carum/chemistry
Seeds/chemistry
Young Adult
RNA, Ribosomal, 16S/genetics
RevDate: 2026-09-16
Microbial diversity: the essential foundation for life on our planet.
Biologia futura [Epub ahead of print].
The biological basis of life on Earth is microbial diversity that ensures human health, agricultural productivity, ecological balance, and ecosystem functioning. Microorganisms enable ecosystem restoration through bioremediation, maintain soil fertility, support plant growth, manage vital biogeochemical cycles, and contribute to climate resilience. Precision probiotics, postbiotics, faecal microbiota transplantation, and personalized microbiome medicine are the examples of emerging microbiome-based therapies that offer promising therapeutic opportunities. In humans, the gut microbial community is essential for immune regulation, metabolism, and disease prevention. In terrestrial ecological systems, interactions between plants, fungi, bacteria, and other soil microorganisms improve carbon sequestration, nutrient cycling, stress resilience, and sustainable agricultural productivity in the given effects of climate change. Emerging uses in agriculture, environmental restoration, and medicine are made possible by advancements in multi-omic techniques, synthetic microbial genomes, microbiome engineering, and artificial intelligence. Considering these developments, issues with ecological complexity, long-term validation, standardization, and field scale application still exist. Therefore, preserving microbial diversity is important for conserving ecological resilience and strengthening the One Health framework, which highlights the mutual dependance of health of animal, human, plant, and environment. This review summarizes what has been discovered about ecological and biomedical relevance of microbiome, identifies important research gaps, highlighting emerging technologies, and evaluates potential future directions for using microbiome to support planetary sustainability.
Additional Links: PMID-42744991
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@article {pmid42744991,
year = {2026},
author = {Singh, K and Julka, JM},
title = {Microbial diversity: the essential foundation for life on our planet.},
journal = {Biologia futura},
volume = {},
number = {},
pages = {},
pmid = {42744991},
issn = {2676-8607},
abstract = {The biological basis of life on Earth is microbial diversity that ensures human health, agricultural productivity, ecological balance, and ecosystem functioning. Microorganisms enable ecosystem restoration through bioremediation, maintain soil fertility, support plant growth, manage vital biogeochemical cycles, and contribute to climate resilience. Precision probiotics, postbiotics, faecal microbiota transplantation, and personalized microbiome medicine are the examples of emerging microbiome-based therapies that offer promising therapeutic opportunities. In humans, the gut microbial community is essential for immune regulation, metabolism, and disease prevention. In terrestrial ecological systems, interactions between plants, fungi, bacteria, and other soil microorganisms improve carbon sequestration, nutrient cycling, stress resilience, and sustainable agricultural productivity in the given effects of climate change. Emerging uses in agriculture, environmental restoration, and medicine are made possible by advancements in multi-omic techniques, synthetic microbial genomes, microbiome engineering, and artificial intelligence. Considering these developments, issues with ecological complexity, long-term validation, standardization, and field scale application still exist. Therefore, preserving microbial diversity is important for conserving ecological resilience and strengthening the One Health framework, which highlights the mutual dependance of health of animal, human, plant, and environment. This review summarizes what has been discovered about ecological and biomedical relevance of microbiome, identifies important research gaps, highlighting emerging technologies, and evaluates potential future directions for using microbiome to support planetary sustainability.},
}
RevDate: 2026-09-16
Correction: Human milk microbiome as a modulator of the early-life gut-brain axis: mechanisms and translational opportunities for neurodevelopment.
Journal of translational medicine, 24(1): pii:10.1186/s12967-026-08990-6.
Additional Links: PMID-42745312
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@article {pmid42745312,
year = {2026},
author = {Alnuaimi, F and Yassin, LK and Alketbi, S and Skrabulyte-Barbulescu, J and Almazrouei, S and Alremeithi, D and Alahbabi, N and Almarzooqi, S and Alkuwaiti, SH and Hamad, MIK},
title = {Correction: Human milk microbiome as a modulator of the early-life gut-brain axis: mechanisms and translational opportunities for neurodevelopment.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
doi = {10.1186/s12967-026-08990-6},
pmid = {42745312},
issn = {1479-5876},
}
RevDate: 2026-09-16
Novel Ferulic Acid Esterase From Human Gut Microbiome: Cloning and Application in Crop Residue Valorization.
Biotechnology and applied biochemistry [Epub ahead of print].
Ferulic acid esterases (FAEs) are enzymes that interact with esterified components of plant cell walls, facilitating the release of free ferulic acid (FA) from plant materials. Therefore, they hold significant importance across multiple industries, including pharma, food, and cosmetics. This investigation involved the cloning, expression, and characterization of FAE from the human fecal metagenome. Sequence analysis revealed that the cloned gene was approximately 750 bp in length and contained an open reading frame encoding a protein of 252 amino acids. The resulting recombinant protein displayed a molecular weight of 28 kDa and 49.7% identity with the chlorogenic acid esterase from Lactobacillus helveticus. The hydrolytic activity of the recombinant FAE was validated using p-nitrophenyl-ferulate (pNPF) as the substrate, with optimal activity at a pH of 7 and a temperature of 35°C. The enzyme showed stability within a pH range of 5.0-7.0 and temperatures from 5°C to 35°C. High-performance liquid chromatography (HPLC) results indicated that the FAE enzyme could release up to 49.7% of total alkali-extractable FA from dehydrated rice bran, followed by wheat bran and sugarcane bagasse. The total phenolic content of sugarcane bagasse increased by approximately 100% after in situ enzymatic fermentation compared with the chemically extracted fraction. These results indicate that cloned FAE can be used as a potential biocatalyst in industrial applications.
Additional Links: PMID-42745387
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@article {pmid42745387,
year = {2026},
author = {Kunnummal, SP and Abdulla, A and Khan, M},
title = {Novel Ferulic Acid Esterase From Human Gut Microbiome: Cloning and Application in Crop Residue Valorization.},
journal = {Biotechnology and applied biochemistry},
volume = {},
number = {},
pages = {},
doi = {10.1002/bab.70208},
pmid = {42745387},
issn = {1470-8744},
support = {5/7/1741/CH/Adhoc/2021-RMBCH//Indian Council of Medical Research/ ; },
abstract = {Ferulic acid esterases (FAEs) are enzymes that interact with esterified components of plant cell walls, facilitating the release of free ferulic acid (FA) from plant materials. Therefore, they hold significant importance across multiple industries, including pharma, food, and cosmetics. This investigation involved the cloning, expression, and characterization of FAE from the human fecal metagenome. Sequence analysis revealed that the cloned gene was approximately 750 bp in length and contained an open reading frame encoding a protein of 252 amino acids. The resulting recombinant protein displayed a molecular weight of 28 kDa and 49.7% identity with the chlorogenic acid esterase from Lactobacillus helveticus. The hydrolytic activity of the recombinant FAE was validated using p-nitrophenyl-ferulate (pNPF) as the substrate, with optimal activity at a pH of 7 and a temperature of 35°C. The enzyme showed stability within a pH range of 5.0-7.0 and temperatures from 5°C to 35°C. High-performance liquid chromatography (HPLC) results indicated that the FAE enzyme could release up to 49.7% of total alkali-extractable FA from dehydrated rice bran, followed by wheat bran and sugarcane bagasse. The total phenolic content of sugarcane bagasse increased by approximately 100% after in situ enzymatic fermentation compared with the chemically extracted fraction. These results indicate that cloned FAE can be used as a potential biocatalyst in industrial applications.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Prevotella intermedia culture supernatant impairs alveolar macrophage function and promotes Mycobacterium avium persistence.
Virulence, 17(1):2728453.
Microbiome analyses using 16S ribosomal RNA gene sequencing have revealed a higher prevalence of Prevotella species in patients with nontuberculous mycobacterial pulmonary disease (NTM-PD) than in those with non-NTM-PD bronchiectasis. Prevotella intermedia culture supernatant (P. int. sup.) has been reported to exacerbate pneumonia, but its effect on Mycobacterium avium infection remains unclear. Thus, we manipulated bone marrow cells to differentiate into alveolar macrophage-like cells (AMLCs), infected them with M. avium in the presence of P. int. sup. or control medium, and analyzed their phagocytic and bactericidal activities. Intracellular bacteria were quantified, and antimicrobial gene expression was assessed using real-time reverse transcription PCR and bulk RNA sequencing. In vivo, female C57BL/6J mice (7-8 weeks old) were oropharyngeally inoculated with M. avium with or without P. int. sup. P. int. sup. impaired intracellular killing of M. avium in AMLCs. RNA sequencing revealed downregulation of autophagy, type I interferon, and anti-mycobacterial genes in the P. int. sup.-treated group. Furthermore, flow cytometry analysis revealed that P. int. sup. increases levels of microtubule-associated protein 1 light chain 3 and may inhibit lysosome maturation. In mice, P. int. sup. increased the pulmonary M. avium load and suppressed type I and II interferon expression in the lungs. In this experimental mouse model of NTM-PD, P. int. sup. increased pulmonary M. avium burden, while in mouse derived AMLCs P. int sup. was associated with impaired autophagy‑related and interferon responses and reduced antimicrobial gene expression, supporting a potential role for P. intermedia in NTM-PD progression.
Additional Links: PMID-42745449
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@article {pmid42745449,
year = {2026},
author = {Fukushima, K and Iwanaga, N and Takeda, K and Hirayama, T and Yoshida, M and Ide, S and Tashiro, M and Takazono, T and Kosai, K and Sakamoto, N and Izumikawa, K and Naito, M and Yanagihara, K and Mukae, H},
title = {Prevotella intermedia culture supernatant impairs alveolar macrophage function and promotes Mycobacterium avium persistence.},
journal = {Virulence},
volume = {17},
number = {1},
pages = {2728453},
doi = {10.1080/21505594.2026.2728453},
pmid = {42745449},
issn = {2150-5608},
mesh = {Animals ; Female ; *Macrophages, Alveolar/microbiology/immunology ; Mice, Inbred C57BL ; *Mycobacterium avium/immunology/physiology ; Mice ; *Prevotella intermedia ; Phagocytosis ; Autophagy ; },
abstract = {Microbiome analyses using 16S ribosomal RNA gene sequencing have revealed a higher prevalence of Prevotella species in patients with nontuberculous mycobacterial pulmonary disease (NTM-PD) than in those with non-NTM-PD bronchiectasis. Prevotella intermedia culture supernatant (P. int. sup.) has been reported to exacerbate pneumonia, but its effect on Mycobacterium avium infection remains unclear. Thus, we manipulated bone marrow cells to differentiate into alveolar macrophage-like cells (AMLCs), infected them with M. avium in the presence of P. int. sup. or control medium, and analyzed their phagocytic and bactericidal activities. Intracellular bacteria were quantified, and antimicrobial gene expression was assessed using real-time reverse transcription PCR and bulk RNA sequencing. In vivo, female C57BL/6J mice (7-8 weeks old) were oropharyngeally inoculated with M. avium with or without P. int. sup. P. int. sup. impaired intracellular killing of M. avium in AMLCs. RNA sequencing revealed downregulation of autophagy, type I interferon, and anti-mycobacterial genes in the P. int. sup.-treated group. Furthermore, flow cytometry analysis revealed that P. int. sup. increases levels of microtubule-associated protein 1 light chain 3 and may inhibit lysosome maturation. In mice, P. int. sup. increased the pulmonary M. avium load and suppressed type I and II interferon expression in the lungs. In this experimental mouse model of NTM-PD, P. int. sup. increased pulmonary M. avium burden, while in mouse derived AMLCs P. int sup. was associated with impaired autophagy‑related and interferon responses and reduced antimicrobial gene expression, supporting a potential role for P. intermedia in NTM-PD progression.},
}
MeSH Terms:
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Animals
Female
*Macrophages, Alveolar/microbiology/immunology
Mice, Inbred C57BL
*Mycobacterium avium/immunology/physiology
Mice
*Prevotella intermedia
Phagocytosis
Autophagy
RevDate: 2026-09-16
CmpDate: 2026-09-16
Diet, the Gut Microbiome, and Mental Health: Mechanistic Perspectives.
Molecular nutrition & food research, 70(18):e70592.
The microbiota-gut-brain axis (MGBA) represents a dynamic, bidirectional communication network linking the gut microbiome with central nervous system function through neural, immune, metabolic, and endocrine pathways. Emerging clinical, observational, and preclinical evidence suggests that special and restrictive dietary patterns-including Mediterranean, ketogenic, vegan, gluten-free, low-FODMAP, sugar-restricted, dairy-free diets, and intermittent fasting (IF)-can substantially modulate the gut microbiota, potentially influencing mental health outcomes. In this review, we first outline the fundamental mechanisms underlying gut-brain communication, emphasizing the roles of microbial metabolites, vagal nerve signaling, immune modulation, and hypothalamic-pituitary-adrenal (HPA) axis interactions. We then examine how distinct dietary interventions may alter gut microbial composition and metabolic activity, with potential implications for neuroimmune regulation, neurotransmitter synthesis, gut barrier integrity, and stress resilience. Current limitations in the field-including population heterogeneity, interindividual microbiome variability, limited longitudinal and mechanistic human studies, and challenges in clinical translation-are critically discussed. Finally, we propose future research directions aimed at developing personalized dietary strategies for mental health support through microbiome-targeted approaches. Understanding how special diets reshape the MGBA may provide promising avenues for the nutritional modulation of emotional and cognitive well-being.
Additional Links: PMID-42745506
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@article {pmid42745506,
year = {2026},
author = {Hetta, HF and Hassan, RAA and Alanazi, FE and Alqifari, SF and Albalwi, MA and Albalawi, AA and Bukhari, SQ and Alatawi, Z and Ellah, NHA and Ramadan, YN},
title = {Diet, the Gut Microbiome, and Mental Health: Mechanistic Perspectives.},
journal = {Molecular nutrition & food research},
volume = {70},
number = {18},
pages = {e70592},
doi = {10.1002/mnfr.70592},
pmid = {42745506},
issn = {1613-4133},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Mental Health ; *Diet ; Animals ; Pituitary-Adrenal System/physiology ; Hypothalamo-Hypophyseal System/physiology ; Intermittent Fasting ; Diet, Ketogenic ; Brain/physiology ; FODMAP Diet ; },
abstract = {The microbiota-gut-brain axis (MGBA) represents a dynamic, bidirectional communication network linking the gut microbiome with central nervous system function through neural, immune, metabolic, and endocrine pathways. Emerging clinical, observational, and preclinical evidence suggests that special and restrictive dietary patterns-including Mediterranean, ketogenic, vegan, gluten-free, low-FODMAP, sugar-restricted, dairy-free diets, and intermittent fasting (IF)-can substantially modulate the gut microbiota, potentially influencing mental health outcomes. In this review, we first outline the fundamental mechanisms underlying gut-brain communication, emphasizing the roles of microbial metabolites, vagal nerve signaling, immune modulation, and hypothalamic-pituitary-adrenal (HPA) axis interactions. We then examine how distinct dietary interventions may alter gut microbial composition and metabolic activity, with potential implications for neuroimmune regulation, neurotransmitter synthesis, gut barrier integrity, and stress resilience. Current limitations in the field-including population heterogeneity, interindividual microbiome variability, limited longitudinal and mechanistic human studies, and challenges in clinical translation-are critically discussed. Finally, we propose future research directions aimed at developing personalized dietary strategies for mental health support through microbiome-targeted approaches. Understanding how special diets reshape the MGBA may provide promising avenues for the nutritional modulation of emotional and cognitive well-being.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Mental Health
*Diet
Animals
Pituitary-Adrenal System/physiology
Hypothalamo-Hypophyseal System/physiology
Intermittent Fasting
Diet, Ketogenic
Brain/physiology
FODMAP Diet
RevDate: 2026-09-16
RAPID: an interactive R/Shiny platform for end-to-end 16S rRNA and ITS amplicon sequence analysis using DADA2.
Bioinformatics (Oxford, England) pii:8800066 [Epub ahead of print].
MOTIVATION: Amplicon sequencing of 16S rRNA and internal transcribed spacer (ITS) gene regions is the most widely used approach for characterizing bacterial and fungal communities. The DADA2 pipeline has become the standard for inferring amplicon sequence variants (ASVs), offering single-nucleotide resolution over traditional OTU clustering. However, executing the full DADA2 workflow requires R programming proficiency and manual coordination of multiple sequential steps, presenting a substantial barrier for researchers in clinical, environmental, and agricultural sciences who lack computational training.
RESULTS: We present RAPID (R-based Amplicon Pipeline for Interactive DADA2), a pair of R/Shiny applications providing complete graphical user interfaces for 16S rRNA and ITS amplicon analysis. The 16S application implements a 10-step guided workflow from raw paired-end FASTQ files through quality filtering, denoising, paired-read merging, chimera removal, SILVA-based taxonomy assignment, phyloseq construction with data transformation (rarefaction, relative abundance, or CLR), visualization (rarefaction curves, alpha diversity, NMDS, PCoA, abundance), PERMANOVA, and ANCOM-BC2 differential abundance analysis. The ITS application extends this to 11 steps, adding automated primer removal via cutadapt with support for multiple primers and length-variable amplicons, and uses the UNITE database for fungal taxonomy. Both applications feature asynchronous background processing, session persistence, real-time progress monitoring, publication-ready figure export at 300 DPI, and comprehensive CSV/PNG result downloads.
AVAILABILITY: Raw 16S rRNA amplicon sequences are available in the NCBI Sequence Read Archive under BioProject accession PRJNA1499817. RAPID is freely available at https://github.com/beantkapoor786/RAPID and archived at 10.5281/zenodo.21628564. Both applications can be installed locally on any system with R (≥4.0) and run as local web applications.
SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.
Additional Links: PMID-42745553
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@article {pmid42745553,
year = {2026},
author = {Kapoor, B and Cregger, MA and Hamilton, J and Mead, A and Ranjan, P},
title = {RAPID: an interactive R/Shiny platform for end-to-end 16S rRNA and ITS amplicon sequence analysis using DADA2.},
journal = {Bioinformatics (Oxford, England)},
volume = {},
number = {},
pages = {},
doi = {10.1093/bioinformatics/btag688},
pmid = {42745553},
issn = {1367-4811},
abstract = {MOTIVATION: Amplicon sequencing of 16S rRNA and internal transcribed spacer (ITS) gene regions is the most widely used approach for characterizing bacterial and fungal communities. The DADA2 pipeline has become the standard for inferring amplicon sequence variants (ASVs), offering single-nucleotide resolution over traditional OTU clustering. However, executing the full DADA2 workflow requires R programming proficiency and manual coordination of multiple sequential steps, presenting a substantial barrier for researchers in clinical, environmental, and agricultural sciences who lack computational training.
RESULTS: We present RAPID (R-based Amplicon Pipeline for Interactive DADA2), a pair of R/Shiny applications providing complete graphical user interfaces for 16S rRNA and ITS amplicon analysis. The 16S application implements a 10-step guided workflow from raw paired-end FASTQ files through quality filtering, denoising, paired-read merging, chimera removal, SILVA-based taxonomy assignment, phyloseq construction with data transformation (rarefaction, relative abundance, or CLR), visualization (rarefaction curves, alpha diversity, NMDS, PCoA, abundance), PERMANOVA, and ANCOM-BC2 differential abundance analysis. The ITS application extends this to 11 steps, adding automated primer removal via cutadapt with support for multiple primers and length-variable amplicons, and uses the UNITE database for fungal taxonomy. Both applications feature asynchronous background processing, session persistence, real-time progress monitoring, publication-ready figure export at 300 DPI, and comprehensive CSV/PNG result downloads.
