@article {pmid41387030,
year = {2025},
author = {Barjij, I and Meliani, M},
title = {The tumor microbiome and cancer immunotherapy: A systematic review of a new frontier beyond the gut.},
journal = {Bulletin du cancer},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.bulcan.2025.09.006},
pmid = {41387030},
issn = {1769-6917},
abstract = {BACKGROUND: While the gut microbiome is known to modulate systemic immunity and response to immune checkpoint inhibitors, the role of tumor-resident microbiota remains underexplored. Recent evidence suggests that these local microbial communities may influence intratumoral immunity and therapeutic outcomes.

METHODS: A systematic review compliant with PRISMA guidelines was conducted to evaluate the impact of tumor-associated bacteria on anti-tumor immune responses. Four databases (PubMed, Scopus, Web of Science and EMBASE) were searched for studies published between January 2010 and April 2025. Eligible studies characterized non-intestinal microbiota within tumor tissue and assessed immune endpoints such as T cell infiltration, cytokine profiles, PD-L1 expression, or immune checkpoint inhibitors responsiveness. Due to endpoint heterogeneity, no meta-analysis was performed. Seventeen studies met inclusion criteria.

RESULTS: In tumors including melanoma, pancreatic, esophageal, gastric, breast, lung, and colorectal cancers, intratumoral bacteria modulated immune responses and immune checkpoint inhibitors efficacy. Three recurring mechanisms emerged: immune activation via antigen presentation and Th1 polarization; immune suppression through regulatory T cell recruitment and stromal remodeling; and checkpoint modulation and T cell exhaustion via microbial signaling. These effects were spatially structured and tumor-context dependent.

CONCLUSION: Tumor-local microbiota represents a distinct and actionable component of the tumor-immune microenvironment. Incorporating microbial profiling into immuno-oncology strategies may enhance biomarker discovery, patient stratification, and development of microbiome-based therapies. Further research is warranted to map spatial microbial heterogeneity, validate functional mechanisms, and translate findings into clinical applications in precision immunotherapy.},
}

@article {pmid41386887,
year = {2025},
author = {Kumagai, K and Chiba, A and Yajima, H},
title = {Design biology and mind-body health.},
journal = {Journal, genetic engineering & biotechnology},
volume = {23},
number = {4},
pages = {100621},
doi = {10.1016/j.jgeb.2025.100621},
pmid = {41386887},
issn = {2090-5920},
abstract = {Recent advances in design biology, including artificial cells, DNA nanostructures, artificial intelligence (AI)-driven molecular design, biofoundries, and next-generation genome editing, are transforming the health sciences of mind and body (HS-MB). Moving beyond traditional observational paradigms, these technologies enable predictive and design-oriented strategies for regulating stress, emotional health, achieving immune homeostasis, and managing lifestyle-related disorders. Psychological and social factors profoundly influence core physiological systems, including neuroendocrine (hypothalamic-pituitary-adrenal [HPA]) axis and cortisol rhythm, autonomic (vagal tone and heart rate variability), immune (cytokine balance and inflammatory control), metabolic (glucose-insulin regulation), and sleep-circadian systems. Artificial cells serve as controllable models for neurotransmitter signaling, immune interactions, and gut-brain communication, while DNA origami provides programmable nanocarriers that complement lipid nanoparticles (LNPs). Genome-editing innovations-such as prime, base, and epigenome editing-facilitate precise and reversible modulation of psychiatric risk genes, particularly when combined with induced pluripotent stem cell (iPSC) and brain-organoid models. Biofoundries integrate AI into Design-Build-Test-Learn (DBTL) cycles, automating molecular discovery and optimization. Ethical and regulatory considerations, including AI transparency, biocontainment, and dual-use governance, must be incorporated from the outset. Collectively, design biology, when strategically aligned with HS-MB, establishes a foundational framework for twenty-first-century medicine that bridges molecular engineering and holistic well-being.},
}

@article {pmid41386833,
year = {2025},
author = {Sarkar, A and Patra, RK and Muthaiyan, M and Mallik, A},
title = {A metagenomic exploration of microbial distribution among the pond sediment, shrimp (Penaeus monodon) tissue and pond water: A special focus on nutrient cycling and shrimp viral pathogens.},
journal = {Journal, genetic engineering & biotechnology},
volume = {23},
number = {4},
pages = {100568},
doi = {10.1016/j.jgeb.2025.100568},
pmid = {41386833},
issn = {2090-5920},
abstract = {Penaeus monodon, a major shrimp species cultivated in Eastern Asia, has faced setbacks in aquaculture due to disease outbreaks. Metagenomic studies offer insights into the pond microbiome, revealing its critical roles in nutrient cycling, water quality, and disease control. This study investigated microbial communities in sediment, water, and shrimp samples from an aquaculture pond in Chaital, West Bengal, India. Shotgun metagenomic sequencing and bioinformatics analyses were used to assess taxonomic and functional profiles, focusing on nutrient cycling genes and viral populations. Sediments showed the highest microbial diversity, contributing to organic matter decomposition and ecological stability. Water microbes played roles in oxygenation and pathogen suppression, while shrimp tissues hosted microbes aiding digestion and immunity. Pathogenic viruses, especially Whispovirus (White Spot Syndrome Virus), dominated shrimp tissues. Functional gene analysis identified key pathways in carbon, nitrogen, and sulfur cycling. Integrating water quality data with microbiome profiles could help identify bioindicators and predict pathogen risks.},
}

@article {pmid41386516,
year = {2025},
author = {Drabesch, S and Mueller, S and Leon Ninin, JM and Planer-Friedrich, B and Kappler, A and Muehe, EM},
title = {Rising temperature and atmospheric CO2 combine to antagonistically alter Cd mobility and biogeochemistry in an agricultural soil.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {127508},
doi = {10.1016/j.envpol.2025.127508},
pmid = {41386516},
issn = {1873-6424},
abstract = {Soil cadmium (Cd) contamination threatens ecosystems and crop safety. Understanding how individual climate change factors influence soil Cd bioavailability is essential for mechanistic understanding and future risk assessments. This study examined individual and combined effects of elevated temperature (+4°C) and doubled atmospheric CO2 (800 ppmv) on soil Cd bioavailability, biogeochemistry, and greenhouse gas emissions in agricultural soils with native (0.13 mg Cd kg-[1]) and high Cd (1.5 mg Cd kg[-1]). Elevated temperature increased porewater Cd up to 50% relative to ambient, while doubled atmospheric CO2 did not alter porewater Cd. Combined future conditions increased porewater Cd by 30% relative to ambient indicating an antagonistic interaction. Doubled atmospheric CO2 enhanced microbial nitrogen fixation and reduced ammonium oxidation, increasing ammonium concentrations up to 10-fold relative to ambient. Elevated temperature stimulated microbiome activity and ammonium oxidation, leading to 1.7-fold more CO2 and 5.5-fold more N2O compared to ambient, both exceeding levels observed under combined future climate. These contrasting single-factor responses highlight the non-additive nature of combined climate factor effects. Warming alone overestimated and CO2 alone underestimated the combined impact on Cd mobility and soil biogeochemistry. Simulating multiple climate drivers is therefore essential for accurate environmental prediction and sustainable Cd management under climate change.},
}

@article {pmid41386393,
year = {2025},
author = {Campanale, A and Mir, HD and Dumais, E and Inserra, A and Flamand, N and Chakravarty, M and Gantois, I and Siddiqui, N and Sonenberg, N and Gobbi, G and Silvestri, C and Di Marzo, V},
title = {Uncovering novel endocannabinoidome-gut microbiome-brain axis-based therapeutic targets in a Fragile X Syndrome mouse model.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111575},
doi = {10.1016/j.pnpbp.2025.111575},
pmid = {41386393},
issn = {1878-4216},
abstract = {BACKGROUND: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition associated with increased risk of psychiatric, gastrointestinal, and metabolic comorbidities. Recent studies highlight the bidirectional role of the gut microbiome (GM) and endocannabinoidome (eCBome) in the eCBome-GM-brain axis, suggesting its therapeutic potential for ASD and comorbidities.

METHODS: We investigated the eCBome-GM-brain axis in the Fragile X Messenger Ribonucleoprotein 1 (Fmr1[-/y]) mouse model, known as a genetic model of ASD, to identify therapeutic targets. Fecal GM composition was analysed via 16S rDNA sequencing, brain eCBome profile via HPLC-MS/MS and qRT-PCR, and fecal short chain fatty acids via GC-FID.

RESULTS: Significant eCBome-GM-brain axis dysregulation was observed in Fmr1[-/y] compared to WT mice. GM analyses revealed gut dysbiosis, increased permeability, and inflammation. Specifically, elevated Akkermansia and Eubacterium siraeum-linked to gut barrier dysfunction-and Ruminococcus and Clostridium, associated with ASD severity, were identified. Concurrently, decreased levels of the gut health biomarker Roseburia and the taxa Helicobacter and Anaeroplasma were observed. Brain region-specific eCBome alterations underscored neuroinflammation. In the HPC, reduced anti-inflammatory dihomogamma-linolenic acid (DGLA) was accompanied by elevated pro-inflammatory 12-hydroxy-heptadecatrienoic acid, a mediator of microglial activation. In the PFC, decreased DGLA, 1/2-linoleoylglycerol, and linoleic acid N-linoleoyl-ethanolamine suggested neuroinflammation; elevated prostaglandin D2, a marker of autophagy impairment, underscores further mechanisms of dysfunction. Upregulation of cannabinoid type 2 and PPAR-γ receptor genes in the PFC suggested a compensatory response to neuroinflammation. Correlations between eCBome and GM alterations highlighted links between dysbiosis, systemic inflammation, and neurodevelopmental atypicalities.

CONCLUSIONS: The Fmr1[-/y] ASD mouse model harbors significant eCBome-GM-brain axis alterations. This study highlights specific GM taxa and eCBome components as potential therapeutic targets for clinical validation in Fragile X Syndrome and ASD.},
}

@article {pmid41386080,
year = {2025},
author = {Thomas, MC and Fisher, R and Luter, HM and Negri, AP},
title = {Making Waves: Advancing environmental risk assessment through the quantification of marine microbial sensitivity thresholds.},
journal = {Water research},
volume = {290},
number = {},
pages = {125102},
doi = {10.1016/j.watres.2025.125102},
pmid = {41386080},
issn = {1879-2448},
abstract = {Microbial communities play a vital role in maintaining marine ecosystem health, yet they remain largely excluded from environmental risk assessments and water quality guideline development. Traditional ecotoxicological and regulatory frameworks predominantly rely on single-species toxicity data from eukaryotes, overlooking microbial responses to environmental stressors. However, microbial communities often respond rapidly to environmental change and can serve as sensitive early indicators of ecological disturbance. Advances in high-throughput sequencing and bioinformatics enable comprehensive assessment of microbial responses across multiple levels of biological organisation. Despite these capabilities, standardised methodologies for deriving quantitative microbial sensitivity thresholds remain lacking. This paper synthesises recent progress and emerging approaches in microbial ecotoxicology to support the incorporation of microbial endpoints into environmental regulatory frameworks. We highlight the potential of combining 16S rRNA gene amplicon sequencing of viable cells with microbial load quantification and advanced Bayesian concentration-response modelling to resolve microbial stress responses and quantify sensitivity thresholds at both community and taxon levels. These thresholds can inform cumulative prokaryotic sensitivity distributions, enabling the derivation of guideline values for microbiomes in alignment with existing approaches used for eukaryotic species. Establishing robust microbial sensitivity thresholds represents a critical step toward incorporating prokaryotes into environmental quality guidelines, improving ecological realism, and enabling earlier, more holistic detection of ecosystem degradation.},
}

@article {pmid41387248,
year = {2025},
author = {Ji, C and Wu, T and Tian, Y and Li, J and Dong, J and Xing, S and Chen, H and Yang, D and Ouyang, S and Li, J and Huang, Y and Hao, Z and Zhang, X and Chen, B and Zhu, Y},
title = {Synergistic response of arbuscular mycorrhizal fungi and hyphosphere microbiome to arsenic contamination in agricultural soils.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.70782},
pmid = {41387248},
issn = {1469-8137},
support = {2023YFF1306004//National Key Research and Development Program of China/ ; 42377299//National Natural Science Foundation of China/ ; 42177109//National Natural Science Foundation of China/ ; U21A2024//National Natural Science Foundation of China/ ; 52504193//National Natural Science Foundation of China/ ; },
abstract = {Arbuscular mycorrhizal fungi (AMF) can modulate arsenic (As) bioavailability through hyphal interactions with microbes. However, whether AMF hyphae assemble a core hyphosphere microbiome adapted to As stress and how this shapes in situ As transformation are still unknown. We conducted field experiments across agricultural soils with an As gradient (21-172 mg kg[-1]), using in situ mesh devices to collect hyphosphere and nonhyphosphere soils during a 98-d wheat growth period. We integrated 16S rRNA and ITS gene sequencing, PICRUSt2-based functional prediction, co-inertia and co-occurrence analyses, and sequential As extraction to investigate the hyphosphere microbiome's structure, functional potential, and AMF-microbe interactions. AMF hyphae significantly increased microbial diversity and niche breadth in the hyphosphere and reshaped community composition. Co-inertia and network analyses showed stronger associations under high As stress. We identified 100 ASVs as a core hyphosphere microbiome - dominated by Proteobacteria, Bacteroidetes, and Verrucomicrobia - rich in arsC, arsH, and arsB/ACR3 genes. Network modules formed by these taxa correlated positively with bioavailable As, suggesting adaptive potential under stress. This study provides the first field-based evidence that AMF hyphae selectively recruit a core microbiome with potential As-transforming functions, offering microbial targets for AMF-assisted remediation of As-contaminated soils.},
}

@article {pmid41387123,
year = {2025},
author = {Guo, J and Kang, SG and Huang, K and Tong, T},
title = {The Gut Microbiota Regulates Motor Deficits via Butyrate in a Gnal[+/-] Mouse Model of DYT25 Dystonia.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e12942},
doi = {10.1002/advs.202512942},
pmid = {41387123},
issn = {2198-3844},
abstract = {Dystonia is the third most common movement disorder, following essential tremor and Parkinson's disease. The underlying mechanisms behind dystonia are still one of the crucial unsolved research topics. Gnal haploinsufficient (Gnal[+/-]) mice are used as a model of DTY25 dystonia to investigate the mechanistic relationship between gut microbiota and dystonia. The present study unveiled Gnal[+/-] mice exhibit significant motor deficits of dystonia, along with a marked gut microbiota dysbiosis. Analysis of the gut microbiota composition and function reveals that Gnal[+/-] mice have decreased butyrate-producing bacteria abundance (such as Lachnospiraceae_NK4A136, Blautia, and Butyricicoccus) and disrupted butanoate metabolism. The targeted metabolomics analysis indicates that the Gnal[+/-] mice exhibit decreased butyrate levels in feces and serum. The colonization of antibiotic-treated wild-type mice with fecal microbiota from Gnal[+/-] mice is sufficient to induce motor deficit symptoms. Oral administration of sodium butyrate ameliorated motor deficits in the Gnal[+/-] mouse model of DYT25 dystonia. Striatal single-nucleus RNA sequencing reveals cell-type-specific gene expression changes, suggesting that butyrate modulates neurotransmitter pathways, particularly GABA signaling. This is confirmed by restored striatal GABA levels after butyrate supplementation. In sum, gut microbiome contributes to dystonia pathogenesis, and butyrate supplementation alleviates the motor deficits of dystonia in Gnal[+/-] mice.},
}

@article {pmid41387111,
year = {2025},
author = {Araujo, ASF and Pereira, APA and de Medeiros, EV and Mendes, LW},
title = {Root-driven microbiome memory enhances plant disease resistance.},
journal = {Trends in plant science},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tplants.2025.12.002},
pmid = {41387111},
issn = {1878-4372},
abstract = {Root-driven microbiome memory imprints biological and chemical legacies in soil, boosting plant disease resistance across generations. In a recent study, Wu et al. found flavonoids acting as key mediators, recruiting protective microbes and lowering pathogen severity beyond one crop cycle. Here, we highlight this concept, its limitations, and opportunities for sustainable disease resistance in agriculture.},
}

@article {pmid41386478,
year = {2025},
author = {Rochman, M and Rothenberg, ME},
title = {Immune Functions of the Esophagus.},
journal = {The Journal of allergy and clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaci.2025.12.001},
pmid = {41386478},
issn = {1097-6825},
abstract = {The esophagus has long been regarded as a simple conduit for food transport. A new paradigm now recognizes it as an immune organ actively involved in environmental sensing, antigen tolerance, and neuroimmune signaling to maintain mucosal homeostasis. The stratified squamous epithelium provides a vital physical barrier, supported by transmembrane mucins and regulated by post-translational modifications, including citrullination mediated by esophagus-enriched peptidyl arginine deiminases. A unique esophageal microbiome, established early in life, shapes epithelial differentiation, gene expression, and immune development and response. Pattern recognition receptors and enriched interleukin 1 (IL-1) family cytokines, including the alarmins IL-33 and thymic stromal lymphopoietin (TSLP), orchestrate rapid immune responses to diverse environmental stimuli, such as allergens. The protease-antiprotease balance, controlled by serine and cysteine proteases, notably kallikreins, and the inhibitors SERPINs and SPINKs, regulates cytokine activity and barrier integrity. Neuroimmune circuits link innate immune activation, sensory perception, and barrier regulation. Disruption of these pathways, including genetic variants in barrier components, proteases, and immune regulators, contributes to disease susceptibility and pathogenesis. Thus, the esophagus is now understood to be an environmental sensing immune organ with functions in health and disease.},
}

@article {pmid41385957,
year = {2025},
author = {Zhang, C and Wang, X and Wang, L and Li, P and Bao, Y and Zhang, Z and Jiang, Z and Feng, C and Chen, L},
title = {Multi-omics reveals gut microbiota-mediated environmental adaptation in Mallards and domesticated Shaoxing ducks.},
journal = {Poultry science},
volume = {105},
number = {1},
pages = {106177},
doi = {10.1016/j.psj.2025.106177},
pmid = {41385957},
issn = {1525-3171},
abstract = {Gut microbiota remodeling is a critical component of the domestication syndrome. However, the structural and functional consequences of domestication on gut microbiomes in ducks remain poorly understood. Understanding how domestication and associated ecological transitions influence gut microbial communities can shed light on host adaptation mechanisms. We performed integrated metagenomic and metabolomic analyses of the ileal and cecal microbiota from Mallards and Shaoxing ducks-two ecotypes of Anas platyrhynchos representing wild and domesticated lineages-to investigate microbial community structure, functional capacity, and host-microbe metabolic interactions. Principal coordinates analysis (PCoA) revealed distinct microbial stratification between intestinal compartments (ileum vs. cecum), with domestication-associated divergence observed primarily in the cecum. Metabolomic profiles were relatively stable across both segments and populations. Mallards harbored a more diverse and metabolically versatile gut microbiota, with significant enrichment in pathways related to carbohydrate, amino acid, and vitamin metabolism. The genus Gemmiger emerged as a key functional contributor, supporting branched-chain amino acid biosynthesis, coenzyme activation, and carbohydrate utilization, thus reflecting enhanced metabolic adaptability. In Shaoxing ducks, the gut microbiome was enriched in the glucagon signaling pathway and glucose-regulatory metabolites such as l-carnitine, myo-inositol, and quinate. Butyricicoccus sp017886875 was identified as a candidate taxon associated with glucose homeostasis. Additionally, immune-related pathways, including the NOD-like receptor signaling and antigen processing and presentation, were significantly enriched and linked to Anaerobiospirillum and Parabasalia, respectively. Co-enrichment of anti-inflammatory metabolites suggests the presence of a host-microbiota feedback mechanism that mitigates inflammation while maintaining immune readiness. These findings reveal that gut microbiota contribute to population-specific environmental adaptation in ducks, with distinct microbiome and functional traits associated with domestication history. The study highlights microbiota-mediated host adaptation as a key feature of domestication-related ecological transitions.},
}

@article {pmid41385919,
year = {2025},
author = {Pan, Q and Zuo, C and Zhao, Y and Zhao, Y and Zhou, Z and Dang, H and Wang, H and Li, S and Liu, F},
title = {Effects of Phthalate Exposure on Oral Microbiome Diversity and Enrichment of Gemella and Streptococcus.},
journal = {International dental journal},
volume = {76},
number = {1},
pages = {109292},
doi = {10.1016/j.identj.2025.109292},
pmid = {41385919},
issn = {1875-595X},
abstract = {AIMS: Phthalates are endocrine-disrupting plasticizers widely used in consumer products, but their effects on oral microbiome diversity remain unclear. To examine associations between phthalate exposure and oral microbiome characteristics.

METHODS: Data were obtained from the 2009 to 2012 cycles of the National Health and Nutrition Examination Survey. Oral microbiome diversity was assessed via 16S rRNA gene sequencing of oral rinse samples. Urinary phthalate metabolites were measured by high performance liquid chromatography-electrospray ionization-tandem mass spectrometry and normalized to uric creatinine. Three microbiome indices were evaluated: α-diversity, β-diversity, and relative abundance. Linear regression and Permutational Multivariate Analysis of Variancetest were employed to examine associations between phthalate exposure and α-diversity and microbial composition, and to assess differences in β-diversity across phthalate exposure tertiles.

RESULTS: Higher concentrations of mono (carboxyoctyl) phthalate (MCOP) and mono-isononyl phthalate (MiNP) were significantly associated with reduced α-diversity (Observed ASVs: β = -0.096 and -0.098; Faith's Phylogenetic Diversity: β = -0.097 and -0.092; Shannon-Weiner index: β = -0.109 and -0.126; Simpson Index: β = -0.078 and -0.110, respectively, with all P < .05). β-diversity, including Bray-Curtis dissimilarity, unweighted UniFrac distance, and weighted UniFrac distance, significantly differed across phthalate exposure tertiles for most phthalates, except for mono-n-butyl phthalate (MBP) and mono-isobutyl phthalate (MiBP). At the genus level, Mono (carboxynonyl) phthalate (MCNP) was positively associated with Gemella (β = 0.099, P = .026), and MiNP with Streptococcus (β = 0.089, P = .026).

CONCLUSIONS: Pphthalate exposure is associated with alterations in oral microbiome diversity and composition, highlighting potential microbiome-mediated pathways underlying phthalate-related health effects.

