@article {pmid42182435,
year = {2026},
author = {Wallace, M and Allen, ML and Karasov, TL and Puri, AW},
title = {A Bacterial Natural Product Reshapes Phyllosphere Microbiome Composition by Blocking Carotenoid Biosynthesis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.05.14.725204},
pmid = {42182435},
issn = {2692-8205},
support = {R35 GM147018/GM/NIGMS NIH HHS/United States ; },
abstract = {The microbial communities that inhabit the phyllosphere, the above-ground portion of plants, are important for plant growth and resilience. However, the natural products that mediate interactions among these organisms and with their environment remain understudied, limiting our molecular-level understanding of how phyllosphere microbial communities are structured and maintained. Natural product-mediated microbial competition is typically associated with growth inhibition, but may also occur through other mechanisms in these communities. Many bacteria produce pigments to mitigate oxidative stress, and here we identify listianol, a previously undescribed natural product that inhibits the pigmentation of diverse bacteria. Listianol blocks carotenoid biosynthesis by targeting the desaturases CrtN and CrtI. This activity sensitizes normally pigmented bacteria to UVB radiation in vitro , and a listianol-producing strain reshapes the composition of a model bacterial community on Arabidopsis thaliana under UVB exposure. Together, these findings identify pigmentation inhibition as a potential form of competition in the phyllosphere.},
}

@article {pmid42551625,
year = {2026},
author = {Poboży, T and Poboży, K and Domańska-Poboża, J and Kotela, A and Konarski, W},
title = {Gut microbiome and avascular necrosis: A scoping review of current evidence and knowledge gaps.},
journal = {Bone},
volume = {},
number = {},
pages = {118041},
doi = {10.1016/j.bone.2026.118041},
pmid = {42551625},
issn = {1873-2763},
abstract = {Avascular necrosis (AVN) is a progressive bone disorder characterized by impaired blood supply, osteocyte death, and structural collapse, most commonly affecting the femoral head. In recent years, growing evidence has suggested that gut microbiota may influence skeletal health through immune, metabolic, and vascular pathways. This scoping review aimed to systematically map current evidence on the relationship between gut microbiota and AVN and to identify key knowledge gaps. Following Joanna Briggs Institute methodology and PRISMA-ScR guidelines, a comprehensive search of PubMed, EMBASE, ScienceDirect, Web of Science Core Collection, ClinicalTrials.gov, and Cochrane CENTRAL was conducted. Thirteen eligible studies, including experimental, clinical, multi-omics, and Mendelian randomization analyses, were included. The available evidence indicates that AVN, particularly glucocorticoid- and alcohol-associated forms, is consistently associated with intestinal dysbiosis, reduced production of short-chain fatty acids, immune activation, vascular impairment, and altered bone remodeling. Animal and translational studies demonstrate partial reversal of pathological changes through microbiota-targeted interventions, while human studies reveal etiology-specific microbiota-metabolome signatures. Genetic analyses further support a potential causal contribution of selected microbial taxa and pathways. Overall, current data support the existence of a multidimensional gut-bone axis in AVN. However, most evidence remains indirect - derived from animal models, cross-sectional human studies, and genetic inference rather than from direct interventional testing in patients. Well-designed longitudinal and interventional investigations are needed to clarify causality and therapeutic potential.},
}

@article {pmid42551693,
year = {2026},
author = {Pedersen, AL and Dayon, L and Affolter, M and Seifert, J},
title = {A streamlined workflow for high throughput metaproteomic analysis of the rumen microbiome.},
journal = {Journal of proteomics},
volume = {},
number = {},
pages = {105721},
doi = {10.1016/j.jprot.2026.105721},
pmid = {42551693},
issn = {1876-7737},
abstract = {Metaproteomics can provide direct functional insights into complex microbial communities, yet its application in rumen research remains limited due to labor-intensive and low-throughput sample preparation workflows before the MS analysis. This work aimed to develop and characterize a streamlined, high throughput metaproteomic workflow optimized for rumen samples. Key steps, including microbial cell extraction, cell lysis, protein digestion, and LC-MS/MS acquisition, were systematically assessed and optimized to reduce hands-on time while maintaining deep proteome coverage. The optimized workflow integrates a minimized cell extraction protocol using 0.5 g starting material and in-solution tryptic digestion. Application of the final workflow to 72 samples from in vitro fermentation revealed that biological variability between inocula dominated technical variability, which remained moderate (median CV of 21-24% across batches). Overall, the optimized workflow supports robust taxonomic and functional characterization of the rumen microbiome with improved scalability. These advances provide a foundation for applying metaproteomics to larger experimental designs, including nutritional trials and cohort studies, thereby enabling broader functional interrogation of rumen microbial ecosystems. SIGNIFICANCE: This study addresses current limitations in the application of metaproteomics to rumen microbiome research by developing a streamlined and scalable sample preparation workflow. By optimizing key steps and reducing sample input while maintaining reproducibility and proteome coverage, this work enables more efficient processing of larger sample sets. These advances support the broader use of metaproteomics in rumen studies and facilitate functional investigations relevant to animal nutrition and sustainable livestock production.},
}