AVAILABILITY: Raw 16S rRNA amplicon sequences are available in the NCBI Sequence Read Archive under BioProject accession PRJNA1499817. RAPID is freely available at https://github.com/beantkapoor786/RAPID and archived at 10.5281/zenodo.21628564. Both applications can be installed locally on any system with R (≥4.0) and run as local web applications.
SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.},
}
RevDate: 2026-09-16
Drought Stress Mediated Changes in Food Crops: Mechanisms and Remediation Strategies.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Climate change has intensified drought frequency and severity, threatening global food security, particularly for staple crops like maize, wheat, and soybean. As central secondary metabolites, flavonoids orchestrate cellular redox homeostasis, stress signal transduction, and metabolic plasticity during plant drought responses. Previous reviews are confined to isolated molecular cascades and separate treatment of flavonoid metabolism, rhizosphere microecology, and agronomic mitigation strategies, failing to establish an integrated multi-scale regulatory framework. To fill this fragmented gap, this review integrates advances in plant physiology, microbial ecology, and nanobiotechnology to construct a cross-scale framework of flavonoid-mediated drought resistance in major food crops. We systematically summarize species-specific flavonoid regulatory networks and metabolic reprogramming triggered by drought-induced oxidative stress, dissect rhizosphere microbiome effects on flavonoid biosynthesis and drought signaling, and elaborate novel mechanisms whereby nanomaterials reshape flavonoid metabolism and boost drought tolerance via tuning ROS homeostasis. Furthermore, this work integrates soil amendment and precision irrigation to decipher synergistic drought-resistance crosstalk among agronomic practices, crop metabolism, and root-associated microbiota. Collectively, this review unifies molecular, microbial, technological, and agronomic perspectives to establish a multi-scale, interdisciplinary framework for crop drought adaptation. It delivers fundamental theoretical support for climate-resilient agriculture and outlines priority research avenues to safeguard global food security.
Additional Links: PMID-42745690
Publisher:
PubMed:
Citation:
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@article {pmid42745690,
year = {2026},
author = {Duan, X and Wang, L and Koski, TM and An, L and Efferth, T and Fu, Y},
title = {Drought Stress Mediated Changes in Food Crops: Mechanisms and Remediation Strategies.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e77194},
doi = {10.1002/advs.77194},
pmid = {42745690},
issn = {2198-3844},
support = {2024YFD2201105//National Key R&D Program of China/ ; 2025XAGG0057//Science and Technology Innovation Program of Xiongan New Area/ ; BLRC2023A01//5·5 Engineering Research & Innovation Team Project of Beijing Forestry University/ ; },
abstract = {Climate change has intensified drought frequency and severity, threatening global food security, particularly for staple crops like maize, wheat, and soybean. As central secondary metabolites, flavonoids orchestrate cellular redox homeostasis, stress signal transduction, and metabolic plasticity during plant drought responses. Previous reviews are confined to isolated molecular cascades and separate treatment of flavonoid metabolism, rhizosphere microecology, and agronomic mitigation strategies, failing to establish an integrated multi-scale regulatory framework. To fill this fragmented gap, this review integrates advances in plant physiology, microbial ecology, and nanobiotechnology to construct a cross-scale framework of flavonoid-mediated drought resistance in major food crops. We systematically summarize species-specific flavonoid regulatory networks and metabolic reprogramming triggered by drought-induced oxidative stress, dissect rhizosphere microbiome effects on flavonoid biosynthesis and drought signaling, and elaborate novel mechanisms whereby nanomaterials reshape flavonoid metabolism and boost drought tolerance via tuning ROS homeostasis. Furthermore, this work integrates soil amendment and precision irrigation to decipher synergistic drought-resistance crosstalk among agronomic practices, crop metabolism, and root-associated microbiota. Collectively, this review unifies molecular, microbial, technological, and agronomic perspectives to establish a multi-scale, interdisciplinary framework for crop drought adaptation. It delivers fundamental theoretical support for climate-resilient agriculture and outlines priority research avenues to safeguard global food security.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
The neonatal and maternal nasal microbiomes are compositionally diverse and functionally distinct within 24 hours of birth.
Frontiers in cellular and infection microbiology, 16:1922369.
BACKGROUND: The nasal microbiome provides a first line of defense at the respiratory mucosa, yet its composition immediately after birth and its relationship to the maternal nasal community remain poorly defined.
METHODS: We used 16S rRNA gene sequencing to compare anterior nares swabs collected within 24 hours of delivery from mothers (n=25) and newborns (n=34), including 22 maternal-newborn dyads.
RESULTS: The neonatal nasal microbiome was significantly more diverse than the maternal microbiome, with higher Shannon diversity, and the two communities were compositionally distinct by weighted UniFrac analysis. Maternal samples were dominated by Corynebacterium and Dolosigranulum, genera characteristic of a stable, healthy adult nares, whereas newborn samples were enriched for Lactobacillus, Burkholderia-Caballeronia-Paraburkholderia, Acinetobacter, and Streptococcus. Predicted functional profiling with PICRUSt2 indicated that, relative to mothers, neonatal communities had greater predicted capacity for degradation of aromatic and xenobiotic compounds, biosynthesis of antimicrobial secondary metabolites (including polyketides, β-lactams, and terpenoids), and lipid metabolism.
CONCLUSIONS: Together, these findings show that the newborn nasal cavity is not a sparsely colonized niche but instead harbors a compositionally diverse and functionally versatile microbial community that is distinct from the maternal nares in both membership and predicted metabolic potential. These results identify the perinatal period as a critical window for nasal microbial colonization, with potential implications for the trajectory of infant respiratory health.
Additional Links: PMID-42745753
PubMed:
Citation:
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@article {pmid42745753,
year = {2026},
author = {Wagner, SB and Keen, KE and Cinco, I and Rincón, M and Marshall, NE and Messaoudi, I},
title = {The neonatal and maternal nasal microbiomes are compositionally diverse and functionally distinct within 24 hours of birth.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1922369},
pmid = {42745753},
issn = {2235-2988},
mesh = {Humans ; Female ; *Microbiota ; RNA, Ribosomal, 16S/genetics ; Infant, Newborn ; DNA, Bacterial/genetics/chemistry ; *Bacteria/classification/genetics/isolation & purification ; Sequence Analysis, DNA ; *Nasal Cavity/microbiology ; Pregnancy ; Mothers ; Biodiversity ; DNA, Ribosomal/genetics/chemistry ; Phylogeny ; },
abstract = {BACKGROUND: The nasal microbiome provides a first line of defense at the respiratory mucosa, yet its composition immediately after birth and its relationship to the maternal nasal community remain poorly defined.
METHODS: We used 16S rRNA gene sequencing to compare anterior nares swabs collected within 24 hours of delivery from mothers (n=25) and newborns (n=34), including 22 maternal-newborn dyads.
RESULTS: The neonatal nasal microbiome was significantly more diverse than the maternal microbiome, with higher Shannon diversity, and the two communities were compositionally distinct by weighted UniFrac analysis. Maternal samples were dominated by Corynebacterium and Dolosigranulum, genera characteristic of a stable, healthy adult nares, whereas newborn samples were enriched for Lactobacillus, Burkholderia-Caballeronia-Paraburkholderia, Acinetobacter, and Streptococcus. Predicted functional profiling with PICRUSt2 indicated that, relative to mothers, neonatal communities had greater predicted capacity for degradation of aromatic and xenobiotic compounds, biosynthesis of antimicrobial secondary metabolites (including polyketides, β-lactams, and terpenoids), and lipid metabolism.
CONCLUSIONS: Together, these findings show that the newborn nasal cavity is not a sparsely colonized niche but instead harbors a compositionally diverse and functionally versatile microbial community that is distinct from the maternal nares in both membership and predicted metabolic potential. These results identify the perinatal period as a critical window for nasal microbial colonization, with potential implications for the trajectory of infant respiratory health.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Microbiota
RNA, Ribosomal, 16S/genetics
Infant, Newborn
DNA, Bacterial/genetics/chemistry
*Bacteria/classification/genetics/isolation & purification
Sequence Analysis, DNA
*Nasal Cavity/microbiology
Pregnancy
Mothers
Biodiversity
DNA, Ribosomal/genetics/chemistry
Phylogeny
RevDate: 2026-09-16
CmpDate: 2026-09-16
Gut microbiota variation in admixed Hispanic populations with polyendocrine metabolic ovarian syndrome.
Frontiers in endocrinology, 17:1890094.
INTRODUCTION: Polyendocrine Metabolic Ovarian Syndrome (PMOS), referred to clinically as polycystic ovary syndrome (PCOS), is a common endocrine disorder associated with reproductive dysfunction, hyperandrogenism, insulin resistance, obesity, and chronic low-grade inflammation. Although gut microbiome alterations have been implicated in PMOS pathophysiology, data from Hispanic populations remain limited.
METHODS: This cross-sectional study evaluated fecal samples from 51 reproductive-age, non-menopausal women living in Puerto Rico, including 41 with PMOS, diagnosed following the Rotterdam criteria, and 10 healthy controls. Genomic DNA was obtained from fecal samples and subjected to 16S rRNA gene sequencing for bacterial identification. Microbial assessment included associations with metabolic, androgenic, and reproductive variables.
RESULTS: After adjustment for age, body mass index (BMI), and recent antibiotic use, PMOS status was not significantly associated with alpha nor beta diversity (p>0.05). However, host factors such as BMI and age explained more variation in microbial communities than PMOS status. Indicator species analysis identified several taxa preferentially associated with controls, including Phocaeicola_A dorei, Alitiscatomonas aceti, Brotaphodocola, and Schaedlerella. Specifically, Fusicatenibacter saccharivorans was significantly reduced in the PMOS group. Metabolic markers, androgen levels, and reproductive features were not significantly associated with global microbiome diversity or composition; however, irregular menses was associated with greater microbiome dispersion.
DISCUSSION: These findings suggest that PMOS is not characterized by major gut microbiome shifts but may involve subtle depletion of health-associated commensals and increased microbial heterogeneity.
Additional Links: PMID-42745765
PubMed:
Citation:
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@article {pmid42745765,
year = {2026},
author = {Gonzalez-Rodriguez, LA and Jimenez-Ortega, KM and Vargas-Robles, D and Martínez-Hernández, CI and Meléndez-Vázquez, NM and Romaguera, J and Godoy-Vitorino, F},
title = {Gut microbiota variation in admixed Hispanic populations with polyendocrine metabolic ovarian syndrome.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1890094},
pmid = {42745765},
issn = {1664-2392},
mesh = {Female ; Humans ; *Polycystic Ovary Syndrome/microbiology/epidemiology ; *Gastrointestinal Microbiome ; Cross-Sectional Studies ; *Hispanic or Latino ; Puerto Rico/epidemiology ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; },
abstract = {INTRODUCTION: Polyendocrine Metabolic Ovarian Syndrome (PMOS), referred to clinically as polycystic ovary syndrome (PCOS), is a common endocrine disorder associated with reproductive dysfunction, hyperandrogenism, insulin resistance, obesity, and chronic low-grade inflammation. Although gut microbiome alterations have been implicated in PMOS pathophysiology, data from Hispanic populations remain limited.
METHODS: This cross-sectional study evaluated fecal samples from 51 reproductive-age, non-menopausal women living in Puerto Rico, including 41 with PMOS, diagnosed following the Rotterdam criteria, and 10 healthy controls. Genomic DNA was obtained from fecal samples and subjected to 16S rRNA gene sequencing for bacterial identification. Microbial assessment included associations with metabolic, androgenic, and reproductive variables.
RESULTS: After adjustment for age, body mass index (BMI), and recent antibiotic use, PMOS status was not significantly associated with alpha nor beta diversity (p>0.05). However, host factors such as BMI and age explained more variation in microbial communities than PMOS status. Indicator species analysis identified several taxa preferentially associated with controls, including Phocaeicola_A dorei, Alitiscatomonas aceti, Brotaphodocola, and Schaedlerella. Specifically, Fusicatenibacter saccharivorans was significantly reduced in the PMOS group. Metabolic markers, androgen levels, and reproductive features were not significantly associated with global microbiome diversity or composition; however, irregular menses was associated with greater microbiome dispersion.
DISCUSSION: These findings suggest that PMOS is not characterized by major gut microbiome shifts but may involve subtle depletion of health-associated commensals and increased microbial heterogeneity.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
Humans
*Polycystic Ovary Syndrome/microbiology/epidemiology
*Gastrointestinal Microbiome
Cross-Sectional Studies
*Hispanic or Latino
Puerto Rico/epidemiology
RNA, Ribosomal, 16S/genetics
Feces/microbiology
RevDate: 2026-09-16
CmpDate: 2026-09-16
Integrated follicular fluid multi-omics identifies steroidogenic dysregulation and a candidate SHBG-associated rescue framework in poor ovarian response.
Frontiers in endocrinology, 17:1909283.
INTRODUCTION: Poor ovarian response (POR) remains a major obstacle in assisted reproductive technology, yet the follicular microenvironmental determinants of impaired ovarian sensitivity are poorly understood. This study aimed to characterize the multi_omics landscape of the follicular fluid in POR and to explore potential therapeutic candidates and underlying mechanisms.
METHODS: We performed 16S rRNA sequencing and untargeted metabolomics on follicular fluid samples from 26 women with POR and 25 normoresponsive controls. Integrated cross_omics analysis, exploratory modelling, and age_adjusted sensitivity assessments were conducted. Candidate metabolites identified by MS/MS annotation were tested in a Tripterygium glycoside_induced ovarian injury mouse model, with subsequent ovarian RNA sequencing, molecular docking, molecular dynamics simulation, qPCR, and SHBG immunohistochemistry to interrogate downstream pathways.
RESULTS: POR was associated with reduced microbial diversity, 55 differential metabolic features, and convergence of 16S_based and metabolomic signals on ABC transporter_related pathways. Age_adjusted analyses indicated that the metabolomic component was more robust than the 16S community_level findings, which are interpreted as exploratory. Two downregulated metabolites --Harmalol and Beraprost --were prioritized for in vivo intervention. Both candidates partially restored follicle counts, reduced ovarian apoptosis, and improved LH/FSH profiles. Mechanistic investigations nominated an SHBG_associated steroidogenic program as a candidate downstream effector.
DISCUSSION: These findings support a working model wherein follicular microenvironment remodelling in POR converges on steroidogenic dysregulation, providing testable rescue hypotheses. The results highlight the relative robustness of metabolomic signatures over microbiome shifts in this context, though further functional validation is required to confirm causality and therapeutic potential.
Additional Links: PMID-42745827
PubMed:
Citation:
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@article {pmid42745827,
year = {2026},
author = {Zheng, R and Jiao, Y and Liu, J and Yang, W and Wang, Z and Tang, W and He, Q and Wu, Z and Xiang, L},
title = {Integrated follicular fluid multi-omics identifies steroidogenic dysregulation and a candidate SHBG-associated rescue framework in poor ovarian response.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1909283},
pmid = {42745827},
issn = {1664-2392},
mesh = {Female ; *Follicular Fluid/metabolism ; Animals ; Humans ; Multiomics ; *Sex Hormone-Binding Globulin/metabolism ; Metabolomics/methods ; Mice ; Adult ; *Ovary/metabolism ; Ovulation Induction ; },
abstract = {INTRODUCTION: Poor ovarian response (POR) remains a major obstacle in assisted reproductive technology, yet the follicular microenvironmental determinants of impaired ovarian sensitivity are poorly understood. This study aimed to characterize the multi_omics landscape of the follicular fluid in POR and to explore potential therapeutic candidates and underlying mechanisms.
METHODS: We performed 16S rRNA sequencing and untargeted metabolomics on follicular fluid samples from 26 women with POR and 25 normoresponsive controls. Integrated cross_omics analysis, exploratory modelling, and age_adjusted sensitivity assessments were conducted. Candidate metabolites identified by MS/MS annotation were tested in a Tripterygium glycoside_induced ovarian injury mouse model, with subsequent ovarian RNA sequencing, molecular docking, molecular dynamics simulation, qPCR, and SHBG immunohistochemistry to interrogate downstream pathways.
RESULTS: POR was associated with reduced microbial diversity, 55 differential metabolic features, and convergence of 16S_based and metabolomic signals on ABC transporter_related pathways. Age_adjusted analyses indicated that the metabolomic component was more robust than the 16S community_level findings, which are interpreted as exploratory. Two downregulated metabolites --Harmalol and Beraprost --were prioritized for in vivo intervention. Both candidates partially restored follicle counts, reduced ovarian apoptosis, and improved LH/FSH profiles. Mechanistic investigations nominated an SHBG_associated steroidogenic program as a candidate downstream effector.
DISCUSSION: These findings support a working model wherein follicular microenvironment remodelling in POR converges on steroidogenic dysregulation, providing testable rescue hypotheses. The results highlight the relative robustness of metabolomic signatures over microbiome shifts in this context, though further functional validation is required to confirm causality and therapeutic potential.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
*Follicular Fluid/metabolism
Animals
Humans
Multiomics
*Sex Hormone-Binding Globulin/metabolism
Metabolomics/methods
Mice
Adult
*Ovary/metabolism
Ovulation Induction
RevDate: 2026-09-16
CmpDate: 2026-09-16
The maternal gut-fetal brain axis: role of maternal microbial metabolome in early neurodevelopment.
Frontiers in nutrition, 13:1903574.
Fetal neurodevelopment is a critical phase modulated by the maternal microbiome. While certain specific signaling pathways have been identified, the complete signaling network and the spatial and temporal complexity remain largely unknown. Maternal metabolites are essential for fetal growth and certain metabolites are subject to dynamic adaptation during pregnancy. Alteration of maternal microbe richness and diversity, caused by malnutrition, psycho-social distress, and or infection, are cues known to impair fetal neural developmental circuits concomitant with increased risk of cognitive dysfunction later in life. This mini review focuses on the role of maternal microbial metabolites in shaping fetal neurodevelopment.
Additional Links: PMID-42745830
PubMed:
Citation:
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@article {pmid42745830,
year = {2026},
author = {Scoglio, MJ and Samala, T and Ghalat, NJ and Jayaraman, A and Pettersson, S},
title = {The maternal gut-fetal brain axis: role of maternal microbial metabolome in early neurodevelopment.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1903574},
pmid = {42745830},
issn = {2296-861X},
abstract = {Fetal neurodevelopment is a critical phase modulated by the maternal microbiome. While certain specific signaling pathways have been identified, the complete signaling network and the spatial and temporal complexity remain largely unknown. Maternal metabolites are essential for fetal growth and certain metabolites are subject to dynamic adaptation during pregnancy. Alteration of maternal microbe richness and diversity, caused by malnutrition, psycho-social distress, and or infection, are cues known to impair fetal neural developmental circuits concomitant with increased risk of cognitive dysfunction later in life. This mini review focuses on the role of maternal microbial metabolites in shaping fetal neurodevelopment.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Cultivation substrates alter plant metabolic profiles with concomitant impacts on herbivore performance.
Frontiers in microbiology, 17:1893579.
INTRODUCTION: Herbivore microbiomes are strongly influenced by host plant quality and diet composition. However, it remains unclear how different cultivation substrates modulate the plant metabolome and how these shifts subsequently influence the performance and microbiome of aboveground herbivores.
METHODS: We utilized common beans cultivated in soil and hydroponic systems to investigate the multi-trophic interactions involving the substrate microbiome, plant metabolome and the polyphagous spider mite Tetranychus pueraricola.