CLINICAL RELEVANCE: phthalate exposure alters oral microbiome diversity, suggesting a potential mechanism linking plasticizers to adverse health outcomes.},
}

@article {pmid41385904,
year = {2025},
author = {Pan, X and Elsayed, SS and van Wezel, GP and Raaijmakers, JM and Carrión, VJ},
title = {Disentangling the molecular mechanisms of disease suppression by endophytic Flavobacterium sp. 98.},
journal = {Microbiological research},
volume = {304},
number = {},
pages = {128415},
doi = {10.1016/j.micres.2025.128415},
pmid = {41385904},
issn = {1618-0623},
abstract = {Endophytic microorganisms colonize internal plant tissues and enhance host resistance to pathogens. We previously showed that endophytic Flavobacterium sp. 98 (Fl98) protects sugar beet against the fungal root pathogen Rhizoctonia solani via biosynthetic gene cluster 298 (BGC298). However, the molecular mechanisms underlying this protection remained poorly understood. Here, comparative metabolomic analyses revealed that knockout of BGC298 led to reduced production of the antifungal compound 5,6-dimethylbenzimidazole (DMB) in Fl98. We hypothesized that BGC298 is involved in regulating DMB biosynthesis and therefore contributes to Fl98's disease suppression as a novel protective mechanism. Subsequent site-directed mutagenesis of the DMB-synthase gene bluB abolished DMB production by Fl98, and both ΔBGC298 and ΔbluB mutants were compromised in protecting sugar beet seedlings in greenhouse bioassays. Bioinformatic analyses further indicated that bluB is widespread across Flavobacterium, while BGC298 is limited to a small subset of plant-associated strains. Together, our findings highlight the pivotal role of BGC298 and DMB biosynthesis in plant protection by endophytic Flavobacterium sp. 98.},
}

@article {pmid41385764,
year = {2025},
author = {Yang, H and Yu, Y and Cui, R and Zhang, Q and Chen, B and Zhang, Z and Xu, N and Sun, L and Lu, T and Qian, H},
title = {Environmental and Microbial Drivers of Global Rhizosphere Resistome Assembly.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c11060},
pmid = {41385764},
issn = {1520-5118},
abstract = {Soil serves as a critical reservoir for antibiotic resistance genes (ARGs); however, the ecological mechanisms driving ARG assembly at the plant-soil interface remain poorly understood. In this study, we analyzed 383 metagenomic samples and identified 4803 predicted ARGs, which were classified into two distinct clusters. The ARG-abundant cluster exhibited higher rhizospheric ARG abundance and diversity but posed a relatively lower health risk compared to the ARG-scarce cluster. Warm and nutrient-rich soils promote diverse resistomes shaped by complex microbial interactions, whereas humid environments promote more homogeneously predicted ARG compositions. Environmental variables such as the temperature and nitrogen were found to indirectly influence resistome composition by modulating microbial diversity. Notably, relatively high proportions of high-risk predicted ARGs were detected in grains and raw-eat vegetables, highlighting a potential threat to public health. Our findings underscore the importance of incorporating both environmental and microbial perspectives into agricultural practices to mitigate ARG dissemination in soil.},
}

@article {pmid41385173,
year = {2025},
author = {Othman, AA and Mohamed Zain, NI and Eshak, Z and Adman, MA and Abd Latif, Z and Aboshanab, KM and Ahmad, A},
title = {Diversity of necrophagous flies and microbiome profiling of Phumosia promittens as a rainforest health indicator.},
journal = {AMB Express},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13568-025-01994-3},
pmid = {41385173},
issn = {2191-0855},
abstract = {Necrophagous flies play a critical role in decomposition and serve as bioindicators of environmental health and pollution. Malaysia's tropical rainforest ecosystems may host many necrophagous fly species, including unique blowflies and their associated bacteria. However, in many forest reserve areas, the diversity of these flies remains poorly studied. This study examines the diversity of necrophagous flies and their associated surface bacteria community, with a particular focus on Phumosia promittens (Walker in J Proc Linn Soc Lond Zool 4:90-96, 1859) in the Bangi Forest Reserve, Universiti Kebangsaan Malaysia. Sampling was conducted across three plots using baited traps, and collected flies were morphologically identified and processed under sterile conditions. Surface bacteria from P. promittens were isolated and analysed through metagenomic analysis targeting the 16S rRNA (V3-V4) amplicon sequencing gene to characterise their microbial communities comprehensively. Among 2,528 individuals collected, Chrysomya megacephala (Fabricius) was the most dominant species overall, while P. promittens was the most abundant among native forest species, suggesting their ecological adaptability and potential as a bioindicator of healthy rainforest. Shannon-Wiener and Simpson's diversity of flies in the study location were 0.67 ± 0.11 and 0.29 ± 0.06, respectively. Meanwhile, the Shannon-Wiener and Simpson's diversity of bacteria from P. promittens were 5.64 ± 0.70 and 0.96 ± 0.02, respectively. Bacterial microbiome analysis revealed the presence of core genera, including Wohlfahrtiimonas, Dysgonomonas, Vagococcus, and Ignatzschineria, which are implicated in both ecological symbiosis and public health concerns. These bacteria may contribute to nutrient cycling, such as heavy metals and antibiotics. Notably, several of these genera are emerging zoonotic pathogens with antimicrobial resistance, highlighting the dual role of necrophagous flies as ecosystem contributors and disease vectors. The findings underscore the importance of monitoring native fly species and their microbiota to assess the integrity of forest ecosystems and potential public health risks.},
}

@article {pmid41385014,
year = {2025},
author = {Sawaran Singh, NS and Gataa, IS and Saleh, LH and Ganesan, S and Kavitha, V and Maharana, L and Sharma, R and Latipova, M and Madatova, N and Jumanazarov, D and Smerat, A},
title = {Lipid nanoparticle-based mRNA platforms for mucosal HIV vaccines: formulation advances, immune mechanisms, and translational pathways.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {68},
pmid = {41385014},
issn = {1432-072X},
mesh = {*AIDS Vaccines/immunology/administration & dosage ; Humans ; *HIV Infections/prevention & control/immunology ; *Nanoparticles/chemistry/administration & dosage ; Immunity, Mucosal ; *RNA, Messenger/immunology/administration & dosage/genetics ; Animals ; *Lipids/chemistry ; Adjuvants, Immunologic ; Mucous Membrane/immunology ; Administration, Mucosal ; Liposomes ; },
abstract = {Developing an effective HIV vaccine remains a major challenge in modern medicine. The majority of HIV transmissions occur across mucosal surfaces, yet the mucosal immune protection provided by current systemic vaccination strategies is limited. However, the potential of lipid nanoparticle (LNP)-based messenger RNA (mRNA) vaccines to revolutionize HIV prevention is a source of hope and optimism. Additionally, circular RNA (circRNA) represents an emergent platform that may offer potential for mucosal HIV vaccine development. This review examines the relationship between mRNA-LNP formulation science and mucosal immunology, with a focus on how adjuvant design, device engineering, and delivery methods interact to influence protective outcomes. We summarize the most recent research on mucosal delivery methods, including nasal, vaginal, rectal, and pulmonary routes, as well as formulation techniques to overcome obstacles such as mucus penetration, enzymatic breakdown, and epithelial absorption. We also examine how mRNA design (including nucleoside modification status) and prime-boost regimens influence the desired immunological outcomes, such as the induction of mucosal secretory IgA (SIgA), tissue-resident memory T cells (TRM), and a balanced systemic-local immune response. The microbiome and mucosal inflammation are examined in relation to safety, tolerability, and regulatory considerations. We stress the importance of future research priorities, including integrated prime-boost schedules, adjuvant tuning, and early human trials, to engage the audience and commit to the advancement of HIV prevention. We also highlight translational roadblocks, such as the lack of standardized mucosal assays, limited preclinical challenge data, and manufacturing challenges. When combined, mucosal delivery of mRNA vaccines made with LNP presents a promising strategy for preventing HIV by focusing immune responses at viral entry points.},
}

*AIDS Vaccines/immunology/administration & dosage
Humans
*HIV Infections/prevention & control/immunology
*Nanoparticles/chemistry/administration & dosage
Immunity, Mucosal
*RNA, Messenger/immunology/administration & dosage/genetics
Animals
*Lipids/chemistry
Adjuvants, Immunologic
Mucous Membrane/immunology
Administration, Mucosal
Liposomes

@article {pmid41384994,
year = {2025},
author = {Zhang, J and Liu, J and Bayani, A},
title = {Phage therapy and the microbiome in hematologic malignancies: opportunities, mechanisms, and early evidence.},
journal = {Journal of cancer research and clinical oncology},
volume = {152},
number = {1},
pages = {8},
pmid = {41384994},
issn = {1432-1335},
mesh = {Humans ; *Hematologic Neoplasms/therapy/microbiology/immunology ; *Phage Therapy/methods ; Animals ; *Bacteriophages ; *Gastrointestinal Microbiome ; *Microbiota ; },
abstract = {Hematologic malignancies remain among the most difficult cancers to treat, challenged by profound heterogeneity, treatment-induced immune dysfunction, and the frequent emergence of drug resistance. Beyond tumor-intrinsic mechanisms, dysbiosis of the gut microbiome is increasingly recognized as a critical determinant of therapeutic outcomes, shaping hematopoiesis, immune responses, and drug metabolism. Bacteriophage (phage) therapy has re-emerged as a precision tool capable of selectively eradicating pathogenic taxa while preserving commensal short-chain fatty acid-producing communities. Preclinical and early human studies demonstrate that phages can recalibrate microbial ecosystems, disrupt antibiotic-tolerant biofilms, and enrich metabolites such as butyrate that support mucosal integrity and immune balance. Mechanistically, phage DNA enriched with CpG motifs engages Toll-like receptor 9, activating dendritic cells and enhancing cytotoxic T lymphocyte responses, suggesting dual benefits in infection control and anti-tumor immunity. Emerging applications extend further, with engineered phages serving as vectors for CRISPR-Cas gene editing, targeted cytokine delivery, and nanocarrier platforms for leukemia therapy. Despite translational promise, major hurdles persist, including immunogenicity, horizontal gene transfer, resistance evolution, and regulatory uncertainty. Addressing these challenges through GMP-compliant manufacturing, metagenomics-guided personalization, and AI-optimized cocktail design could establish phage therapy as a microbiome-informed adjunct to overcome drug resistance in blood cancers. However, direct clinical evidence of phage therapy efficacy in hematologic malignancies remains limited, and current data are largely derived from preclinical and compassionate-use contexts.},
}

Humans
*Hematologic Neoplasms/therapy/microbiology/immunology
*Phage Therapy/methods
Animals
*Bacteriophages
*Gastrointestinal Microbiome
*Microbiota

@article {pmid41384800,
year = {2025},
author = {Moxon, SAT and Solbrig, H and Harris, NL and Kalita, P and Miller, MA and Patil, S and Schaper, K and Bizon, C and Caufield, JH and Cuesta, SC and Cox, C and Dekervel, F and Dooley, DM and Duncan, WD and Fliss, T and Gehrke, S and Graefe, ASL and Hegde, H and Ireland, AJ and Jacobsen, JOB and Krishnamurthy, M and Kroll, C and Linke, D and Ly, R and Matentzoglu, N and Overton, JA and Saunders, JL and Unni, DR and Vaidya, G and Vierdag, WAM and Ruebel, O and Chute, CG and Brush, MH and Haendel, MA and Mungall, CJ},
title = {LinkML: An Open Data Modeling Framework.},
journal = {GigaScience},
volume = {},
number = {},
pages = {},
doi = {10.1093/gigascience/giaf152},
pmid = {41384800},
issn = {2047-217X},
abstract = {BACKGROUND: Scientific research relies on well-structured, standardized data; however, much of it is stored in formats such as free-text lab notebooks, non-standardized spreadsheets, or data repositories. This lack of structure challenges interoperability, making data integration, validation, and reuse difficult.

FINDINGS: LinkML (Linked Data Modeling Language) is an open framework that simplifies the process of authoring, validating, and sharing data. LinkML can describe a range of data structures, from flat, list-based models to complex, interrelated, and normalized models that utilize polymorphism and compound inheritance. It offers an approachable syntax that is not tied to any one technical architecture and can be integrated seamlessly with many existing frameworks. The LinkML syntax provides a standard way to describe schemas, classes, and relationships, allowing modelers to build well-defined, stable, and optionally ontology-aligned data structures. Once defined, LinkML schemas may be imported into other LinkML schemas. These key features make LinkML an accessible platform for interdisciplinary collaboration and a reliable way to define and share data semantics.

CONCLUSIONS: LinkML helps reduce heterogeneity, complexity, and the proliferation of single-use data models while simultaneously enabling compliance with FAIR data standards. LinkML has seen increasing adoption in various fields, including biology, chemistry, biomedicine, microbiome research, finance, electrical engineering, transportation, and commercial software development. In short, LinkML makes implicit models explicitly computable and allows data to be standardized at its origin. LinkML documentation and code are available at linkml.io.},
}

@article {pmid41384525,
year = {2025},
author = {Amirova, TO and Moskalev, AA},
title = {[Biomarkers of aging mechanisms].},
journal = {Voprosy kurortologii, fizioterapii, i lechebnoi fizicheskoi kultury},
volume = {102},
number = {5. Vyp. 2},
pages = {108-119},
doi = {10.17116/kurort2025102052108},
pmid = {41384525},
issn = {0042-8787},
mesh = {Humans ; *Biomarkers/urine/metabolism ; *Aging/metabolism ; Cellular Senescence ; },
abstract = {OBJECTIVE: To systematize current knowledge on biomarkers of fundamental aging mechanisms, their reference and target values for practical application in longevity medicine.

MATERIAL AND METHODS: Analysis of scientific literature on 14 key aging mechanisms according to the modern gerontological concept, including genomic instability, telomere shortening, epigenetic alterations, loss of proteostasis, impaired macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, microbiome dysbiosis, extracellular matrix stiffness and barrier dysfunction, as well as circadian rhythm disruption.

RESULTS: A comprehensive system of 30+biomarkers with detailed reference and target values is presented. Key biomarkers include: urinary 8-OHdG (target values<5.0 ng/mg creatinine), leukocyte telomere length (target >6000 base pairs), N7-methylguanine (<6-7 μg/g creatinine), dityrosine (≤10-12 μmol/mol creatinine), p62 and Beclin-1 for autophagy assessment, HOMA-IR (<1.5), IGF-1 (100-150 ng/ml), mitochondrial markers, senescence-associated β-galactosidase (<3% positive cells), inflammatory cytokines, microbiome-associated markers, and circadian biomarkers.

CONCLUSION: The developed biomarker panel provides a scientifically grounded foundation for personalized assessment of aging rate and correction of age-associated changes, requiring regular monitoring every 3-6 months for effective interpretation of biomarker dynamics.},
}

Humans
*Biomarkers/urine/metabolism
*Aging/metabolism
Cellular Senescence

@article {pmid41384457,
year = {2025},
author = {Igídio, CED and Brito, CB and Bezerra, RO and Oliveira, SN and Teixeira, CF and Amorim-Santos, BM and Andrade, ACO and Rios, DL and Pedroso, SHSP and Santos, SGD and Teixeira, MM and Souza, DDG and Mata, CPSMD and Fagundes, CT},
title = {Indole-Acetic Acid Impairs Pseudomonas aeruginosa Virulence and Alters Lung Infection in Mice.},
journal = {MicrobiologyOpen},
volume = {14},
number = {6},
pages = {e70185},
doi = {10.1002/mbo3.70185},
pmid = {41384457},
issn = {2045-8827},
support = {//Instituto Nacional de Ciencia e Tecnologia em Dengue-INCT Dengue (408527/2024-2), Fundação do Amparo a pesquisa de Minas Gerais (FAPEMIG) (APQ-00897-22), Pró-reitoria de Pesquisa da UFMG (edital01/2024), and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (88882.348380/2010-1)./ ; },
mesh = {Animals ; *Pseudomonas aeruginosa/drug effects/pathogenicity/genetics ; *Indoleacetic Acids/pharmacology/metabolism ; Virulence/drug effects ; Biofilms/drug effects/growth & development ; Mice ; *Pseudomonas Infections/microbiology/drug therapy ; Disease Models, Animal ; Humans ; Indoles/pharmacology/metabolism ; Lung/microbiology ; Female ; Tryptophan/metabolism ; Pyocyanine/metabolism ; },
abstract = {Patients in intensive care units, especially those immunocompromised, are prone to opportunistic infections, such as respiratory and urinary tract infections. Extended antibiotic use disrupts the production of microbiome-derived metabolites, including those involved in colonization resistance to Pseudomonas aeruginosa, which is known for its multidrug resistance. Hence, prior antibiotic treatment has been shown to increase susceptibility to P. aeruginosa infection, but the role of microbiota-derived metabolic cues in this context is still elusive. This study investigates how tryptophan metabolites from the indigenous microbiota affect P. aeruginosa virulence. In vitro tests on motility, biofilm production, and pigment quantification (pyocyanin and pyoverdine) were performed on P. aeruginosa strains (PAO1, PA103, PA14) and clinical isolates. Additionally, gene expression related to virulence was analyzed, and the effects of tryptophan metabolites on experimental lung infection in mice were evaluated. Indole, indoleacetic acid (IAA), and indoleacrylic acid (IA) reduced motility and pigment production. IAA and indole promoted biofilm formation, with indole having a stronger effect. Clinical isolates showed significant phenotypic diversity, and IAA was more effective at inhibiting virulence traits than indole or IA. Mice infected with bacteria grown in the presence of IAA had lower lethality and fewer polymorphonuclear leukocyte influx compared to the control group. This suggests that tryptophan metabolites, especially IAA, can modulate P. aeruginosa virulence and may help control infection progression.},
}

Animals
*Pseudomonas aeruginosa/drug effects/pathogenicity/genetics
*Indoleacetic Acids/pharmacology/metabolism
Virulence/drug effects
Biofilms/drug effects/growth & development
Mice
*Pseudomonas Infections/microbiology/drug therapy
Disease Models, Animal
Humans
Indoles/pharmacology/metabolism
Lung/microbiology
Female
Tryptophan/metabolism
Pyocyanine/metabolism

@article {pmid41384120,
year = {2025},
author = {Li, X and Guo, G and Shi, Q and Chen, Q and Li, L},
title = {Association study between intestinal microbiota dysbiosis in inflammatory bowel disease and the global disease burden growth trend.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1635242},
pmid = {41384120},
issn = {2296-858X},
abstract = {BACKGROUND: Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a group of chronic intestinal inflammatory diseases. Its incidence and prevalence have been on the rise globally, imposing a heavy burden on patients' health and social medical resources. Intestinal microbiota dysbiosis is believed to play a crucial role in the occurrence and development of IBD, but the association between them and the global disease burden growth trend remains unclear.

METHODS: By searching the Global Burden of Disease (GBD) study database, we collected IBD disease burden data from 180 countries and regions between 1990 and 2023, including key indicators such as incidence, prevalence, mortality, and disability-adjusted life years (DALYs). Intestinal microbiota data were sourced from two parts: (1) Independent collection: A total of 20,000 healthy individuals and IBD patients were selected as research subjects from 180 countries and regions using a stratified random sampling method. Fecal samples (2-5 grams per person) were collected and immediately stored in a -80 °C ultra-low temperature refrigerator to avoid changes in the microbial community structure; (2) Supplementary data from public databases: Published intestinal microbiota sequencing data of corresponding regions from 1990 to 2023 were extracted from the MGnify (https://www.ebi.ac.uk/metagenomics/), Human Microbiome Project (HMP), and GMrepo (https://gmrepo.humangut.info/) databases. The sample size for each country and region was no less than 500 to cover populations of different ages (18-70 years), genders (male/female ratio approximately 1:1), and dietary habits (high-fiber diet, high-sugar and high-fat diet). Technologies like metagenomic sequencing and 16S rRNA gene sequencing were used to obtain data on the composition, abundance, and diversity of the intestinal microbiota of the corresponding regional populations. For metagenomic sequencing, the Illumina HiSeq or NovaSeq platform was used. Linear regression models, time-series analysis, and causal inference methods were applied to evaluate the correlation between intestinal microbiota dysbiosis and the growth trends of various disease burden indicators, and to explore the potential impact mechanisms.

RESULTS: The global incidence of IBD increased from 12.3 per 100,000 in 1990 to 25.6 per 100,000 in 2023, the prevalence rose from 396 per 100,000 to 523 per 100,000, and the DALY value also increased significantly (from 230 per 100,000 in 1990 to 380 per 100,000 in 2023). The average annual growth rates of the above indicators were 2.8% (95% CI: 2.5-3.1%, p < 0.001), 1.0% (95% CI: 0.8-1.2%, p < 0.001), and 1.5% (95% CI: 1.3-1.7%, p < 0.001), respectively. Further analysis showed that intestinal microbiota dysbiosis was closely related to the growth of the disease burden. In regions with severe microbiota dysbiosis, the annual growth rate of the IBD incidence was 3.2 times higher than that in balanced regions (β = 3.2, 95% CI: 2.8-3.6, p < 0.001); when the average abundance of beneficial bacteria such as Bifidobacterium and Lactobacillus in the intestine decreased by 40% (relative to the average abundance of healthy populations) and the abundance of harmful bacteria such as Escherichia coli increased by 60%, the annual growth rate of IBD incidence in this region was as high as 8.5% (95% CI: 7.9-9.1%, p < 0.001); in regions where the Shannon index decreased by 10%, the incidence of IBD increased by an average of 15% (β = 0.15, 95% CI: 0.12-0.18, p < 0.001). A positive correlation was observed between the degree of intestinal microbiota dysbiosis and disease severity (measured by DALYs): in regions where the intestinal F/B ratio deviated from the normal range by more than 30%, DALYs were 40% higher than those in regions with a normal ratio (β = 0.40, 95% CI: 0.35-0.45, p < 0.001); in regions where the content of short-chain fatty acids (SCFAs) decreased by 20%, DALYs increased by approximately 25% (β = 0.25, 95% CI: 0.21-0.29, p < 0.001). Among IBD patients with different severity levels in the Asian region, the abundance of specific bacterial genera related to inflammation regulation (e.g., Faecalibacterium) in the intestines of severe patients decreased by more than 50% compared with healthy populations, and their DALY values were 60% higher than those of mild patients (95% CI: 55-65%, p < 0.001). Additionally, the SCFA levels of severe patients were significantly lower than those of mild patients and healthy populations (median SCFA level: 2.1 mmol/L in severe patients; 4.5 mmol/L in mild patients; 6.8 mmol/L in healthy populations, p < 0.001).

CONCLUSION: This study confirms a close association between intestinal microbiota dysbiosis in inflammatory bowel disease and the global disease burden growth trend. Intestinal microbiota dysbiosis can be used as a key indicator to predict the growth of the IBD disease burden, providing an important theoretical basis for formulating targeted prevention, control strategies, and treatment methods.},
}

@article {pmid41384118,
year = {2025},
author = {Bautista, J and Cardona-Maya, WD and Gancino-Guevara, K and López-Cortés, A},
title = {Reprogramming prostate cancer through the microbiome.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1690498},
pmid = {41384118},
issn = {2296-858X},
abstract = {Prostate cancer (PCa) is a major global public health challenge, driven by a multifactorial interplay of genetic, epigenetic, hormonal and environmental determinants. In recent years, the human microbiome has emerged as a critical and previously underappreciated contributor to PCa initiation, progression, and therapeutic response. Emerging high-resolution multi-omics studies have demonstrated that microbial communities across the gut, urinary tract and prostate form a functional axis that shapes immune surveillance, hormonal metabolism, inflammatory tone and epigenetic regulation. Dysbiosis in these compartments promotes chronic inflammation, modulates androgen receptor signaling, and produces bioactive metabolites, including short-chain fatty acids, that activate oncogenic IGF-1/MAPK/PI3K and NF-κB/JAK/STAT pathways. Cross-compartmental trafficking of bacterial taxa and metabolites reinforces tumor-promoting circuits, while specific commensals such as Akkermansia muciniphila enhance antitumor immunity and improve responses to androgen deprivation therapy. Importantly, microbiota-derived factors also modulate microRNA (miRNAs) expression and epigenetic signatures, thereby affecting tumor plasticity and resistance to therapy. These mechanistic insights have catalyzed interest in microbiome-based therapeutic approaches, including probiotics, prebiotics, fecal microbiota transplantation, dietary modulation and bacteriophage therapy, which hold promise for restoring eubiosis and enhancing treatment efficacy. Nevertheless, clinical translation remains limited by inter-individual variability and the need for well-designed, longitudinal studies integrating shotgun metagenomics, metabolomics and host-microbe interactomics. Overall, the prostate, urinary and gut microbiomes represent interconnected targets that may inform precision diagnostics and novel therapeutic strategies in PCa.},
}

@article {pmid41384017,
year = {2025},
author = {Long, XF and Fang, YQ and Li, YH and Li, JY and Wang, XP and Wang, XL and Zhang, L and Liu, Y},
title = {Combination metformin and liraglutide in PCOS: clinical efficacy in women and preclinical insights from gut microbiome modulation in rats.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1599879},
pmid = {41384017},
issn = {1664-2392},
mesh = {Animals ; Female ; *Metformin/therapeutic use/administration & dosage/pharmacology ; *Polycystic Ovary Syndrome/drug therapy/microbiology/pathology ; *Liraglutide/therapeutic use/administration & dosage/pharmacology ; Rats ; *Gastrointestinal Microbiome/drug effects ; Humans ; Rats, Sprague-Dawley ; Adult ; *Hypoglycemic Agents/therapeutic use/administration & dosage/pharmacology ; Drug Therapy, Combination ; Young Adult ; Treatment Outcome ; },
abstract = {BACKGROUND: Metformin and liraglutide have been gradually used in the treatment of polycystic ovary syndrome (PCOS) due to their metabolic benefits, but also with some adverse reactions. Evidence suggests that gut microbiota imbalance plays an important role in the pathogenesis of PCOS. This study comprised a clinical trial to evaluate the efficacy of metformin, liraglutide, and their combination in PCOS women, and a parallel animal experiment to explore the potential involvement of gut microbiota.

METHODS: In an open-label randomized controlled trial, sixty overweight/obese women with PCOS were randomized to: the MET group received oral metformin (0.85 g twice daily; n=20), the LIRA group received subcutaneous liraglutide (1.2 mg once daily; n=20), and the COM group received both treatments (n=20) for 12 weeks. In a separate animal study, female Sprague-Dawley rats were divided into five groups: (1) PCOS model group (letrozole 1 mg/kg orally); (2) MET group (letrozole + metformin 200 mg/kg orally); (3) LIRA group (letrozole + liraglutide 0.2 mg/kg subcutaneously); (4) COM group (letrozole + metformin + liraglutide at above doses); and (5) healthy controls (no treatment). All treatments lasted 4 weeks.

RESULTS: In the clinical trial, women in MET, LIRA, and COM groups showed significant reductions in body weight, blood glucose, blood lipid, and the LH/FSH ratio. Notably, body weight, BMI, visceral fat area, and body fat percentage decreased more significantly in the COM group than in the MET group (P<0.05). Compared with the MET group, the COM group was more effective in reducing free testosterone (P=0.01). In the animal experiment, the body weight, estrus cycle, and ovarian morphology of rats in the COM group were significantly improved. Letrozole-induced PCOS rats showed intestinal flora disorder, which was improved by metformin, liraglutide, and their combination by altering the alpha and beta diversity and relative abundance of the gut microbiota.