@article {pmid42551765,
year = {2026},
author = {Battelli, MG and Bortolotti, M and Bolognesi, A and Polito, L},
title = {XANTHINE OXIDOREDUCTASE IN DIGESTIVE DISEASES: A CONTEXT-DEPENDENT REDOX SWITCH LINKING INFLAMMATION, METABOLISM AND CARCINOGENESIS.},
journal = {Free radical biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.freeradbiomed.2026.08.007},
pmid = {42551765},
issn = {1873-4596},
abstract = {Xanthine oxidoreductase (XOR) is a molybdenum-containing enzyme that catalyzes the final steps of purine catabolism, generating uric acid and, under specific conditions, reactive oxygen species (ROS) and reactive nitrogen species. Due to its high expression in the liver and gastrointestinal tract, XOR has emerged as an important regulator of redox homeostasis, innate immunity and metabolic adaptation in digestive diseases. This review examines the role of XOR in hepatic disorders, intestinal ischemia-reperfusion (I/R) injury and inflammatory bowel disease (IBD), focusing on oxidative stress, tissue injury, host-microbiome interactions and carcinogenesis. Evidence indicates increased XOR activity in inflammatory and fibrotic liver diseases, where ROS generation contributes to hepatocellular damage, fibrosis and disease progression. In intestinal I/R injury, XOR links ATP depletion and hypoxanthine accumulation to reperfusion-associated oxidative stress, barrier dysfunction, bacterial translocation and systemic inflammation. In IBD, XOR participates in cytokine amplification, redox imbalance, thiopurine metabolism and inflammation-associated colorectal carcinogenesis. Emerging evidence also supports bidirectional interactions between XOR/urate metabolism and the gut microbiota, suggesting a broader role for XOR in regulating intestinal immune homeostasis. However, the biological significance of XOR is strongly context dependent. Whereas increased XOR activity promotes inflammatory tissue injury, advanced gastrointestinal malignancies are frequently characterized by reduced XOR expression, loss of cellular differentiation and enhanced de novo purine synthesis. Overall, XOR emerges as a central, but highly plastic, regulator at the interface between metabolism, inflammation and host-microbiome interactions in digestive diseases. Its clinical exploitation will depend on the ability to understand, rather than oversimplifying, this complexity.},
}

@article {pmid42551774,
year = {2026},
author = {Cheng, Y and Yu, S and Huang, Y and Liu, B},
title = {Engineered microorganisms and nanomaterials in cancer therapy: Emerging hybrid systems and translational challenges.},
journal = {Nanomedicine : nanotechnology, biology, and medicine},
volume = {},
number = {},
pages = {103002},
doi = {10.1016/j.nano.2026.103002},
pmid = {42551774},
issn = {1549-9642},
abstract = {The convergence of synthetic biology and nanotechnology has created new opportunities for cancer diagnosis and therapy. Engineered microorganisms exhibit unique tumor-targeting, colonization, and immunomodulatory capabilities, while nanomaterials provide versatile platforms for drug delivery, imaging, and controlled therapeutic release. This review summarizes recent advances in the application of engineered microorganisms and nanomaterials in oncology, with a focus on their mechanisms of action, therapeutic potential, and translational challenges. We discuss the roles of the tumor microbiome in cancer progression, microbial engineering strategies for tumor targeting and immune regulation, and the development of nanomaterial-based delivery systems and immunotherapies. Particular attention is given to microbe-nanomaterial hybrid platforms, which combine the advantages of both systems to enhance therapeutic efficacy and modulate the tumor microenvironment. Finally, key challenges related to biosafety, biocompatibility, regulatory approval, and clinical translation are highlighted. The integration of engineered microorganisms and nanomaterials represents a promising strategy for next-generation precision oncology and may accelerate the development of more effective and personalized cancer therapies.},
}