RESULTS: Our results showed that while T. pueraricola exhibited an increased oviposition on hydroponic leaves, they achieved markedly higher biomass when reared on soil-grown common beans. The beta diversity of the mite microbiome differed markedly between two systems and showed close associations with substrate microbial composition. Metabolomic profiling revealed significant enrichment in isoflavonoid biosynthesis and carbon metabolism pathways between hydroponic and soil-grown leaves. Specifically, the upregulation of key secondary metabolites in hydroponic leaves correlated with suppressed mite weight. Comprehensive correlation analyses further indicated that cultivation substrate affected multi-scale associations among substrate microbiome and leaf metabolome and mite microbiome.
DISCUSSION: Our results demonstrate that growth substrates potentially contribute to divergence in herbivore microbiome and performance, as well as plant metabolism. These findings highlight the significant influence of cultivation substrate on aboveground plant-herbivore interactions, providing new insights for optimizing crop management and ecological pest control.
Additional Links: PMID-42746029
PubMed:
Citation:
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@article {pmid42746029,
year = {2026},
author = {Huo, S and Xie, K and Chen, L and Sun, J and Wang, S},
title = {Cultivation substrates alter plant metabolic profiles with concomitant impacts on herbivore performance.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1893579},
pmid = {42746029},
issn = {1664-302X},
abstract = {INTRODUCTION: Herbivore microbiomes are strongly influenced by host plant quality and diet composition. However, it remains unclear how different cultivation substrates modulate the plant metabolome and how these shifts subsequently influence the performance and microbiome of aboveground herbivores.
METHODS: We utilized common beans cultivated in soil and hydroponic systems to investigate the multi-trophic interactions involving the substrate microbiome, plant metabolome and the polyphagous spider mite Tetranychus pueraricola.
RESULTS: Our results showed that while T. pueraricola exhibited an increased oviposition on hydroponic leaves, they achieved markedly higher biomass when reared on soil-grown common beans. The beta diversity of the mite microbiome differed markedly between two systems and showed close associations with substrate microbial composition. Metabolomic profiling revealed significant enrichment in isoflavonoid biosynthesis and carbon metabolism pathways between hydroponic and soil-grown leaves. Specifically, the upregulation of key secondary metabolites in hydroponic leaves correlated with suppressed mite weight. Comprehensive correlation analyses further indicated that cultivation substrate affected multi-scale associations among substrate microbiome and leaf metabolome and mite microbiome.
DISCUSSION: Our results demonstrate that growth substrates potentially contribute to divergence in herbivore microbiome and performance, as well as plant metabolism. These findings highlight the significant influence of cultivation substrate on aboveground plant-herbivore interactions, providing new insights for optimizing crop management and ecological pest control.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Microbial diversity, antimicrobial resistance and zoonotic implications of the reptile gut microbiota: an updated review.
Frontiers in microbiology, 17:1913228.
The reptilian gastrointestinal tract harbors a complex and dynamic ecosystem of microorganisms that plays a fundamental and multifaceted role in host nutrition, immune function, and overall physiological homeostasis. This gut microbiome exhibited remarkable phylogenetic and functional diversity, intricately shaped by a confluence of host evolutionary history, dietary strategy, environmental context, captive status, and life history traits. Beyond its critical importance for reptilian health and fitness, this internal microbial reservoir is of significant and growing concern from a public health perspective, serving as a major source of zoonotic pathogens, most notably non-typhoidal Salmonella, and as a critical and underexplored hotspot for the emergence, amplification, and dissemination of antimicrobial resistance genes (ARGs), a dimension that forms the central theme of this review and is systematically examined across host ecology, captive management, and the global pet trade continuum. This comprehensive review synthesizes contemporary research on the gut microbiota across key reptilian taxa, including popular companion species such as lizards such as Eublepharis macularius and Tiliqua scincoides, snakes such as Pantherophis guttatus, Python regius and chelonians. We undertake a detailed analysis of the foundational drivers shaping microbial community structure, assembly and stability, exploring the delicate balance between core symbiotic residents, putatively beneficial probiotic candidates, and pathogenic entities. A critical and extensive focus is placed on the distribution, ecological drivers, and transmission pathways of antimicrobial resistance genes within this ecosystem, highlighting its underappreciated role in the global One Health continuum. The review further elaborates on the indispensable metabolic contributions of the microbiota to host fitness, the complex tripartite interactions involving host, microbiome and parasitic helminths or protozoa, and the implications of dysbiosis. Finally, we evaluated practical and emerging strategies for targeted microbiome modulation aimed at enhancing captive management, supporting conservation breeding outcomes, mitigating zoonotic risks and promoting sustainable herpetoculture.
Additional Links: PMID-42746048
PubMed:
Citation:
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@article {pmid42746048,
year = {2026},
author = {Kong, D and Zhang, Y and Li, Z and Chen, L and Nie, J and Jiang, X and Cao, H and Ma, Y},
title = {Microbial diversity, antimicrobial resistance and zoonotic implications of the reptile gut microbiota: an updated review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1913228},
pmid = {42746048},
issn = {1664-302X},
abstract = {The reptilian gastrointestinal tract harbors a complex and dynamic ecosystem of microorganisms that plays a fundamental and multifaceted role in host nutrition, immune function, and overall physiological homeostasis. This gut microbiome exhibited remarkable phylogenetic and functional diversity, intricately shaped by a confluence of host evolutionary history, dietary strategy, environmental context, captive status, and life history traits. Beyond its critical importance for reptilian health and fitness, this internal microbial reservoir is of significant and growing concern from a public health perspective, serving as a major source of zoonotic pathogens, most notably non-typhoidal Salmonella, and as a critical and underexplored hotspot for the emergence, amplification, and dissemination of antimicrobial resistance genes (ARGs), a dimension that forms the central theme of this review and is systematically examined across host ecology, captive management, and the global pet trade continuum. This comprehensive review synthesizes contemporary research on the gut microbiota across key reptilian taxa, including popular companion species such as lizards such as Eublepharis macularius and Tiliqua scincoides, snakes such as Pantherophis guttatus, Python regius and chelonians. We undertake a detailed analysis of the foundational drivers shaping microbial community structure, assembly and stability, exploring the delicate balance between core symbiotic residents, putatively beneficial probiotic candidates, and pathogenic entities. A critical and extensive focus is placed on the distribution, ecological drivers, and transmission pathways of antimicrobial resistance genes within this ecosystem, highlighting its underappreciated role in the global One Health continuum. The review further elaborates on the indispensable metabolic contributions of the microbiota to host fitness, the complex tripartite interactions involving host, microbiome and parasitic helminths or protozoa, and the implications of dysbiosis. Finally, we evaluated practical and emerging strategies for targeted microbiome modulation aimed at enhancing captive management, supporting conservation breeding outcomes, mitigating zoonotic risks and promoting sustainable herpetoculture.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Grand challenge: building a digitally enabled one health future for pediatric infectious diseases.
Frontiers in pediatrics, 14:1967922.
Additional Links: PMID-42746073
PubMed:
Citation:
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@article {pmid42746073,
year = {2026},
author = {Zama, D},
title = {Grand challenge: building a digitally enabled one health future for pediatric infectious diseases.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1967922},
pmid = {42746073},
issn = {2296-2360},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Antibiotic-induced gut microbiota dysbiosis in the PICU: mechanisms, clinical outcomes, and management strategies - a narrative review.
Frontiers in immunology, 17:1910105.
BACKGROUND: Antibiotic exposure is highly prevalent in the paediatric intensive care unit (PICU) and constitutes a major modifiable driver of gut microbiota dysbiosis. However, a systematic synthesis focusing specifically on the PICU population has been lacking. This narrative review addresses how antibiotic exposure drives gut dysbiosis in the PICU, its clinical consequences with emphasis on immunological pathways, and its management.
METHODS: This review was informed by a structured search of PubMed, Web of Science, Cochrane Library, and Chinese databases up to June 2026, including studies on antibiotic exposure, microbiota alterations, clinical outcomes, and management in critically ill children.
RESULTS: Antibiotic use in PICU children ranges from 58% to 94%, with broad-spectrum and combination therapy being common. Anti-anaerobic antibiotics-particularly piperacillin-tazobactam, meropenem, and clindamycin-cause the most pronounced disruption, as quantified in adult ICU cohorts. In PICU children, clinical consequences include a higher incidence of Clostridioides difficile infection and an increased risk of ventilator-associated pneumonia following carbapenem exposure. Antibiotic stewardship, encompassing de-escalation and avoidance of unnecessary anaerobic coverage, is the first-line microbiota protection strategy. Probiotics reduce ventilator-associated pneumonia and shorten PICU stay, but should not be used routinely in high-risk children. High-fibre enteral nutrition has shown feasibility, whereas postbiotics and faecal microbiota transplantation lack PICU-specific trial data.
CONCLUSIONS: Antibiotics are among the most significant modifiable drivers of gut dysbiosis in the PICU, with dose-dependent, class-specific effects. Antibiotic stewardship should be prioritised before any microbiota-directed intervention. Live probiotics require caution in high-risk populations, while non-live interventions are promising but need larger trials. Future research should employ longitudinal, multicentre studies with standardised reporting to elucidate host-microbe interactions in critically ill children.
Additional Links: PMID-42746112
PubMed:
Citation:
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@article {pmid42746112,
year = {2026},
author = {Yang, C and Wang, D and Peng, W},
title = {Antibiotic-induced gut microbiota dysbiosis in the PICU: mechanisms, clinical outcomes, and management strategies - a narrative review.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1910105},
pmid = {42746112},
issn = {1664-3224},
mesh = {Humans ; *Dysbiosis/chemically induced/therapy ; *Gastrointestinal Microbiome/drug effects ; *Intensive Care Units, Pediatric ; *Anti-Bacterial Agents/adverse effects ; Child ; Critical Illness ; },
abstract = {BACKGROUND: Antibiotic exposure is highly prevalent in the paediatric intensive care unit (PICU) and constitutes a major modifiable driver of gut microbiota dysbiosis. However, a systematic synthesis focusing specifically on the PICU population has been lacking. This narrative review addresses how antibiotic exposure drives gut dysbiosis in the PICU, its clinical consequences with emphasis on immunological pathways, and its management.
METHODS: This review was informed by a structured search of PubMed, Web of Science, Cochrane Library, and Chinese databases up to June 2026, including studies on antibiotic exposure, microbiota alterations, clinical outcomes, and management in critically ill children.
RESULTS: Antibiotic use in PICU children ranges from 58% to 94%, with broad-spectrum and combination therapy being common. Anti-anaerobic antibiotics-particularly piperacillin-tazobactam, meropenem, and clindamycin-cause the most pronounced disruption, as quantified in adult ICU cohorts. In PICU children, clinical consequences include a higher incidence of Clostridioides difficile infection and an increased risk of ventilator-associated pneumonia following carbapenem exposure. Antibiotic stewardship, encompassing de-escalation and avoidance of unnecessary anaerobic coverage, is the first-line microbiota protection strategy. Probiotics reduce ventilator-associated pneumonia and shorten PICU stay, but should not be used routinely in high-risk children. High-fibre enteral nutrition has shown feasibility, whereas postbiotics and faecal microbiota transplantation lack PICU-specific trial data.
CONCLUSIONS: Antibiotics are among the most significant modifiable drivers of gut dysbiosis in the PICU, with dose-dependent, class-specific effects. Antibiotic stewardship should be prioritised before any microbiota-directed intervention. Live probiotics require caution in high-risk populations, while non-live interventions are promising but need larger trials. Future research should employ longitudinal, multicentre studies with standardised reporting to elucidate host-microbe interactions in critically ill children.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dysbiosis/chemically induced/therapy
*Gastrointestinal Microbiome/drug effects
*Intensive Care Units, Pediatric
*Anti-Bacterial Agents/adverse effects
Child
Critical Illness
RevDate: 2026-09-16
CmpDate: 2026-09-16
Disrupting the vicious cycle of malnutrition and enteropathy: advancing strategies to improve child physical and neurocognitive outcomes.
Frontiers in public health, 14:1792466.
BACKGROUND: Recognition of the synergistic cycle of malnutrition, immune dysfunction, and recurrent enteric infection in children and its role in linear growth stunting and impaired cognitive development (the "stunting syndrome"), dates back to the 1960s. Early hypotheses emphasized reduced intestinal absorption associated with diarrhea as the primary enteropathy driving malnutrition and developmental deficits. However, recent evidence indicates that a subclinical condition termed environmental enteropathy (EE), or environmental enteric dysfunction (EED), may be a more critical contributor. Mitigating the adverse impacts of EE/EED requires a holistic, integrated approach that combines improved nutrition, water, sanitation, and hygiene (WASH), appropriate vaccination, and targeted non-pharmaceutical hygiene interventions designed to prevent recurrent enteric infections. These interventions aim to reduce pathogen exposure in infants' immediate environments, a prerequisite for achieving sustained physical and neurocognitive development and, ultimately, economic progress in low- and middle-income countries (LMICs).
OBJECTIVE: This Hypothesis and Theory article synthesizes current understanding of EE/EED as a proximate driver of chronic childhood malnutrition and its major sequelae: stunting, impaired neurocognitive development, immune dysfunction (including poor pediatric vaccine response), and nutrient malabsorption. We hypothesize the necessity of reducing enteric infection occurrence as a cornerstone for breaking the malnutrition-infection cycle and propose that non-pharmaceutical interventions targeting pathogen exposure in household and infant play environments are essential. In addition to pathogen exposure, we examine other determinants of malnutrition, including microbiome dysbiosis and epigenetic alterations as possible targets for therapeutic interventions intended to mitigate negative outcomes on health and nutrition.
METHODS: We reviewed literature addressing malnutrition, immune impacts, enteric infections, EE, growth stunting, cognitive impairment, epigenetic alterations, and mitigation strategies including WASH, baby WASH, hand and surface hygiene, and vaccination, using databases such as PubMed, Embase, and Google Scholar.
RESULTS: The synergistic malnutrition and infection cycle underlying the stunting syndrome comprises multiple interdependent components: chronic malnutrition, immune dysfunction, recurrent pathogen assault, microbiome dysbiosis, and EE/EED. Previous interventions have largely failed, likely because they targeted isolated components rather than the entire cycle. Here, we describe this cycle, its interactions, and prior attempts at disruption. We advocate for a novel, integrated approach, termed baby WASH or environmental hygiene, focused on creating hygienically clean environments where infants live and play, thereby reducing exposure to enteric pathogens. We also explore the link between malnutrition, EE/EED, and epigenetic reprogramming, as a contributor to health risks. Importantly, malnutrition is linked to epigenetic reprogramming, which contributes to neurocognitive impairment. We hypothesize that by combining baby WASH strategies with emerging pharmaceutical interventions addressing epigenetic and nutritional deficits, and associated socioeconomic and political factors, a comprehensive maternal-child health framework may be established to interrupt this vicious cycle.
CONCLUSION: Preventing recurrent pathogen exposure during both prenatal and postnatal periods is hypothesized to be essential to interrupting the malnutrition and infection cycle and reducing stunting. Interventions must address infants' immediate living, feeding, and educational environments, as well as maternal environments during gestation. Early-life nutritional deficiencies may influence epigenetic programming, with developmental consequences. Breaking this cycle remains an unmet global health priority, warranting urgent international attention due to the human and economic tolls in resource-limited settings LMICs.
Additional Links: PMID-42746172
PubMed:
Citation:
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@article {pmid42746172,
year = {2026},
author = {Ijaz, MK and Nims, RW and Rubino, JR and Hasan, BSF and Ijaz, MK and Xu, FY and Gerba, CP},
title = {Disrupting the vicious cycle of malnutrition and enteropathy: advancing strategies to improve child physical and neurocognitive outcomes.},
journal = {Frontiers in public health},
volume = {14},
number = {},
pages = {1792466},
pmid = {42746172},
issn = {2296-2565},
mesh = {Humans ; Hygiene ; *Growth Disorders/prevention & control/etiology ; Infant ; Sanitation ; *Intestinal Diseases/complications/prevention & control ; Child ; Child, Preschool ; *Malnutrition/complications/prevention & control ; *Child Nutrition Disorders/prevention & control ; Developing Countries ; },
abstract = {BACKGROUND: Recognition of the synergistic cycle of malnutrition, immune dysfunction, and recurrent enteric infection in children and its role in linear growth stunting and impaired cognitive development (the "stunting syndrome"), dates back to the 1960s. Early hypotheses emphasized reduced intestinal absorption associated with diarrhea as the primary enteropathy driving malnutrition and developmental deficits. However, recent evidence indicates that a subclinical condition termed environmental enteropathy (EE), or environmental enteric dysfunction (EED), may be a more critical contributor. Mitigating the adverse impacts of EE/EED requires a holistic, integrated approach that combines improved nutrition, water, sanitation, and hygiene (WASH), appropriate vaccination, and targeted non-pharmaceutical hygiene interventions designed to prevent recurrent enteric infections. These interventions aim to reduce pathogen exposure in infants' immediate environments, a prerequisite for achieving sustained physical and neurocognitive development and, ultimately, economic progress in low- and middle-income countries (LMICs).
OBJECTIVE: This Hypothesis and Theory article synthesizes current understanding of EE/EED as a proximate driver of chronic childhood malnutrition and its major sequelae: stunting, impaired neurocognitive development, immune dysfunction (including poor pediatric vaccine response), and nutrient malabsorption. We hypothesize the necessity of reducing enteric infection occurrence as a cornerstone for breaking the malnutrition-infection cycle and propose that non-pharmaceutical interventions targeting pathogen exposure in household and infant play environments are essential. In addition to pathogen exposure, we examine other determinants of malnutrition, including microbiome dysbiosis and epigenetic alterations as possible targets for therapeutic interventions intended to mitigate negative outcomes on health and nutrition.
METHODS: We reviewed literature addressing malnutrition, immune impacts, enteric infections, EE, growth stunting, cognitive impairment, epigenetic alterations, and mitigation strategies including WASH, baby WASH, hand and surface hygiene, and vaccination, using databases such as PubMed, Embase, and Google Scholar.
RESULTS: The synergistic malnutrition and infection cycle underlying the stunting syndrome comprises multiple interdependent components: chronic malnutrition, immune dysfunction, recurrent pathogen assault, microbiome dysbiosis, and EE/EED. Previous interventions have largely failed, likely because they targeted isolated components rather than the entire cycle. Here, we describe this cycle, its interactions, and prior attempts at disruption. We advocate for a novel, integrated approach, termed baby WASH or environmental hygiene, focused on creating hygienically clean environments where infants live and play, thereby reducing exposure to enteric pathogens. We also explore the link between malnutrition, EE/EED, and epigenetic reprogramming, as a contributor to health risks. Importantly, malnutrition is linked to epigenetic reprogramming, which contributes to neurocognitive impairment. We hypothesize that by combining baby WASH strategies with emerging pharmaceutical interventions addressing epigenetic and nutritional deficits, and associated socioeconomic and political factors, a comprehensive maternal-child health framework may be established to interrupt this vicious cycle.
CONCLUSION: Preventing recurrent pathogen exposure during both prenatal and postnatal periods is hypothesized to be essential to interrupting the malnutrition and infection cycle and reducing stunting. Interventions must address infants' immediate living, feeding, and educational environments, as well as maternal environments during gestation. Early-life nutritional deficiencies may influence epigenetic programming, with developmental consequences. Breaking this cycle remains an unmet global health priority, warranting urgent international attention due to the human and economic tolls in resource-limited settings LMICs.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Hygiene
*Growth Disorders/prevention & control/etiology
Infant
Sanitation
*Intestinal Diseases/complications/prevention & control
Child
Child, Preschool
*Malnutrition/complications/prevention & control
*Child Nutrition Disorders/prevention & control
Developing Countries
RevDate: 2026-09-16
CmpDate: 2026-09-16
Subconscious Restructuring Protocol in a Mental Health Quality Improvement Study: Reduced Treatment Duration and Improvement Across 17 Psychometric Outcomes in Adult Civilians, Veterans, and Adolescents.