CONCLUSION: Metformin combined with liraglutide significantly improved metabolic and endocrine characteristics in PCOS women. The associated amelioration of gut microbiota dysbiosis in PCOS rats suggests a potential mechanistic link, which warrants verification in future clinical studies.},
}

Animals
Female
*Metformin/therapeutic use/administration & dosage/pharmacology
*Polycystic Ovary Syndrome/drug therapy/microbiology/pathology
*Liraglutide/therapeutic use/administration & dosage/pharmacology
Rats
*Gastrointestinal Microbiome/drug effects
Humans
Rats, Sprague-Dawley
Adult
*Hypoglycemic Agents/therapeutic use/administration & dosage/pharmacology
Drug Therapy, Combination
Young Adult
Treatment Outcome

@article {pmid41383770,
year = {2025},
author = {ElNaggar, S and Chen, WC and Prodehl, LM and Marumo, TK and Khan, MU and Mathew, CG and Ruff, P and Jin, Z and Neugut, AI and Rustgi, AK and Uhlemann, AC and Korem, T and Abrams, JA},
title = {A generalizable cross-continent prediction of esophageal squamous cell carcinoma using the oral microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.23.690048},
pmid = {41383770},
issn = {2692-8205},
abstract = {Esophageal squamous cell carcinoma (ESCC) is a disease with limited tools for early screening and a poor prognosis. Symptoms typically appear late, and early cancer is hard to detect without endoscopic screening, which is inaccessible in most high-risk areas. Saliva is easily accessible, and its microbiome composition can serve as a marker for upper gastrointestinal tract disease. We studied the potential utility of an oral microbiome signature for ESCC in South Africa, a region with a high incidence of the disease. In a cohort of 48 ESCC patients and 110 controls, we found marked alterations in the oral microbiome in patients with ESCC, including significantly reduced alpha diversity and increased Fusobacterium nucleatum . We devised machine learning models that classify ESCC using microbiome data, finding good performance on held-out samples (area under receiver operating characteristic curve of 0.96), and demonstrated generalization to data across independent studies conducted in different geographic regions (0.64-0.81). Overall, our results demonstrate the potential of the oral microbiome to serve as a non-invasive screening tool for ESCC.},
}

@article {pmid41383769,
year = {2025},
author = {Shen, BA and Asfahl, KL and Lim, B and Bertolli, SK and Minot, SS and Radey, MC and Penewit, K and Ngo, B and Salipante, SJ and Johnston, CD and Peterson, SB and Goodman, AL and Mougous, JD},
title = {The type VI secretion system governs strain maintenance in a wild mammalian gut microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.29.690828},
pmid = {41383769},
issn = {2692-8205},
abstract = {Bacteria inhabiting the mammalian gut coexist in dense communities where contact-dependent antagonism mechanisms are widespread. The type VI secretion system (T6SS) is an interbacterial toxin delivery pathway prevalent among gut Bacteroidales, yet its function in naturally evolved microbiomes remains poorly defined. Here, we examine the physiological role of the T6SS in Bacteroides within a gut community derived from wild mice (the WildR microbiome). Using newly developed genetic tools and a strategy for functional replacement of strains within the WildR community, we demonstrate that the WildR isolate B. acidifaciens employs a T6SS to antagonize co-resident Bacteroidales. We also show that loss of T6SS function compromises the long-term maintenance of B. acidifaciens in the community but not its initial colonization, establishing the system as a determinant of strain persistence. The T6SS we identified resides on an integrative and conjugative element (ICE). ICE-seq, a targeted sequencing approach, reveals that the T6SS-ICE is distributed among select Bacteroidales and Muribaculaceae species in the WildR microbiome, between which it appears to be recently exchanged. We also show that transfer of the T6SS-ICE to WildR isolate Phocaeicola vulgatus confers transient colonization benefits in mice, but an eventual fitness cost. Our findings demonstrate that the T6SS can stabilize the presence of specific strains within a complex, co-evolved gut microbiome, yet its value is context dependent and constrained by the ecological and physiological landscape of the host community.},
}

@article {pmid41383765,
year = {2025},
author = {Satten, GA and Li, M and Zhao, N},
title = {CAFT: A Compositional Log-Linear Model for Microbiome Data with Zero Cells.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.26.690468},
pmid = {41383765},
issn = {2692-8205},
abstract = {BACKGROUND: Differential abundance analysis is fundamental to microbiome research and provides valuable insights into host-microbe interactions. However, microbiome data are compositional, highly sparse (with many zero counts), and influenced by differential experimental biases across taxa. Standard statistical methods often overlook these features. Many approaches analyze relative abundances without accounting for compositionality or rely on pseudocounts, potentially leading to spurious associations and inadequate false discovery rate (FDR) control.

METHODS: We introduce a novel framework for differential abundance analysis of microbiome data: the Compositional Accelerated Failure Time (CAFT) model. CAFT addresses zero read counts by treating them as censored observations that are below a detection limit. This approach is inherently resistant to multiplicative technical bias, eliminates the need for pseudocounts, and addresses compositional bias through the establishment of appropriate score test procedures.

RESULTS: Extensive simulations show that CAFT outperforms competing compositional differential abundance methods, including LOCOM, LinDA, ANCOM-BC2, its robust variant, and LDM-clr by offering more robust type I error and FDR control with or without technical bias. Additionally, we applied CAFT to microbiome data on inflammatory bowel disease (IBD) and the upper respiratory tract (URT) to identify differentially abundant gut microbial taxa between IBD patients and healthy controls, as well as URT taxa distinguishing smokers from non-smokers.

CONCLUSION: We present CAFT, a powerful, robust, and efficient approach for compositional differential abundance analysis. CAFT effectively controls Type I error and maintains FDR control, while demonstrating enhanced power in statistical testing. These capabilities render CAFT a useful tool for compositional microbiome data analysis.},
}

@article {pmid41383742,
year = {2025},
author = {Bian, X and Xu, H and Li, J and Kuang, J and Shi, F and Li, X and Li, J},
title = {Integrated multi-omics reveals distinct maternal and neonatal gut microbial and metabolic signatures associated with small for gestational age status.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1668148},
pmid = {41383742},
issn = {1664-302X},
abstract = {INTRODUCTION: Children born small for gestational age (SGA) have an elevated risk of developing metabolic disorders in later life. However, the underlying gut microbiota and metabolomic alterations in SGA mother-infant dyads remain poorly understood.

METHODS: We performed an integrated analysis of fecal metagenomics, metabolomics, and short-chain fatty acids (SCFAs) profiling in 10 SGA and 10 appropriate for gestational age (AGA) mother-infant dyads at term. Taxonomic composition, microbial functional pathways, carbohydrate-active enzyme (CAZyme) profiles, differential metabolites, and metabolite pathway enrichment were systematically evaluated.

RESULTS AND DISCUSSION: SGA neonates exhibited reduced microbial richness (Chao1 index), distinct beta-diversity, and differential abundance of key bacterial species including increased Enterococcus faecalis and Escherichia coli. Functionally, SGA maternal subjects showed divergent profiles in CAZyme genes, with lower abundance of glycoside hydrolase family 13 subfamily 16, glycosyl transferase family 66, and carbohydrate-binding module family 6, and altered structural polysaccharide degradation capacity. Metabolomic profiling revealed significant perturbations in tryptophan metabolism pathways, notably enriched in kynurenine and taurine derivatives in SGA mother and neonates. Notably, SCFA profiles were disrupted, with increased butyrate in SGA mother and reduced propionate and isobutyrate in SGA neonates. Microbe-metabolite correlation networks revealed strong associations between SGA-specific bacterial taxa and fecal metabolites. In conclusion, our analysis identifies distinct features of the early fecal microbiome and metabolome within 48 h of birth in SGA neonates compared with AGA peers, reflecting differences in initial colonization and metabolism that warrant longitudinal follow-up.},
}

@article {pmid41383738,
year = {2025},
author = {Chen, G and Wiegand, C and Willett, A and Herr, C and Müller, R and Bals, R and Kalinina, OV},
title = {Comparative metagenomic analysis on COPD and health control samples reveals taxonomic and functional motifs.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1636322},
pmid = {41383738},
issn = {1664-302X},
abstract = {Chronic obstructive pulmonary disease (COPD) is a progressive lung condition marked by persistent respiratory symptoms and airflow limitation and significantly affects global health. The intricate relationship between COPD and the lung microbiome has garnered attention, with metagenomic analyses revealing critical insights into microbial community dynamics and their functional roles. In this study, we conducted a comprehensive metagenomic analysis comparing throat samples from COPD patients (n = 26) and healthy controls (n = 32) derived from a large cohort analyzed at the Saarland University Hospital. Taxonomic profiling and differential abundance analysis indicated a significant reduction of the microbial diversity in COPD patients, with notable overrepresentation of pathogenic bacteria, such as Veillonella parvula (NCBI:txid29466), Streptococcus gordonii (NCBI:txid1302), Scardovia wiggsiae (NCBI:txid230143), as well as a less stable microbiome composition than in healthy individuals. Functional profiling identified alterations in metabolic pathways implicating microbial dysbiosis in disease progression. The study also highlighted enrichment of inflammation-related pathways in COPD samples, emphasizing the microbiome's role in inflammatory processes. Comparative analysis of bronchoalveolar lavage (BAL) and throat samples collected from the same 11 individuals further underscored distinct microbial compositions across respiratory tract regions, suggesting spatial variability in microbial communities. Metagenomic approaches including analysis of metabolic pathways showed significant alteration of the microbiome of the lung in COPD.},
}

@article {pmid41383725,
year = {2025},
author = {Zeng, Y and Wu, H and Zhang, H and Ye, X and Chen, L and Ye, Y},
title = {Dexmedetomidine modulates gut microbiota and improves long-term survival in sepsis patients with pre-existing malignancies: a propensity-matched analysis.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1720867},
pmid = {41383725},
issn = {1664-302X},
abstract = {BACKGROUND: The interplay between sedative agents and the gut microbiome may influence long-term outcomes in sepsis, but data are scarce. This study compared the effects of dexmedetomidine vs. propofol sedation on long-term survival in mechanically ventilated sepsis adults, with an exploratory focus on the gut microbiome and pre-existing malignancies.

METHODS: In this multicenter, retrospective cohort study, 1,295 mechanically ventilated adults with sepsis (2013-2020) were analyzed. Propensity score matching (1:1) balanced 27 baseline covariates, producing 177 matched pairs. Primary outcomes were 30-day, 90-day, and 5-year mortality. Secondary outcomes included delirium/coma-free days, cardiovascular safety, and 6-month functional status. Subgroup analyses assessed pre-existing malignancies and high antibiotic exposure (≥7 days before enrollment) as proxies for microbiome disruption. Gut microbiota composition was characterized via 16S rRNA sequencing in a pre-specified subcohort (n = 89).

RESULTS: After matching, dexmedetomidine was associated with significantly lower 5-year mortality (34.5% vs. 45.2%; HR 0.64, 95% CI 0.52-0.79; p = 0.039). Survival curves progressively diverged beyond 180 days. No differences were observed in short-term neurological outcomes or cardiovascular safety. Subgroup analyses showed enhanced survival benefits with dexmedetomidine in patients aged >65, females, those with pulmonary-source sepsis, SOFA >10, baseline delirium, pre-existing malignancies (OR 2.10, 95% CI 1.15-3.85; p = 0.015), and high antibiotic exposure as a proxy for gut dysbiosis (OR 1.95, 95% CI 1.08-3.52; p = 0.028). Exploratory 16S rRNA analysis in a subset (n = 89) revealed that dexmedetomidine was associated with enriched beneficial genera such as Faecalibacterium and Bifidobacterium, while propofol correlated with increased Enterococcusand Escherichia/Shigella.

CONCLUSIONS: Dexmedetomidine sedation is associated with a significant 5-year survival benefit in mechanically ventilated sepsis patients, particularly among those with malignancies or factors predisposing to gut dysbiosis. The observed modulation of the gut microbiome toward a more symbiotic state provides a plausible mechanistic insight into these clinical findings, highlighting a potential role for microbiota-centric strategies in critical care.},
}

@article {pmid41383635,
year = {2025},
author = {Zhu, W and Ni, R and Cai, B and Ma, S and Jiang, J and Wang, B},
title = {In-situ diet-microbiota associations across taxonomic scales in desert-dwelling amphibians and reptiles.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf213},
pmid = {41383635},
issn = {2730-6151},
abstract = {Understanding how host and environmental factors shape gut microbiota is central to microbial ecology and evolution. However, the extent to which gut microbes covary with diet and how such variation reflects host phylogeny, remains unclear under natural conditions. Here, we used DNA metabarcoding of gut contents to analyze the dietary arthropod composition and gut microbiota of four amphibian and three reptile species from the Tarim Desert, Xinjiang, China. These species showed pronounced differences in both diet and microbial profiles. Dominant dietary arthropod families exhibited generally low overlap among species, and dietary variation did not align with host phylogeny. Interestingly, Bufotes pewzowi (amphibian) and Teratoscincus przewalskii (reptile)-the most common species in their respective groups-both primarily consumed ants (Formicidae). Conversely, gut microbial composition more closely reflected host phylogeny than diet, with a clear separation between amphibians and reptiles, particularly in the relative abundances of Bacteroidetes and the genera Bacteroides and Blautia. These findings suggest that the previously reported phylosymbiosis in these species is not primarily driven by dietary overlap. Significant diet-microbiota correlations were observed across all species and within each taxonomic class but were largely absent within species. This highlights taxonomic-level differences in the diet-microbiota relationship, indicating that diet-microbiota covariation is more pronounced over evolutionary timescales than in response to real-time dietary variation. Taken together, our results show that gut microbiota and diet exhibit distinct phylogenetic patterns, with microbiota showing both associations with diet and resilience to short-term dietary changes, underscoring the importance of considering timescales in diet-microbiota studies.},
}

@article {pmid41383632,
year = {2025},
author = {González-Hermosillo, LM and Ávila-Soto, KI and Méndez-García, LA and Cérbulo-Vázquez, A and Esquivel-Velázquez, M and Bueno-Hernández, N and Fonseca-Sánchez, MÁ and Escobedo, G},
title = {The molecular interplay among gut dysbiosis, adipose tissue, and metabolite-derived damage-associated molecular patterns in metainflammation and atherogenesis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1694061},
pmid = {41383632},
issn = {1664-3224},
mesh = {Humans ; *Dysbiosis/immunology/metabolism ; *Atherosclerosis/metabolism/immunology/etiology/pathology ; *Gastrointestinal Microbiome/immunology ; Animals ; *Adipose Tissue/metabolism/immunology/pathology ; *Inflammation/immunology/metabolism ; Macrophages/immunology ; },
abstract = {Metainflammation is a low-grade systemic inflammatory response that can persist for months or even years, during which monocytes, macrophages, and other immune cells become hyperactivated, contributing to metabolic disease and atherogenesis. Although we now better understand the role of metainflammation in atherosclerosis, uncertainty persists about how gut dysbiosis, adipose tissue expansion, and metabolite-derived damage-associated molecular patterns (Md-DAMPs) can trigger metainflammation and promote atherogenesis. In this comprehensive review, we summarize the role of gut dysbiosis in lipopolysaccharide (LPS) production, a component of gram-negative bacteria that can trigger metainflammation by stimulating circulating monocytes and tissue-resident macrophages. We also outline adipose tissue expansion as an additional igniter of metainflammation by driving the expression of hypoxia-inducible factor 1α (HIF-1α), a master transcription factor that leads to nuclear factor kappa B (NFκB)-dependent proinflammatory cytokine production. Furthermore, we thoroughly explored the precise nature of Md-DAMPs, including glutamate, bile acids, lipoproteins, short-chain fatty acids (SCFAs), uric acid, and excess glucose, with emphasis on the molecular mechanisms that mediate their roles in metainflammation and atherosclerosis. Finally, we integrate the molecular interplay among gut dysbiosis, adipose tissue expansion, and Md-DAMPs to a scenario in which circulating monocytes, macrophages, and foam cells contribute to atherosclerotic plaque formation, instability, and rupture. In conclusion, the information examined here may help refresh our conceptual understanding of atherogenesis, incorporating novel actors as gut dysbiosis, adipose tissue expansion, and Md-DAMPs in the complex network that leads to metainflammation and cardiovascular disease.},
}

Humans
*Dysbiosis/immunology/metabolism
*Atherosclerosis/metabolism/immunology/etiology/pathology
*Gastrointestinal Microbiome/immunology
Animals
*Adipose Tissue/metabolism/immunology/pathology
*Inflammation/immunology/metabolism
Macrophages/immunology

@article {pmid41383524,
year = {2025},
author = {Zhang, X and Zhong, M and Li, Y and Wang, H and Xi, G and Wang, F and Cheng, C and Shi, Y},
title = {Oral microbiota and central nervous system diseases: A review.},
journal = {Neuroprotection (Chichester, England)},
volume = {3},
number = {1},
pages = {79-94},
pmid = {41383524},
issn = {2770-730X},
abstract = {Oral microbiota is the second largest microbial colony in the body and forms a complex ecological community that influences oral and brain health. Impaired homeostasis of the oral microbiota can lead to pathological changes, resulting in central nervous system (CNS) diseases. However, the mechanisms and clinical value of how the oral microbiome influences the brain remain unclear. This review summarizes recent clinical findings on the role of the oral microbiota in CNS diseases and proposes potential approaches to understand the way the oral microbiota and brain communicate. We propose three underlying patterns involving neuroinflammation, neuroendocrine regulation, and CNS signaling between oral microbiota and CNS diseases. We also summarize the clinical characteristics and potential utilization of the oral microbiota in ischemic stroke, Alzheimer's and Parkinson's disease, intracranial aneurysms, and mental disorders. Although the current findings are preliminary and clinical evidence is incomplete, oral microbiota is a potential biomarker for the clinical diagnosis and treatment of CNS diseases.},
}

@article {pmid41383079,
year = {2025},
author = {Wilcox, RS and Marenda, MS and Devlin, JM and Pritchett-Corning, KR and Wilks, CR},
title = {Widespread antimicrobial use in laboratory rodent vivaria in North America revealed by a cross-sectional survey of American College of Laboratory Animal Medicine certified veterinarians.},
journal = {Laboratory animals},
volume = {},
number = {},
pages = {236772251385020},
doi = {10.1177/00236772251385020},
pmid = {41383079},
issn = {1758-1117},
abstract = {Antimicrobial resistance (AMR) is a major global threat to human health, animal welfare and sustainable development. Whilst resistance can arise naturally, inappropriate antimicrobial exposure accelerates its emergence. Recognizing this risk, international One Health initiatives emphasize reducing antimicrobial use, especially of drugs considered critical for human medicine. Much of the evidence guiding these efforts comes from food-producing and companion animals, but antimicrobial use in laboratory animals, particularly rodents, remains poorly described. To address this gap, we surveyed all veterinarians certified by the American College of Laboratory Animal Medicine in the United States (921) and Canada (10). A total of 157 veterinarians completed the survey, resulting in a 16.9% overall response rate. The response rate was 16.6% for participants in the United States and 40.0% for those in Canada. Despite a strong response, the small number of eligible veterinarians restricts data extrapolation in the Canadian context. Survey results showed that antimicrobial use is common and routine in rodent vivaria. Overall, 91.7% of respondents reported regular antimicrobial use. Applications included both clinical treatment and research purposes such as induction of microbiome dysbiosis, prophylaxis in immunocompromised rodents and gene induction. Reported drug classes included fluoroquinolones and third-generation cephalosporins, with some use of glycopeptides and carbapenems, all considered critically important to human health. Disposal practices often involved release into sewerage or landfill without inactivation, raising environmental concerns. These findings suggest that antimicrobial use in laboratory rodents may represent an underrecognized contributor to AMR and highlight the importance of targeted stewardship.},
}

@article {pmid41382996,
year = {2025},
author = {Xie, Y and Zeng, J},
title = {[Mechanisms and protective strategies for astronaut skin injury in deep space environments].},
journal = {Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences},
volume = {50},
number = {8},
pages = {1346-1354},
doi = {10.11817/j.issn.1672-7347.2025.250443},
pmid = {41382996},
issn = {1672-7347},
support = {2024RC3064//the Science and Technology Innovation Program of Hunan Province/ ; },
mesh = {Humans ; *Astronauts ; *Skin/injuries/radiation effects ; *Space Flight ; *Weightlessness/adverse effects ; Wound Healing ; Extraterrestrial Environment ; },
abstract = {With the continuous advancement of deep space exploration missions, maintaining astronaut skin health has become a critical medical issue affecting the safety and effectiveness of long-duration missions. Deep space environmental stressors, including microgravity, ionizing radiation, lunar dust exposure, and microbiome dysbiosis, can synergistically disrupt the skin barrier structure, leading to immune homeostasis imbalance and impaired wound healing. In recent years, research on skin protection in deep space has gradually evolved into a systematic "multi-dimensional integrated protective" framework. From the engineering protection perspective, optimization of multi-layer composite spacesuit structures, the use of hydrogen-rich and boron-containing shielding materials, as well as cabin temperature-humidity regulation and debris-resistant technologies, have greatly enhanced environmental defense capacity. From the biomedical protection perspective, functional hydrogels, antimicrobial dressings, and active compounds derived from traditional Chinese medicine have demonstrated remarkable potential in repairing the skin barrier, modulating immunity, and providing antioxidant defense. Meanwhile, the development of skin microecological interventions and wearable physiological monitoring systems has fostered a trend toward personalized health management. Future research should focus on elucidating the interactive mechanisms among the space environment, skin, and immune barrier, while exploring intelligent monitoring and nanotechnology-based protection strategies. Establishing a predictive and preventive skin health safeguarding system will provide comprehensive medical support for future deep space missions.},
}

Humans
*Astronauts
*Skin/injuries/radiation effects
*Space Flight
*Weightlessness/adverse effects
Wound Healing
Extraterrestrial Environment

@article {pmid41382286,
year = {2025},
author = {Rousseau, C and Tanguy, G and Legeay, E and Blanquart, S and Belcour, A and Rousvoal, S and Potin, P and Leblanc, C and Dittami, SM},
title = {A duo of fungi and complex and dynamic bacterial community networks contribute to shape the Ascophyllum nodosum holobiont.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-025-00825-z},
pmid = {41382286},
issn = {2524-6372},
support = {AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; AAPG2020//ANR-20-CE43-0013/ ; },
abstract = {BACKGROUND: The brown alga Ascophyllum nodosum and its microbiota form a dynamic functional entity named holobiont. Some microbial partners may play a role in seaweed health through bioactive compounds crucial for normal morphology, development, and physiological acclimation. However, the full spectrum of the microbial diversity and its variations according to algal life stage, season, and location have not been comprehensively studied. This study uses 208 short-read metabarcoding samples to characterize the bacterial, archaeal, and microeukaryotic communities of A. nodosum across three nearby sites, four thallus parts, and a monthly survey, aiming to explore the dynamics of ecological interactions within the holobiont.

RESULTS: Our results revealed that A. nodosum harbors a predominantly bacterial microbiota, varying significantly across all covariables, while archaea were virtually absent. An innovative normalization using the co-amplified host reads provided an estimation of bacterial abundance, revealing a drastic decline in May, potentially linked to epidermal shedding. In contrast, fungal communities were stable, dominated by Mycophycias ascophylli and Moheitospora sp., which remained closely associated with the host year-round. We identified a core microbiome of 22 ASVs, consistently found in all samples, including Granulosicoccus, a genus consistently abundant in other brown algal microbiota. Sequence clustering revealed multiple species which vary according seasons, even in the overall stable Granulosicoccus genus. Co-occurrence network analysis revealed putative interactions between microbial groups in response to ecological niches.

CONCLUSIONS: Overall, these findings highlight the dynamic of bacterial interactions and stable fungal associations within the A. nodosum holobiont, providing new insights into the ecology of its microbiota.},
}

@article {pmid41382248,
year = {2025},
author = {Gurung, A and Callens, M and Massol, F and Souffreau, C and Mukherjee, S and Houwenhuyse, S and Stoks, R and De Meester, L and Decaestecker, E},
title = {Investigating the core microbiome concept: Daphnia as a case study.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-025-00834-y},
pmid = {41382248},
issn = {2524-6372},
support = {C16/23/003//Onderzoeksraad, KU Leuven , Belgium/ ; G092619N, G014423N and G061824N//Fonds Wetenschappelijk Onderzoek/ ; },
abstract = {BACKGROUND: Host-associated microbiomes play an important role in the ecology and fitness of organisms. Given their significance, it is much debated to what extent these associations are widespread and even obligatory. Such frequent associations are captured by the concept of the core microbiome. The cladoceran Daphnia is a pivotal genus in freshwater ecosystems occupying a central position in the food webs of standing waters. With its unique standing in pelagic waters, Daphnia serves as a key grazer, regulating algal populations and nutrient cycling, making its microbiome essential to understanding ecosystem function and stability. In recent years, Daphnia has become an increasingly popular study system for exploring host‒microbiota interactions. There is, however, limited knowledge on the baseline taxa that consistently inhabit this host and potentially contribute to its fitness. Identifying whether such a host-associated "core microbiome" exists for Daphnia and, if so, which microbial taxa it comprises is important both for enhancing our ecological understanding of this genus and its ecosystem function and for interpreting future experiments.

RESULTS: We compiled a dataset on Daphnia magna microbiome based on 12 published studies, comprising gut and whole microbiome samples of both laboratory-cultured and field-grown animals across five countries spanning three continents. To identify core taxa, we employ quantification metrics based on prevalence and a combination of prevalence and relative abundance. Our analysis demonstrates that the D. magna microbiome is highly variable, yet, a consistent association with specific taxa, notably Limnohabitans planktonicus, is observed especially under laboratory conditions. However, this pattern is tempered by the observation that field-grown animals exhibit a more diverse microbiome with a weaker presence of L. planktonicus, challenging its status as a core member.

CONCLUSIONS: Our analysis suggests that the D. magna microbiome is defined by its high variability and few conserved associations, with L. planktonicus being the most stable taxon in laboratory settings but not necessarily a core member in natural environments. These findings underscore the need for caution when using laboratory results to interpret natural microbiome compositions and emphasize the need for further research on field-grown animals to better understand the structuring of microbial communities under natural settings.},
}

@article {pmid41382244,
year = {2025},
author = {Bae, IH and Kim, H and Kim, SM and Lee, YH},
title = {Multi-meta-omics reveal unique symbiotic synchronization between ectomycorrhizal fungus and soil microbiome in Tricholoma matsutake habitat.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02292-7},
pmid = {41382244},
issn = {2049-2618},
support = {RS-2022-NR072199//National Research Foundation of Korea/ ; RS-2025-00512558//National Research Foundation of Korea/ ; },
abstract = {BACKGROUND: Ectomycorrhizal (ECM) fungi establish symbiotic relationships with plant roots, enhancing nutrient uptake, improving plant health, and boosting ecosystem resilience. Although previous studies reported molecular interactions among plant-ECM fungi-surrounding microbes near plant roots, microbiome-wide metabolic shifts and associations with the fungi remain unclear.

RESULTS: Using Tricholoma matsutake as a model, we initially found that T. matsutake induced remarkable microbial community turnover linked to altered soil moisture, nitrogen, and phosphorus levels. Parallel with the compositional alteration, microbiome-wide metabolic capacities, including glutamate metabolism, oligopeptide transport, and siderophore activity, were enriched in the T. matsutake-colonizing soil compared to the soils where the fungus was not colonized. From metatranscriptome data, we found that T. matsutake induced functional remodeling in nitrogen metabolism. Notably, the fungus and soil microbiome were metabolically synchronized with the upregulation of nitrate reduction, glutamate biosynthesis, tryptophan biosynthesis, and indole-3-acetic acid (IAA) biosynthesis. Metabarcoding and metatranscriptome-guided microbial associations revealed potential T. matsutake helper bacteria consisting of Conexibacter and Paraburkholderia. Phage community analyses further showed that the colonization of the ECM fungus influenced phage distributions along with the increase in temperate phage populations. The differential expression of auxiliary metabolic genes also demonstrated that phages could influence bacterial fitness in response to T. matsutake colonization.

CONCLUSION: Our multi-meta-omics-based approaches revealed unique environmental changes by T. matsutake compared to other mycorrhizal systems, as well as metabolic synchronization between the ECM fungus and surrounding microbiomes. These findings will expand our understanding of ECM symbiotic frameworks by highlighting integrated microbial and viral metabolic dynamics. Video Abstract.},
}

@article {pmid41382235,
year = {2025},
author = {Ventura, JP and Lacerda-Júnior, GV and Rados, T and Bisson, A and Fernandes-Júnior, PI and Melo, IS},
title = {Harnessing haloarchaea from halophyte Atriplex nummularia rhizosphere to enhance salt stress tolerance in maize seedlings.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-025-00698-2},
pmid = {41382235},
issn = {2524-6372},
abstract = {Soil salinization is a critical global issue threatening agricultural productivity and significantly reducing the availability of arable land. Effective mitigation and recovery strategies are vital for sustaining food production, especially in the context of climate change. Halophytic plants, such as Atriplex nummularia, have shown potential for remediating saline soils, though their large-scale application remains limited. An alternative approach involves leveraging microorganisms adapted to saline environments to enhance plant stress tolerance. In this study, we investigated the microbiome of A. nummularia under saline and non-saline irrigation conditions to identify extremophilic microorganisms that promote salt stress tolerance. Through 16S rRNA analysis, we identified members of the genus Haladaptatus exclusively in the rhizosphere of salt-irrigated plants. These microorganisms were isolated and inoculated into maize crop systems to evaluate their ability to confer salt tolerance. Our results demonstrate that Haladaptatus strains significantly enhance salinity tolerance in maize, with a marked increase in the relative abundance of archaeal 16S rRNA in soils as NaCl irrigation levels rise. This study provides the first evidence that Haladaptatus, an archaeon isolated from the rhizosphere of a halophyte, can significantly enhance salt tolerance in an agriculturally important crop. These findings suggest a promising biotechnological application for improving crop resilience in saline environments, offering a sustainable strategy for addressing soil salinization and securing food production in the context of global climate challenges.},
}

@article {pmid41382117,
year = {2025},
author = {Wang, Y and Bai, Z and Sun, J and Gong, Q and Miao, W and Niu, Z and Li, X and Xu, J and Lai, Z},
title = {Intestinal congestion-driven gut dysbiosis: a cross-disease hemodynamic mechanism in liver cirrhosis and heart failure.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-025-07547-3},
pmid = {41382117},
issn = {1479-5876},
support = {SYYYRC-2022006//First Hospital of Shanxi Medical University/ ; 202103021224408//Natural Science Foundation of Shanxi Province/ ; 202203021221248//Natural Science Foundation of Shanxi Province/ ; 202204010931008//Shanxi Provincial Science and Technology Department/ ; YDZJSX2021B012//Shanxi Provincial Science and Technology Department/ ; 82470693//Innovative Research Group Project of the National Natural Science Foundation of China/ ; 2023065//Health Commission of Shanxi Province/ ; },
}

@article {pmid41381939,
year = {2025},
author = {Spychała, K and Piecuch, A and Korzekwa, K and Szleszkowski, Ł and Thannhäuser, A and Siuta, J and Kadej, M and Ogórek, R},
title = {Myco- and microbiological profiling of a human cadaver reveals drug-resistant strains and new fungal records.},
journal = {Applied microbiology and biotechnology},
volume = {109},
number = {1},
pages = {268},
pmid = {41381939},
issn = {1432-0614},
mesh = {Humans ; Cadaver ; *Fungi/drug effects/isolation & purification/classification/genetics ; Microbial Sensitivity Tests ; *Bacteria/drug effects/isolation & purification/classification/genetics ; Antifungal Agents/pharmacology ; *Drug Resistance, Fungal ; *Mycobiome ; Anti-Bacterial Agents/pharmacology ; Microbiota ; },
abstract = {In this study, the composition of the postmortem mycobiome and microbiome of a cadaver in an advanced stage of decomposition, had been deposited outdoors and showed extensive mycelial growth, was characterized using culture methods. This approach allowed for the identification of a total of 26 fungal and 16 bacterial species. The dominant fungal species were Penicillium polonicum, Debaryomyces hansenii, and Penicillium commune. Sensitivity tests for voriconazole and amphotericin B were also performed, to which several isolates were resistant. In the case of bacteria, the distribution of dominant species differed between samples taken from outside the body and samples taken from inside the body. Sensitivity tests for 16 antibiotics showed that 23.08% of isolates were resistant to the tested drugs. Importantly, to the best of our knowledge, we detected several species that have not been previously associated with cadavers: Botryotrichum domesticum, Chaetomium subaffine, Penicillium allii, Scopulariopsis crassa, Scopulariopsis fusca and Yarrowia deformans. These results not only expand our understanding of the ecological roles of fungi in cadaver decomposition but also highlight their potential forensic value. First and foremost, it broadens our understanding of local fungal communities associated with human remains, which in the future may provide valuable information about the location or environmental conditions of body deposition, while specific taxa could assist in estimating the postmortem interval. Moreover, the identification of drug-resistant strains underscores the importance of biosafety in forensic practice and raises awareness of the potential for pathogen dissemination from decomposing remains. KEY POINTS: • Twenty-six fungi and sixteen bacterial species were identified from the cadaver • New fungal records isolated from human remains, expanding forensic mycology knowledge • Antimicrobial susceptibility testing revealed the presence of drug-resistant fungal and bacterial isolates.},
}

Humans
Cadaver
*Fungi/drug effects/isolation & purification/classification/genetics
Microbial Sensitivity Tests
*Bacteria/drug effects/isolation & purification/classification/genetics
Antifungal Agents/pharmacology
*Drug Resistance, Fungal
*Mycobiome
Anti-Bacterial Agents/pharmacology
Microbiota

@article {pmid41381886,
year = {2025},
author = {Fu, C and Li, T and Hao, Y and Lin, Y and Qiu, Y and Jia, Y and Yang, J and Liu, B and Hua, D and Wang, C and Chen, T and Piron, A and Cnop, M and Ni, Q and Zheng, J and Ning, G and Gu, Y},
title = {Declining FXR expression coordinates neonatal beta cell mass development with microbial bile acid metabolism maturation in mice.},
journal = {Diabetologia},
volume = {},
number = {},
pages = {},
pmid = {41381886},
issn = {1432-0428},
support = {82100835//National Natural Science Foundation of China/ ; 92157112//National Natural Science Foundation of China/ ; },
abstract = {AIMS/HYPOTHESIS: Diet switch during weaning induces gut microbiome maturation, accompanied by the formation of adequate functional beta cell mass. Bile acid (BA), an essential microbial metabolite, regulates host glucose homeostasis by binding to its main receptor, farnesoid X receptor (FXR, encoded by NR1H4). However, the precise roles of microbial BA metabolism and FXR signalling in neonatal beta cell development are still unclear.

METHODS: Islet FXR levels were determined at different perinatal stages. Postnatal changes in gut microbiome and BA profiles were examined in mice, with changes in germ-free mouse BAs serving as the control. We genetically modified beta cells to sustain FXR expression after birth (using Nr1h4-knockin [βFxrKI] mice) and performed morphological and functional analysis on murine islets. Single-cell RNA-seq and single-cell assay for transposase-accessible chromatin sequencing of islet cells were used to study FXR-mediated downstream regulation in islets. Lineage tracing was performed to evaluate beta cell fate transition. Mendelian randomisation (MR) and human islet proteomics data analysis were applied to study the pathological relevance in human diabetes.

RESULTS: FXR expression in beta cells declined after birth (positive cell proportion, 29.1 ± 3.1% at embryonic day 18.5 vs 4.2 ± 2.4% at 3 weeks postnatal in mice, p<0.001). This physiological change paralleled the ascending of FXR-agonistic BAs derived from gut microbiome maturation (unconjugated BA proportion, 0.9 ± 0.6% at 1 week vs 14.0 ± 5.6% at 3 weeks, p<0.05). βFxrKI mice had limited beta cell mass growth (approximately 70% of the control level at 1 week of age and only 15% of the control level at 8 weeks of age) and developed high blood glucose levels by weaning (random blood glucose, 15.2 ± 1.7 mmol/l in βFxrKI vs 7.7 ± 0.5 mmol/l in control, p<0.001), mainly resulting from elevated cell apoptosis (1.95-, 1.79-, and 3.27-fold increase vs control at 1, 2 and 3 weeks, respectively) and altered beta cell identity. Casp6 was identified as a key downstream target in beta cell FXR. Intervention with antibiotics or a specific caspase-6 (CASP6) inhibitor partially recovered the phenotypes of βFxrKI mice. Further validation in humans showed that islet FXR/CASP6 levels were elevated in individuals with type 2 diabetes (FXR, -0.039 ± 1.257 a.u. in donors without diabetes vs 0.646 ± 1.140 a.u. in donors with diabetes, p=0.0371; CASP6, -1.575 ± 0.307 a.u. in donors without diabetes vs -1.325 ± 0.381 a.u. in donors with diabetes, p=0.011). MR analysis further supported the effect of human islet FXR expression in elevating HbA1c (β=0.006, p<0.001) with lowering fasting insulin level (β=-0.009, p=0.02) and the effect of CASP6 expression in enhancing 2 h glucose (β=0.039, p=0.01).

CONCLUSIONS/INTERPRETATION: The declining FXR-CASP6 signals in neonatal beta cells could serve as a programmed host response to the maturing gut microbial BA metabolism to maintain normal postnatal beta cell mass development and ensure glycaemic homeostasis in adults.

DATA AVAILABILITY: Raw data of scRNA-seq and scATAC-seq are deposited in the Gene Expression Omnibus (GEO) database under the accession number GSE241408. The code used in this Mendelian randomisation study is publicly available at https://github.com/Angela-linyt/Gene_Glu_MR.git .},
}

@article {pmid41381881,
year = {2025},
author = {Park, G and Chung, H},
title = {Endoscopic swab sampling as a novel method for gastric Microbiome profiling: A pilot study compared with tissue biopsy.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-025-32028-4},
pmid = {41381881},
issn = {2045-2322},
}

@article {pmid41381410,
year = {2025},
author = {Abutaleb, NS and Holly, KJ and Metcalfe, CK and Abouelkhair, AA and Tharra, PR and Shrinidhi, A and Abdelsattar, AS and Burgo, V and Melotte, G and Akin-Olabiyi, T and Knoblauch, S and Ramaswamy, R and Woodson, C and Thirumalaikumar, VP and Rodriguez, JA and Yeo, FJ and Snell, OC and Nocentini, A and Sundararajan, A and Olson, MR and Supuran, CT and Seleem, MN and Flaherty, DP},
title = {Bacterial Carbonic Anhydrase Inhibitor CAI0019 Demonstrates Efficacy in Enterococcus faecium Septicemic Peritonitis Mouse Model While Sparing the Microbiome.},
journal = {ACS infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1021/acsinfecdis.5c00736},
pmid = {41381410},
issn = {2373-8227},
abstract = {Vancomycin-resistant enterococci are multidrug-resistant bacteria that as of 2021 continue to pervade the U.S. healthcare system as the second-most prevalent source of healthcare-acquired infections behind Escherichia coli. Given the limited treatment options for vancomycin-resistant enterococci and growing concerns about antibiotic-induced gut microbiome dysbiosis, there is an urgent need for narrow-spectrum antibiotics that can selectively target vancomycin-resistant enterococci while preserving the integrity of the gut microbiome. Previous studies have demonstrated the in vivo potential of orally dosed acetazolamide-based compounds to reduce vancomycin-resistant enterococci bioburden in the gastrointestinal tract and internal organs of mice. However, while it is hypothesized that these molecules inhibit bacterial carbonic anhydrases, the exact target of the acetazolamide scaffold in vancomycin-resistant enterococci has remained unconfirmed. Additionally, the impact of the scaffold on in vivo gut microbiome diversity remains uncharacterized. The work herein reports the chemoproteomic identification of α-carbonic anhydrase as the primary target of the acetazolamide scaffold in E. faecium and presents its uniqueness as a narrow-spectrum antibiotic target that can be exploited by CAI0019, a lead acetazolamide derivative with in vivo efficacy, while sparing gut microbiome diversity in mice. This work presents compelling data that not only confirm α-carbonic anhydrase as an antibiotic target in Enterococcus but also demonstrate that narrow-spectrum in vivo antienterococcal efficacy can be achieved through targeting α-carbonic anhydrase such that gut commensal microbiota remain unimpacted.},
}

@article {pmid41381080,
year = {2025},
author = {Chantakhow, S and Kunasol, C and Khorana, J and Tepmalai, K and Chattipakorn, N and Chattipakorn, SC},
title = {Longitudinal analysis of gut microbiota dysbiosis and bacterial signatures predictive of postoperative enterocolitis in children with Hirschsprung disease.},
journal = {Clinical and experimental pediatrics},
volume = {},
number = {},
pages = {},
doi = {10.3345/cep.2025.01886},
pmid = {41381080},
issn = {2713-4148},
abstract = {BACKGROUND: We aimed to investigate differences in gut microbiota between patients with Hirschsprung disease (HSCR) and healthy children; assess longitudinal changes in the microbiota of patients with HSCR from diagnosis through postoperative period; and identify microbial markers predictive of postoperative HSCR-associated enterocolitis (HAEC).

PURPOSE: To investigate alterations in the gut microbiota of patients with HSCR by assessing longitudinal microbiome changes after surgery and identifying microbial signatures predictive of postoperative HAEC.

METHODS: A case-control study of 20 patients with HSCR and 20 controls was conducted at Maharaj Nakorn Chiang Mai Hospital. Fecal specimens were collected from patients with HSCR at initial diagnosis and from age-matched controls. Additional samples were obtained from patients intraoperatively and at 1 and 6 months postoperatively. A microbial analysis was performed using 16S rRNA gene sequencing (V3-V4 hypervariable regions).

RESULTS: Compared to controls, patients with HSCR exhibited gut dysbiosis characterized by reduced microbial diversity and altered community composition as determined by Analysis of Compositions of Microbiomes with Bias Correction. Increased relative abundances of Robinsoniella, Fusobacterium, Cutibacterium, Citrobacter, and Eubacterium fissicatena were observed in patients with HSCR, whereas NK4A214, Lachnospiraceae XPB1014 groups, Acinetobacter and Acetitomaculum were decreased (q< 0.05). Alpha diversity in patients with HSCR was significantly increased at 6 months postoperatively versus at theinitial diagnosis (P<0.05). Longitudinal changes in Eubacterium and Eubacteriales suggest their potential use as markers of treatment efficacy. In patients who developed postoperative HAEC, Olsenella was enriched in the proximal intestine, whereas Holdemanella, Corynebacterium, Collinsella, and CAG-352 were elevated in the distal intestine (q<0.05).

CONCLUSION: Patients with HSCR exhibited distinct alterations in the gut microbiota, with significant shifts observed between the pretreatment period and 6 months postoperatively. Specific bacterial taxa were identified as potential markers for HAEC development. Future microbiome- targeted.},
}

@article {pmid41381065,
year = {2025},
author = {Benga, L and Benten, WPM and Bischoff, SJ and Christensen, H},
title = {Why Is the Current Monitoring of Rodentibacter spp. Exclusively by Molecular Methods Insufficient?.},
journal = {Journal of the American Association for Laboratory Animal Science : JAALAS},
volume = {},
number = {},
pages = {1-4},
doi = {10.30802/AALAS-JAALAS-25-143},
pmid = {41381065},
issn = {2769-6677},
abstract = {The former [Pasteurella] pneumotropica complex has rendered until now 12 Rodentibacter species, which has implications in the monitoring of these highly prevalent laboratory rodent microorganisms. Rodentibacter spp. are known as classic opportunistic pathogens of laboratory rodents and represent noteworthy members of the oral and genital microbiome, with potential pathophysiological interferences in colonized animals. Laboratory mice and rats are predominantly colonized by host-specific Rodentibacter spp., with R. pneumotropicus and R. heylii as mouse-specific species and R. ratti, R. heidelbergensis, R. rarus, and R. trehalosifermentans as rat-specific species; however, host specificity of R. haemolyticus, currently prevalent in both species, remains to be elucidated. Nevertheless, cross contaminations with the taxa from the opposite host occurs between mice and rats. The monitoring occurs by classic culture and/or by molecular techniques, although the latter are currently available only for a few Rodentibacter taxa. Unfortunately, many current health monitoring strategies do not take into consideration the host specificities of these taxa and are often focused nearly exclusively on the molecular diagnostics of R. pneumotropicus and R. heylii, thus neglecting the remaining taxa. Until future research addresses the lack of molecular tests available for all relevant Rodentibacter spp. and a host-specific monitoring is implemented, we consider that monitoring exclusively by current molecular methods risks missing opportunistic members of this genus. Importing laboratory rodents based on health reports relying solely on molecular assays is currently associated with an increased risk of accepting Rodentibacter-positive animals.},
}

@article {pmid41380668,
year = {2025},
author = {Sumner, JT and Huttelmaier, S and Pickens, CI and Moghadam, AA and Abdala-Valencia, H and Shen, J and , and Hauser, AR and Seed, PC and Wunderink, RG and Hartmann, EM},
title = {Transitions in lung microbiota landscape associate with distinct patterns of pneumonia progression.},
journal = {Cell host & microbe},
volume = {33},
number = {12},
pages = {2148-2166.e8},
doi = {10.1016/j.chom.2025.11.011},
pmid = {41380668},
issn = {1934-6069},
mesh = {Humans ; *Microbiota/genetics ; *Lung/microbiology ; Disease Progression ; RNA, Ribosomal, 16S/genetics ; *Pneumonia/microbiology/pathology ; Metagenomics ; Bacteria/classification/genetics/isolation & purification ; Male ; Female ; Bacterial Load ; Middle Aged ; Aged ; },
abstract = {The precise microbial determinants driving clinical outcomes in severe pneumonia are unknown. Competing ecological forces produce dynamic microbiota states in health and disease, and a more thorough understanding of these states has the potential to improve pneumonia therapy. Here, we leverage a large collection of bronchoscopic samples from patients with suspected pneumonia to determine lung microbial ecosystem dynamics throughout the course of pneumonia. We combine 16S rRNA gene, metagenomic, and metatranscriptomic sequencing with bacterial-load quantification to reveal clinically relevant drivers of pneumonia progression. Microbiota states are predictive of pneumonia subtypes and exhibit differential stability and pneumonia therapy response. Disruptive forces, such as aspiration, are associated with cohesive changes in gene expression and microbial community structure. In summary, we show that host and microbiota landscapes change in unison with clinical phenotypes and that microbiota state dynamics reflect pneumonia progression. We suggest that distinct pathways of lung microbial community succession mediate pneumonia progression.},
}

Humans
*Microbiota/genetics
*Lung/microbiology
Disease Progression
RNA, Ribosomal, 16S/genetics
*Pneumonia/microbiology/pathology
Metagenomics
Bacteria/classification/genetics/isolation & purification
Male
Female
Bacterial Load
Middle Aged
Aged

@article {pmid41380664,
year = {2025},
author = {Ramírez-Sánchez, D and Weigel, D},
title = {Pseudomonas can make or break a happy phyllosphere microbiota.},
journal = {Cell host & microbe},
volume = {33},
number = {12},
pages = {2004-2007},
doi = {10.1016/j.chom.2025.11.006},
pmid = {41380664},
issn = {1934-6069},
mesh = {*Pseudomonas/physiology ; *Microbiota ; *Fusarium/pathogenicity/growth & development ; *Triticum/microbiology ; *Plant Diseases/microbiology ; Hydrogen-Ion Concentration ; },
abstract = {In this issue of Cell Host & Microbe, Xu and colleagues investigate host pH modulation as a microbiome-mediated defense mechanism. Pseudomonas strains can protect wheat against the pathogenic fungus Fusarium graminearum by counteracting alkalinization of the host environment by the fungus, although other Pseudomonas strains support the fungus by further alkalinization.},
}

*Pseudomonas/physiology
*Microbiota
*Fusarium/pathogenicity/growth & development
*Triticum/microbiology
*Plant Diseases/microbiology
Hydrogen-Ion Concentration

@article {pmid41384134,
year = {2023},
author = {Clegg, TJ and Kawmi, N and Graziane, NM},
title = {Different Classes of Antibiotics Have Varying Effects on the Risk of Developing Opioid Use Disorder: A National Database Study.},
journal = {Journal of substance use},
volume = {28},
number = {1},
pages = {101-111},
pmid = {41384134},
issn = {1465-9891},
abstract = {OBJECTIVE: To examine whether different classes of antibiotics in combination with opioids differentially affect the risk of developing opioid use disorder (OUD).

METHODS: A cohort study was conducted to identify adult subjects (18-65 years old) with no previous history of OUD. Two cohorts were defined: subjects who were prescribed an opioid or an opioid in combination with antibiotics in the emergency department or inpatient unit, from the years 2015 to 2018. The diagnosis of an Opioid Related Disorder (F11.10-F11.20) 12 months following discharge from the emergency department or inpatient unit was then observed within the cohorts following the index event as identified by the ICD-10 procedural coding system.

RESULTS: Primary analysis showed that penicillin G had no statistically significant effect, while the following list of antibiotics were associated with increased risk of developing OUD in order from highest to lowest risk: cefepime > tazobactam > ertapenem > doxycycline > ceftriaxone, sulfamethoxazole > clindamycin > azithromycin > ciprofloxacin > penicillins > cefazolin > amoxicillin > penicillin V.