Cureus, 18(8):e114583.
BACKGROUND: Conventional psychiatric and psychotherapeutic services typically require extended treatment durations while collecting limited outcome data, producing inconsistent care. Subconscious Restructuring (SR) uses a behavioral microbiome model treating psychological symptoms and gut barrier integrity as a single clinical target, on the premise that a compromised gut barrier permits translocation of lipopolysaccharide and Candida, activating microglia and the neuroinflammation implicated in depression, anxiety, and post-traumatic stress disorder (PTSD). The model is the rationale for the protocol's dual target, not a hypothesis tested here. SR is cloud-based, scripted, and auditable, capturing session-level client-generated data, and has been in clinical use since 1990; it is mechanistic rather than symptom-based, so no personal history is required for delivery. This quality improvement (QI) initiative aimed to improve the efficiency and clinical outcomes of care by delivering a standardized brief emotional fitness protocol through the SR framework.
METHODOLOGY: This initiative used Plan-Do-Study-Act cycles with 50 clients across three populations (20 adult civilians, 20 military veterans, 10 adolescents) in multi-site clinical practices. The protocol comprised two two-hour sessions on consecutive days plus three one-hour follow-ups for adult civilians, two two-hour sessions for veterans, and a single four-hour session for adolescents, delivered as extended workshop-format blocks rather than 50-minute appointments. Sixteen psychometric metrics and a derived Stress Load Index were measured, alongside adherence, completion, and safety. The Gut Health Symptom Checklist was completed at every session as a physician-referral gate, not an outcome measure; no gut health data were analyzed. Change was summarized as the mean change in scale points with SD, 95% CI, percent improvement, and within-subject standardized mean change (d_z); paired t-tests are descriptive.
RESULTS: Treatment duration was reduced by 67.5% relative to the 16-hour midpoint of the conventional 12-20-session benchmark, ranging from 56.7% to 74.0% against its 12-hour and 20-hour bounds. Adherence and assessment completion were 100% with no adverse events. Mean improvement across the 17 outcomes was 35.2% for adults, 47.3% for veterans, and 19.1% for adolescents; pooled across 50 clients, depression (Emotional Checklist total) improved 46.63%. Veterans achieved the strongest gains (depression: 57.87%, anger: 63.95%, Stress Load Index: 46.25%). Every outcome improved in raw scale points in all three cohorts, but the adolescent response was smaller and more variable, with 10 of 16 intervals, including zero; its two negative percentages are floor and ceiling artifacts on hopelessness and relationship satisfaction. Standardized Cronbach's alpha was 0.93 for the valence-aligned overall scale, and d_z ranged from 0.04 to 2.04. Reliable improvement on the primary symptom instrument reached 90.0% of veterans, 60.0% of adults, and 50.0% of adolescents; on at least one instrument, these were 95.0%, 95.0%, and 50.0%, respectively.
CONCLUSIONS: Standardized brief emotional fitness protocols were associated with improvements in both clinical outcomes and service delivery efficiency. This model offers a replicable framework for reducing treatment timelines; controlled studies are needed to confirm effects on mental health outcomes.
Additional Links: PMID-42746181
PubMed:
Citation:
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@article {pmid42746181,
year = {2026},
author = {Burris, K},
title = {Subconscious Restructuring Protocol in a Mental Health Quality Improvement Study: Reduced Treatment Duration and Improvement Across 17 Psychometric Outcomes in Adult Civilians, Veterans, and Adolescents.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e114583},
pmid = {42746181},
issn = {2168-8184},
abstract = {BACKGROUND: Conventional psychiatric and psychotherapeutic services typically require extended treatment durations while collecting limited outcome data, producing inconsistent care. Subconscious Restructuring (SR) uses a behavioral microbiome model treating psychological symptoms and gut barrier integrity as a single clinical target, on the premise that a compromised gut barrier permits translocation of lipopolysaccharide and Candida, activating microglia and the neuroinflammation implicated in depression, anxiety, and post-traumatic stress disorder (PTSD). The model is the rationale for the protocol's dual target, not a hypothesis tested here. SR is cloud-based, scripted, and auditable, capturing session-level client-generated data, and has been in clinical use since 1990; it is mechanistic rather than symptom-based, so no personal history is required for delivery. This quality improvement (QI) initiative aimed to improve the efficiency and clinical outcomes of care by delivering a standardized brief emotional fitness protocol through the SR framework.
METHODOLOGY: This initiative used Plan-Do-Study-Act cycles with 50 clients across three populations (20 adult civilians, 20 military veterans, 10 adolescents) in multi-site clinical practices. The protocol comprised two two-hour sessions on consecutive days plus three one-hour follow-ups for adult civilians, two two-hour sessions for veterans, and a single four-hour session for adolescents, delivered as extended workshop-format blocks rather than 50-minute appointments. Sixteen psychometric metrics and a derived Stress Load Index were measured, alongside adherence, completion, and safety. The Gut Health Symptom Checklist was completed at every session as a physician-referral gate, not an outcome measure; no gut health data were analyzed. Change was summarized as the mean change in scale points with SD, 95% CI, percent improvement, and within-subject standardized mean change (d_z); paired t-tests are descriptive.
RESULTS: Treatment duration was reduced by 67.5% relative to the 16-hour midpoint of the conventional 12-20-session benchmark, ranging from 56.7% to 74.0% against its 12-hour and 20-hour bounds. Adherence and assessment completion were 100% with no adverse events. Mean improvement across the 17 outcomes was 35.2% for adults, 47.3% for veterans, and 19.1% for adolescents; pooled across 50 clients, depression (Emotional Checklist total) improved 46.63%. Veterans achieved the strongest gains (depression: 57.87%, anger: 63.95%, Stress Load Index: 46.25%). Every outcome improved in raw scale points in all three cohorts, but the adolescent response was smaller and more variable, with 10 of 16 intervals, including zero; its two negative percentages are floor and ceiling artifacts on hopelessness and relationship satisfaction. Standardized Cronbach's alpha was 0.93 for the valence-aligned overall scale, and d_z ranged from 0.04 to 2.04. Reliable improvement on the primary symptom instrument reached 90.0% of veterans, 60.0% of adults, and 50.0% of adolescents; on at least one instrument, these were 95.0%, 95.0%, and 50.0%, respectively.
CONCLUSIONS: Standardized brief emotional fitness protocols were associated with improvements in both clinical outcomes and service delivery efficiency. This model offers a replicable framework for reducing treatment timelines; controlled studies are needed to confirm effects on mental health outcomes.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Microbiota-mitochondria axis in neurodegenerative disorders and retinal dysfunction: mechanisms and emerging therapeutic opportunities.
Frontiers in pharmacology, 17:1889898.
The gut microbiota crucial role in maintaining host metabolism, immune homeostasis, intestinal integrity, and mitochondrial function. Emerging evidence suggests that dysregulation of the microbiota-mitochondria axis represents one of the key mechanisms linking gut dysbiosis to the development of neurodegenerative and ocular diseases. The dysbiosis causes disruptions in mitochondrial physiology due to lower levels of short-chain fatty acids, increased intestinal permeability, endotoxemia, oxidative stress, and inflammation. These mechanisms contribute to the pathogenesis of Alzheimer's disease, Parkinson's disease, age-related macular degeneration, diabetic retinopathy, retinitis pigmentosa, and central serous chorioretinopathy. Environmental factors such as unhealthy dietary patterns, excessive antibiotic use, and prolonged exposure to artificial blue light may exacerbate dysbiosis and further disrupt mitochondrial homeostasis, thereby contributing to disease progression. We also elaborated the emerging therapeutic strategies targeting both the gut microbiota and mitochondrial function, including next-generation probiotics, postbiotics, dietary interventions, mitochondria-targeted antioxidants, NAD[+] precursors, and precision medicine approaches. Collectively, current evidence represents the microbiota-mitochondria axis as a one of the promising mechanistic and therapeutic targets for neurodegenerative and ocular diseases. However, most therapeutic evidence discussed in this review is derived from preclinical studies, with relatively limited clinical validation. Future well-designed longitudinal studies and randomized clinical trials are essential to establish efficacy, safety, and translational applicability in humans.
Additional Links: PMID-42746219
PubMed:
Citation:
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@article {pmid42746219,
year = {2026},
author = {Samaiya, PK and Agrawal, A and Kesharwani, S and Sathe, R and Prajapati, SK and Majumdar, S},
title = {Microbiota-mitochondria axis in neurodegenerative disorders and retinal dysfunction: mechanisms and emerging therapeutic opportunities.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1889898},
pmid = {42746219},
issn = {1663-9812},
abstract = {The gut microbiota crucial role in maintaining host metabolism, immune homeostasis, intestinal integrity, and mitochondrial function. Emerging evidence suggests that dysregulation of the microbiota-mitochondria axis represents one of the key mechanisms linking gut dysbiosis to the development of neurodegenerative and ocular diseases. The dysbiosis causes disruptions in mitochondrial physiology due to lower levels of short-chain fatty acids, increased intestinal permeability, endotoxemia, oxidative stress, and inflammation. These mechanisms contribute to the pathogenesis of Alzheimer's disease, Parkinson's disease, age-related macular degeneration, diabetic retinopathy, retinitis pigmentosa, and central serous chorioretinopathy. Environmental factors such as unhealthy dietary patterns, excessive antibiotic use, and prolonged exposure to artificial blue light may exacerbate dysbiosis and further disrupt mitochondrial homeostasis, thereby contributing to disease progression. We also elaborated the emerging therapeutic strategies targeting both the gut microbiota and mitochondrial function, including next-generation probiotics, postbiotics, dietary interventions, mitochondria-targeted antioxidants, NAD[+] precursors, and precision medicine approaches. Collectively, current evidence represents the microbiota-mitochondria axis as a one of the promising mechanistic and therapeutic targets for neurodegenerative and ocular diseases. However, most therapeutic evidence discussed in this review is derived from preclinical studies, with relatively limited clinical validation. Future well-designed longitudinal studies and randomized clinical trials are essential to establish efficacy, safety, and translational applicability in humans.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Autoimmune disease-associated pathobionts: mechanisms and therapeutic potential of phage-based approaches.
Frontiers in immunology, 17:1884094.
The gut microbiota is a critical regulator of systemic immune homeostasis; accumulating evidence implicates specific commensal bacteria, termed "pathobionts," in autoimmune disease pathogenesis. However, the definition of pathobionts remains context-dependent, as their effects are influenced by host genetics and host-microbe interactions. In this review, we summarize representative pathobionts supported by functional evidence in selected extraintestinal autoimmune diseases and discuss how these mechanisms may inform phage-based microbiome-targeted interventions. Mechanistically, pathobionts contribute to autoimmune disease through multiple pathways, including molecular mimicry, induction of intestinal T helper 17 and T follicular helper cell responses, disruption of regulatory T cell homeostasis, intestinal barrier dysfunction, and bacterial translocation from the gut to extraintestinal sites. These processes highlight the central role of gut-associated lymphoid tissue in initiating systemic autoimmunity, and targeting disease-associated microbes represents a promising therapeutic strategy. Whole-phage therapy, which enables highly specific bacterial elimination, has shown efficacy in preclinical immune-mediated disease models, but may be affected by variable in vivo replication, bacterial receptor-mediated resistance, anti-phage immune responses, and ecological effects on the resident microbiome. Phage-derived enzymes that lyse bacterial cell walls, such as endolysins, represent a complementary therapeutic modality that specifically targets bacterial peptidoglycan through cell wall-binding and catalytic domains. Collectively, these findings support the concept that pathobiont-targeted interventions, particularly phage-based strategies, may provide microbiome-directed, immunosuppression-sparing therapeutic approaches for selected patient subsets.
Additional Links: PMID-42746328
PubMed:
Citation:
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@article {pmid42746328,
year = {2026},
author = {Kuzuya, K and Maeda, Y and Funakoshi, K and Mizuno, Y and Fujimoto, K},
title = {Autoimmune disease-associated pathobionts: mechanisms and therapeutic potential of phage-based approaches.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1884094},
pmid = {42746328},
issn = {1664-3224},
mesh = {Humans ; *Autoimmune Diseases/therapy/immunology/microbiology ; Animals ; *Phage Therapy/methods ; *Gastrointestinal Microbiome/immunology ; *Bacteriophages/immunology ; Bacteria/immunology/virology ; Host Microbial Interactions/immunology ; },
abstract = {The gut microbiota is a critical regulator of systemic immune homeostasis; accumulating evidence implicates specific commensal bacteria, termed "pathobionts," in autoimmune disease pathogenesis. However, the definition of pathobionts remains context-dependent, as their effects are influenced by host genetics and host-microbe interactions. In this review, we summarize representative pathobionts supported by functional evidence in selected extraintestinal autoimmune diseases and discuss how these mechanisms may inform phage-based microbiome-targeted interventions. Mechanistically, pathobionts contribute to autoimmune disease through multiple pathways, including molecular mimicry, induction of intestinal T helper 17 and T follicular helper cell responses, disruption of regulatory T cell homeostasis, intestinal barrier dysfunction, and bacterial translocation from the gut to extraintestinal sites. These processes highlight the central role of gut-associated lymphoid tissue in initiating systemic autoimmunity, and targeting disease-associated microbes represents a promising therapeutic strategy. Whole-phage therapy, which enables highly specific bacterial elimination, has shown efficacy in preclinical immune-mediated disease models, but may be affected by variable in vivo replication, bacterial receptor-mediated resistance, anti-phage immune responses, and ecological effects on the resident microbiome. Phage-derived enzymes that lyse bacterial cell walls, such as endolysins, represent a complementary therapeutic modality that specifically targets bacterial peptidoglycan through cell wall-binding and catalytic domains. Collectively, these findings support the concept that pathobiont-targeted interventions, particularly phage-based strategies, may provide microbiome-directed, immunosuppression-sparing therapeutic approaches for selected patient subsets.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Autoimmune Diseases/therapy/immunology/microbiology
Animals
*Phage Therapy/methods
*Gastrointestinal Microbiome/immunology
*Bacteriophages/immunology
Bacteria/immunology/virology
Host Microbial Interactions/immunology
RevDate: 2026-09-16
CmpDate: 2026-09-16
Beyond the Pancreas: The Gut Microbiota in Acute Pancreatitis - From Mechanisms to Therapeutic Perspectives.
Clinical and experimental gastroenterology, 19:636881.
Acute pancreatitis is a heterogeneous inflammatory disease in which severe forms are frequently complicated by intestinal barrier failure, dysbiosis, bacterial translocation, infected necrosis, systemic inflammation, and organ dysfunction. Growing clinical and experimental evidence suggests that the gut microbiota may contribute to disease progression and represents a potential, although incompletely validated, therapeutic target. Importantly, acute pancreatitis-associated dysbiosis involves not only taxonomic shifts but also functional metabolic reprogramming, including reduced short-chain fatty acid production, altered microbial bile acid transformation, and disturbances in amino acid and lipid metabolism that may contribute to barrier dysfunction and systemic inflammation. This review synthesizes current evidence on microbiota-oriented strategies in acute pancreatitis, with emphasis on clinical applicability, mechanistic rationale, and safety. This narrative review integrates clinical guidelines, randomized trials, meta-analyses, cohort studies, metagenomic and metabolomic investigations, and experimental studies published mainly between 2002 and 2026. Among clinically supported strategies, early oral or enteral nutrition has the strongest evidence base and may help preserve mucosal integrity while limiting the ecological consequences of fasting and critical illness. Antimicrobial stewardship is also fundamental, because unnecessary antibiotic exposure may aggravate dysbiosis, impair colonization resistance, and promote resistant organisms. Selective digestive decontamination has historical clinical evidence but is not established for routine contemporary practice. Prebiotics, dietary fibers, postbiotics, and metabolite-oriented approaches are mechanistically promising, but clinical evidence remains limited. GV-971 is currently supported predominantly by preclinical experimental data. Probiotics and synbiotics require caution, particularly in predicted severe disease, because clinical benefits are inconsistent and important safety concerns have been reported. Fecal microbiota transplantation and washed microbiota transplantation remain investigational and should not be used routinely outside controlled protocols. At present, microbiota-oriented management should prioritize evidence-based supportive measures, particularly early oral or enteral nutrition and rational antimicrobial use. Future studies should combine clinical outcomes with standardized microbiome, metabolome, barrier, and resistance endpoints to determine whether direct microbiota modulation can become a safe and reproducible component of personalized therapy.
Additional Links: PMID-42746344
PubMed:
Citation:
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@article {pmid42746344,
year = {2026},
author = {Chooklin, S and Chuklin, S},
title = {Beyond the Pancreas: The Gut Microbiota in Acute Pancreatitis - From Mechanisms to Therapeutic Perspectives.},
journal = {Clinical and experimental gastroenterology},
volume = {19},
number = {},
pages = {636881},
pmid = {42746344},
issn = {1178-7023},
abstract = {Acute pancreatitis is a heterogeneous inflammatory disease in which severe forms are frequently complicated by intestinal barrier failure, dysbiosis, bacterial translocation, infected necrosis, systemic inflammation, and organ dysfunction. Growing clinical and experimental evidence suggests that the gut microbiota may contribute to disease progression and represents a potential, although incompletely validated, therapeutic target. Importantly, acute pancreatitis-associated dysbiosis involves not only taxonomic shifts but also functional metabolic reprogramming, including reduced short-chain fatty acid production, altered microbial bile acid transformation, and disturbances in amino acid and lipid metabolism that may contribute to barrier dysfunction and systemic inflammation. This review synthesizes current evidence on microbiota-oriented strategies in acute pancreatitis, with emphasis on clinical applicability, mechanistic rationale, and safety. This narrative review integrates clinical guidelines, randomized trials, meta-analyses, cohort studies, metagenomic and metabolomic investigations, and experimental studies published mainly between 2002 and 2026. Among clinically supported strategies, early oral or enteral nutrition has the strongest evidence base and may help preserve mucosal integrity while limiting the ecological consequences of fasting and critical illness. Antimicrobial stewardship is also fundamental, because unnecessary antibiotic exposure may aggravate dysbiosis, impair colonization resistance, and promote resistant organisms. Selective digestive decontamination has historical clinical evidence but is not established for routine contemporary practice. Prebiotics, dietary fibers, postbiotics, and metabolite-oriented approaches are mechanistically promising, but clinical evidence remains limited. GV-971 is currently supported predominantly by preclinical experimental data. Probiotics and synbiotics require caution, particularly in predicted severe disease, because clinical benefits are inconsistent and important safety concerns have been reported. Fecal microbiota transplantation and washed microbiota transplantation remain investigational and should not be used routinely outside controlled protocols. At present, microbiota-oriented management should prioritize evidence-based supportive measures, particularly early oral or enteral nutrition and rational antimicrobial use. Future studies should combine clinical outcomes with standardized microbiome, metabolome, barrier, and resistance endpoints to determine whether direct microbiota modulation can become a safe and reproducible component of personalized therapy.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Microbiota-driven metabolic-immune crosstalk in breast cancer.
Frontiers in pharmacology, 17:1931829.
Cancer continues to pose a significant risk to women's health globally, as its progression and treatment resistance arise from an intricate interplay between metabolic reprogramming, immunological evasion, and the tumor microbiome. Augmented glycolysis has emerged as a pivotal element in cancer pathogenesis, altering the tumor microenvironment via the buildup of immune-regulated metabolites that directly influence the activation of the cGAS-STING pathway. This pathway is regarded as a significant modulator of cancer immunity, but new studies indicate that its persistent activation generally results in an immunosuppressive tumor microenvironment instead of robust antitumor immunity. Developments in multi-omics technology have revealed the therapeutic importance of the tumor microbiome, and thus, we focus on recent advancements in tumor microbiota that modify glycolytic pathways to influence the cGAS-STING signaling threshold, thereby impacting cancer immunotherapy.