CONCLUSIONS: These findings suggest that the type of antibiotic prescribed in combination with opioid treatment may have important implications on the risk of developing OUD at later time points following hospital discharge.},
}

@article {pmid41380402,
year = {2025},
author = {Huang, Q and Khan, NA and Tang, S and Zhou, C and He, Z and Tan, Z and Liu, Y},
title = {Ecological resilience of the rectal microbiome to environmental stressors in Hulunbuir grazing sheep: response to feed restriction and extreme cold challenge.},
journal = {Journal of thermal biology},
volume = {134},
number = {},
pages = {104351},
doi = {10.1016/j.jtherbio.2025.104351},
pmid = {41380402},
issn = {0306-4565},
abstract = {The gut microbiota is essential for helping animals to adapt to food shortages and extreme environments. In China's Hulunbuir region, local grazing sheep endure harsh winters characterized by intense cold and limited food supply. Uncovering the adaptive mechanisms that underpin their resilience is essential for improving their productivity, breeding practices, and management strategies. This research investigated the effects of feed restriction (set at 40 % of ad libitum intake) and extreme cold stress (temperature-humidity index set at 22.27) on the dynamics of gut microbiota in Hulunbuir sheep. We employed 16S rRNA gene sequencing to investigate alterations in rectal microbial diversity, community composition, and functional pathways in response to these stressors. Our findings revealed a significant reduction in bacterial diversity and microbial community structure in response to both stressors (P < 0.05), with cold stress exerting a more pronounced impact than feed restriction. Several key bacterial genera, including Akkermansia, Christensenellaceae, Monoglobus, Bacteroides, Alistipes, and Solibacillus, were identified as major contributors to the adaptive microbiota-drives responses of Hulunbuir sheep under environmental stress. A Spearman correlation analysis revealed strong associations between these genera and essential functional pathways such as fat digestion and absorption, quorum sensing, and mineral uptake, all of which were differentially regulated in response to stress (|r| > 0.6, Padj < 0.05). These findings offer novel insights into how the gut microbiota in Hulunbuir sheep supports physiological adaptation to extreme cold and nutritional stress, laying a robust foundation for creating microbiota-targeted strategies to enhance resilience, promote animal health, and improve productivity of grazing ruminants in harsh winter environments.},
}

@article {pmid41380320,
year = {2025},
author = {Hundam, S and Al-Zghoul, MB and Almaasfeh, M},
title = {The impact of embryonic thermal manipulation on the microbiome of the jejunum and cecum in response to post-hatch acute heat stress.},
journal = {Poultry science},
volume = {105},
number = {1},
pages = {106212},
doi = {10.1016/j.psj.2025.106212},
pmid = {41380320},
issn = {1525-3171},
abstract = {Thermal manipulation (TM) during embryogenesis has been proposed as a sustainable strategy to enhance thermotolerance and resilience in broiler chickens. However, its long-term Influence on gut microbiota composition, particularly under post-hatch acute heat stress (AHS), remains unclear. This study investigated the effects of TM on the jejunal and cecal microbiota of Ross broilers following AHS. Fertile eggs (n = 182) were incubated under standard conditions (37.8°C and 56 % relative humidity), while the thermally manipulated group (n = 182) was incubated at 38.5°C and 65 % relative humidity for 18 h/day during embryonic days 10-18. On day 35 post-hatch, birds were exposed to 35°C and 60-65 % RH for three hours to induce AHS, and jejunal and cecal contents were analyzed by 16S rRNA gene sequencing (V3-V4 region, Illumina MiSeq). Alpha diversity indices (Shannon, evenness) did not differ significantly between treatments (P > 0.05), although the cecum consistently exhibited higher richness and evenness than the jejunum (P < 0.05). Beta diversity analysis revealed strong separation between intestinal segments but no treatment-driven clustering. Firmicutes and Bacteroidota dominated all groups, with regional enrichment of Lactobacillus and Ligilactobacillus in the jejunum, and Faecalibacterium in the cecum. Differential abundance analysis revealed 30 taxa that differed significantly (q < 0.05) at the family level across intestinal segments. In contrast, comparing the TM, AHS, and control groups within any single segment yielded no significant taxonomic differences after false discovery rate (FDR) correction. These results indicate that anatomical location within the intestine exerts a more substantial influence on microbial community composition than either embryonic or post-hatch heat exposure. The stability of microbial diversity under acute thermal challenge suggests that the beneficial effects of TM on thermotolerance, as reported in the literature, are likely mediated through host physiological or epigenetic mechanisms rather than microbiome remodeling.},
}

@article {pmid41380282,
year = {2025},
author = {Xu, X and Wang, J and Deng, C and Yu, X and Nie, R and Wang, S and Huang, W},
title = {Metagenomic insights into rhizosphere microbiome dynamics of Oenanthe javanica in ecological floating beds under different hydrodynamic regimes.},
journal = {Journal of contaminant hydrology},
volume = {277},
number = {},
pages = {104795},
doi = {10.1016/j.jconhyd.2025.104795},
pmid = {41380282},
issn = {1873-6009},
abstract = {Ecological floating beds (EFBs) are a cost-effective and sustainable technology that utilizes macrophyte to remove nutrients from aquatic ecosystems, where rhizosphere bacterial degradation and assimilation play a key role in nutrient removal. However, the current knowledge about how hydrodynamic regimes impact the rhizosphere bacterial community on EFB systems remains limited. Here, we investigated the effects of different hydrodynamic regimes (i.e., stagnant water, pulsed water, and flowing water conditions) on the rhizosphere bacterial community structure and function of Oenanthe javanica in an experimental EFB system based on metagenomic sequencing. We observed that bacterial community compositions on the roots of O. javanica were significantly differed across the three hydrodynamic regimes, with the highest bacterial biodiversity captured from the flowing water condition. Moreover, a total of 65 nitrogen functional genes (NFGs) were identified in the rhizosphere bacterial community, with nitrate reduction pathways dominating the nitrogen cycling processes. In contrast, totally 139 phosphorus functional genes (PFGs) were detected, primarily involved in purine metabolism, which drove the phosphorus cycling dynamics. We found the distinct nitrogen and phosphorus metabolic strategies of rhizosphere bacterial communities in response to hydrodynamic regime changes. Specifically, the relative abundances of NFGs like nasB, narl, and ansB were significantly increased under the pulsed water condition, whereas gdh_K00262 were relative abundant under the flowing condition. Moreover, pulsed water condition promoted the relative abundances of PFGs such asas phnC, phoD, and pgtP in rhizosphere bacterial communities, in contrast to the stagnant condition, which favored genes like ugpC, purK, phoH, and purA. Our study offers technical support for regulating plant degradation of pollutants to improve EFB's performance in engineering applications.},
}

@article {pmid41380257,
year = {2025},
author = {Zeng, C and Wu, D and Yang, J and Chen, J and Tan, C and Wang, D and Zhang, G},
title = {The effect of maternal exposure to Tris(n-butyl) phosphate on the gut microbiome of SD rats and offspring.},
journal = {Journal of hazardous materials},
volume = {501},
number = {},
pages = {140763},
doi = {10.1016/j.jhazmat.2025.140763},
pmid = {41380257},
issn = {1873-3336},
abstract = {Tris (n-butyl) phosphate (TnBP), a heavily utilized organophosphate ester, remains poorly characterized with respect to its long-term effects on the structure and metabolic capacity of the gut microbiota. The purpose of this study is to explore how TnBP exposure affects the intestinal microbiota of maternal Sprague-Dawley (SD) rats and their corresponding progeny, as well as the impact of its metabolite, dibutyl phosphate (DBP), in the human population. A cross-sectional analysis revealed a significant positive correlation between DBP concentrations and the C-reactive protein/albumin ratio (CAR) in the United States population. Results of 16S rRNA gene sequencing revealed that maternal TnBP exposure significantly increased gut bacterial α-diversity in both dams and their F1-generation offspring (Shannon index, P < 0.05). Principal-coordinate analysis (PCoA) based on Bray-Curtis dissimilarity showed distinct clustering of the microbial communities, and PERMANOVA confirmed significant differences between the exposed and control groupsAt the phylum level, TnBP exposure elicited a proportional expansion of Proteobacteria coupled with concomitant reductions in Bacillota and Bacteroidetes in both dams and their F1 offspring. Genus-level profiling further revealed a selective enrichment of Bifidobacterium and significant perturbations in Lactobacillus, Limosilactobacillus, Muribaculum, Turicibacter, Allobaculum, and Clostridium.Furthermore, TnBP exposure significantly elevated total short-chain fatty acid (SCFA) levels in the offspring, indicating a functional shift in microbial metabolism. Correlation analysis further revealed that under TnBP treatment the relative abundances of Allobaculum and Collinsella were positively associated with the concentrations of acetate, propionate, and butyrate (P < 0.05 for each). Quantitative PCR and histopathological examination collectively demonstrated a pronounced inflammatory signature in the colons of juvenile offspring exposed to TnBP. These observations underscore the potential for persistent adverse health outcomes following developmental exposure and warrant comprehensive mechanistic and epidemiological investigations.},
}

@article {pmid41379981,
year = {2025},
author = {Nicholson, MR and Ma, S and Strickland, BA and Cecala, M and Zhang, L and Reasoner, S and Guiberson, ER and Munneke, MJ and Shilts, MH and Skaar, EP and Das, SR},
title = {The Gut Microbiome and Butyrate Differentiate Clostridioides difficile Colonization and Infection in Children.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiaf631},
pmid = {41379981},
issn = {1537-6613},
abstract = {BACKGROUND AND AIMS: Symptomatic Clostridioides difficile infection (CDI) can cause significant morbidity and mortality. Conversely, patients can be colonized with toxigenic C. difficile in the absence of symptoms, termed asymptomatic colonization. We previously demonstrated that the presence and function of C. difficile toxins do not differentiate between asymptomatic colonization and CDI in children, suggesting the influence of other factors. This study aimed to interrogate the intestinal microbiome and butyrate in stool samples from children with CDI and asymptomatic colonization.

METHODS: Design: Case-control studySetting: Tertiary care children's hospitalParticipants and measures: Asymptomatic children had stool tested for C. difficile by nucleic-acid amplification-based testing (NAAT) and were considered colonized if positive (N=50). Residual stool was also obtained from symptomatic children who tested positive for C. difficile by NAAT (N=55). The microbiome was assessed via 16S rRNA sequencing and butyrate via liquid chromatography-mass spectrometry.

RESULTS: Compared to clinical co-variates and comorbidities, C. difficile symptom status (i.e., asymptomatic colonization versus symptomatic CDI) demonstrated the strongest differential abundance association on gut microbes. Symptomatic CDI was associated with increased abundance of Escherichia/Shigella (Benjamini-Hochberg adjusted q=3.94x10-5), Haemophilus (q=0.022), and Gemella (q=0.085), and depleted abundance of gut commensals such as Faecalibacterium (q=0.041), Blautia (q=0.041), and Bifidobacterium (q=0.063). We also observed depletion in the abundance of microbial butyrate producers and fecal butyrate in participants with symptomatic CDI versus asymptomatic colonization.

CONCLUSION: The gut microbiota and butyrate differ between participants with asymptomatic C. difficile colonization and symptomatic CDI, suggesting their potential role in symptom development.},
}

@article {pmid41379255,
year = {2025},
author = {Špiljak, B and Ozretić, P and Brailo, V and Škrinjar, I and Lončar Brzak, B and Andabak Rogulj, A and Butić, I and Tambić Andrašević, A and Vidović Juras, D},
title = {Microbial dysbiosis and host-microbe interactions in proliferative verrucous leukoplakia: insights into carcinogenic potential.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {65},
pmid = {41379255},
issn = {1432-072X},
mesh = {Humans ; *Dysbiosis/microbiology ; *Leukoplakia, Oral/microbiology/pathology ; Microbiota ; *Host Microbial Interactions ; Carcinogenesis ; Mouth Neoplasms/microbiology/pathology ; },
abstract = {Proliferative verrucous leukoplakia (PVL) is a rare and aggressive oral potentially malignant disorder (OPMD) characterized by multifocal keratotic plaques, progressive expansion, high recurrence, and a strong risk of malignant transformation. Although its etiology remains unclear, recent evidence emphasizes the role of the oral microbiome as a key factor in disease progression. Alterations in microbial diversity and ecological balance create a shift toward dysbiosis, supporting a chronic inflammatory microenvironment that favors epithelial transformation. Specific taxa, including Fusobacterium and Porphyromonas, have been implicated in biofilm formation, immune evasion, and modulation of epithelial signaling pathways. These interactions highlight the potential of microbial communities to drive oncogenic processes through host-microbe crosstalk. Advanced methodological approaches such as metagenomics, functional microbiome profiling, and multi-omics integration provide novel opportunities to unravel the mechanisms of dysbiosis in PVL. Beyond pathogenesis, microbiome research opens perspectives for the identification of predictive biomarkers, targeted prevention, and microbiome-based therapeutics. This review synthesizes current insights into the microbial basis of PVL and outlines future directions aimed at improving understanding of host-microbe interactions and their role in oral carcinogenesis. Relevant literature was identified through PubMed and Web of Science searches (1985-2025) using terms related to PVL, oral leukoplakia, OPMD, oral microbiome, and oral squamous cell carcinoma. In conclusion, current evidence suggests that while microbial dysbiosis is not an isolated driver, it likely synergizes with genetic, epigenetic, and immunological factors in PVL progression, offering opportunities for biomarker discovery and novel therapeutic strategies. This study also provides a potential direction for the early diagnosis of PVL and the development of microecologically targeted interventions.},
}

Humans
*Dysbiosis/microbiology
*Leukoplakia, Oral/microbiology/pathology
Microbiota
*Host Microbial Interactions
Carcinogenesis
Mouth Neoplasms/microbiology/pathology

@article {pmid41379245,
year = {2025},
author = {Namadara, S and Pragadeesh, ARU and Uthandi, S and Rangasamy, A and Malaichamy, K and Venkatesan, M and Narayanan, MB and Murugaiyan, S},
title = {Comparative metagenomic analysis of bacterial communities associated with two mealybug species, Phenacoccus saccharifolii and Dysmicoccus carens infesting sugarcane in Tamil Nadu, India.},
journal = {World journal of microbiology & biotechnology},
volume = {41},
number = {12},
pages = {504},
pmid = {41379245},
issn = {1573-0972},
support = {DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; },
mesh = {*Saccharum/parasitology ; Animals ; India ; *Bacteria/classification/genetics/isolation & purification ; *Hemiptera/microbiology ; RNA, Ribosomal, 16S/genetics ; *Metagenomics/methods ; *Gastrointestinal Microbiome/genetics ; Phylogeny ; DNA, Bacterial/genetics ; },
abstract = {This study presents a comparative metagenomic analysis of the gut bacterial communities of two sugarcane-infesting mealybug species, Phenacoccus saccharifolii (WR) and Dysmicoccus carens (RR), from Tamil Nadu, India. Using Oxford Nanopore sequencing of the 16s rRNA gene spanning the hypervariable regions V1 - V9 and predictive metagenomics, differences in microbial diversity, taxonomy, and functional potential were assessed to explore the ecological adaptations of the gut microbiota in mealybugs. The D. carens gut microbiome showed higher species richness than P. saccharifolii (WR) (125 vs. 45 species, p < 0.05) but lower community evenness (0.43 vs. 0.61, p < 0.05), resulting in similar overall Shannon diversity (2.08 vs. 2.30) despite markedly different community structures, which may be influenced by their different feeding niches, including the sugarcane crown region, leaf sheath tissues, and basal stem and root portions. Both mealybug species exhibited contrasting bacterial community structures. D. carens (RR) harbored high abundances of endosymbionts (43.8%), Gilliamella (22.3%), Enterobacter (18.3%), and Candidatus Tremblaya (9.3%), representing a symbiont-dominated microbiome typical of many hemipteran insects. P. saccharifolii (WR) displayed a distinct profile with Serratia as the dominant genus (43.2%), followed by Enterobacter (20.1%), Klebsiella (14.6%), and substantially reduced endosymbiont abundances (14.8%). Beta diversity analysis revealed distinct community clustering of species, highlighting the variation driven by feeding habitat and host genotype. Functional profiling indicated largely conserved metabolic capabilities dominated by amino acid and carbohydrate metabolism, which was a key to compensate the nutrient-poor phloem sap diet. The core microbiome identified several genera that form complex ecological networks, emphasizing their importance in community stability. These findings provide insights into the role of symbiotic bacteria in mealybug adaptation to different ecological niches within the sugarcane agroecosystem. Understanding these host-microbiome interactions may facilitate the development of targeted, microbiome-based biocontrol strategies for sustainable mealybug management in sugarcane cultivation.},
}

*Saccharum/parasitology
Animals
India
*Bacteria/classification/genetics/isolation & purification
*Hemiptera/microbiology
RNA, Ribosomal, 16S/genetics
*Metagenomics/methods
*Gastrointestinal Microbiome/genetics
Phylogeny
DNA, Bacterial/genetics

@article {pmid41379184,
year = {2025},
author = {DE Souza, GC and Araujo Filho, HB and DE Oliveira, CZ and Paiotti, APR and Forones, NM},
title = {EFFICACY OF PROBIOTICS IN PREVENTING CHEMOTHERAPY-INDUCED DIARRHEA IN GASTROINTESTINAL CANCER PATIENTS.},
journal = {Arquivos de gastroenterologia},
volume = {62},
number = {},
pages = {e25020},
doi = {10.1590/S0004-2803.24612025-020},
pmid = {41379184},
issn = {1678-4219},
mesh = {Humans ; *Probiotics/therapeutic use ; *Diarrhea/prevention & control/chemically induced ; Female ; Male ; Middle Aged ; *Gastrointestinal Neoplasms/drug therapy ; Aged ; Treatment Outcome ; *Antineoplastic Agents/adverse effects ; Bifidobacterium ; Lactobacillus ; Gastrointestinal Microbiome/drug effects ; Adult ; Double-Blind Method ; },
abstract = {BACKGROUND: Chemotherapy-induced diarrhea is a common and distressing side effect experienced by patients undergoing cancer treatment, particularly those with gastrointestinal cancer. It can lead to significant health complications, including dehydration, electrolyte imbalances, and treatment interruptions. Recent studies have shown that the gut microbiome plays an important role in the development and severity of chemotherapy-induced diarrhea. Modulating the gut microbiome with probiotics has emerged as a potential strategy for preventing and managing chemotherapy-induced diarrhea.

OBJECTIVE: In this study we aimed to evaluate the efficacy of one probiotic containing a mixture of several strains of Lactobacillus and Bifidobacterium species in prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.

METHODS: Between April 2022 and June 2024, a total of 28 patients diagnosed with gastrointestinal cancer who were intended to receive chemotherapy based on fluoropyrimidine, oxaliplatin, and/or irinotecan were randomized in a ratio 1:1 to receive either a placebo or 20 billion colony-forming units (CFU) of a mixture containing five viable strains including 335 mg of Lactobacillus acidophilus NCFM®, Lactobacillus paracasei Lpc-37TM, Bifidobacterium lactis Bi-04TM, Bifidobacterium lactis Bi-07TM, and Bifidobacterium bifidum Bb-02TM. Patients were instructed to take the product orally once daily for 90 days and to record their bowel habits in a diary using the Bristol stool scale.

RESULTS: The use of probiotics, compared to placebo, did not result in reduction of grade 2/3 diarrhea episodes (placebo arm 55.56% vs probiotic arm 44.44%; P=1). Likewise, no statistically significant difference was observed in the overall incidence of diarrhea between the two groups (71.43% vs 64.29%; P=1). The median number of diarrhea episodes during the 90-day follow-up tended to be lower in the probiotic group (eight episodes) compared to the placebo group (9 episodes) (P=0.639) Subgroup analyses failed to identify any specific patient characteristics that associated any benefit from the probiotic use, regardless of diarrhea grade. Also, no infections related to the probiotic strains administered in this study were detected.

CONCLUSION: Probiotic in comparison to a placebo did not result in a statistically significant effect, suggesting a lack of benefit of administered probiotic for prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.},
}

Humans
*Probiotics/therapeutic use
*Diarrhea/prevention & control/chemically induced
Female
Male
Middle Aged
*Gastrointestinal Neoplasms/drug therapy
Aged
Treatment Outcome
*Antineoplastic Agents/adverse effects
Bifidobacterium
Lactobacillus
Gastrointestinal Microbiome/drug effects
Adult
Double-Blind Method

@article {pmid41379027,
year = {2025},
author = {Esvap, E and Ulgen, KO},
title = {Community Modeling Reveals Disrupted Gut Microbial Secretion in Autism Associated With Redox and Neurometabolic Alterations.},
journal = {Biotechnology journal},
volume = {20},
number = {12},
pages = {e70164},
doi = {10.1002/biot.70164},
pmid = {41379027},
issn = {1860-7314},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/genetics ; Oxidation-Reduction ; Child ; Male ; Feces/microbiology ; *Autism Spectrum Disorder/microbiology/metabolism ; Female ; Child, Preschool ; Metagenomics ; Metabolomics ; Bacteria/metabolism/classification/genetics ; *Autistic Disorder/microbiology/metabolism ; },
abstract = {Emerging evidence suggests that disruptions in the gut microbiome may influence autism spectrum disorder (ASD) through altered microbial metabolism and gut-brain communication. However, the specific metabolic impacts of these microbial changes remain unclear. Community-scale metabolic modeling was applied to shotgun metagenomics data from children with ASD and neurotypical controls to predict secretion of host-impacting metabolites. Modeled ASD-associated communities exhibited altered predicted secretion of metabolites related to redox balance and neurotransmission, including increased 2-ketobutyrate and GABA and reduced riboflavin and inositol, with microbiota transfer therapy (MTT) shifting these profiles toward NT. Empirical fecal metabolomics data showed generally consistent directional trends with model predictions. Reductions in autism severity scores following MTT were associated with increased predicted secretion potentials for inositol and arginine. Taxonomic analysis revealed a depletion of beneficial and an enrichment of pro-inflammatory species, such as Escherichia and Flavonifractor, in ASD. Associations between microbial taxa (e.g., Bacteroides, Bifidobacterium) and neuroactive metabolites highlight microbial modulation as a promising therapeutic strategy in ASD. These results emphasize microbial metabolism as a contributor to ASD traits and a target for therapeutic intervention.},
}

Humans
*Gastrointestinal Microbiome/physiology/genetics
Oxidation-Reduction
Child
Male
Feces/microbiology
*Autism Spectrum Disorder/microbiology/metabolism
Female
Child, Preschool
Metagenomics
Metabolomics
Bacteria/metabolism/classification/genetics
*Autistic Disorder/microbiology/metabolism

@article {pmid41378921,
year = {2025},
author = {Montini, A and Pellegrini, C and Loddo, G and Ravaioli, F and Baldelli, L and Mainieri, G and Pirazzini, C and Mazzotta, E and Carano, F and Sala, C and De Fanti, S and Bacalini, MG and Provini, F},
title = {Analysis of gut microbiota in Restless Legs Syndrome: searching for a metagenomic signature.},
journal = {Sleep},
volume = {},
number = {},
pages = {},
doi = {10.1093/sleep/zsaf383},
pmid = {41378921},
issn = {1550-9109},
abstract = {STUDY OBJECTIVES: We aim to analyse the microbiota composition in RLS patients and its relationship with the different RLS phenotypes.

METHODS: We recruited idiopathic RLS (RLS) and insomnia (INS) patients and healthy subjects (CTRL). Validated questionnaires (PSQI, IRLS, ISI, BDI-II) were administered in the RLS and INS. Fecal microbiota was analysed by 16S rRNA gene sequencing according to Illumina metagenomics standard procedure on MiSeq Platform. Dada2 pipeline was used to process sequencing data, while DESeq2 and Aldex2 tools were used to calculate differential abundance taxa, correcting for age, sex, Body Mass Index, sequencing run and presence of mood disorders.

RESULTS: The sample included 37 RLS (28 females, mean age 64.78 years), 31 INS (22 females, mean age 60.64 years) and 33 CTRL (24 females, mean age 62.54 years). Differential abundance analysis revealed a statistically significant decrease in the abundance of Lachnoclostridium and Flavonifractor genera in RLS compared to CTRL and INS, but not in the INS compared to CTRL. Lachnoclostridium abundance tended to decrease with long disease duration and a predominant motor phenotype. In the RLS group, several genera were identified as significantly associated with IRLS and PSQI scores.

CONCLUSIONS: Although only a few previous studies have reported the presence of small intestinal bacterial overgrowth (SIBO) in RLS, to the best of our knowledge this is the first study to highlight significant differences in the gut microbiota composition of RLS compared to both CTRL and INS, identifying a specific RLS metagenomic signature.},
}

@article {pmid41378889,
year = {2025},
author = {Gerna, D and Chadelaud, T and Lamouche, F and Barret, M and Darrasse, A and Simonin, M},
title = {Dormancy and reactivation of the seed and its microbiome: a holobiont perspective.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0114025},
doi = {10.1128/msystems.01140-25},
pmid = {41378889},
issn = {2379-5077},
abstract = {Desiccation-tolerant seeds provide an intriguing system for studying microbial dormancy, which includes reversible inactivation and reactivation in response to stress. Focusing on bacterial responses to desiccation and rehydration, we offer a holistic interpretation of dormancy and quiescence within the seed holobiont, highlighting both parallels and distinctions between microbes and their plant host. Based on pilot evidence, we propose that microbial dormancy supports persistence throughout the life cycle of desiccation-tolerant seeds. Transcriptomic analyses of seed-transmitted bacteria have identified genes implicated in inactivation and the viable-but-nonculturable state. Our analysis of Xanthomonas citri pv. fuscans illustrates this during seed maturation. However, the signals triggering microbial reactivation and the potential reciprocal interactions between seed dormancy and quiescence, and microbial dormancy, remain unknown. Elucidating this interplay within the seed holobiont could enhance plant growth and health either by promoting seed germination through microbial inoculation or by enabling early detection of seed-transmitted phytopathogens.},
}

@article {pmid41378888,
year = {2025},
author = {Gao, J-H and Li, L-X and Li, W-J and Wang, X and Lyu, D-p and Xie, X-R and Li, S-Y and Zuo, X-L and Li, Y-Q},
title = {Inhibition of PFKFB3 in macrophages ameliorates intestinal inflammation by modulating gut microbiota in DSS-induced colitis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0063225},
doi = {10.1128/msystems.00632-25},
pmid = {41378888},
issn = {2379-5077},
abstract = {UNLABELLED: Phosphofructo-2-kinase/fructose-2,6-biophosphatase 3 (PFKFB3), a key glycolytic enzyme, has attracted increasing attention for its essential roles in various inflammatory responses and immune-related diseases. But the functional relevance and mechanistic basis of the PFKFB3 on ulcerative colitis (UC) remain unclear. Immunohistochemical staining and publicly available data sets were used to analyze PFKFB3 expression in healthy controls (HCs) and UC patients. The role of PFKFB3 on colitis and gut microbiota was investigated by deficiency of PFKFB3 in macrophages (PFKFB3[fl/fl]Lyz2-Cre) mice. In silico meta- and Spearman's correlation analysis of published high-throughput transcriptomic data analyzed the correlation between PFKFB3 and microbiome-associated genes. The expression of PFKFB3 was significantly upregulated in the colon of both human UC cohorts and colitis mice. Pharmacological inhibition of PFKFB3 by 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO) diminished the severity of colitis. Single-cell RNA sequencing and flow analysis revealed that the upregulated PFKFB3 was predominantly contributed by colonic macrophages. PFKFB3[fl/fl]Lyz2-Cre mice alleviated experimental colitis in contrast to littermate control (PFKFB3[fl/fl]). Concomitantly, PFKFB3[fl/fl]Lyz2-Cre mice exhibited a remarkably Faecalibaculum genus-enhanced microenvironment, which can be horizontally transmitted to co-housed wild-type mice, leading to an attenuation of DSS-induced colitis. However, when antibiotics were administered to PFKFB3[fl/fl]Lyz2-Cre mice, the transmission effect was lost. By analyzing the UC patient cohort, Spearman's correlation provided additional evidence for a significant positive correlation between PFKFB3 and microbiota-associated genes expression. This study demonstrated that PFKFB3 deficiency in macrophages could effectively ameliorate colonic inflammation, providing the first evidence that gut microbiota from PFKFB3-deficient mice may represent a novel therapeutic strategy for UC.

IMPORTANCE: PFKFB3 expression was upregulated in the colon of both ulcerative colitis (UC) patients and colitis mice, and this differential expression was predominantly contributed by colonic lamina propria macrophages. Knockout of PFKFB3 in macrophages significantly alleviated DSS-induced colitis. Knockout of PFKFB3 in macrophage mice exhibited a remarkably Faecalibaculum genus-enhanced microenvironment, which can be horizontally transmitted to co-housed wild-type mice, leading to an attenuation of DSS-induced colitis; however, when administered to antibiotics, the transmission effect was lost. By analyzing the UC patient cohort, we demonstrated significant positive correlation between PFKFB3 and microbiota-associated gene expression. Our study first elucidates the relationship of PFKFB3 in macrophages with intestinal inflammation and gut microbiota in UC, which may provide a new strategy for the treatment.},
}

@article {pmid41378649,
year = {2025},
author = {May, W and Goedecke, JH and Conradie-Smit, M},
title = {The science of obesity.},
journal = {South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde},
volume = {115},
number = {9b},
pages = {e3600},
doi = {10.7196/SAMJ.2025.v115i9b.3600},
pmid = {41378649},
issn = {2078-5135},
mesh = {Humans ; *Obesity/genetics/physiopathology/etiology/therapy ; Energy Metabolism ; Body Mass Index ; Appetite ; },
abstract = {KEY MESSAGES • Obesity arises from a complex interplay of genetic, biological, behavioural, psychosocial and environmental factors. • Obesity has a strong genetic component, with twin studies indicating a 50 - 80% concordance in body mass index (BMI) and regional fat distribution. A Swedish study on identical twins raised apart found no correlation between BMI and their adoptive families but a strong correlation with their biological twin, despite being raised in separate households. • The regulation of appetite, body weight and energy balance is highly complex, governed by a network of hormonal signals from the gut, adipose tissue and other organs, as well as neural signals that shape eating behaviours. Many of these signalling pathways are disrupted in people living with obesity. • Since body weight is homeostatically regulated, weight loss triggers physiological adaptations that promote weight regain. These include a decrease in energy expenditure, and hormonal changes that enhance appetite while reducing satiety. • Adipose tissue influences the central regulation of energy homeostasis, and excess adiposity can become dysfunctional, with production of proinflammatory cytokines and associated metabolic health complications. • Individual variations in body composition, fat distribution and function result in a highly variable threshold at which excess adiposity begins to negatively affect health. • Emerging research in obesity science has widened to include brown fat, the gut microbiome, immune system regulation, and the intricate mechanisms that regulate body weight. • Obesity can be classified as primary, secondary and genetic obesity. • In the current management of primary obesity, prevention (the path in) and treatment (the path out) need to be distinctly separated. • Effective primary obesity treatment requires an integrated approach that addresses the non-modifiable cause (increased appetite) together with modifiable contributors (poor diet quality, increased stress, poor sleep, reduced physical activity and increased sedentary behaviour). Behavioural modification and psychological support provide additional benefit. • Effective treatment in genetic and secondary obesity requires treatment of the underlying causes along with modification of the contributors.},
}

Humans
*Obesity/genetics/physiopathology/etiology/therapy
Energy Metabolism
Body Mass Index
Appetite

@article {pmid41378491,
year = {2025},
author = {Manzoor, M and Zaric, S and Dong, A and Leskelä, J and Pietiäinen, M and Könönen, E and Ylikotila, P and Enzinger, C and Ropele, S and Gattringer, T and Eppinger, S and Sinisalo, J and Putaala, J and Pussinen, PJ and Paju, S},
title = {Association of Subgingival Microbiota Composition With Risk, Severity, and Outcome of Cryptogenic Ischemic Stroke in Young Adults.},
journal = {Journal of the American Heart Association},
volume = {},
number = {},
pages = {e043495},
doi = {10.1161/JAHA.125.043495},
pmid = {41378491},
issn = {2047-9980},
abstract = {BACKGROUND: Oral and gut dysbiosis has been linked to stroke pathogenesis and its prognosis. However, the relationship between the subgingival microbiota and cryptogenic ischemic stroke (CIS) remains unclear. We compared the subgingival microbiota of patients with CIS and their age-and sex-matched stroke-free controls to identify the specific microbiota associated with CIS, stroke symptom severity, and clinical outcome.

METHODS: This multicenter, case-control study was conducted between 2013 and 2019 as part of a screening protocol for the SECRETO (Searching for Explanations for Cryptogenic Stroke in the Young: Revealing the Etiology, Triggers, and Outcome) study (NCT01934725). Stroke severity was assessed using the National Institutes of Health Stroke Scale score. After thorough clinical and radiographic oral examinations, subgingival samples were collected and analyzed using 16S rRNA gene sequencing.

RESULTS: A total of 272 participants (134 patients and 138 controls) were included. There were no differences in the following clinical characteristics between patients and controls: diabetes, hypertension, smoking, alcohol use, abdominal obesity, physical activity, and chronic multiorgan disease. Beta diversity differed significantly between patients and controls (P<0.05). The abundance of Spirochaetota and Treponema was higher and Pseudomonadota, Veillonella, and Capnocytophaga were lower in patients than in controls (P<0.05). The abundance of T. denticola was associated with an increased risk of CIS (odds ratio [OR], 1.002 [95% CI, 1.000-1.003], P=0.023), and this association persisted after adjusting for relevant comorbidities and medications (OR, 1.002 [95% CI, 1.000-1.003], P=0.021).

CONCLUSIONS: The subgingival microbiota is associated with CIS, suggesting a possible link between oral health and stroke pathophysiology. Although causality cannot be proven, oral microbiota may be a modifiable treatment target for the prevention of CIS and improving its outcome.},
}

@article {pmid41378445,
year = {2025},
author = {Behling, AH and Portlock, T and Ho, D and Wilson, BC and Paramsothy, S and Kamm, MA and Cutfield, WS and Kaakoush, NO and O'Sullivan, JM and Vatanen, T},
title = {Cohort-specific determinants of donor strain engraftment following multi-donor faecal microbiota transplantation in two randomised clinical trials.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2597628},
doi = {10.1080/19490976.2025.2597628},
pmid = {41378445},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; *Colitis, Ulcerative/therapy/microbiology ; Tissue Donors ; Feces/microbiology ; *Obesity/therapy/microbiology ; Bacteria/classification/isolation & purification/genetics ; Randomized Controlled Trials as Topic ; Male ; Female ; Adult ; Middle Aged ; Cohort Studies ; },
abstract = {Disrupted human gut microbiota have been associated with the development of certain disease states, including obesity and ulcerative colitis (UC). Faecal microbiota transplantation (FMT) from healthy donors is a promising avenue to shift the microbiome profile of the recipient towards that of the donor, potentially ameliorating related symptoms. Several recent meta-analyses have investigated the clinical and microbial determinants that influence the retention of transplanted donor microbial strains within the recipient gut microbiome following FMT (i.e. engraftment). However, the specific factors that affect donor strain engraftment in different disease states require further exploration. Here, we perform a strain engraftment analysis on data from two multi-donor FMT clinical trials: the Gut Bugs Trial for obesity and the FOCUS Trial for UC. Using donor strain matching, the donor-recipient pairings of the FOCUS Trial were first predicted in a blinded manner. The subsequent, unblinded, strain engraftment analysis of both datasets highlighted a differential effect of donor-recipient microbiome complementarity on engraftment across the two disease cohorts; greater engraftment efficiency was associated with increased donor-recipient microbial similarity in the FOCUS Trial, and decreased similarity in the Gut Bugs Trial, suggesting that the factors influencing engraftment may differ across disease cohorts.},
}

Humans
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
*Colitis, Ulcerative/therapy/microbiology
Tissue Donors
Feces/microbiology
*Obesity/therapy/microbiology
Bacteria/classification/isolation & purification/genetics
Randomized Controlled Trials as Topic
Male
Female
Adult
Middle Aged
Cohort Studies

@article {pmid41378387,
year = {2025},
author = {Niu, G and Liu, W and Zhang, T and Ma, J and Yuan, X and Xie, P and Yang, S and Ding, Z and Fang, J and Zeng, J and Wen, T and Shen, Q and Yuan, J},
title = {Deciphering Conserved Rhizosphere Metabolite-Microbiome Interactions for Crop Drought Resistance.},
journal = {Global change biology},
volume = {31},
number = {12},
pages = {e70652},
doi = {10.1111/gcb.70652},
pmid = {41378387},
issn = {1365-2486},
support = {2025FRF05007//Central Guidance on Local Science and Technology Development Fund of Ningxia/ ; 42322708//Natural Science Foundation of China/ ; CARS-23//China Agriculture Research System/ ; 202302140601007//Key Research and Development Program of Shanxi Province/ ; KJJQ2025017//Fundamental Research Funds for the Central Universities/ ; },
mesh = {*Rhizosphere ; *Droughts ; *Crops, Agricultural/microbiology/physiology ; *Microbiota ; *Soil Microbiology ; Drought Resistance ; },
abstract = {Drought stress is a major threat to global food security. It remains uncertain whether conserved drought-responsive microbes can be recruited by different crop species to help their adaptation to drought and how this recruitment occurs. Herein, we identified drought-responsive rhizosphere microbial genera conserved across multiple crop species under drought stress and elucidated their in situ regulatory mechanisms. Integrated amplicon sequencing of rhizosphere microbiomes from 26 crop species indicated 6 core genera (Streptomyces, Glycomyces, Inquilinus, Amycolatopsis, Acinetobacter, and Promicromonospora) consistently enriched under drought. Soil conditioning with 46 shared rhizosphere metabolites among multiple crops demonstrated that trehalose, myo-inositol, and phenylalanine synergistically enrich the six genera. The soil microbiome conditioned with three compounds significantly increased root length and leaf water content when evaluated in greenhouse trials (tomato, cucumber, and watermelon) and sorghum field studies. Furthermore, the conditioned soil microbiome exhibited enrichment in pathways related to energy supply, protective compound synthesis, and plant interaction signaling, driven by six core genera. Pure culture experiments revealed a potential cross-phylum interaction; that is, Streptomyces could synthesize phenylalanine to recruit Acinetobacter. Our findings reveal a potential conserved rhizosphere metabolite-microbiome interactions across multiple crops, offering a talent pathway to steer soil microbiome for drought resistance.},
}

*Rhizosphere
*Droughts
*Crops, Agricultural/microbiology/physiology
*Microbiota
*Soil Microbiology
Drought Resistance

@article {pmid41378343,
year = {2025},
author = {Shah, SS and Jackovic, A and Alhilli, M},
title = {Dietary and Physical Activity Interventions in Gynecologic Oncology: Mechanisms, Guidelines, and Clinical Evidence.},
journal = {American journal of lifestyle medicine},
volume = {},
number = {},
pages = {15598276251405209},
pmid = {41378343},
issn = {1559-8284},
abstract = {Background: Obesity and modifiable lifestyle factors contribute significantly to the rising global burden of cancer, particularly gynecologic malignancies such as endometrial and ovarian cancer. Despite strong biological plausibility, the role of lifestyle interventions in improving outcomes for women with gynecologic cancers remains underexplored. Objective: This review synthesizes current evidence on the impact of dietary and physical activity interventions on gynecologic cancer outcomes, highlighting links and existing clinical guidelines. Methods: Literature exploring the influence of obesity, inflammation hormonal dysregulation, insulin resistance, and gut microbiome alterations on cancer progression were assessed, and studies assessing the effects of lifestyle interventions in gynecologic cancers were explored. Results: Obesity-induced inflammation and hormonal imbalances are key drivers of tumorigenesis. Structured exercise and adherence to anti-inflammatory diets, such as the Mediterranean diet, can reduce pro-inflammatory cytokines, improve insulin sensitivity, regulate estrogen metabolism, and enhance immune function. These interventions also modulate angiogenesis and promote a favorable gut microbiome, offering a biologically plausible approach to slowing cancer progression. Conclusion: Diet and exercise represent promising, low-risk strategies to improve quality of life and potentially enhance survival in women with gynecologic cancers. Greater integration of lifestyle interventions into gynecologic oncology care is warranted, guided by evidence and recommendations from national cancer organizations.},
}

@article {pmid41378331,
year = {2025},
author = {Zalzman, M and Banerjee, A},
title = {Herbal formulas and gastrointestinal motility: Bridging traditional medicine and mechanistic insights.},
journal = {World journal of gastroenterology},
volume = {31},
number = {45},
pages = {113332},
pmid = {41378331},
issn = {2219-2840},
mesh = {Humans ; *Gastrointestinal Motility/drug effects ; Animals ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Transit/drug effects ; *Gastrointestinal Diseases/drug therapy ; Mice ; Phytotherapy/methods ; },
abstract = {Wang et al provide preclinical evidence that specific traditional herbal formulas, like Pyeongwi-san, can improve gastrointestinal (GI) motility under stress. Pyeongwi-san enhances GI transit, boosts serotonin levels, restores short-chain fatty acid balance, and reduces inflammation. The clinical significance of this research is its potential for standardized herbal remedies for GI disorders, such as dyspepsia and irritable bowel syndrome. At the same time, using only male mice, a single dose regimen, and relatively small cohorts highlights the need for further validation, including sex-specific responses, dose-effect relationships, and translational clinical studies. In summary, readers will find value in this article because it provides mechanistic details, bridges tradition with modern science, deals transparently with its limitations, and paves the way for clinically relevant innovation in GI health. Future investigations should focus on clinical validation and personalized therapeutic strategies that harness both microbiome-gut-brain interactions and the long history of herbal medicine.},
}

Humans
*Gastrointestinal Motility/drug effects
Animals
*Drugs, Chinese Herbal/pharmacology/therapeutic use
Gastrointestinal Microbiome/drug effects
Gastrointestinal Transit/drug effects
*Gastrointestinal Diseases/drug therapy
Mice
Phytotherapy/methods

@article {pmid41378248,
year = {2025},
author = {Abdulaal, R and Afara, I and Harajli, A and Al Mashtoub, E and Tarchichi, A and Hassan, K and Afara, A and Abou Fakher, J and Salhab, S and Fassih, I and Tlais, M},
title = {Gut microbiome and chemotherapy-induced cardiotoxicity: A systematic review of evidence and emerging therapies.},
journal = {World journal of biological chemistry},
volume = {16},
number = {4},
pages = {112221},
pmid = {41378248},
issn = {1949-8454},
abstract = {BACKGROUND: Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy, limiting treatment efficacy and worsening patient outcomes. Recent studies have implicated the gut microbiome and its key metabolites, such as short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO), in mediating inflammation, oxidative stress, and cardiac damage. The gut-heart axis is increasingly recognized as a pivotal pathway linking microbiota dysregulation to chemotherapy-related cardiac dysfunction.

AIM: To systematically review existing evidence on the role of gut microbiome alterations in chemotherapy-induced cardiotoxicity and evaluate emerging microbiome-based therapeutic strategies aimed at mitigating cardiovascular risk in cancer patients.

METHODS: A systematic literature search was conducted in PubMed, Scopus, and Web of Science for studies published between January 2013 and December 2024. Studies were included if they examined chemotherapy-induced cardiotoxicity in relation to gut microbiota composition, microbial metabolites (e.g., SCFAs, TMAO), or microbiome-targeted interventions. Selection followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Data extraction focused on microbiota alterations, mechanistic pathways, cardiac outcomes, and quality assessments using standardized risk-of-bias tools.

RESULTS: Eighteen studies met the inclusion criteria. Chemotherapy was consistently associated with gut dysbiosis characterized by reduced SCFA-producing bacteria and increased TMAO-producing strains. This imbalance contributed to gut barrier disruption, systemic inflammation, and oxidative stress, all of which promote myocardial damage. SCFA depletion weakened anti-inflammatory responses, while elevated TMAO levels exacerbated cardiac fibrosis and dysfunction. Preclinical studies showed promising cardioprotective effects from probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation, though human data remain limited.

CONCLUSION: Gut microbiome dysregulation plays a crucial role in the development of chemotherapy-induced cardiotoxicity. Altered microbial composition and metabolite production trigger systemic inflammation and cardiac injury. Microbiome-targeted therapies represent a promising preventive and therapeutic approach in cardio-oncology, warranting further clinical validation through well-designed trials.},
}

@article {pmid41378121,
year = {2025},
author = {Liu, C and Wang, L and Huai, J and He, S and Su, Q and Min, Q and An, Z},
title = {TMOD2 and DOCK4 as Novel Gut Microbiota-Associated Biomarkers for Colorectal Adenoma: Integrated Transcriptomic Analysis and Therapeutic Target Identification.},
journal = {Mediators of inflammation},
volume = {2025},
number = {},
pages = {6267309},
pmid = {41378121},
issn = {1466-1861},
mesh = {Humans ; *Colorectal Neoplasms/metabolism/genetics/microbiology ; *Gastrointestinal Microbiome/genetics/physiology ; *Adenoma/metabolism/genetics/microbiology ; Gene Expression Profiling ; Biomarkers, Tumor/metabolism/genetics ; Transcriptome/genetics ; ROC Curve ; },
abstract = {Colorectal adenomas (CRA) represent critical precursors to colorectal cancer (CRC), yet reliable transcriptomic biomarkers for early detection and therapeutic targeting remain limited. Integration of gut microbiota (GM) genetics with transcriptomics offers a novel approach to identify disease-associated molecular signatures. We sought to identify GM-associated molecular signatures that could serve as early intervention targets. We integrated transcriptomic data with Mendelian randomization (MR) analysis to establish causal relationships between GM and CRA development. Machine learning algorithms identified robust biomarkers, which we validated through expression analysis and receiver operating characteristic (ROC) analysis to construct predictive nomogram models. Comprehensive molecular characterization included Gene Set Enrichment Analysis (GSEA), immune profiling, and regulatory network analysis. Single-cell RNA sequencing (scRNA-seq) analysis further validated biomarker expression patterns across distinct cell populations in the tumor microenvironment. We discovered 12 GM species with significant causal relationships to CRA risk. Two biomarkers, TMOD2 and DOCK4, emerged as powerful predictive indicators with strong correlation (r = 0.66, p < 0.001). These biomarkers demonstrated excellent diagnostic performance in ROC analysis and revealed previously unrecognized connections to cell adhesion pathways critical for adenoma progression. Single-cell analysis revealed TMOD2 expression across multiple cell clusters with notable exclusion in mast cells, while DOCK4 expression was predominantly restricted to fibroblasts, myeloid, and epithelial cells. Notably, we identified distinct immune cell infiltration patterns, including altered naive B cells and macrophage populations, suggesting immune dysregulation as a key mechanism. GSEA revealed enrichment in cell adhesion molecule (CAM) pathways. Regulatory network analysis uncovered complex control by 18 microRNAs (miRNAs), 40 long noncoding RNAs (lncRNAs), and 10 transcription factors (TFs), with EIF3A emerging as a key m6A reader protein. Drug screening identified 22 potential therapeutic compounds, with trichostatin A showing optimal binding affinity. These findings establish TMOD2 and DOCK4 as novel biomarkers linking GM dysbiosis to CRA development, opening new avenues for microbiome-targeted early intervention strategies.},
}

Humans
*Colorectal Neoplasms/metabolism/genetics/microbiology
*Gastrointestinal Microbiome/genetics/physiology
*Adenoma/metabolism/genetics/microbiology
Gene Expression Profiling
Biomarkers, Tumor/metabolism/genetics
Transcriptome/genetics
ROC Curve

@article {pmid41378079,
year = {2025},
author = {Jeyaraman, N and Jeyaraman, M and Mariappan, T and Nallakumarasamy, A and Subramanian, P and T, P and Vetrivel, VN},
title = {Harnessing postbiotics for liver health: Emerging perspectives.},
journal = {World journal of gastrointestinal pharmacology and therapeutics},
volume = {16},
number = {4},
pages = {109177},
pmid = {41378079},
issn = {2150-5349},
abstract = {With emerging scientific breakthroughs, it has been established that gut microbiome dysbiosis has an undeniable correlation with hepatic diseases through complex interlinked metabolic pathways. There's always been a need for new therapeutic options to deal with the rising prevalence of metabolic dysfunction-associated steatotic liver disease, liver cirrhosis, alcoholic liver disease, hepatocellular carcinoma etc. Several researchers have studied the role of probiotics and prebiotics in altering gut microbiome to tackle microbial dysbiosis which has been proven to be the cause of several metabolic disorders. However, postbiotics remain an untapped potential due to the limited literature on their intake and associated benefits. These bioactive compounds include short chain fatty acids such as butyrate, propionate and acetate, exopolysaccharides, inactivated strains such as Akkermansia muciniphila and Bacillus coagulans etc., have hepatoprotective effects which are highlighted in this article. This review aims to discuss the findings of postbiotics research, their classification and their diverse role in serving as a therapeutic option for liver diseases.},
}

@article {pmid41378067,
year = {2025},
author = {Vargas-Beltran, AM and Mialma-Omana, SJ and Vivanco-Tellez, DO},
title = {Targeting gut microbiota in liver disease: A pharmacological approach for hepatic encephalopathy and beyond.},
journal = {World journal of gastrointestinal pharmacology and therapeutics},
volume = {16},
number = {4},
pages = {110271},
pmid = {41378067},
issn = {2150-5349},
abstract = {The gut microbiota plays a pivotal role in the pathogenesis of liver diseases, particularly hepatic encephalopathy (HE), in which dysbiosis contributes to ammonia production, systemic inflammation, and neurocognitive dysfunction. Emerging evidence suggests that targeting the gut-liver axis through pharmacological and microbiota-based interventions can mitigate liver disease progression and HE severity. This review explored the latest therapeutic strategies aimed at modulating gut microbiota in liver disease, focusing on traditional approaches such as non-absorbable disaccharides (lactulose, lactitol), antibiotics (rifaximin), and probiotics as well as novel interventions, including postbiotics, synbiotics, and fecal microbiota transplantation. Additionally, bile acid modulators, short-chain fatty acid derivatives, and microbiome-targeted small molecules are being investigated for their potential to restore gut-liver homeostasis. We also discussed the implications of gut microbiota modulation in conditions beyond HE, such as metabolic dysfunction-associated steatotic liver disease and cirrhosis. By integrating gut microbiota-targeted therapies into liver disease management, we may develop more effective, personalized approaches to improve patient outcomes and reduce complications.},
}

@article {pmid41377991,
year = {2025},
author = {Blaser, M and Zhang, XS and Zhang, M and Wang, Y and Sun, H and Scarnati, M and Gao, Z and Yin, Y and Zerbe, C and Falcone, E and Lally, M and Joshi, J and Bhattacharya, S and Diaz-Rubio, M and Bharj, D and Patel, D and Pan, S and Ro, G and Grenard, J and Armstrong, A and Valvezan, A and Holland, S and Mulle, J and Dominguez-Bello, M and Su, X},
title = {Gut microbiota phospholipids regulate intestinal gene expression and can counteract the effects of antibiotic treatment.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-7924457/v1},
pmid = {41377991},
issn = {2693-5015},
abstract = {Early-life antibiotic exposure perturbs the developing gut microbiome and increases risk for immune disorders such as type 1 diabetes (T1D) in non-obese diabetic (NOD) mice. Comparing germ-free and conventional mice, we identified 747 intestinal lipid compounds and defined a subset of gut microbially-produced lipids (GMPLs). Antibiotic treatment disrupted GMPL profiles in mice and in human volunteers, with partial restoration in mice after cecal microbiota transplantation. Among affected compounds, four phospholipids: LPG(13:0), LPG(16:0), LPG(18:0), and PG(15:0_15:0), were structurally defined and tested functionally. These lipids suppressed LPS-induced NFκB activation, modulated innate immune gene expression in intestinal epithelial cells, and enhanced epithelial cell mitochondrial respiration. Oral administration of LPG(16:0) or LPG(18:0) to antibiotic-treated NOD mice partially restored microbiome composition, normalized ileal gene expression, and improved epithelial transport and metabolic pathways. These findings identify bacterial phospholipids as regulators of intestinal immunity and metabolism, with potential therapeutic applications for inflammatory diseases.},
}

@article {pmid41377969,
year = {2025},
author = {McReynolds, M and Alsaadi, A and Welz, L and Pothakamury, A and Gilloteau, C and Prasad, P and Yahia, M and Sadler, J and Smith, J and Jenkins, B and Diven, G and Bornhäuser, J and Mekdoud, T and Tian, S and Rosenstiel, P and Schreiber, S and Bisanz, J and Aden, K},
title = {Tracing NAD[+] metabolism uncovers adaptive coordination between host and microbiome during colitis.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-8195970/v1},
pmid = {41377969},
issn = {2693-5015},
abstract = {Host-microbiota metabolic interactions critically regulate nicotinamide adenine dinucleotide (NAD+) homeostasis, and their disruption is increasingly linked to chronic diseases including inflammatory bowel disease (IBD). However, it remains unclear whether NAD+ dysregulation in IBD arises from impaired production, enhanced consumption, or both. Using multi-omics approaches and stable isotope-labeled NAD+ precursors administered via intravenous infusion in a murine model of dextran sulfate sodium (DSS)-induced colitis, we mapped tissue- and lumen-specific NAD+ metabolism under inflammatory stress. Our results reveal tissue-specific rewiring of NAD+ metabolism, with increased flux through the salvage pathway compensating for reduced de novo NAD+ synthesis from tryptophan. In parallel, microbial de novo NAD+ production was elevated, highlighting a cooperative host-microbiota response to inflammatory stress. These findings demonstrate differential regulation of NAD+ biosynthesis during acute colitis and underscore the dynamic interplay between host and microbial metabolism in maintaining NAD+ homeostasis under inflammatory conditions.},
}

@article {pmid41377758,
year = {2026},
author = {Benjamin, K and Yuan, Q and Boyer, J},
title = {Increased gut Saccharomyces and decreased pathogenic fungi associated with food protein-induced enterocolitis syndrome resolution.},
journal = {The journal of allergy and clinical immunology. Global},
volume = {5},
number = {1},
pages = {100598},
pmid = {41377758},
issn = {2772-8293},
abstract = {BACKGROUND: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated allergy, primarily affecting infants and children, with potentially severe gastrointestinal impacts. As with other allergic diseases, the cause of FPIES is unknown. Preliminary research suggests that the gut microbiome may play a role in FPIES, as well as other allergy, yet data on the mycobiome are limited.