Additional Links: PMID-42746350
PubMed:
Citation:
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@article {pmid42746350,
year = {2026},
author = {Guan, J and Zhou, Q and Chen, J and Zhang, J and Yang, S and Xiong, Q and Ye, J and Zeng, Y and Ren, GH and Zhang, M},
title = {Microbiota-driven metabolic-immune crosstalk in breast cancer.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1931829},
pmid = {42746350},
issn = {1663-9812},
abstract = {Cancer continues to pose a significant risk to women's health globally, as its progression and treatment resistance arise from an intricate interplay between metabolic reprogramming, immunological evasion, and the tumor microbiome. Augmented glycolysis has emerged as a pivotal element in cancer pathogenesis, altering the tumor microenvironment via the buildup of immune-regulated metabolites that directly influence the activation of the cGAS-STING pathway. This pathway is regarded as a significant modulator of cancer immunity, but new studies indicate that its persistent activation generally results in an immunosuppressive tumor microenvironment instead of robust antitumor immunity. Developments in multi-omics technology have revealed the therapeutic importance of the tumor microbiome, and thus, we focus on recent advancements in tumor microbiota that modify glycolytic pathways to influence the cGAS-STING signaling threshold, thereby impacting cancer immunotherapy.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Age and sex: dual drivers remodeling the anti-tumor immune microenvironment and shaping personalized immuno-oncology.
Frontiers in immunology, 17:1918543.
Despite breakthrough advancements in cancer immunotherapy, significant inter-individual heterogeneity in clinical outcomes persists, bringing the regulatory roles of intrinsic host biological variables into sharp focus. Accumulating fundamental and clinical evidence indicates that age and sex play crucial roles in determining tumor susceptibility, disease progression, and the remodeling of the anti-tumor immune microenvironment. This review systematically delineates the profound impacts of the dual dimensions of age and sex on anti-tumor immune responses and immune evasion mechanisms. In the dimension of age, this article outlines the progressive functional decline of T/B lymphocytes and innate immune subsets driven by immunosenescence, and emphatically reveals how inflammaging and its associated senescence-associated secretory phenotype (SASP) orchestrate the formation of an immunosuppressive tumor microenvironment. In the dimension of sex, we deeply explore four core mechanisms comprising sex chromosome genomics (e.g., escape from X-chromosome inactivation and loss of Y chromosome), sex hormone networks, microenvironmental metabolic reprogramming, and the host gut microbiome, elucidating the molecular basis driving the disparities in innate and adaptive immunity between males and females. In summary, thoroughly deciphering the complex immune regulatory networks driven by age and sex not only helps elucidate the disparities in efficacy and toxicity observed in patients undergoing immune checkpoint inhibitors, but also provides crucial theoretical foundations and translational insights for the future development of "age-tailored" and "sex-specific" strategies in personalized immuno-oncology.
Additional Links: PMID-42746406
PubMed:
Citation:
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@article {pmid42746406,
year = {2026},
author = {Wang, Y and Wang, T and Xi, Y and Wang, Y and Bai, Y and Zhang, T},
title = {Age and sex: dual drivers remodeling the anti-tumor immune microenvironment and shaping personalized immuno-oncology.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1918543},
pmid = {42746406},
issn = {1664-3224},
mesh = {Humans ; *Tumor Microenvironment/immunology ; *Neoplasms/immunology/therapy ; Female ; Animals ; Male ; Precision Medicine ; Sex Factors ; Age Factors ; Tumor Escape ; Immunosenescence ; Immunotherapy/methods ; Immunity, Innate ; *Aging/immunology ; Senescence-Associated Secretory Phenotype ; },
abstract = {Despite breakthrough advancements in cancer immunotherapy, significant inter-individual heterogeneity in clinical outcomes persists, bringing the regulatory roles of intrinsic host biological variables into sharp focus. Accumulating fundamental and clinical evidence indicates that age and sex play crucial roles in determining tumor susceptibility, disease progression, and the remodeling of the anti-tumor immune microenvironment. This review systematically delineates the profound impacts of the dual dimensions of age and sex on anti-tumor immune responses and immune evasion mechanisms. In the dimension of age, this article outlines the progressive functional decline of T/B lymphocytes and innate immune subsets driven by immunosenescence, and emphatically reveals how inflammaging and its associated senescence-associated secretory phenotype (SASP) orchestrate the formation of an immunosuppressive tumor microenvironment. In the dimension of sex, we deeply explore four core mechanisms comprising sex chromosome genomics (e.g., escape from X-chromosome inactivation and loss of Y chromosome), sex hormone networks, microenvironmental metabolic reprogramming, and the host gut microbiome, elucidating the molecular basis driving the disparities in innate and adaptive immunity between males and females. In summary, thoroughly deciphering the complex immune regulatory networks driven by age and sex not only helps elucidate the disparities in efficacy and toxicity observed in patients undergoing immune checkpoint inhibitors, but also provides crucial theoretical foundations and translational insights for the future development of "age-tailored" and "sex-specific" strategies in personalized immuno-oncology.},
}
MeSH Terms:
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Humans
*Tumor Microenvironment/immunology
*Neoplasms/immunology/therapy
Female
Animals
Male
Precision Medicine
Sex Factors
Age Factors
Tumor Escape
Immunosenescence
Immunotherapy/methods
Immunity, Innate
*Aging/immunology
Senescence-Associated Secretory Phenotype
RevDate: 2026-09-16
CmpDate: 2026-09-16
A metagenomic analysis of the gut microbiota in a mouse model of fish allergy.
Frontiers in microbiology, 17:1886359.
BACKGROUND: Fish are among the most frequent causes of immunoglobulin E (IgE)-mediated food allergies (Type I). Currently, there is no known cure for fish allergy and individuals who are sensitized have to practice strict, lifelong avoidance of fish products in their diets. The relationship between gut microbiome and food allergies is currently a major topic of discussion; these pathologies involve the development of dysbiosis, which is a microbial imbalance resulting from immune-related mechanisms. Recent studies have provided evidence that individuals suffering from food allergies, display an intestinal microbiota with a different microbial composition compared to healthy subjects.
OBJECTIVES AND METHODS: In this work, we have described for the first time the differences in microbiome composition in a mouse model of fish allergy with previous sensitization to the main allergen, beta-Parvalbumin (β-PRVB), compared to mouse individuals without allergic response.
RESULTS: The metagenomic analysis has shown differences in taxonomic composition between the treatments. Regarding phyla, an increase in the relative abundance of Patescibacteria, specifically Saccharimonas genus and Candidatus_Saccharimonas group, were observed in the allergic animals (Prvb_Alum group) when compared to the other groups. In contrast, the relative abundance of the RF39 group (Bacilli), Atopobiaceae family, Erysipelotrichaceae, and the Coriobacteriaceae_UCG-002 group, was higher in the animals that did not develop an allergic response, despite being exposed to the allergen (Prvb group). Furthermore, an increase in the relative abundance of Lachnospiraceae ASF356 group was observed in the control group compared to the other treatments. This family, has been reported to be inversely associated with the progression of intestinal inflammation and anaphylactic diseases. For the first time, the gut microbiota composition of individual mice with and without fish allergies is described in detail in this work. This study may shed light on the potential contribution of gut microbiota to the onset and avoidance of food allergies.
Additional Links: PMID-42746455
PubMed:
Citation:
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@article {pmid42746455,
year = {2026},
author = {Abril, AG and Freire, J and Magadán, S and Villa, TG and Pazos, M and Carrera, M},
title = {A metagenomic analysis of the gut microbiota in a mouse model of fish allergy.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1886359},
pmid = {42746455},
issn = {1664-302X},
abstract = {BACKGROUND: Fish are among the most frequent causes of immunoglobulin E (IgE)-mediated food allergies (Type I). Currently, there is no known cure for fish allergy and individuals who are sensitized have to practice strict, lifelong avoidance of fish products in their diets. The relationship between gut microbiome and food allergies is currently a major topic of discussion; these pathologies involve the development of dysbiosis, which is a microbial imbalance resulting from immune-related mechanisms. Recent studies have provided evidence that individuals suffering from food allergies, display an intestinal microbiota with a different microbial composition compared to healthy subjects.
OBJECTIVES AND METHODS: In this work, we have described for the first time the differences in microbiome composition in a mouse model of fish allergy with previous sensitization to the main allergen, beta-Parvalbumin (β-PRVB), compared to mouse individuals without allergic response.
RESULTS: The metagenomic analysis has shown differences in taxonomic composition between the treatments. Regarding phyla, an increase in the relative abundance of Patescibacteria, specifically Saccharimonas genus and Candidatus_Saccharimonas group, were observed in the allergic animals (Prvb_Alum group) when compared to the other groups. In contrast, the relative abundance of the RF39 group (Bacilli), Atopobiaceae family, Erysipelotrichaceae, and the Coriobacteriaceae_UCG-002 group, was higher in the animals that did not develop an allergic response, despite being exposed to the allergen (Prvb group). Furthermore, an increase in the relative abundance of Lachnospiraceae ASF356 group was observed in the control group compared to the other treatments. This family, has been reported to be inversely associated with the progression of intestinal inflammation and anaphylactic diseases. For the first time, the gut microbiota composition of individual mice with and without fish allergies is described in detail in this work. This study may shed light on the potential contribution of gut microbiota to the onset and avoidance of food allergies.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Plant-food components at the microbiota-neuroinflammation interface: human evidence, translational limits, and sustainable dietary translation.
Frontiers in nutrition, 13:1907913.
This narrative review evaluates how convincingly plant-food components and plant-rich dietary patterns influence neuroinflammation and whether those mechanisms translate into neurological benefit. Infection is treated as one possible initiating exposure, neuroinflammation as a context-dependent mechanism, and neurological complications as clinical outcomes. Targeted literature searches and reference verification prioritized original human trials, mechanistic studies and balanced evidence syntheses. The most coherent pathways are modulation of microglial inflammatory signaling, including NLRP3-related processes, by selected phytochemicals, and microbial production of short-chain fatty acids from fermentable fiber, with effects on intestinal barrier function, systemic immune tone and microglial homeostasis. Cell and animal evidence is substantial, but human findings are heterogeneous. Randomized studies of whole dietary patterns and selected foods report both favorable and null cognitive, vascular, inflammatory, and microbiome outcomes. Trials of formulated curcumin and resveratrol show selective signals rather than consistent disease-modifying efficacy, underscoring problems of dose, metabolism, formulation and target engagement. Direct human evidence that plant foods prevent or modify infection-specific neurological outcomes remains insufficient. Translation also depends on food-system conditions: affordability, cultural acceptability, local availability, processing, safety, environmental burden and the foods displaced by a plant-forward intervention. Plant foods should therefore be framed as components of nutritionally adequate and context-specific sustainable diets, not as universally low-impact products or substitutes for clinical care. Future studies should integrate defined food exposures, pharmacokinetics, microbial function, inflammatory and vascular measures, neurological outcomes, safety, cost and environmental indicators.
Additional Links: PMID-42746492
PubMed:
Citation:
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@article {pmid42746492,
year = {2026},
author = {Dunga, KE and Izah, SC and Dunkwu-Okafor, A and Promise, VI and Alum, EU and Aliu, OO and Aseibai, ER and Ogwu, MC},
title = {Plant-food components at the microbiota-neuroinflammation interface: human evidence, translational limits, and sustainable dietary translation.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1907913},
pmid = {42746492},
issn = {2296-861X},
abstract = {This narrative review evaluates how convincingly plant-food components and plant-rich dietary patterns influence neuroinflammation and whether those mechanisms translate into neurological benefit. Infection is treated as one possible initiating exposure, neuroinflammation as a context-dependent mechanism, and neurological complications as clinical outcomes. Targeted literature searches and reference verification prioritized original human trials, mechanistic studies and balanced evidence syntheses. The most coherent pathways are modulation of microglial inflammatory signaling, including NLRP3-related processes, by selected phytochemicals, and microbial production of short-chain fatty acids from fermentable fiber, with effects on intestinal barrier function, systemic immune tone and microglial homeostasis. Cell and animal evidence is substantial, but human findings are heterogeneous. Randomized studies of whole dietary patterns and selected foods report both favorable and null cognitive, vascular, inflammatory, and microbiome outcomes. Trials of formulated curcumin and resveratrol show selective signals rather than consistent disease-modifying efficacy, underscoring problems of dose, metabolism, formulation and target engagement. Direct human evidence that plant foods prevent or modify infection-specific neurological outcomes remains insufficient. Translation also depends on food-system conditions: affordability, cultural acceptability, local availability, processing, safety, environmental burden and the foods displaced by a plant-forward intervention. Plant foods should therefore be framed as components of nutritionally adequate and context-specific sustainable diets, not as universally low-impact products or substitutes for clinical care. Future studies should integrate defined food exposures, pharmacokinetics, microbial function, inflammatory and vascular measures, neurological outcomes, safety, cost and environmental indicators.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Current Concepts in Periprosthetic Joint Infection: Modern Biomarkers, Microbiome Insights, Molecular Diagnostics, and Emerging Prevention Strategies.
Orthopedic research and reviews, 18:634292.
AIM: Periprosthetic joint infection (PJI) remains one of the leading causes of revision arthroplasty and is associated with substantial morbidity, mortality, and healthcare costs. Diagnosis remains challenging because of heterogeneous clinical presentations, the limited sensitivity of conventional inflammatory markers in chronic and low-grade infections, culture-negative cases, and biofilm-mediated pathogen persistence. This narrative review summarizes recent advances in the diagnosis and prevention of PJI, with a particular focus on synovial and serum biomarkers, microbiome-related susceptibility, molecular diagnostics, artificial intelligence, and emerging anti-biofilm and implant-surface technologies. Synovial biomarkers, including alpha-defensin, leukocyte esterase, calprotectin, and D-lactate, have demonstrated improved diagnostic performance, particularly in equivocal and culture-negative cases. However, none has sufficient evidence to replace established diagnostic criteria, and current data support their use as adjunctive tools in selected clinical scenarios rather than as standalone tests. Serum biomarkers beyond erythrocyte sedimentation rate and C-reactive protein, such as fibrinogen and protein fraction alterations, may provide additional diagnostic value but require further validation and standardized diagnostic thresholds. Molecular approaches, particularly metagenomic next-generation sequencing, improve pathogen detection in complex infections but remain limited by cost, protocol variability, and challenges in distinguishing clinically relevant pathogens from contaminants. Preventive strategies targeting bacterial adhesion and biofilm formation through local antibiotic delivery, surface modification, and nanotechnology-enabled implants are promising, although long-term efficacy, safety, and cost-effectiveness remain to be established. Overall, PJI management is evolving toward integrated, multimodal diagnostic strategies and biologically informed prevention. Current evidence supports the selective clinical use of synovial biomarker testing as an adjunctive tool within established diagnostic criteria, while continued research is needed before widespread routine implementation can be recommended.
Modern synovial biomarkers provide valuable adjunctive information that may improve diagnostic confidence in challenging periprosthetic joint infection cases when incorporated into a multidisciplinary diagnostic approach involving clinical assessment, laboratory evaluation, microbiological analysis, and established consensus criteria. Emerging preventive strategies targeting biofilm formation and host-microbe interactions represent promising approaches, although their ability to reduce revision rates and improve patient outcomes requires further clinical validation.
Additional Links: PMID-42746583
PubMed:
Citation:
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@article {pmid42746583,
year = {2026},
author = {Saadeh, JE and Saad, R and Assaf, F and Osman, R and Chami, AA and Harb, BA and Ghanem, W and Badra, M and Moucharafieh, R},
title = {Current Concepts in Periprosthetic Joint Infection: Modern Biomarkers, Microbiome Insights, Molecular Diagnostics, and Emerging Prevention Strategies.},
journal = {Orthopedic research and reviews},
volume = {18},
number = {},
pages = {634292},
pmid = {42746583},
issn = {1179-1462},
abstract = {AIM: Periprosthetic joint infection (PJI) remains one of the leading causes of revision arthroplasty and is associated with substantial morbidity, mortality, and healthcare costs. Diagnosis remains challenging because of heterogeneous clinical presentations, the limited sensitivity of conventional inflammatory markers in chronic and low-grade infections, culture-negative cases, and biofilm-mediated pathogen persistence. This narrative review summarizes recent advances in the diagnosis and prevention of PJI, with a particular focus on synovial and serum biomarkers, microbiome-related susceptibility, molecular diagnostics, artificial intelligence, and emerging anti-biofilm and implant-surface technologies. Synovial biomarkers, including alpha-defensin, leukocyte esterase, calprotectin, and D-lactate, have demonstrated improved diagnostic performance, particularly in equivocal and culture-negative cases. However, none has sufficient evidence to replace established diagnostic criteria, and current data support their use as adjunctive tools in selected clinical scenarios rather than as standalone tests. Serum biomarkers beyond erythrocyte sedimentation rate and C-reactive protein, such as fibrinogen and protein fraction alterations, may provide additional diagnostic value but require further validation and standardized diagnostic thresholds. Molecular approaches, particularly metagenomic next-generation sequencing, improve pathogen detection in complex infections but remain limited by cost, protocol variability, and challenges in distinguishing clinically relevant pathogens from contaminants. Preventive strategies targeting bacterial adhesion and biofilm formation through local antibiotic delivery, surface modification, and nanotechnology-enabled implants are promising, although long-term efficacy, safety, and cost-effectiveness remain to be established. Overall, PJI management is evolving toward integrated, multimodal diagnostic strategies and biologically informed prevention. Current evidence supports the selective clinical use of synovial biomarker testing as an adjunctive tool within established diagnostic criteria, while continued research is needed before widespread routine implementation can be recommended.
Modern synovial biomarkers provide valuable adjunctive information that may improve diagnostic confidence in challenging periprosthetic joint infection cases when incorporated into a multidisciplinary diagnostic approach involving clinical assessment, laboratory evaluation, microbiological analysis, and established consensus criteria. Emerging preventive strategies targeting biofilm formation and host-microbe interactions represent promising approaches, although their ability to reduce revision rates and improve patient outcomes requires further clinical validation.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Gut Microbial Metabolites as a Bridge in Osteoporotic Rehabilitation for the Elderly: From Aging-Related Dysbiosis to Precision Non-Pharmacological Strategies.
International journal of general medicine, 19:637308.
BACKGROUND AND OBJECTIVE: Osteoporosis in the elderly represents a major public health challenge in aging societies. Although non-pharmacological rehabilitation has become a core intervention strategy, standard protocols yield highly variable responses across individuals. This review aims to systematically examine the bridging role of gut microbial metabolites in the pathogenesis and rehabilitation of osteoporosis in the elderly, explore the hypothesis that baseline microbial status influences the heterogeneity of rehabilitation outcomes, and propose a microbiota-targeted precision rehabilitation framework for older populations.
METHODS: This narrative review systematically searched PubMed, Web of Science, Embase, Cochrane Library, Scopus, and CINAHL databases (January 2016 to May 2026). Original studies and reviews on naturally aged animal models and populations aged ≥60 years were included, with 56 articles retained for narrative synthesis.