OBJECTIVE: We sought to examine the role of the gut mycobiome in FPIES by comparing the stool mycobiome of children with FPIES to that of children who have outgrown FPIES.

METHODS: Caregivers of children with FPIES and children who had outgrown FPIES completed a demographic and lifestyle survey. DNA was extracted and sequenced from stool samples of 23 children with FPIES and 17 children with resolved FPIES. Fungal diversity and composition between the 2 groups were compared using QIIME2 (Quantitative Insights Into Microbial Ecology 2).

RESULTS: Children with resolved FPIES had significantly more Saccharomyces than children with current FPIES. Children with current FPIES had significantly more diverse samples and included opportunistic pathogens, such as Candida spp. Children with resolved FPIES reported significantly less infant antibiotic usage and proton pump inhibitor usage.

DISCUSSION: This study identified distinct mycobiome profiles in children with current versus resolved FPIES. Resolved FPIES was associated with Saccharomyces enrichment, whereas children with current FPIES had more diverse, opportunistic pathogen-associated communities and greater infant antibiotic and proton pump inhibitor usage. Although these associations do not establish causality, they underscore the need for larger, longitudinal studies to determine whether the mycobiome and early-life exposures influence FPIES outcomes, because it could have implications for treatment and prevention.},
}

@article {pmid41377665,
year = {2025},
author = {Xia, J and Shao, Y and Li, B and Wu, T and He, Z and Feng, Z and Zhang, Z and Yin, S and Wang, Y and Yu, J and Wang, J and Sun, G},
title = {Integrative analysis of the gut microbiota, bile acid pathways, and immune dysregulation in dyslipidemia models.},
journal = {iScience},
volume = {28},
number = {12},
pages = {114001},
pmid = {41377665},
issn = {2589-0042},
abstract = {Emerging evidence suggests a link between gut microbiota, bile acid metabolism, and immune dysregulation in dyslipidemia. Through a case-control study involving 140 participants and an animal experiment, we identified significantly elevated counts of peripheral blood CD3[+] T cells, CD4[+] T cells, CD8[+] T cells, and CD19[+] B cells in patients with dyslipidemia, alongside increased specific bile acids in fecal samples and distinct alterations in gut microbiota composition. The animal model confirmed changes in gut microbiota, bile acid metabolism, and percentage of specific lymphocyte subsets. Also, we identified downregulated hepatic expressions of bile acid metabolism-related proteins in hyperlipidemic rats. Integrated analysis suggested potential associations among gut microbiota, bile acid pathways, and immune dysregulation. Overall, these data highlight the critical role of the potential gut microbiota-bile acid metabolism-immune axis in dyslipidemia, providing potential therapeutic targets for diseases associated with lipid metabolism disorders.},
}

@article {pmid41377642,
year = {2025},
author = {Edpuganti, S and Subhash, S and Subrahmaniyan, SL and Latheef, S and Albarari, SS},
title = {Gut Microbiome and Cardiovascular Health: Mechanisms, Therapeutic Potential and Future Directions.},
journal = {Heart international},
volume = {19},
number = {2},
pages = {12-20},
pmid = {41377642},
issn = {2036-2579},
abstract = {BACKGROUND: The gut microbiome has a crucial role in host metabolism and immune regulation, and there is growing evidence that dysbiosis may be associated with the pathogenesis of cardiovascular disease (CVD). This narrative review provides an overview of the recent literature on mechanistic connections between the gut and heart, as well as on the therapeutic strategies and research gaps in the gut-heart axis.

METHODS: We conducted a systematic literature search on PubMed and Embase databases with MeSH and keyword terms: 'gut microbiome', 'cardiovascular disease', 'TMAO', 'short-chain fatty acids', 'probiotics' and 'faecal microbiota transplantation'. We considered human and relevant animal studies focusing on mechanistic pathways or microbiome treatments and excluded editorials, small (less than 10 subjects) case series and articles not published in the English language.

RESULTS: Key microbiota-derived metabolites, trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), contribute to atherogenesis, blood pressure and myocardial inflammation. Dysbiosis-induced barrier dysfunction and disturbed bile acid signalling also serve as the mediators of cardiac remodelling. Dietary fibre, probiotics/prebiotics, postbiotics and faecal microbiota transplantation are emerging interventions for the modulation of CVD risk. Nevertheless, most result from observational studies, whilst such are heterogeneous in sequencing platforms and too small to draw any definitive conclusions.

CONCLUSION: The modulation of gut microbiome might be a new target for CVD prevention and treatment. Large-scale, standardized randomized trials with hard cardiovascular endpoints, as well as integrated multi-omics profiling, will be required to validate microbial biomarkers and to optimize microbiome-based interventions.},
}

@article {pmid41377590,
year = {2025},
author = {Bolgova, O and Shypilova, I and Mavrych, V},
title = {Natural strategies to optimize estrogen levels in aging women: mini review.},
journal = {Frontiers in aging},
volume = {6},
number = {},
pages = {1706117},
pmid = {41377590},
issn = {2673-6217},
abstract = {INTRODUCTION: Menopause triggers declining estradiol, causing vasomotor symptoms, bone loss, and urogenital changes. Despite hormone therapy's effectiveness, safety concerns drive 40%-50% of Western women toward natural alternatives.

AIM: To evaluate evidence supporting non-pharmacological interventions that modulate endogenous estrogen activity in postmenopausal women.

METHODS: 48 high-quality publications (2015-2025) examining dietary interventions, micronutrient supplementation, gut microbiome modulation, lifestyle modifications, and botanical remedies for menopausal symptoms were analyzed and included in this review. Selection criteria included randomized controlled trials, systematic reviews, meta-analyses, and cohort studies specifically addressing natural interventions in perimenopausal and postmenopausal women.

RESULTS: Multiple natural approaches demonstrated clinically meaningful effects. Dietary phytoestrogens (50-80 mg/day isoflavones) reduced severe hot flashes by up to 92%, improved metabolic parameters, and were confirmed safe for reproductive tissues. Flaxseed lignans reduced perimenopausal symptoms. Combined vitamin E and omega-3 lowered hot flush intensity, while vitamin E alone showed estrogenic receptor activation. Curcumin (500 mg/day) reduced hot flashes after 4 weeks and improved metabolic profiles. Probiotics containing L. brevis KABP052 increased circulating estrogens by up to 26% over 12 weeks. Stress reduction interventions improved quality of life, and cognitive behavioral therapy reduced insomnia severity. Botanicals including black cohosh, red clover, and rhapontic rhubarb reduced vasomotor symptoms, while resveratrol (75 mg twice daily) significantly improved bone mineral density over 12 months. Research gaps remain regarding dosing and genetic variability.

CONCLUSION: A multi-domain approach incorporating phytoestrogen-rich foods, targeted micronutrients, gut microbiome optimization, and regular exercise provides evidence-based options for managing estrogen decline. While these approaches cannot fully replace hormone therapy, they provide valuable alternatives for women with contraindications or preferences against pharmaceutical intervention. Future research should focus on personalized approaches incorporating genetic profiling.},
}

@article {pmid41377560,
year = {2025},
author = {Liu, S and Cao, H and Wang, L and Li, S and Liang, Y and Feng, Y and Gao, Z and Wang, S and Lian, X},
title = {Sarcopenia and lower urinary tract diseases: links, mechanisms, and clinical implications.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1704456},
pmid = {41377560},
issn = {2296-861X},
abstract = {Lower urinary tract diseases (LUTDs), including lower urinary tract symptoms (LUTS), overactive bladder (OAB), urinary incontinence (UI), bladder cancer (BC), prostate cancer (PCa), and benign prostatic hyperplasia (BPH), severely impair the quality of life of the elderly. Emerging evidence highlights a strong association between sarcopenia (progressive loss of muscle mass, strength, and function) and the prevalence, severity, and progression of LUTDs, as well as poorer treatment responses in affected patients-though most supporting studies are cross-sectional or retrospective, with prospective trials needed to confirm causality. Potential mechanisms linking sarcopenia to LUTDs include pelvic floor muscle weakening, neuromuscular dysfunction, metabolic/endocrine disturbances, genetic factors, and gut microbiome dysregulation. Clinically, interventions such as resistance exercise, nutritional support, gut microbiome-targeted strategies, pelvic floor training, and pharmacological therapies show promise in mitigating LUTDs symptoms by targeting sarcopenia. Integrating sarcopenia assessment into LUTDs management could improve patient care; future research should prioritize large-scale prospective trials to validate causal relationships, clarify key mediating mechanisms (e.g., specific gut microbial taxa, neuromuscular signaling pathways), and develop personalized intervention protocols tailored to distinct LUTD subtypes and patient characteristics.},
}

@article {pmid41377537,
year = {2025},
author = {Merhavy, ZI and Raeburn, T and Torres-Ayala, GM and McCulloch, MA and Varkey, TC},
title = {Sedation and analgesia strategies in the neuro intensive care unit.},
journal = {World journal of critical care medicine},
volume = {14},
number = {4},
pages = {111787},
pmid = {41377537},
issn = {2220-3141},
abstract = {Intensivists are often plagued with the challenges of managing critically ill patients in the neurocritical intensive care unit (neuro ICU); one such challenge is the level of illness and the need for sedation, inhibiting the provider's ability to adequately assess the patient. Most sedatives alter neurological and physical exam findings, only compounding potential barriers to providing the best care for each patient. It is important to emphasize that even in the altered mentation of these patients, physical and neurological exams reign supreme as diagnostic tools and should be used in conjunction with multimodal neuromonitoring methods, rather than labs or imaging alone. Additionally, selecting the appropriate analgesic(s) and sedative(s) based on these findings are highly important when determining the best course of individualized management. Thus, providers in the neuro ICU should be highly familiar with the appropriate analgesic and sedative options available in order to determine not only which may be best for each patient, but to also better understand how each drug may impact assessment findings. This comprehensive review aims to provide a structured overview of the pertinent sedatives commonly used in neuro ICUs, their risks and benefits, and how providers can best utilize each in practice to further improve patient outcomes. The novel contribution of this work provides comparative drug tables, dosing guidance for pediatric and very elderly (> 85-years-old) populations, and an exploration into the future possibilities of utilizing artificial intelligence and the human gut microbiome to further enhance the prospects of precision medicine.},
}

@article {pmid41377497,
year = {2025},
author = {Ran, D and Zhang, Y and An, Y and Hu, Y and Xia, Y and Sun, J},
title = {Disrupted tRNA modification leads to intestinal mitochondrial dysfunction and microbial dysbiosis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.27.690007},
pmid = {41377497},
issn = {2692-8205},
abstract = {BACKGROUND AND AIMS: Transfer RNA (tRNA) modifications determine translation fidelity and efficiency. It occurs through the action of specific enzymes that modify the nucleotides within the tRNA molecule. Our previous study demonstrated tRNA modopathies and altered queuine-related metabolites in inflammatory bowel diseases. Queuine tRNA-ribosyltransferase catalytic subunit 1 (QTRT1) and QTRT 2 co-localize in mitochondria and form a heterodimeric TGT participating in tRNA Queuosine (tRNA-Q) modification. Human body acquires Queuine/Vitamin Q from intestinal microbiota or from diet. However, the roles of tRNA-Q modifications in the maintenance of intestinal mitochondrial homeostasis and microbiome are still unclear.

METHODS: We used publicly available human IBD datasets, QTRT1 knockout (KO) mice, QTRT1 intestinal epithelial conditional KO (QTRT1 [ΔIEC]) mice, cultured cell lines with QTRT1-specific siRNA, and organoids from patients with IBD to investigate the mechanism of tRNA-Q modifications in intestinal mitochondrial homeostasis and therapeutic potential in anti-inflammation.

RESULTS: In single cell RNA sequencing datasets of human IBD, we identified significant reduced intestinal epithelial QTRT1 expression in the patients with Crohn's Disease. Using publicly available datasets, we identified significantly changes of Vitamin Q-associated bacteria in human IBD, compared to the healthy control. Qtrt1 [-/-] mice had significant reduction of Q-associated bacteria, e.g., Bacteroides . Alcian Blue and Mucin-2 staining revealed mucosal barrier damage and disrupted homeostasis, with reduced colonic cell proliferation. Intestinal tight junction integrity was impaired in QTRT1-KO mice, as evidenced by reduced ZO-1 and increased Claudin-10 expression. QTRT1 [ΔIEC] mice also showed dysbiosis and disrupted TJs. ATP synthesis was significantly decreased in the colon of QTRT1-KO mice, accompanied by severe mitochondrial dysfunction: reduced mitochondrial quality, Cytochrome-C release, and mitochondrial DNA (mtDNA) leakage. Mitochondrial dysfunction contributed to colonic cell death, as shown by elevated expressions of Cleaved Caspase-3 and Cleaved Caspase-1, increased BAX/Bcl-2 ratio, and positive TUNEL signals. Elevated CDC42, CD14, and CD4 levels in QTRT1-KO colon suggested mucosal immune activation and tissue repair responses. QTRT1-deficient CaCO2-BBE cells showed mitochondrial dysfunction. Cytochrome-C and mito-DNA release leading to cell death characterized by elevated expressions of Cleaved Caspase-3 and Caspase-1, increased BAX/Bcl-2 ratio, and higher apoptosis rate. Organoids isolated from patients with IBD showed reduced levels of QTRT1 and dysfunctional mitochondria. Restoring mitochondrial function leads to enhanced QTRT1.

CONCLUSIONS: These findings underscore the critical role of QTRT1/Q-tRNA modification in maintaining intestinal and microbial homeostasis. Mechanistically, QTRT1 loss impacts mitochondrial integrity and mucosal homeostasis. Our study highlights the novel roles of tRNA-Q modification in maintaining mucosal barriers and innate immunity in intestinal health.

Eukaryotes acquire queuine (q), also known as Vitamin Q, as a micronutrient factor from intestinal microbiota or from diet.Vitamin Q is needed for queuosine (Q) modification of tRNAs for the protein translation rate and fidelity.Queuine tRNA-ribosyltransferase catalytic subunit 1 (QTRT1) is reduced in human IBD.However, health consequences of disturbed availability of queuine and altered Q-tRNA modification in digestive diseases remain to be investigated.

WHAT ARE THE NEW FINDINGS?: QTRT1 deficiency leads to altered microbiome and reduced Vitamin Q-associated bacteria in human IBD and a QTRT1 KO animal model.QTRT1 protects the host against losing intestinal integrity during inflammation.QTRT1 localizes in mitochondria and plays novel functions by maintaining intestinal mitochondrial function. QTRT1 loss impacts tRNA modification in the intestine, linking to mitochondrial integrity and mucosal homeostasis.Human IBD showed reduced levels of QTRT1 and dysfunctional mitochondria. Restoring mitochondrial function leads to enhanced QTRT1.

Targeting tRNA-Q modification in enhancing mitochondrial function will be a novel method to maintain intestinal health.},
}

@article {pmid41377425,
year = {2025},
author = {Nawaz, S and Nadeem, IA and Talha, M and Irshad, NUN and Imran, SB},
title = {Engineered microbes over immunosuppression: MAGIC as a transformative strategy for vasculitides.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9131-9132},
pmid = {41377425},
issn = {2049-0801},
}

@article {pmid41377407,
year = {2025},
author = {Mehmood, MS and Hajj, F},
title = {Reassessment of microbial DNA in cancer genomes: addressing contamination controversies.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9085-9086},
pmid = {41377407},
issn = {2049-0801},
abstract = {The proposed existence of a widespread "tumor microbiome" has sparked considerable interest, yet recent evidence suggests many microbial DNA signals in cancer genomes arise from contamination rather than true colonization. A September 2025 Science Translational Medicine analysis of over 5700 cancer genomes demonstrated that most detected sequences reflected artifacts, underscoring earlier concerns about low-biomass sequencing studies. While enthusiasm for a universal tumor microbiome must be tempered, robust associations remain in specific cancers, including Helicobacter pylori in gastric carcinoma, Fusobacterium nucleatum in colorectal cancer, and human papillomavirus in cervical malignancies. This reassessment highlights the urgent need for rigorous methodological standards, such as robust negative controls, contamination-aware pipelines, and transparent reporting, to ensure reproducibility. Rather than discouragement, this represents an opportunity to refocus research on biologically plausible, clinically relevant cancer-microbe interactions.},
}

@article {pmid41377390,
year = {2025},
author = {Mehmood, MS and Iqbal, I and Hajj, F},
title = {Intratumoral microbiota as prognostic biomarkers in gastrointestinal cancers.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9137-9138},
pmid = {41377390},
issn = {2049-0801},
abstract = {Recent evidence highlights that the tumor microenvironment in gastrointestinal (GI) cancers harbors distinct microbial communities with potential prognostic value. GI malignancies account for nearly 25% of all cancer-related deaths worldwide, yet patients with comparable histopathological features often display markedly different clinical outcomes. Emerging multi-omics studies involving over 3000 tumor specimens have revealed that specific microbial taxa, including Granulicella, Fusobacterium nucleatum, and Parvimonas micra, are linked to advanced disease stages, lymphatic spread, and poorer overall survival. F. nucleatum, in particular, has been implicated in promoting chemoresistance via Toll-like receptor 4 activation and modulation of the immune microenvironment. Reduced microbial alpha diversity within tumors has also been correlated with disease aggressiveness, suggesting a dysbiosis-mediated influence on tumor immunity. Integration of microbial profiles with transcriptomic and immunologic datasets has produced hybrid models that outperform conventional TNM staging in predicting recurrence and therapy response. Standardizing sampling, sequencing, and analytical methodologies remains a critical challenge. The incorporation of microbiome profiling into diagnostic and registry systems could enable routine use of intratumoral microbial signatures as prognostic biomarkers, paving the way toward microbiome-informed precision oncology.},
}

@article {pmid41377381,
year = {2025},
author = {Memon, U and Memon, D and Talha, M and Fatima, M},
title = {Zero-gravity microbiome vortices: decoding orbital sepsis mimics and probiotic dysregulation in space health systems.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9208-9210},
pmid = {41377381},
issn = {2049-0801},
}

@article {pmid41377324,
year = {2025},
author = {Abedin, ZU and Iqbal, MU and Shahriar, Z},
title = {Microbiome-gut-heart axis in cardiac complications of Gaucher disease type 3.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9091-9092},
pmid = {41377324},
issn = {2049-0801},
}

@article {pmid41377295,
year = {2025},
author = {Talha, M and Bilal, M and Fatima, M and Hassan, M and Gill, OA},
title = {From microbiome dysbiosis to virtual reality and nanomedicine: a multidisciplinary roadmap for pediatric glaucoma care.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9115-9116},
pmid = {41377295},
issn = {2049-0801},
}

@article {pmid41377246,
year = {2025},
author = {Singh, PK and Rathi, D and Shweliya, MA and Farooq, A and Anfaal, Z and Saleem, NUA and Hamza, M and Qadri, M and Rath, S and Hemida, MF and Rani, H and Mahgoub, AMA and Wazir, HU},
title = {The interplay of the microbiome and breast cancer: beyond the gut: a narrative review.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {8496-8507},
pmid = {41377246},
issn = {2049-0801},
abstract = {Breast cancer remains a leading cause of morbidity and mortality among women worldwide, with emerging evidence underscoring the microbiota's pivotal role in its etiology, progression, and therapeutic response. This narrative review synthesizes the intricate interplay between the breast tissue, skin, and lung microbiomes in breast cancer pathogenesis, with particular emphasis on inflammatory breast cancer (IBC) and metastatic dissemination. The healthy breast microbiome, dominated by Firmicutes, Proteobacteria, Actinobacteria, and Bacteroidetes, maintains tissue homeostasis through pH regulation, metabolite production, and immune modulation. Dysbiosis disrupts this equilibrium, fostering carcinogenesis via chronic inflammation, estrogen deconjugation, and DNA damage-induced genomic instability, with subtype-specific microbial signatures influencing tumor growth and therapy resistance. In IBC, skin microbiome alterations characterized by overgrowth of pathogens like Pseudomonas aeruginosa and Staphylococcus aureus exacerbate inflammation, epithelial-mesenchymal transition (EMT), and lymphatic invasion, while promoting a pro-tumorigenic microenvironment enriched in regulatory T cells and M2 macrophages. Concurrently, lung microbiota dysbiosis impairs immune surveillance, remodels the extracellular matrix, and facilitates metastatic seeding through neutrophil extracellular traps and cytokine storms. Cross-talk among these microbiomes amplifies systemic effects, highlighting their synergistic contributions to disease aggressiveness. Advanced analytical techniques, including 16S rRNA sequencing, metagenomics, and metabolomics, offer promising microbial biomarkers for early detection and risk stratification. By elucidating these host-microbe dynamics, this review advocates for microbiome-centric interventionssuch as probiotics, fecal microbiota transplantation, and targeted antimicrobials to enhance precision diagnostics and therapies, ultimately improving outcomes in breast cancer management.},
}

@article {pmid41377223,
year = {2025},
author = {Mehmood, MS and Hajj, F},
title = {Microbiome modulation strategies to enhance chemotherapy response and minimize toxicity.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9087-9088},
pmid = {41377223},
issn = {2049-0801},
}

@article {pmid41377184,
year = {2025},
author = {Ayilaran, E and McHugh, O and Jung, Y},
title = {Metagenomic sequencing dataset of microbial communities in onion and cabbage microgreens across substrates, Salmonella inoculation, and bacteriophage application.},
journal = {Data in brief},
volume = {63},
number = {},
pages = {112297},
pmid = {41377184},
issn = {2352-3409},
abstract = {This dataset comprises shotgun metagenomic sequencing results from edible portion of onion (Allium cepa) and cabbage (Brassica oleracea) microgreens cultivated on soil, biostrate, and jute fiber substrates, with and without Salmonella inoculation and bacteriophage application. Table 1 contains detailed sequencing quality metrics and National Center for Biotechnology Information Sequence Read Archive accession numbers (BioProject: PRJNA1327464) for all 24 samples. Figure 1 provides a species-level (≥5% relative abundance) heatmap highlighting microbial community clustering by seed type. These data can be reused for comparative microbiome analyses, evaluation of pathogen-phage-substrate interactions, and benchmarking of metagenomic workflows.},
}

@article {pmid41377121,
year = {2025},
author = {Umphonsathien, M and Prutanopajai, P and Cheibchalard, T and Somboonna, N},
title = {Low-calorie diet intervention ameliorates gut microbiota dysbiosis and metabolic changes in obese patients with type 2 diabetes under standard care.},
journal = {Computational and structural biotechnology journal},
volume = {27},
number = {},
pages = {5307-5317},
pmid = {41377121},
issn = {2001-0370},
abstract = {BACKGROUND: Dietary interventions can modulate the gut bacteria community (microbiota) and offer a complementary strategy for improving metabolic control in type 2 diabetes (T2D). This pilot study evaluated clinical clinical outcomes and gut microbiota changes following a structured low-calorie diet (LCD) intervention in obese T2D individuals under standard care.