KEY FINDINGS: Aging drives gut dysbiosis characterized by depletion of short-chain fatty acid (SCFA)-producing bacteria, accumulation of lipopolysaccharide (LPS) and trimethylamine N-oxide (TMAO), and disrupted bile acid metabolism. These alterations compromise intestinal barrier integrity and induce chronic low-grade inflammation, ultimately shifting the osteoblast-osteoclast balance toward bone resorption. Exercise training and dietary fiber supplementation can partially reverse these changes by elevating SCFA levels, suppressing NF-κB-mediated inflammatory pathways, and restoring intestinal barrier function. However, the translational gap between animal models and elderly populations, confounding effects of polypharmacy, poor long-term adherence, and inter-individual baseline differences constitute major barriers to translating mechanistic evidence into clinical rehabilitation.
CLINICAL IMPLICATIONS: Baseline gut microbial status may be a core predictor of rehabilitation response, though this hypothesis requires prospective cohort validation. A stratified rehabilitation strategy based on microbial typing-"sensitive" individuals receiving standard protocols and "resistant" individuals receiving combined microbiome-targeted adjunctive therapy (including specific probiotic strains or synbiotics)-offers an actionable research direction for precision rehabilitation. Candidate stratification biomarkers such as the fecal SCFA-to-calprotectin ratio require prospective validation, and the development of home-detectable biomarkers remains a critical translational priority. The clinical translation of this framework depends on the accumulation of long-term follow-up data and the resolution of implementation barriers in real-world primary care settings. Notably, the mechanistic evidence underpinning this framework derives predominantly from animal and in vitro studies (high mechanistic certainty, low translational certainty), whereas clinical trial evidence remains limited to small, short-term, predominantly exploratory trials (low to moderate certainty for efficacy, very low for precision targeting); prospective clinical validation is therefore essential before routine implementation.
Additional Links: PMID-42746595
PubMed:
Citation:
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@article {pmid42746595,
year = {2026},
author = {Tu, M and Jiang, W and Huang, Y},
title = {Gut Microbial Metabolites as a Bridge in Osteoporotic Rehabilitation for the Elderly: From Aging-Related Dysbiosis to Precision Non-Pharmacological Strategies.},
journal = {International journal of general medicine},
volume = {19},
number = {},
pages = {637308},
pmid = {42746595},
issn = {1178-7074},
abstract = {BACKGROUND AND OBJECTIVE: Osteoporosis in the elderly represents a major public health challenge in aging societies. Although non-pharmacological rehabilitation has become a core intervention strategy, standard protocols yield highly variable responses across individuals. This review aims to systematically examine the bridging role of gut microbial metabolites in the pathogenesis and rehabilitation of osteoporosis in the elderly, explore the hypothesis that baseline microbial status influences the heterogeneity of rehabilitation outcomes, and propose a microbiota-targeted precision rehabilitation framework for older populations.
METHODS: This narrative review systematically searched PubMed, Web of Science, Embase, Cochrane Library, Scopus, and CINAHL databases (January 2016 to May 2026). Original studies and reviews on naturally aged animal models and populations aged ≥60 years were included, with 56 articles retained for narrative synthesis.
KEY FINDINGS: Aging drives gut dysbiosis characterized by depletion of short-chain fatty acid (SCFA)-producing bacteria, accumulation of lipopolysaccharide (LPS) and trimethylamine N-oxide (TMAO), and disrupted bile acid metabolism. These alterations compromise intestinal barrier integrity and induce chronic low-grade inflammation, ultimately shifting the osteoblast-osteoclast balance toward bone resorption. Exercise training and dietary fiber supplementation can partially reverse these changes by elevating SCFA levels, suppressing NF-κB-mediated inflammatory pathways, and restoring intestinal barrier function. However, the translational gap between animal models and elderly populations, confounding effects of polypharmacy, poor long-term adherence, and inter-individual baseline differences constitute major barriers to translating mechanistic evidence into clinical rehabilitation.
CLINICAL IMPLICATIONS: Baseline gut microbial status may be a core predictor of rehabilitation response, though this hypothesis requires prospective cohort validation. A stratified rehabilitation strategy based on microbial typing-"sensitive" individuals receiving standard protocols and "resistant" individuals receiving combined microbiome-targeted adjunctive therapy (including specific probiotic strains or synbiotics)-offers an actionable research direction for precision rehabilitation. Candidate stratification biomarkers such as the fecal SCFA-to-calprotectin ratio require prospective validation, and the development of home-detectable biomarkers remains a critical translational priority. The clinical translation of this framework depends on the accumulation of long-term follow-up data and the resolution of implementation barriers in real-world primary care settings. Notably, the mechanistic evidence underpinning this framework derives predominantly from animal and in vitro studies (high mechanistic certainty, low translational certainty), whereas clinical trial evidence remains limited to small, short-term, predominantly exploratory trials (low to moderate certainty for efficacy, very low for precision targeting); prospective clinical validation is therefore essential before routine implementation.},
}
RevDate: 2026-09-16
The Relationship Between the Gut Microbiome and Executive Function in Adolescents With Overweight and Obesity.
Journal of paediatrics and child health [Epub ahead of print].
OBJECTIVES: Excess weight affects both brain structure and function. Among the structures affected by excess weight, the prefrontal cortex, a key structure for executive functions, appears to be especially vulnerable. Beyond genetic, cognitive and social factors, recent research has highlighted the role of the gut microbiome on excess weight.
METHODS: In this cross-sectional study, the relationship between gut microbiome composition and executive functioning was assessed in adolescents classified into obesity, overweight and normoweight groups according to their body mass index.
RESULTS: Genera Bacteroides and Ruthenibacterium were more abundant in controls with normoweight compared to participants with overweight. Genus Alistipes was more abundant in controls with normoweight compared to participants with obesity. The Shannon's alpha diversity index was negatively correlated with the inhibition index of the Five Digit Test in participants with overweight. The Firmicutes/Bacteroidetes ratio was negatively correlated with the number of commission errors of the Continuous Performance Test in participants with obesity. Further, several components of the microbiome were differentially related to executive functions depending on weight status.
CONCLUSIONS: Our results suggest that the microbiome composition differs between adolescents with different weight status. Further, the relative abundance of specific members of the microbiome is related to executive function.
Additional Links: PMID-42747142
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PubMed:
Citation:
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@article {pmid42747142,
year = {2026},
author = {Caldú, X and Jurado, MÁ and Prunell-Castañé, A and Sánchez-Garre, C and Sender-Palacios, MJ and Garolera, M},
title = {The Relationship Between the Gut Microbiome and Executive Function in Adolescents With Overweight and Obesity.},
journal = {Journal of paediatrics and child health},
volume = {},
number = {},
pages = {},
doi = {10.1111/jpc.70596},
pmid = {42747142},
issn = {1440-1754},
support = {//European Regional Development Fund/ ; PRE2019-087430//Ministerio de Ciencia, Innovación y Universidades/ ; PSI2017-86536-C2-1-R//Ministerios de Economía, Industria y Competitividad/ ; PSI2017-86536-C2-2-R//Ministerios de Economía, Industria y Competitividad/ ; },
abstract = {OBJECTIVES: Excess weight affects both brain structure and function. Among the structures affected by excess weight, the prefrontal cortex, a key structure for executive functions, appears to be especially vulnerable. Beyond genetic, cognitive and social factors, recent research has highlighted the role of the gut microbiome on excess weight.
METHODS: In this cross-sectional study, the relationship between gut microbiome composition and executive functioning was assessed in adolescents classified into obesity, overweight and normoweight groups according to their body mass index.
RESULTS: Genera Bacteroides and Ruthenibacterium were more abundant in controls with normoweight compared to participants with overweight. Genus Alistipes was more abundant in controls with normoweight compared to participants with obesity. The Shannon's alpha diversity index was negatively correlated with the inhibition index of the Five Digit Test in participants with overweight. The Firmicutes/Bacteroidetes ratio was negatively correlated with the number of commission errors of the Continuous Performance Test in participants with obesity. Further, several components of the microbiome were differentially related to executive functions depending on weight status.
CONCLUSIONS: Our results suggest that the microbiome composition differs between adolescents with different weight status. Further, the relative abundance of specific members of the microbiome is related to executive function.},
}
RevDate: 2026-09-16
Prevotella-dominated dysbiosis and predicted suppression of sulfur biosynthesis pathways associated with halitosis in Korean adults.
Microbiology spectrum [Epub ahead of print].
Halitosis affects a substantial proportion of adults worldwide, yet the compositional and functional basis of the oral microbiome in halitosis remains incompletely understood, particularly in East Asian populations. We performed 16S rRNA gene amplicon sequencing of oral gargle samples from 45 individuals with halitosis and 45 healthy controls in South Korea, generating approximately 4,600 amplicon sequence variants. Beta diversity analysis revealed significant community-level separation (PERMANOVA, P = 0.001) and an elevated Firmicutes/Bacteroidota ratio in halitosis, although alpha diversity did not differ between groups. Because the halitosis group was significantly older than controls, age-adjusted PERMANOVA and age-matched sensitivity analyses confirmed that separation persisted independent of age (age-adjusted R[2] = 0.030, P = 0.003). Halitosis-associated microbiomes were enriched for Prevotella melaninogenica and Peptostreptococcus stomatis, whereas healthy microbiomes were distinguished by Haemophilus parainfluenzae and Veillonella rogosae (LEfSe). Functional profiling using PICRUSt2 revealed a counterintuitive, predicted suppression of sulfur metabolism in halitosis: pathways for sulfate assimilation, cysteine, and methionine biosynthesis were predicted to be significantly reduced relative to healthy controls. This predicted shift was significantly inversely correlated with directly measured volatile sulfur compounds (H2S and methyl mercaptan; Spearman ρ = -0.54 and -0.64, both P < 0.0001), providing phenotypic support for the predicted signature. These findings suggest healthy oral microbiomes efficiently channel sulfur into anabolic pathways, whereas dysbiotic microbiomes may lose this capacity, allowing volatile sulfur compounds to accumulate. Our study provides a species-resolved, functionally annotated reference framework for halitosis-associated oral dysbiosis in a Korean cohort, and identifies candidate targets for diagnosis and intervention.IMPORTANCEHalitosis (bad breath) affects up to 30% of adults worldwide and is caused by volatile sulfur compounds (VSCs) produced by oral bacteria, yet the underlying microbial mechanisms remain poorly understood. Our study of 90 Korean adults reveals that halitosis is associated not only with an overgrowth of Prevotella species but also with a predicted, paradoxical suppression of the microbial community's capacity to assimilate sulfur into anabolic biosynthetic pathways. This predicted "sulfur assimilation failure" was associated with elevated VSC accumulation, supporting a reframing of halitosis as a community-level metabolic dysfunction rather than simple bacterial overproduction. These findings have direct clinical implications: the identified Prevotella-dominated dysbiosis and associated sulfur pathway signatures represent candidate biomarkers for objective halitosis diagnosis, and the restoration of microbial sulfur-channeling capacity offers a rational target for probiotic and prebiotic interventions. This work also contributes a well-characterized oral microbiome reference data set from an underrepresented East Asian population.
Additional Links: PMID-42747185
Publisher:
PubMed:
Citation:
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@article {pmid42747185,
year = {2026},
author = {Eom, J-H and Cho, M-Y and Kim, J-W and Kim, Y and Yang, S-J and Hwang, J and Lee, D and Kim, H-S and Baek, H and Kim, Y-Y},
title = {Prevotella-dominated dysbiosis and predicted suppression of sulfur biosynthesis pathways associated with halitosis in Korean adults.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0090626},
doi = {10.1128/spectrum.00906-26},
pmid = {42747185},
issn = {2165-0497},
abstract = {Halitosis affects a substantial proportion of adults worldwide, yet the compositional and functional basis of the oral microbiome in halitosis remains incompletely understood, particularly in East Asian populations. We performed 16S rRNA gene amplicon sequencing of oral gargle samples from 45 individuals with halitosis and 45 healthy controls in South Korea, generating approximately 4,600 amplicon sequence variants. Beta diversity analysis revealed significant community-level separation (PERMANOVA, P = 0.001) and an elevated Firmicutes/Bacteroidota ratio in halitosis, although alpha diversity did not differ between groups. Because the halitosis group was significantly older than controls, age-adjusted PERMANOVA and age-matched sensitivity analyses confirmed that separation persisted independent of age (age-adjusted R[2] = 0.030, P = 0.003). Halitosis-associated microbiomes were enriched for Prevotella melaninogenica and Peptostreptococcus stomatis, whereas healthy microbiomes were distinguished by Haemophilus parainfluenzae and Veillonella rogosae (LEfSe). Functional profiling using PICRUSt2 revealed a counterintuitive, predicted suppression of sulfur metabolism in halitosis: pathways for sulfate assimilation, cysteine, and methionine biosynthesis were predicted to be significantly reduced relative to healthy controls. This predicted shift was significantly inversely correlated with directly measured volatile sulfur compounds (H2S and methyl mercaptan; Spearman ρ = -0.54 and -0.64, both P < 0.0001), providing phenotypic support for the predicted signature. These findings suggest healthy oral microbiomes efficiently channel sulfur into anabolic pathways, whereas dysbiotic microbiomes may lose this capacity, allowing volatile sulfur compounds to accumulate. Our study provides a species-resolved, functionally annotated reference framework for halitosis-associated oral dysbiosis in a Korean cohort, and identifies candidate targets for diagnosis and intervention.IMPORTANCEHalitosis (bad breath) affects up to 30% of adults worldwide and is caused by volatile sulfur compounds (VSCs) produced by oral bacteria, yet the underlying microbial mechanisms remain poorly understood. Our study of 90 Korean adults reveals that halitosis is associated not only with an overgrowth of Prevotella species but also with a predicted, paradoxical suppression of the microbial community's capacity to assimilate sulfur into anabolic biosynthetic pathways. This predicted "sulfur assimilation failure" was associated with elevated VSC accumulation, supporting a reframing of halitosis as a community-level metabolic dysfunction rather than simple bacterial overproduction. These findings have direct clinical implications: the identified Prevotella-dominated dysbiosis and associated sulfur pathway signatures represent candidate biomarkers for objective halitosis diagnosis, and the restoration of microbial sulfur-channeling capacity offers a rational target for probiotic and prebiotic interventions. This work also contributes a well-characterized oral microbiome reference data set from an underrepresented East Asian population.},
}
RevDate: 2026-09-16
Seasonal Gut Microbiome Variation Associated With Both Climate and Wildlife Tourism in Asian Elephants (Elephas maximus).
Integrative zoology [Epub ahead of print].
The health, survival, and fitness of wild animals depend on their responses to seasonal variation in natural and anthropogenic environmental factors. The gut microbiome is a unique, non-invasive tool for assessing the magnitude of these responses, but few studies collect longitudinal gut microbiome data from wild populations. Here, we begin to address this gap in a population of Asian elephants in Sri Lanka that experience variation in both natural and anthropogenic factors across seasons. Using 16S rRNA gene amplicon data from elephants in two national parks collected over 6 months, we test the hypothesis that Asian elephant gut microbiome composition varies across months in association with both climate and tourist activity. We find that both national park and sampling month are associated with significant differences in elephant gut microbiome composition, and a portion of the observed temporal variation is associated with tourist vehicle traffic. These results provide an important foundation from which to build knowledge regarding how natural and anthropogenic factors interact with and affect elephant health.
Additional Links: PMID-42747284
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PubMed:
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@article {pmid42747284,
year = {2026},
author = {Amato, KR and Kelleher, E and Savo Sardaro, ML and Jayarathna, KHDL and Jayawardena, PDPJ and Warnapura, AGSM and LaDue, CA and Vandercone, R},
title = {Seasonal Gut Microbiome Variation Associated With Both Climate and Wildlife Tourism in Asian Elephants (Elephas maximus).},
journal = {Integrative zoology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1749-4877.70174},
pmid = {42747284},
issn = {1749-4877},
abstract = {The health, survival, and fitness of wild animals depend on their responses to seasonal variation in natural and anthropogenic environmental factors. The gut microbiome is a unique, non-invasive tool for assessing the magnitude of these responses, but few studies collect longitudinal gut microbiome data from wild populations. Here, we begin to address this gap in a population of Asian elephants in Sri Lanka that experience variation in both natural and anthropogenic factors across seasons. Using 16S rRNA gene amplicon data from elephants in two national parks collected over 6 months, we test the hypothesis that Asian elephant gut microbiome composition varies across months in association with both climate and tourist activity. We find that both national park and sampling month are associated with significant differences in elephant gut microbiome composition, and a portion of the observed temporal variation is associated with tourist vehicle traffic. These results provide an important foundation from which to build knowledge regarding how natural and anthropogenic factors interact with and affect elephant health.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Enterocloster citroniae and related gut microbiome species modulate Vibrio cholerae biofilm formation through the production of bioactive small molecules.
Virulence, 17(1):2712696.
Cholera is a diarrheal disease that affects millions of people globally. Although the causative agent, Vibrio cholerae, has been extensively studied in isolation, investigation of its interactions with the gut microbiota started relatively recently. We and others previously showed that microbiota-derived metabolites significantly influence V. cholerae behavior. By investigating how an organic extract of human feces affects V. cholerae gene expression, we showed that gut metabolites strongly suppress swimming motility, a trait important for host colonization. Interestingly, extracts of pure cultures of a gut commensal, Enterocloster citroniae, recapitulated this inhibition. Here, we present a comprehensive examination of the effect of small molecules produced by E. citroniae and related species on V. cholerae behavior. We show that E. citroniae small molecules inhibit motility by various V. cholerae strains, and that several phylogenetically related species produce this activity, although the magnitude of the effect varies between strains. Using biofilm formation assays in static and flow conditions, we show that V. cholerae strongly induces biofilm formation in response to E. citroniae metabolites. Transcriptome and reporter analyses showed that several genes involved in the synthesis of an extracellular polysaccharide are induced by E. citroniae metabolites. Finally, we show that V. cholerae interactions with host cells are also modulated by this commensal. These findings advance our understanding of microbiome-pathogen interactions and how commensal bacteria influence V. cholerae virulence through the production of small molecules. In the future, this knowledge may be used to design novel microbiome-based therapeutic approaches to combat cholera and other infections.
Additional Links: PMID-42747286
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@article {pmid42747286,
year = {2026},
author = {Pauer, H and Nasiri, S and Magalhães, NS and Nguyen, VT and Ferreira, NV and Ferreira, LDS and Bradshaw, AB and Kirby, KE and Sabapathy, T and Udensi, CG and Feofanova, V and Moreira, DA and Parente, TE and Wilde, J and Pride, DT and Allen-Vercoe, E and Antunes, LCM},
title = {Enterocloster citroniae and related gut microbiome species modulate Vibrio cholerae biofilm formation through the production of bioactive small molecules.},
journal = {Virulence},
volume = {17},
number = {1},
pages = {2712696},
doi = {10.1080/21505594.2026.2712696},
pmid = {42747286},
issn = {2150-5608},
mesh = {*Vibrio cholerae/drug effects/physiology/genetics/pathogenicity ; *Biofilms/growth & development/drug effects ; Humans ; *Gastrointestinal Microbiome ; Gene Expression Regulation, Bacterial ; Cholera/microbiology ; },
abstract = {Cholera is a diarrheal disease that affects millions of people globally. Although the causative agent, Vibrio cholerae, has been extensively studied in isolation, investigation of its interactions with the gut microbiota started relatively recently. We and others previously showed that microbiota-derived metabolites significantly influence V. cholerae behavior. By investigating how an organic extract of human feces affects V. cholerae gene expression, we showed that gut metabolites strongly suppress swimming motility, a trait important for host colonization. Interestingly, extracts of pure cultures of a gut commensal, Enterocloster citroniae, recapitulated this inhibition. Here, we present a comprehensive examination of the effect of small molecules produced by E. citroniae and related species on V. cholerae behavior. We show that E. citroniae small molecules inhibit motility by various V. cholerae strains, and that several phylogenetically related species produce this activity, although the magnitude of the effect varies between strains. Using biofilm formation assays in static and flow conditions, we show that V. cholerae strongly induces biofilm formation in response to E. citroniae metabolites. Transcriptome and reporter analyses showed that several genes involved in the synthesis of an extracellular polysaccharide are induced by E. citroniae metabolites. Finally, we show that V. cholerae interactions with host cells are also modulated by this commensal. These findings advance our understanding of microbiome-pathogen interactions and how commensal bacteria influence V. cholerae virulence through the production of small molecules. In the future, this knowledge may be used to design novel microbiome-based therapeutic approaches to combat cholera and other infections.},
}
MeSH Terms:
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hide MeSH Terms
*Vibrio cholerae/drug effects/physiology/genetics/pathogenicity
*Biofilms/growth & development/drug effects
Humans
*Gastrointestinal Microbiome
Gene Expression Regulation, Bacterial
Cholera/microbiology
RevDate: 2026-09-16
CmpDate: 2026-09-16
Gut microbiota functional remodeling and butyrate depletion amplify anti-Ro/La antibody-driven type I interferon activation in neonatal lupus.
Gut microbes, 18(1):2728464.
The early-life gut microbiome may influence susceptibility to antibody-mediated neonatal autoimmunity, but the underlying mechanisms remain poorly understood. We investigated whether gut microbial functional capacity and metabolites influence autoantibody-dependent immune activation in 90 neonates, including healthy controls, anti-Ro/La-exposed neonates without neonatal lupus erythematosus (No-NLE), and neonates with NLE (n = 30 per group). Shotgun metagenomic profiling demonstrated progressive remodeling of the neonatal gut microbiome across the three groups, with anti-Ro/La exposure associated with depletion of early-life commensal-associated taxa, including Bifidobacterium, Rothia, and Clostridium, and enrichment of taxa with opportunistic potential, including Klebsiella and Enterococcus, with greatest ecological divergence in neonates with NLE. Functional profiling identified altered microbial carbohydrate-processing capacity, marked by enrichment of glycosyltransferase family 4 (GT4) and depletion of GT2 in NLE. These alterations coincided with broad reductions in plasma short-chain fatty acid metabolites, most prominently butyrate, together with increased serum immunoglobulin G (IgG) and interferon-α (IFN-α) and decreased complement component 4 (C4). A GT4-Klebsiella-Rothia-IFN-α signature distinguished NLE from No-NLE (AUC = 0.883; 95% CI, 0.799-0.967). In functional assays, pooled bacteria-depleted fecal filtrates from neonates with NLE potentiated IFN-α production by neonatal peripheral blood mononuclear cells in the presence of anti-Ro/La-positive plasma. Conversely, sodium butyrate suppressed anti-Ro/La-associated IFN-α production and reduced 28 inflammation-related proteins, including CXCL10, ADA, and PD-L1, involved in cytokine, IL-17, and TNF signaling. Together, these findings provide functional evidence supporting a microbiota-associated butyrate-type I interferon pathway that may amplify maternal autoantibody-dependent immune activation and contribute to the clinical manifestation of NLE.
Additional Links: PMID-42747315
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PubMed:
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@article {pmid42747315,
year = {2026},
author = {Sun, W and Li, Y and Liu, X and Yu, S and Li, W and Wang, H and Geng, H and Li, L and Hu, J and Huo, J and Zhang, W and Fu, J and Jin, X and Li, H and Zhou, X and Zhu, X},
title = {Gut microbiota functional remodeling and butyrate depletion amplify anti-Ro/La antibody-driven type I interferon activation in neonatal lupus.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2728464},
doi = {10.1080/19490976.2026.2728464},
pmid = {42747315},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Interferon Type I/immunology ; Infant, Newborn ; *Autoantibodies/immunology/blood ; *Lupus Erythematosus, Systemic/immunology/microbiology ; *Butyrates/metabolism ; Female ; Bacteria/classification/genetics/isolation & purification/metabolism ; Male ; },
abstract = {The early-life gut microbiome may influence susceptibility to antibody-mediated neonatal autoimmunity, but the underlying mechanisms remain poorly understood. We investigated whether gut microbial functional capacity and metabolites influence autoantibody-dependent immune activation in 90 neonates, including healthy controls, anti-Ro/La-exposed neonates without neonatal lupus erythematosus (No-NLE), and neonates with NLE (n = 30 per group). Shotgun metagenomic profiling demonstrated progressive remodeling of the neonatal gut microbiome across the three groups, with anti-Ro/La exposure associated with depletion of early-life commensal-associated taxa, including Bifidobacterium, Rothia, and Clostridium, and enrichment of taxa with opportunistic potential, including Klebsiella and Enterococcus, with greatest ecological divergence in neonates with NLE. Functional profiling identified altered microbial carbohydrate-processing capacity, marked by enrichment of glycosyltransferase family 4 (GT4) and depletion of GT2 in NLE. These alterations coincided with broad reductions in plasma short-chain fatty acid metabolites, most prominently butyrate, together with increased serum immunoglobulin G (IgG) and interferon-α (IFN-α) and decreased complement component 4 (C4). A GT4-Klebsiella-Rothia-IFN-α signature distinguished NLE from No-NLE (AUC = 0.883; 95% CI, 0.799-0.967). In functional assays, pooled bacteria-depleted fecal filtrates from neonates with NLE potentiated IFN-α production by neonatal peripheral blood mononuclear cells in the presence of anti-Ro/La-positive plasma. Conversely, sodium butyrate suppressed anti-Ro/La-associated IFN-α production and reduced 28 inflammation-related proteins, including CXCL10, ADA, and PD-L1, involved in cytokine, IL-17, and TNF signaling. Together, these findings provide functional evidence supporting a microbiota-associated butyrate-type I interferon pathway that may amplify maternal autoantibody-dependent immune activation and contribute to the clinical manifestation of NLE.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
*Interferon Type I/immunology
Infant, Newborn
*Autoantibodies/immunology/blood
*Lupus Erythematosus, Systemic/immunology/microbiology
*Butyrates/metabolism
Female
Bacteria/classification/genetics/isolation & purification/metabolism
Male
RevDate: 2026-09-16
Cross-domain cooperation drives nutrient acquisition and metabolism in the bark beetle holobiont.
The ISME journal pii:8802131 [Epub ahead of print].
Microbial symbiosis underpins host adaptation, yet mechanisms of metabolic integration in holobionts remain unclear. Using metatranscriptomics, genomics, and metabolic assays, we investigated gut microbiome interactions in the European spruce bark beetle (Ips typographus). We observed metabolic complementarity among symbionts and host, forming cross-domain networks that support nutrient acquisition. Nitrogen recycling revealed strong interdependence: no single partner possessed a complete uric acid degradation pathway, but combined evidence supports a distributed pathway spanning beetle, Bacteria, and fungi. Additionally, bacterial nitrate reduction to ammonia indicates a potential nitrogen influx, making otherwise inaccessible inorganic nitrogen available to the host. Shaped by microbial interactions, symbionts also likely supply specific amino acids, while vitamin metabolism showed cross-domain co-metabolism, with Bacteria as main producers of B vitamins, while host and fungi modulated interconversion. Carbohydrate degradation was highly partitioned; bacteria target xylan and pectin, while fungi contribute to glucan breakdown. Crucially, our data provide indirect evidence that the beetle may contribute to complete cellulose degradation, highlighting an underappreciated host role in lignocellulose processing. In terms of enzymatic functional diversity, the bacteriome emerged as the most important microbiome component-an observation that contrasts with the traditional focus on fungi and underscores the need to consider bacterial contributions in insect symbioses. Despite life-stage variation, core metabolic functions remained stable. Overall, metabolic interdependence, rather than microbial composition alone, structures holobiont function. These results highlight functional redundancy and ecological resilience, emphasizing the importance of microbial cooperation and host-microbe metabolic evolution.
Additional Links: PMID-42747345
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@article {pmid42747345,
year = {2026},
author = {Saati-Santamaría, Z and Veselská, T and Švec, K and Kostovčík, M and Peral-Aranega, E and Křížková, B and García-Fraile, P and Kolařík, M},
title = {Cross-domain cooperation drives nutrient acquisition and metabolism in the bark beetle holobiont.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag227},
pmid = {42747345},
issn = {1751-7370},
abstract = {Microbial symbiosis underpins host adaptation, yet mechanisms of metabolic integration in holobionts remain unclear. Using metatranscriptomics, genomics, and metabolic assays, we investigated gut microbiome interactions in the European spruce bark beetle (Ips typographus). We observed metabolic complementarity among symbionts and host, forming cross-domain networks that support nutrient acquisition. Nitrogen recycling revealed strong interdependence: no single partner possessed a complete uric acid degradation pathway, but combined evidence supports a distributed pathway spanning beetle, Bacteria, and fungi. Additionally, bacterial nitrate reduction to ammonia indicates a potential nitrogen influx, making otherwise inaccessible inorganic nitrogen available to the host. Shaped by microbial interactions, symbionts also likely supply specific amino acids, while vitamin metabolism showed cross-domain co-metabolism, with Bacteria as main producers of B vitamins, while host and fungi modulated interconversion. Carbohydrate degradation was highly partitioned; bacteria target xylan and pectin, while fungi contribute to glucan breakdown. Crucially, our data provide indirect evidence that the beetle may contribute to complete cellulose degradation, highlighting an underappreciated host role in lignocellulose processing. In terms of enzymatic functional diversity, the bacteriome emerged as the most important microbiome component-an observation that contrasts with the traditional focus on fungi and underscores the need to consider bacterial contributions in insect symbioses. Despite life-stage variation, core metabolic functions remained stable. Overall, metabolic interdependence, rather than microbial composition alone, structures holobiont function. These results highlight functional redundancy and ecological resilience, emphasizing the importance of microbial cooperation and host-microbe metabolic evolution.},
}
RevDate: 2026-09-16
CmpDate: 2026-09-16
Time to rethink prevention of neonatal group B streptococcal disease.
Seminars in immunopathology, 48(1):.
Group B Streptococci (GBS) are both natural colonizers and important invasive pathogens in newborns. The introduction of intrapartum antibiotic prophylaxis has led to a significant decrease in the incidence of early onset sepsis. In contrast, late onset sepsis, which accounts for up to 50% of cases, has not declined. IAP impacts microbiome development during infancy, specifically it reduces the abundance of Bifidobacterium and Bacteroides spp., which might be associated with long-term health outcomes such as asthma development and obesity. This review highlights the challenges and risks associated with GBS colonization in neonates, including the role of virulence factors and specific contribution of host immunity. Bacterial pathogenicity factors involved in adhesion and colonization, e.g. GBS pilus islands, barrier disruption, e.g. pore-forming toxin ß-hemolysin, or evasion of neonatal immune defense mediated by GBS capsular polysaccharide and membrane glycolipids are important targets to suppress the translocation of GBS and progression to invasive disease. In line with this, metabolic programming of neonatal immune cells, e.g. glycolytic capacity, is GBS strain-specific which also argues for a more tailored strategy of prevention. Given the benefits and risks of IAP, it is important to rethink strategies of preventing GBS disease including alternative strategies such as vaccination and probiotic supplementation. Further studies need to focus on modulating the developing immune-microbiome interplay including the metabolic milieu to the advantage of the vulnerable newborn.
Additional Links: PMID-42747473
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Citation:
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@article {pmid42747473,
year = {2026},
author = {Teuscher, JL and Lohrmann, F and Herting, E and Sugihara, F and Henneke, P and Härtel, C},
title = {Time to rethink prevention of neonatal group B streptococcal disease.},
journal = {Seminars in immunopathology},
volume = {48},
number = {1},
pages = {},
pmid = {42747473},
issn = {1863-2300},
mesh = {Humans ; *Streptococcus agalactiae/immunology ; *Streptococcal Infections/prevention & control/microbiology/epidemiology/immunology ; Infant, Newborn ; Antibiotic Prophylaxis ; Animals ; Host-Pathogen Interactions/immunology ; Virulence Factors ; Microbiota ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Group B Streptococci (GBS) are both natural colonizers and important invasive pathogens in newborns. The introduction of intrapartum antibiotic prophylaxis has led to a significant decrease in the incidence of early onset sepsis. In contrast, late onset sepsis, which accounts for up to 50% of cases, has not declined. IAP impacts microbiome development during infancy, specifically it reduces the abundance of Bifidobacterium and Bacteroides spp., which might be associated with long-term health outcomes such as asthma development and obesity. This review highlights the challenges and risks associated with GBS colonization in neonates, including the role of virulence factors and specific contribution of host immunity. Bacterial pathogenicity factors involved in adhesion and colonization, e.g. GBS pilus islands, barrier disruption, e.g. pore-forming toxin ß-hemolysin, or evasion of neonatal immune defense mediated by GBS capsular polysaccharide and membrane glycolipids are important targets to suppress the translocation of GBS and progression to invasive disease. In line with this, metabolic programming of neonatal immune cells, e.g. glycolytic capacity, is GBS strain-specific which also argues for a more tailored strategy of prevention. Given the benefits and risks of IAP, it is important to rethink strategies of preventing GBS disease including alternative strategies such as vaccination and probiotic supplementation. Further studies need to focus on modulating the developing immune-microbiome interplay including the metabolic milieu to the advantage of the vulnerable newborn.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Streptococcus agalactiae/immunology
*Streptococcal Infections/prevention & control/microbiology/epidemiology/immunology
Infant, Newborn
Antibiotic Prophylaxis
Animals
Host-Pathogen Interactions/immunology
Virulence Factors
Microbiota
Anti-Bacterial Agents/therapeutic use
RevDate: 2026-09-16
CmpDate: 2026-09-16
Castration-resistant prostate cancer as an adaptive tumor ecosystem: coupling tumor evolution with microenvironmental reprogramming.
Cancer metastasis reviews, 45(4):.
Castration-resistant prostate cancer (CRPC) represents a lethal stage of prostate cancer that emerges following sustained androgen deprivation therapy (ADT) and remains a major clinical challenge in the era of androgen receptor (AR)-targeted therapies. Although AR reactivation and lineage plasticity are recognized as central mechanisms of resistance, these tumor-intrinsic processes alone cannot fully explain the profound heterogeneity and therapeutic failure observed during CRPC evolution. Here, integrating recent advances in single-cell and spatial profiling, we propose a unified framework in which CRPC is viewed as an adaptive tumor ecosystem shaped by evolutionary selection, cellular plasticity, and microenvironmental co-evolution under therapeutic pressure. ADT not only selects pre-existing resistant populations but also induces cellular reprogramming, expanding tumor state diversity and adaptive capacity. Concurrently, the tumor microenvironment is extensively remodeled to support and stabilize therapy-adapted states. Immune compartments evolve toward myeloid-dominant immunosuppressive configurations characterized by T cell dysfunction and exclusion, whereas cancer-associated fibroblasts (CAFs) promote tumor persistence through stromal remodeling, metabolic coupling, and alternative steroidogenic pathways. Neural remodeling represents an additional regulatory layer that enhances cellular plasticity, stress adaptation, and neuroendocrine differentiation. Together, these alterations establish a multicompartmental and self-reinforcing tumor-microenvironment network that sustains adaptation during AR suppression. This ecosystem framework further extends beyond the primary tumor to distal niches, including bone metastases and the gut microbiome, where tumor-osteoblast-osteoclast interactions and microbial regulation of androgen metabolism and immunity contribute to therapeutic adaptation. By integrating tumor evolution with immune, stromal, neural, and distal ecosystem remodeling, this perspective provides a system-level framework for understanding CRPC progression and highlights therapeutic strategies aimed at reprogramming or destabilizing adaptive tumor ecosystems rather than targeting individual resistance pathways alone.
Additional Links: PMID-42747576
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Citation:
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@article {pmid42747576,
year = {2026},
author = {Wang, S and Xu, X and Xu, M and Wei, Y and Qiao, Y and Song, X and Xie, C and Zhou, C and Yuan, F},
title = {Castration-resistant prostate cancer as an adaptive tumor ecosystem: coupling tumor evolution with microenvironmental reprogramming.},
journal = {Cancer metastasis reviews},
volume = {45},
number = {4},
pages = {},
pmid = {42747576},
issn = {1573-7233},
mesh = {Humans ; *Tumor Microenvironment ; Male ; *Prostatic Neoplasms, Castration-Resistant/pathology/drug therapy/immunology/metabolism ; Animals ; Cellular Reprogramming ; Receptors, Androgen/metabolism ; },
abstract = {Castration-resistant prostate cancer (CRPC) represents a lethal stage of prostate cancer that emerges following sustained androgen deprivation therapy (ADT) and remains a major clinical challenge in the era of androgen receptor (AR)-targeted therapies. Although AR reactivation and lineage plasticity are recognized as central mechanisms of resistance, these tumor-intrinsic processes alone cannot fully explain the profound heterogeneity and therapeutic failure observed during CRPC evolution. Here, integrating recent advances in single-cell and spatial profiling, we propose a unified framework in which CRPC is viewed as an adaptive tumor ecosystem shaped by evolutionary selection, cellular plasticity, and microenvironmental co-evolution under therapeutic pressure. ADT not only selects pre-existing resistant populations but also induces cellular reprogramming, expanding tumor state diversity and adaptive capacity. Concurrently, the tumor microenvironment is extensively remodeled to support and stabilize therapy-adapted states. Immune compartments evolve toward myeloid-dominant immunosuppressive configurations characterized by T cell dysfunction and exclusion, whereas cancer-associated fibroblasts (CAFs) promote tumor persistence through stromal remodeling, metabolic coupling, and alternative steroidogenic pathways. Neural remodeling represents an additional regulatory layer that enhances cellular plasticity, stress adaptation, and neuroendocrine differentiation. Together, these alterations establish a multicompartmental and self-reinforcing tumor-microenvironment network that sustains adaptation during AR suppression. This ecosystem framework further extends beyond the primary tumor to distal niches, including bone metastases and the gut microbiome, where tumor-osteoblast-osteoclast interactions and microbial regulation of androgen metabolism and immunity contribute to therapeutic adaptation. By integrating tumor evolution with immune, stromal, neural, and distal ecosystem remodeling, this perspective provides a system-level framework for understanding CRPC progression and highlights therapeutic strategies aimed at reprogramming or destabilizing adaptive tumor ecosystems rather than targeting individual resistance pathways alone.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Tumor Microenvironment
Male
*Prostatic Neoplasms, Castration-Resistant/pathology/drug therapy/immunology/metabolism
Animals
Cellular Reprogramming
Receptors, Androgen/metabolism
RevDate: 2026-09-16
CmpDate: 2026-09-16
Gut Dysbiosis, Sex, and Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysms.
Current atherosclerosis reports, 28(1):.
PURPOSE OF REVIEW: This paper reviews the present literature on how sex-related differences in gut dysbiosis influence vascular smooth muscle cell behavior in the pathogenesis of abdominal aortic aneurysms.
RECENT FINDINGS: Emerging research has linked gut microbial metabolites, such as trimethylamine oxide and phenylacetyl glutamine, to abdominal aortic aneurysm pathogenesis via inflammation and vascular damage. Sex hormones also directly influence vascular smooth muscle cell phenotype switching, as estrogen has been found to be protective, while testosterone may enhance inflammation. Novel biomarkers and molecular regulators have emerged as potential targets, revealing new avenues for abdominal aortic aneurysm treatment. Gut dysbiosis contributes to abdominal aortic aneurysm progression through inflammation, vascular smooth muscle cell dysfunction, and immune activation. These effects vary by sex and are influenced by sex hormones and structural differences in vascular smooth muscle cells but require further investigation to establish a clear relationship.