METHODS: Twenty obese T2D patients were randomized into an intervention group (n = 15) (6-week 1000-1200 kcal/day of glycemic and metabolic control LCD), or a matched control group (n = 5). Clinical parameters and fecal microbiota profiles were assessed at baseline, week 6, and week 12.

RESULTS: The intervention group showed clinical trends toward improved glycemic and metabolic parameters, including reductions in fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), and lipid levels (i.e., cholesterol) (P > 0.05), accompanied by significant loss of body weight, body mass index (BMI), and body fat (P < 0.05). Four intervention participants (26.7 %) achieved normoglycemia without glucose-lowering medication. Gut microbiota analyses revealed significant alterations in alpha and beta diversity over time in the intervention group (AMOVA: P(control baseline, intervention 12-week) = 0.025 and P(intervention baseline, intervention 12-week) = 0.002), with increased abundance of beneficial genera i.e. Streptococcus, Bifidobacterium and Lactobacillus, and enrichment of Actinobacteria, Candidatus Saccharibacteria (TM7), and Firmicutes at week 12. Linear discriminant analysis effect size (LEfSe) analysis identified distinct microbial biomarkers differentiating groups. Microbial functional predictions revealed significantly decreased inferred activity in pathways related to adipocytokine signaling, D-glutamine and D-glutamate metabolism, and type I diabetes mellitus (P < 0.05); however, these predictions were computational inferences and not experimentally validated.

CONCLUSION: A structured LCD combined with standard care led to metabolic improvement and remodeling of gut microbiota trend in obese Thai individuals with T2D. The findings support the dietary interventions to beneficially modulate the gut microbiome and metabolic health, while highlighting the need for larger studies and functional validation.},
}

@article {pmid41377050,
year = {2025},
author = {An, Y and Yu, X and Wang, C and Yu, X and Zheng, J and Lin, H},
title = {Integrative network pharmacology, transcriptomics, and microbiomics elucidate the therapeutic mechanism of Polygala tenuifolia Willd water extract in chronic obstructive pulmonary disease.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1703853},
pmid = {41377050},
issn = {1664-302X},
abstract = {BACKGROUND: Polygala tenuifolia Willd (PT) is a plant with both medicinal and edible values. Traditionally, it has been used for sedation, enhancing cognition, resolving phlegm, and relieving cough. However, its protective effects and mechanisms against chronic obstructive pulmonary disease (COPD) remain unclear.

AIM OF THE STUDY: This study aims to observe the protective effects of the water extract of Polygala tenuifolia Willd (WEPT) on COPD, and to preliminarily elucidate its potential therapeutic mechanisms by integrating network pharmacology, molecular docking, multi-omics analysis, and molecular experiments.

METHODS AND MATERIALS: HPLC quantified WEPT constituents. COPD mice models established via chronic smoke exposure underwent WEPT treatment, and the therapeutic effect was evaluated by lung function test, histopathology and cytokine profiling. Integrated multi-omics analyses (network pharmacology, transcriptomics, microbiomics) identified bioactive compounds, therapeutic targets, pathway regulations, and microbiota dynamics. Molecular docking validated compound-target interactions, while immunohistochemical/fluorescence assays confirmed key protein expression in lung tissues.

RESULTS: WEPT administration effectively reduced inflammatory cytokine levels in COPD mice, improved lung function, and alleviated histopathological damage like alveolar structural injury and airway inflammation. Network pharmacology and transcriptomic analyses identified Norhyoscyamine and Onjixanthone I as key active components, targeting PIK3CA and AKT1 via PI3K-AKT pathway regulation. Microbiome analysis showed WEPT restored gut microbiota balance. Molecular docking confirmed strong binding of bioactive compounds to core targets, while immunostaining assays demonstrated WEPT suppressed p-PI3K and p-AKT protein expression.

CONCLUSION: WEPT may exert its intervention effects on COPD through a multi-target and multi-level comprehensive regulatory mechanism.},
}

@article {pmid41377043,
year = {2025},
author = {Batur, M and Li, X and Liu, B and Wang, S and Dong, Q and Abudurexiti, N and Liu, Z},
title = {Characterization of gut microbiome dysbiosis in calcium oxalate stone patients with comorbid metabolic syndrome.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1644416},
pmid = {41377043},
issn = {1664-302X},
abstract = {OBJECTIVE: Metabolic syndrome is an important risk factor for calcium oxalate stone, yet the underlying mechanism remain unclear. Gut microbiota is involved in human metabolic processes and is associated with both metabolic syndrome and calcium oxalate stone formation.

METHODS: In this study, 100 subjects were divided into four groups: calcium oxalate stone with metabolic syndrome (Group A), metabolic syndrome only (Group B), calcium oxalate stone only (Group C), and healthy controls (Group D), with 25 cases in each group. Gut microbiota composition and function were analyzed using 16S rRNA gene sequencing. Microbiota diversity, species differences, and metabolic function changes were assessed by combining clinical parameters and metabolic pathway (KEGG) annotation.

RESULTS: The α diversity in Group A was significantly lower than in the other three groups (Shannon index, P < 0.05), and β diversity analysis revealed significant differences in bacterial community structure among all four groups (ANOSIM, P < 0.05). In Group A, short-chain fatty acid (SCFA)-producing probiotics (e.g., Faecalibacterium, Faecalibacillus, Prevotella) were reduced, while pro-inflammatory bacteria (e.g., Eggerthella and Anaerobacteriaceae) were enriched. RDA correlation analysis indicated that Faecalibacterium is negatively correlated with blood glucose levels, Faecalibacterium and Roseburia are positively correlated with urinary pH. KEGG analysis showed that the bisphenol degradation pathway was reduced (logFC = -1.45, P = 0.027) and the retinol metabolism pathway was enriched (logFC = 0.928, P = 0.006) in Group A compared to Group B.

CONCLUSION: Patients with calcium oxalate stone and metabolic syndrome exhibit a "double imbalance" in gut microbiota: on the one hand, the reduced diversity of the microbiota and the decrease of SCFAs-producing microbiota weakened the metabolic protective effect of the gut microbiota; on the other hand, the enrichment of pro-inflammatory and pathogenic bacteria exacerbated metabolic disorders and inflammatory reactions. The present study reveals that gut microbiota play a role in the mechanism of metabolic syndrome promoting calcium oxalate stone formation, and these findings provide a theoretical basis for the use of probiotics to prevent calcium oxalate stone.},
}

@article {pmid41377037,
year = {2025},
author = {Thornval, NR and Lacy-Roberts, N and Nilsson, P and Espinosa-Gongora, C and Hasman, H and Mourão, J and Rasmussen, A and Rebelo, AR and Gibson, C and Hendriksen, RS},
title = {Evaluation of four DNA extraction kits for implementation of nanopore sequencing in routine surveillance of antimicrobial resistance in low-resource settings.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1715467},
pmid = {41377037},
issn = {1664-302X},
abstract = {INTRODUCTION: Whole genome sequencing (WGS) is a valuable tool in surveillance of antimicrobial resistance (AMR). However, the technology faces several implementation challenges in low-resource settings. While advances in Oxford Nanopore Technologies (ONT) field sequencing have enabled sequencing in low-resource settings, DNA extraction remains a critical barrier to implementation.

METHODS: We evaluated four commercially available DNA extraction kits: QIAGEN DNeasy Blood & Tissue, NEB Monarch® HMW, Thermo Fisher MagMAX™ Microbiome, and Thermo Fisher MagMax™ Viral/Pathogen, for their suitability in ONT-based AMR surveillance across Gram-positive and Gram-negative bacterial strains. Kits were evaluated for DNA purity, yield, and fragment length, as well as sequencing metrics including mean read quality, read N50, sequencing depth, multilocus sequence typing concordance, and AMR gene detection. Practical parameters such as cost, hand-on time, and equipment requirements were also assessed.

RESULTS: The DNeasy Blood & Tissue kit consistently produced DNA of sufficient quality and quantity to enable high-sequencing depth ONT sequencing, enabling robust multi-locus sequence typing and AMR gene recovery, while remaining cost-effective and requiring minimal technical expertise.

DISCUSSION: These findings support the integration of optimized DNA extraction workflows into public health surveillance systems. The DNeasy Blood & Tissue kit offers a reliable and scalable solution for real-time genomic monitoring of antimicrobial resistance in resource-limited settings.},
}

@article {pmid41376894,
year = {2026},
author = {Kamath, A and Patel, D and Saraf, M and Patel, S},
title = {Rooted intelligence: Integrating AI, Omics, and Synthetic biology to engineer the plant microbiome.},
journal = {3 Biotech},
volume = {16},
number = {1},
pages = {10},
pmid = {41376894},
issn = {2190-572X},
abstract = {This review synthesizes recent advances in the integration of omics, synthetic biology, and artificial intelligence (AI) to deepen understanding of plant-microbe interactions and support sustainable agriculture. Omics approaches have provided molecular-level insights into microbial diversity, functional genes, and regulatory pathways shaping rhizosphere dynamics. Synthetic biology has enabled the design of microbial strains and synthetic communities (SynComs) with enhanced traits such as nutrient solubilization, stress tolerance, and pathogen suppression, offering targeted solutions for crop improvement. AI-driven tools have accelerated these advances by enabling predictive modelling, multi-omics data integration, and real-time phenotyping, while also enhancing disease forecasting and microbiome-informed crop management. The combined application of these technologies demonstrates potential for the rational design of next-generation plant growth-promoting rhizobacteria and synthetic microbial consortia optimized for diverse agroecosystems. Key challenges remain in translating laboratory findings to field conditions, ensuring biosafety of engineered microbes, and addressing ethical and regulatory issues. Addressing these barriers through interdisciplinary frameworks and responsible innovation will pave the way for climate specific high-yielding, and sustainable cropping systems.},
}

@article {pmid41376863,
year = {2025},
author = {Rakow, A and Lebek, S and Renz, N and Funk, J},
title = {Sonication findings do not support routine removal of paediatric orthopaedic implants.},
journal = {Journal of children's orthopaedics},
volume = {},
number = {},
pages = {18632521251400162},
pmid = {41376863},
issn = {1863-2521},
abstract = {PURPOSE: The risk of implant-associated infection (IAI) is occasionally cited as an indication for routine removal of orthopaedic implants in children, but evidence is lacking. This study aimed at exploring the frequency of microbial colonization of paediatric orthopaedic implants by sonication, a gold standard for diagnosing IAI.

METHODS: Data of all patients aged <18 years at index implantation who underwent implant removal over a 34-month period at a single institution were retrospectively reviewed. Sonication culture results were classified according to microbial growth as negative (no/non-significant growth) or positive (significant growth/colonization). Descriptive statistics were performed, correlations were analysed via crosstabs and univariate ANOVA (p < 0.05).

RESULTS: One hundred and twenty-nine sonicated devices from 63 patients were included. Mean patient age at implantation was 9.8 years (standard deviation (SD) 3.4; range 3.0-15.6), mean implant in situ time was 2.2 years (SD 1.5; range 0.6-8.8). In all, 63 tension band plates, 35 locking screw plates, 26 cannulated screws, 3 intramedullary nails and 2 K-wires were evaluated. In total, 128/129 (99%) of implant sites were asymptomatic. Sonication fluid cultures of 24/128 (19%) implants from 21 asymptomatic patients showed non-significant growth of pathogens mainly related to the human skin microbiome, suggesting contamination.

CONCLUSIONS: Sonication of implants removed from asymptomatic implant sites showed no significant microbial growth. Thus, the risk of IAI should be irrelevant for scheduling implant removal in children without signs and symptoms of infection.

SIGNIFICANCE OF STUDY: This study investigates for the first time the role of sonication in non-spinal paediatric orthopaedics and provides important insights into the question of routine implant removal in children, providing a foundation for future research.},
}

@article {pmid41376848,
year = {2025},
author = {Naegele, C and Jones, G},
title = {Capitalizing on the GLP-1 RA revolution for behavioral health through digital companions.},
journal = {Digital health},
volume = {11},
number = {},
pages = {20552076251406308},
pmid = {41376848},
issn = {2055-2076},
}

@article {pmid41376716,
year = {2025},
author = {Abarca-Castro, EA and Reyes-Lagos, JJ and Guzmán Ramos, K and Montiel-Castro, AJ and Arano-Varela, H and Mayer-Villa, PA and Aguilar-Toalá, JE and Montesillo-Cedillo, JL and Talavera-Peña, AK},
title = {Fetal development and the air pollution exposome: an integrative perspective of health pathways.},
journal = {Frontiers in cellular neuroscience},
volume = {19},
number = {},
pages = {1688437},
pmid = {41376716},
issn = {1662-5102},
abstract = {We offer an integrative perspective on how the air-pollution exposome shapes fetal development during the first 1,000 days and reverberates across mental health and behavior. Pregnant individuals and young children are disproportionately exposed to particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and volatile organic compounds (VOCs) with social disadvantage amplifying risk. We bridge exposure to biology through three conduits. First, the placenta acts as a sensor and recorder, transducing signals that alter growth, immune tone, and neuroendocrine programming. Second, fetal autonomic control-captured by beat-to-beat fetal heart rate variability (fHRV) offers a relevant biomarker of neurodevelopmental integrity; the absence of direct ambient-pollution-fHRV studies is a pressing gap. Third, maternal immune activation, oxidative and endoplasmic reticulum (ER) stress, and disrupted morphogenesis reshape developing circuits, changes now traceable in utero by advanced fetal MRI. These pathways fit a developmental-programming frame: epigenetic remodeling, gene-environment interplay, endocrine-disrupting co-exposures, and gut-microbiome shifts create durable susceptibility. Clinically, the result is structural and functional brain alterations and child phenotypes spanning attention, executive control, affecting regulation, and learning, with clear pediatric and educational implications. We propose an exposome-based research agenda coupling high-resolution exposure assessment with placental molecular profiling, fetal/neonatal autonomic biomarkers (including fHRV), fetal/child neuroimaging, and longitudinal microbiome readouts in harmonized cohorts. In parallel, multisectoral actions-clean air urban design, targeted protection of pregnancy and early childhood, chemical regulation, and risk communication-should narrow exposure inequities while trials test biomarker-guided prevention. Aligning placental biology, autonomic metrics, and exposome science may transform risk stratification and safeguard the developing brain.},
}

@article {pmid41376623,
year = {2025},
author = {Khilwani, R and Singh, S},
title = {Dual signaling cascade regulating gut-lung axis in Interleukin-6/Interleukin-17 for NSCLC immuno pathogenesis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1649517},
pmid = {41376623},
issn = {1664-3224},
mesh = {Humans ; *Carcinoma, Non-Small-Cell Lung/immunology/metabolism/pathology/microbiology/etiology ; *Gastrointestinal Microbiome/immunology ; *Lung Neoplasms/immunology/metabolism/pathology/microbiology/etiology ; *Interleukin-17/metabolism/immunology ; *Interleukin-6/metabolism/immunology ; *Signal Transduction/immunology ; Animals ; *Lung/immunology/metabolism/microbiology ; },
abstract = {Non-small cell lung cancer is the leading cause of death globally, affecting both men and women. Emerging evidence has highlighted the apparent role of gut microbiota in reshaping the lung microbial community. Notably, imbalances in the gut microbiome disrupt lung physiology, which increases an individual's susceptibility to lung diseases. The homing of gut residents to pulmonary sites prompts tumorigenic processes by altering microbial synergism that metabolically reprograms immune effectors to complement tumor growth. Nevertheless, the additive effect of microbiomes induces immune-responsive mechanisms that excessively induce IL-6 and IL-17 at the inflamed site. Consequently, perturbations in cytokine pool boost inflammatory responses toward a pro-tumor effect, implying cytokine duality and the role of these interleukins in regulating gut-lung crosstalk. Inflammation is a natural host defense mechanism activated against foreign stimulants to mount an immune response. At later stages, the inductive effect of IL-6/17 triggers inflammasome assembly where their accelerated response induces lung epithelial damage, leading to cellular transformation. This implies that the unexplored interconnections between microbiomes and interleukin biology influence immune dynamics that regulate the processes of neoplastic transformation. Here, in this comprehensive review, we comment on the gut-lung crosstalk along with the role of resident microbes in generating immunological responses. Besides, we discuss the IL-6/17-mediated activation of the inflammasome in attuning tumoral immunity. These dictate the potential of microbiotal lifeforms in generating inflammatory responses, which can therefore serve as potential diagnostic markers in NSCLC.},
}

Humans
*Carcinoma, Non-Small-Cell Lung/immunology/metabolism/pathology/microbiology/etiology
*Gastrointestinal Microbiome/immunology
*Lung Neoplasms/immunology/metabolism/pathology/microbiology/etiology
*Interleukin-17/metabolism/immunology
*Interleukin-6/metabolism/immunology
*Signal Transduction/immunology
Animals
*Lung/immunology/metabolism/microbiology

@article {pmid41376600,
year = {2025},
author = {Yang, K and Liu, Z and Wang, H and Xiao, Z and Zhao, W and Gong, W},
title = {Microbial metabolite trimethylamine-N-oxide facilitates colorectal inflammation-cancer transformation by blocking lysosomal degradation of Wnt signaling.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2597626},
doi = {10.1080/19490976.2025.2597626},
pmid = {41376600},
issn = {1949-0984},
mesh = {Animals ; *Methylamines/metabolism ; Mice ; *Gastrointestinal Microbiome ; Humans ; *Wnt Signaling Pathway/drug effects ; *Colorectal Neoplasms/metabolism/pathology/microbiology ; *Lysosomes/metabolism ; Bacteria/metabolism/genetics/classification ; Mice, Inbred C57BL ; Disease Models, Animal ; *Cell Transformation, Neoplastic ; beta Catenin/metabolism ; Colitis/microbiology ; Inflammation ; },
abstract = {Chronic inflammation is closely related to the occurrence and development of many tumors, including colorectal cancer (CRC), a typical inflammation-dependent cancer. The gut bacteria and their metabolites, as signaling molecules or substrates of metabolic processes, have attracted increasing attention during the colorectal inflammation-cancer transformation process. However, how commensal microbiota-derived metabolites create a favorable internal environment for carcinogenesis through the chronic inflammatory response is not entirely understood. Here, we conducted multiomics analysis, including single-cell RNA-sequencing (scRNA-seq), microbiome and metabolome to explore the intricate cross-talk of host-microbe-metabolite. By employing colitis-associated CRC mice models, as well as patient-derived CRC organoids, we identified that trimethylamine n-oxide (TMAO), a metabolic product derived from the gut microbiota, was crucial for inflammation-mediated colorectal carcinogenesis by enhancing Wnt signaling. Further mechanistic studies revealed that TMAO interacted with heat shock protein family A member 8 (Hspa8, also known as Hsc70), a molecular chaperone that mediates autophagy, to block the lysosomal degradation of the β-catenin protein, leading to an increase in the downstream targets cyclin D1 and c-Myc, thus contributing to colorectal carcinogenesis. Our results indicated that TMAO serves as a bridge to establish the connection between microbiota and colorectal carcinogenesis, playing a critical pathogenic role during CRC progression and therefore provides novel mechanistic insights into the intestinal inflammation in colorectal neoplasia progression.},
}

Animals
*Methylamines/metabolism
Mice
*Gastrointestinal Microbiome
Humans
*Wnt Signaling Pathway/drug effects
*Colorectal Neoplasms/metabolism/pathology/microbiology
*Lysosomes/metabolism
Bacteria/metabolism/genetics/classification
Mice, Inbred C57BL
Disease Models, Animal
*Cell Transformation, Neoplastic
beta Catenin/metabolism
Colitis/microbiology
Inflammation

@article {pmid41376147,
year = {2025},
author = {Wang, J and Chen, P and Deng, Y and Yu, L and Tu, C and Xu, X and Fang, X and Li, W},
title = {Akkermansia muciniphila Alleviates Olanzapine-Induced Hepatic Steatosis via the Gut Microbiota-IGFBP2/APOA1-Liver Axis.},
journal = {Microbial biotechnology},
volume = {18},
number = {12},
pages = {e70281},
doi = {10.1111/1751-7915.70281},
pmid = {41376147},
issn = {1751-7915},
support = {82173903//National Natural Science Foundation of China/ ; 81903686//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Olanzapine/adverse effects ; Humans ; *Fatty Liver/chemically induced/metabolism ; Rats ; Male ; Liver/metabolism/pathology/drug effects ; *Apolipoprotein A-I/metabolism/genetics ; *Akkermansia ; Disease Models, Animal ; Rats, Sprague-Dawley ; Antipsychotic Agents/adverse effects ; },
abstract = {Olanzapine is associated with a high risk of hepatic steatosis as a commonly used atypical antipsychotic. In this study, we observed differential susceptibility to olanzapine-induced fatty liver disease in both rats and patients. Notably, patients with olanzapine-induced liver damage exhibited an altered gut microbiota composition, with Akkermansia muciniphila showing the most pronounced alteration. To explore its therapeutic potential, we administered A. muciniphila to olanzapine-treated rats, which significantly reduced hepatic lipid accumulation and liver injury. Gut microbiome analysis revealed significant alterations in microbial diversity and composition following A. muciniphila treatment. Transcriptomic analysis further identified differentially expressed genes in the liver, highlighting the involvement of IGFBP2 and APOA1 in the protective effects of A. muciniphila . Functional validation demonstrated that overexpression of IGFBP2 and APOA1 alleviated olanzapine-induced hepatic steatosis in both cellular and animal models. These findings suggest that A. muciniphila exerts hepatoprotective effects via the gut microbiota-IGFBP2/APOA1-liver axis, offering a potential microbiota-targeted strategy to mitigate olanzapine-induced metabolic dysfunction.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Olanzapine/adverse effects
Humans
*Fatty Liver/chemically induced/metabolism
Rats
Male
Liver/metabolism/pathology/drug effects
*Apolipoprotein A-I/metabolism/genetics
*Akkermansia
Disease Models, Animal
Rats, Sprague-Dawley
Antipsychotic Agents/adverse effects

@article {pmid41376027,
year = {2025},
author = {Takahashi, H and Fujii, T and Yamada, C and Kondo, N and Kuramitsu, K and Funasaka, K and Ohno, E and Hirooka, Y and Tochio, T and Fujiki, K},
title = {Host Dietary Nutrients Shape GH32-Mediated Microbial Responses to Prebiotic Fructans: A Randomized Trial.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/foods14234090},
pmid = {41376027},
issn = {2304-8158},
support = {JP24K14784//JSPS KAKENHI/ ; No grant number//The Anzu no Mori Foundation 2024 Research Grant/ ; },
abstract = {Prebiotics, such as short- and long-chain fructans, beneficially modulate the microbiota; however, individual variability in response remains unclear. In this randomized, double-blind, placebo-controlled trial, 40 healthy adults received either a combined fructan supplement-1-Kestose (Kes) and inulin (Inu)-or a placebo (maltose + cornstarch) for 4 weeks. We investigated the fecal microbiome, bacterial growth, and glycoside hydrolase family 32 (GH32) gene abundance, and further examined the association between dietary intake and GH32. Kes and Inu co-supplementation selectively increased Bifidobacterium adolescentis and B. longum, harboring the GH32 genes inuA and cscA, respectively. Growth assays revealed that B. longum, which expresses cscA, grew only on Kes, whereas B. adolescentis, which expresses inuA, showed growth on Kes and Inu. Only responders-participants showing increases in both species-exhibited consistent upregulation of GH32 genes and were associated with higher retinol and C16:3 (n-6) fatty acid intake, as well as greater green leafy vegetable and canned tuna consumption. This study provides insights into species level responses to prebiotics, supporting personalized dietary strategies for gut microbiota modulation.},
}