Additional Links: PMID-42747626
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@article {pmid42747626,
year = {2026},
author = {Hatcher, G and Kazaleh, M and Patil, R and Ailawadi, G and Salmon, M},
title = {Gut Dysbiosis, Sex, and Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysms.},
journal = {Current atherosclerosis reports},
volume = {28},
number = {1},
pages = {},
pmid = {42747626},
issn = {1534-6242},
mesh = {Humans ; *Muscle, Smooth, Vascular/pathology ; *Aortic Aneurysm, Abdominal/pathology/microbiology/metabolism ; *Dysbiosis/complications ; *Gastrointestinal Microbiome ; Animals ; *Myocytes, Smooth Muscle/pathology ; Gonadal Steroid Hormones/metabolism ; Sex Factors ; Male ; Inflammation ; },
abstract = {PURPOSE OF REVIEW: This paper reviews the present literature on how sex-related differences in gut dysbiosis influence vascular smooth muscle cell behavior in the pathogenesis of abdominal aortic aneurysms.
RECENT FINDINGS: Emerging research has linked gut microbial metabolites, such as trimethylamine oxide and phenylacetyl glutamine, to abdominal aortic aneurysm pathogenesis via inflammation and vascular damage. Sex hormones also directly influence vascular smooth muscle cell phenotype switching, as estrogen has been found to be protective, while testosterone may enhance inflammation. Novel biomarkers and molecular regulators have emerged as potential targets, revealing new avenues for abdominal aortic aneurysm treatment. Gut dysbiosis contributes to abdominal aortic aneurysm progression through inflammation, vascular smooth muscle cell dysfunction, and immune activation. These effects vary by sex and are influenced by sex hormones and structural differences in vascular smooth muscle cells but require further investigation to establish a clear relationship.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Muscle, Smooth, Vascular/pathology
*Aortic Aneurysm, Abdominal/pathology/microbiology/metabolism
*Dysbiosis/complications
*Gastrointestinal Microbiome
Animals
*Myocytes, Smooth Muscle/pathology
Gonadal Steroid Hormones/metabolism
Sex Factors
Male
Inflammation
RevDate: 2026-09-16
CmpDate: 2026-09-16
Antimicrobial-resistant organism carriage and metagenomic characterization of the microbiome and resistome in veterinary workers.
Veterinary research communications, 50(6):.
BACKGROUND: Veterinary personnel work in environments with high exposure to antimicrobials and antimicrobial-resistant pathogens. However, the extent to which these occupational exposures influence their carriage of antimicrobial-resistant (AMR) organisms and the composition of their microbiome and resistome remains poorly understood. The objective of this study was to characterize AMR pathogen carriage and microbiome/resistome composition in veterinary personnel and to assess whether workplace setting and patient-related exposures were associated with detectable differences in these outcomes.
METHODS: Personnel from a large academic veterinary hospital and a convenience sample of private-practice small-animal veterinary hospitals provided nasal swabs, stool samples, and exposure survey data; environmental samples were also collected from the academic hospital. Nasal swabs were cultured for methicillin-resistant Staphylococcus aureus, and stool samples were cultured for extended spectrum cephalosporin resistance (ESCR) Escherichia coli. Samples also underwent shotgun metagenomic sequencing or 16S rRNA gene sequencing for taxonomic and antimicrobial resistance gene profiling. Alpha/beta diversity were compared across groups, beta diversity by Permutational Multivariate Analysis of Variance, linear models tested differential abundance, and logistic regression was used to assess covariates associated with MRSA and ESCR carriage. A subset of academic-hospital participants also submitted additional samples after time away (1-2 weeks) from the hospital.
RESULTS: Among academic-hospital personnel (n = 38), MRSA and ESCR-E. coli carriage prevalence were 18.4% and 11.1%, respectively. In private-practice personnel (n = 8), carriage was 12.5% and 25%, respectively. Within the academic hospital, MRSA carriage was associated with administering antibiotics to patients. Microbial composition differed modestly by worksite (R[2] = 0.02) when assessed using unweighted UniFrac metrics only, suggesting subtle site-related differences in low-abundance phylogenetically distinct taxa. Global resistome composition did not differ significantly by site or clinical exposure, although a small number of individual AMR ontologies and broad AMR gene families varied across groups, including those associated with commonly-administered oral antibiotics at the hospital. Paired on/off-clinic analyses did not show a clear directional shift after time away from the hospital.
CONCLUSIONS: Veterinary personnel carried MRSA at a notable frequency, while workplace effects on the microbiome and resistome were subtle, with limited evidence for large-scale shifts in community structure by site or patient exposure.
Additional Links: PMID-42747640
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@article {pmid42747640,
year = {2026},
author = {Redding, LE and Hu, W and Daniel, S and Okumura, M and Hiehle, ME and David, MZ and Hunter, L and Cole, SD},
title = {Antimicrobial-resistant organism carriage and metagenomic characterization of the microbiome and resistome in veterinary workers.},
journal = {Veterinary research communications},
volume = {50},
number = {6},
pages = {},
pmid = {42747640},
issn = {1573-7446},
support = {NI25AHDRXXXXG042 Formula Funds//U.S. Department of Agriculture/ ; },
mesh = {Humans ; *Microbiota ; *Drug Resistance, Bacterial ; Hospitals, Animal ; Methicillin-Resistant Staphylococcus aureus/isolation & purification/drug effects/genetics ; Animals ; Anti-Bacterial Agents/pharmacology ; Male ; Escherichia coli/drug effects/isolation & purification/genetics ; Female ; *Animal Technicians ; *Carrier State/microbiology/epidemiology ; *Veterinarians ; Feces/microbiology ; Metagenome ; RNA, Ribosomal, 16S ; Adult ; },
abstract = {BACKGROUND: Veterinary personnel work in environments with high exposure to antimicrobials and antimicrobial-resistant pathogens. However, the extent to which these occupational exposures influence their carriage of antimicrobial-resistant (AMR) organisms and the composition of their microbiome and resistome remains poorly understood. The objective of this study was to characterize AMR pathogen carriage and microbiome/resistome composition in veterinary personnel and to assess whether workplace setting and patient-related exposures were associated with detectable differences in these outcomes.
METHODS: Personnel from a large academic veterinary hospital and a convenience sample of private-practice small-animal veterinary hospitals provided nasal swabs, stool samples, and exposure survey data; environmental samples were also collected from the academic hospital. Nasal swabs were cultured for methicillin-resistant Staphylococcus aureus, and stool samples were cultured for extended spectrum cephalosporin resistance (ESCR) Escherichia coli. Samples also underwent shotgun metagenomic sequencing or 16S rRNA gene sequencing for taxonomic and antimicrobial resistance gene profiling. Alpha/beta diversity were compared across groups, beta diversity by Permutational Multivariate Analysis of Variance, linear models tested differential abundance, and logistic regression was used to assess covariates associated with MRSA and ESCR carriage. A subset of academic-hospital participants also submitted additional samples after time away (1-2 weeks) from the hospital.
RESULTS: Among academic-hospital personnel (n = 38), MRSA and ESCR-E. coli carriage prevalence were 18.4% and 11.1%, respectively. In private-practice personnel (n = 8), carriage was 12.5% and 25%, respectively. Within the academic hospital, MRSA carriage was associated with administering antibiotics to patients. Microbial composition differed modestly by worksite (R[2] = 0.02) when assessed using unweighted UniFrac metrics only, suggesting subtle site-related differences in low-abundance phylogenetically distinct taxa. Global resistome composition did not differ significantly by site or clinical exposure, although a small number of individual AMR ontologies and broad AMR gene families varied across groups, including those associated with commonly-administered oral antibiotics at the hospital. Paired on/off-clinic analyses did not show a clear directional shift after time away from the hospital.
CONCLUSIONS: Veterinary personnel carried MRSA at a notable frequency, while workplace effects on the microbiome and resistome were subtle, with limited evidence for large-scale shifts in community structure by site or patient exposure.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
*Drug Resistance, Bacterial
Hospitals, Animal
Methicillin-Resistant Staphylococcus aureus/isolation & purification/drug effects/genetics
Animals
Anti-Bacterial Agents/pharmacology
Male
Escherichia coli/drug effects/isolation & purification/genetics
Female
*Animal Technicians
*Carrier State/microbiology/epidemiology
*Veterinarians
Feces/microbiology
Metagenome
RNA, Ribosomal, 16S
Adult
RevDate: 2026-09-15
CmpDate: 2026-09-14
Sex and stress paradigm influence behavioural, neuroimmune, and microbiome responses in pubertal CD-1 mice.
Brain, behavior, & immunity - health, 56:101341.
Puberty is a critical developmental period marked by heightened vulnerability to stress. Exposure to pubertal stress can have lasting effects on behaviour, immune function, and the gut-brain axis. The NLRP3 inflammasome and gut microbiome are key regulators of neuroinflammation, yet their roles across distinct pubertal stress paradigms remain unclear. This study compared behavioural, immune, and microbial outcomes in 100 CD-1 mice following chronic unpredictable stress (CUS; 14 or 28 days) or 7-day sleep disruption (SD) in pubertal males and females. Behavioural testing revealed stressor- and sex-specific effects: females spent more time in the open arms of the elevated plus maze, SD reduced open-arm exploration, 14-day CUS reduced centre activity in the open field, and SD increased immobility in the forced swim test. Plasma cytokines showed divergent patterns, with IL-22 elevated across stress conditions and IL-17A highest following 28-day CUS and in females overall. In the prefrontal cortex, SD males exhibited increased NLRP3 and CASP1 mRNA expression, whereas 28-day CUS females showed reduced NFκB1, and NFκB2 expression was elevated in stress-exposed males. In the hippocampus, 28-day CUS females demonstrated coordinated reductions in NFκB1, NLRP3, and CASP1 expression. Microbiome analyses indicated that SD and 14-day CUS produced the most substantial alterations, characterized by reductions in short-chain fatty acid-producing taxa (Ligilactobacillus, Acetatifactor, Christensenella) and enrichment of stress-associated genera (Flintibacter, Oscillospiraceae). Together, these findings indicate that stressor type and sex differentially shape behavioural, neuroimmune, and microbial profiles during puberty, with sleep disruption exerting particularly strong effects on behavioural and gut-immune regulation.
Additional Links: PMID-42733488
PubMed:
Citation:
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@article {pmid42733488,
year = {2026},
author = {Dworsky-Fried, M and Iqbal, UH and Bronner, S and Auger, J and Mathieu, O and Auclair-Ouellet, N and Liang, J and Ismail, N},
title = {Sex and stress paradigm influence behavioural, neuroimmune, and microbiome responses in pubertal CD-1 mice.},
journal = {Brain, behavior, & immunity - health},
volume = {56},
number = {},
pages = {101341},
pmid = {42733488},
issn = {2666-3546},
abstract = {Puberty is a critical developmental period marked by heightened vulnerability to stress. Exposure to pubertal stress can have lasting effects on behaviour, immune function, and the gut-brain axis. The NLRP3 inflammasome and gut microbiome are key regulators of neuroinflammation, yet their roles across distinct pubertal stress paradigms remain unclear. This study compared behavioural, immune, and microbial outcomes in 100 CD-1 mice following chronic unpredictable stress (CUS; 14 or 28 days) or 7-day sleep disruption (SD) in pubertal males and females. Behavioural testing revealed stressor- and sex-specific effects: females spent more time in the open arms of the elevated plus maze, SD reduced open-arm exploration, 14-day CUS reduced centre activity in the open field, and SD increased immobility in the forced swim test. Plasma cytokines showed divergent patterns, with IL-22 elevated across stress conditions and IL-17A highest following 28-day CUS and in females overall. In the prefrontal cortex, SD males exhibited increased NLRP3 and CASP1 mRNA expression, whereas 28-day CUS females showed reduced NFκB1, and NFκB2 expression was elevated in stress-exposed males. In the hippocampus, 28-day CUS females demonstrated coordinated reductions in NFκB1, NLRP3, and CASP1 expression. Microbiome analyses indicated that SD and 14-day CUS produced the most substantial alterations, characterized by reductions in short-chain fatty acid-producing taxa (Ligilactobacillus, Acetatifactor, Christensenella) and enrichment of stress-associated genera (Flintibacter, Oscillospiraceae). Together, these findings indicate that stressor type and sex differentially shape behavioural, neuroimmune, and microbial profiles during puberty, with sleep disruption exerting particularly strong effects on behavioural and gut-immune regulation.},
}
RevDate: 2026-09-14
CmpDate: 2026-09-14
Corrigendum to "Urinary Microbiome Dysbiosis in Children With Congenital Uropathies at Varying Risk for Urinary Tract Infections" [Kidney International Reports Volume 11, Issue 4, April 2026, 103799].
Kidney international reports, 11(10):107043 pii:S2468-0249(26)03275-4.
[This corrects the article DOI: 10.1016/j.ekir.2026.103799.].
Additional Links: PMID-42733517
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Citation:
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@article {pmid42733517,
year = {2026},
author = {Anand, S and Shete, O and Srivastava, A and Verma, A and Goswami, S and Aggarwal, S and Luthra, K and Ghosh, TS},
title = {Corrigendum to "Urinary Microbiome Dysbiosis in Children With Congenital Uropathies at Varying Risk for Urinary Tract Infections" [Kidney International Reports Volume 11, Issue 4, April 2026, 103799].},
journal = {Kidney international reports},
volume = {11},
number = {10},
pages = {107043},
doi = {10.1016/j.ekir.2026.107043},
pmid = {42733517},
issn = {2468-0249},
abstract = {[This corrects the article DOI: 10.1016/j.ekir.2026.103799.].},
}
RevDate: 2026-09-15
CmpDate: 2026-09-14
Water-responsive injectable hydrogel achieving rapid in situ gelation and long-term colonic mucoadhesion for efficient fecal microbiota transplantation.
Bioactive materials, 68:135-147.
Gut microbiota dysbiosis is a critical factor in numerous diseases, yet current fecal microbiota (FM) transplantation therapies suffer from poor retention and inconsistent engraftment due to harsh gastric conditions or rapid clearance by bowel peristalsis. Herein, we report a thioester pre-crosslinked, low-viscosity injectable sol (Alg-NHS@αLA) formulated by directly mixing α-lipoic acid (αLA) and N-hydroxysuccinimide ester-modified sodium alginate (Alg-NHS) in a biocompatible polyethylene glycol solvent. This formulation remains flowable for minimally invasive transanal administration. Critically, upon contact with the wet colonic mucosa, tissue-derived water triggers a rapid ring-opening polymerization of αLA, inducing an in situ sol-gel transition to form a robust hydrogel network. Simultaneously, abundant carboxyl groups and unreacted NHS esters establish strong hydrogen bonds and covalent linkages with the mucosal surface, enabling robust and durable wet adhesion that conventional injectables fail to achieve. More importantly, this hydrogel harnesses continuous mucus secretion to facilitate conformal coating, achieving exceptional long-term retention exceeding 72 h while preserving the viability of the incorporated microbiota. The translational potential of this platform is validated through successful endoscopic delivery in a porcine model. By integrating rapid water-triggered gelation with robust mucosal adhesion, our Alg-NHS@αLA/FM system significantly enhances FM transplantation efficacy in a mouse colitis model, offering a promising strategy for colonic microbiome-based therapeutics.
Additional Links: PMID-42733554
PubMed:
Citation:
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@article {pmid42733554,
year = {2027},
author = {Chen, Z and Li, Y and Xiong, W and Ma, P and Liu, W and Zhou, H and Wang, X and Tang, Y and Cai, J and Su, M and Chen, Z and Xiong, W},
title = {Water-responsive injectable hydrogel achieving rapid in situ gelation and long-term colonic mucoadhesion for efficient fecal microbiota transplantation.},
journal = {Bioactive materials},
volume = {68},
number = {},
pages = {135-147},
pmid = {42733554},
issn = {2452-199X},
abstract = {Gut microbiota dysbiosis is a critical factor in numerous diseases, yet current fecal microbiota (FM) transplantation therapies suffer from poor retention and inconsistent engraftment due to harsh gastric conditions or rapid clearance by bowel peristalsis. Herein, we report a thioester pre-crosslinked, low-viscosity injectable sol (Alg-NHS@αLA) formulated by directly mixing α-lipoic acid (αLA) and N-hydroxysuccinimide ester-modified sodium alginate (Alg-NHS) in a biocompatible polyethylene glycol solvent. This formulation remains flowable for minimally invasive transanal administration. Critically, upon contact with the wet colonic mucosa, tissue-derived water triggers a rapid ring-opening polymerization of αLA, inducing an in situ sol-gel transition to form a robust hydrogel network. Simultaneously, abundant carboxyl groups and unreacted NHS esters establish strong hydrogen bonds and covalent linkages with the mucosal surface, enabling robust and durable wet adhesion that conventional injectables fail to achieve. More importantly, this hydrogel harnesses continuous mucus secretion to facilitate conformal coating, achieving exceptional long-term retention exceeding 72 h while preserving the viability of the incorporated microbiota. The translational potential of this platform is validated through successful endoscopic delivery in a porcine model. By integrating rapid water-triggered gelation with robust mucosal adhesion, our Alg-NHS@αLA/FM system significantly enhances FM transplantation efficacy in a mouse colitis model, offering a promising strategy for colonic microbiome-based therapeutics.},
}
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RJR Experience and Expertise
Researcher
Robbins holds BS, MS, and PhD degrees in the life sciences. He served as a tenured faculty member in the Zoology and Biological Science departments at Michigan State University. He is currently exploring the intersection between genomics, microbial ecology, and biodiversity — an area that promises to transform our understanding of the biosphere.
Educator
Robbins has extensive experience in college-level education: At MSU he taught introductory biology, genetics, and population genetics. At JHU, he was an instructor for a special course on biological database design. At FHCRC, he team-taught a graduate-level course on the history of genetics. At Bellevue College he taught medical informatics.
Administrator
Robbins has been involved in science administration at both the federal and the institutional levels. At NSF he was a program officer for database activities in the life sciences, at DOE he was a program officer for information infrastructure in the human genome project. At the Fred Hutchinson Cancer Research Center, he served as a vice president for fifteen years.
Technologist
Robbins has been involved with information technology since writing his first Fortran program as a college student. At NSF he was the first program officer for database activities in the life sciences. At JHU he held an appointment in the CS department and served as director of the informatics core for the Genome Data Base. At the FHCRC he was VP for Information Technology.
Publisher
While still at Michigan State, Robbins started his first publishing venture, founding a small company that addressed the short-run publishing needs of instructors in very large undergraduate classes. For more than 20 years, Robbins has been operating The Electronic Scholarly Publishing Project, a web site dedicated to the digital publishing of critical works in science, especially classical genetics.
Speaker
Robbins is well-known for his speaking abilities and is often called upon to provide keynote or plenary addresses at international meetings. For example, in July, 2012, he gave a well-received keynote address at the Global Biodiversity Informatics Congress, sponsored by GBIF and held in Copenhagen. The slides from that talk can be seen HERE.
Facilitator
Robbins is a skilled meeting facilitator. He prefers a participatory approach, with part of the meeting involving dynamic breakout groups, created by the participants in real time: (1) individuals propose breakout groups; (2) everyone signs up for one (or more) groups; (3) the groups with the most interested parties then meet, with reports from each group presented and discussed in a subsequent plenary session.
Designer
Robbins has been engaged with photography and design since the 1960s, when he worked for a professional photography laboratory. He now prefers digital photography and tools for their precision and reproducibility. He designed his first web site more than 20 years ago and he personally designed and implemented this web site. He engages in graphic design as a hobby.
RJR Picks from Around the Web (updated 11 MAY 2018 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.