@article {pmid42552038,
year = {2026},
author = {Peter L, IR and Chatterjee, D and Chrishone, AF and Francis, D},
title = {Metabolic therapeutic targets in Alzheimer's disease.},
journal = {International review of neurobiology},
volume = {188},
number = {},
pages = {1-32},
doi = {10.1016/bs.irn.2026.05.010},
pmid = {42552038},
issn = {2162-5514},
mesh = {Humans ; *Alzheimer Disease/metabolism/drug therapy ; Animals ; *Energy Metabolism/physiology/drug effects ; *Brain/metabolism ; *Mitochondria/metabolism ; Glucose/metabolism ; },
abstract = {Alzheimer's disease (AD) is increasingly recognized as a disorder marked not only by amyloid-β and tau pathology, but also by profound disturbances in brain energy metabolism that arise early in disease progression. Accumulating evidence indicates that impairments in glucose utilization, insulin signaling, and mitochondrial function precede neurodegeneration and contribute directly to synaptic failure and cognitive decline. This chapter presents a comprehensive overview of Alzheimer's disease through the lens of metabolic dysfunction, highlighting disrupted neuronal bioenergetics as a central and unifying feature of pathogenesis. We examine key metabolic pathways implicated in AD, including cerebral glucose hypometabolism, brain insulin resistance, impaired glycolysis, mitochondrial oxidative phosphorylation deficits, oxidative stress, and altered mitochondrial dynamics. The chapter further discusses therapeutic strategies aimed at restoring metabolic homeostasis, such as insulin sensitization, enhancement of glucose transport, activation of mitochondrial biogenesis, modulation of the electron transport chain, and the use of mitochondria-targeted antioxidants. In parallel, alternative energy approaches-including ketone metabolism, fatty acid oxidation, and pentose phosphate pathway activation-are explored as promising avenues to bypass glucose-dependent energy deficits and reinforce neuronal resilience. Emerging directions in metabolic therapeutics are also highlighted, including combination treatment strategies, NAD[+]-sirtuin and AMPK signaling, and the expanding role of the gut microbiome-brain metabolism axis. By integrating insights from experimental models, neuroimaging studies, and clinical trials, this chapter underscores the potential of metabolic interventions to enable early, disease-modifying strategies for Alzheimer's disease.},
}

Humans
*Alzheimer Disease/metabolism/drug therapy
Animals
*Energy Metabolism/physiology/drug effects
*Brain/metabolism
*Mitochondria/metabolism
Glucose/metabolism

@article {pmid42552151,
year = {2026},
author = {Bai, QX and Luo, KM and Jia, LH and Jia, J and Kantawong, F and Tan, RZ and Wang, L},
title = {The Therapeutic Application of Epigenetic Regulation by Natural Herbal Compounds in Kidney Diseases.},
journal = {Seminars in nephrology},
volume = {},
number = {},
pages = {151711},
doi = {10.1016/j.semnephrol.2026.151711},
pmid = {42552151},
issn = {1558-4488},
abstract = {Kidney diseases, represented by chronic kidney disease (CKD) and acute kidney injury (AKI), pose significant global public health challenges due to their complex pathogenesis and limited therapeutic options. In recent years, epigenetic regulation-including DNA methylation, histone modifications, and non-coding RNAs-has been shown to play a crucial role in the progression of kidney diseases, offering new directions for therapeutic strategies. Natural herbal compounds have emerged as a research focus for modulating epigenetic mechanisms owing to their multi-target effects, low toxicity, and broad bioactivity. This review outlines the regulatory functions of epigenetic mechanisms across various kidney diseases and illustrates how natural herbal compounds can mitigate renal injury via multi-target epigenetic modulation. These compounds have been shown to reverse renal fibrosis, attenuate inflammatory responses, suppress oxidative stress, and protect podocytes and renal tubular epithelial cells by targeting DNA methyltransferases, histone-modifying enzymes, and non-coding RNAs, including microRNAs and long non-coding RNAs. However, challenges such as limited bioavailability and insufficiently elucidated in vivo mechanisms impede clinical translation. Future research should prioritize structural optimization, advanced delivery systems, and investigations into gut microbiome interactions to enhance therapeutic applicability. Overall, this review highlights the promise of epigenetics-based therapeutic strategies using herbal active ingredients for kidney disease intervention, though further validation and optimization are needed for clinical application.},
}

@article {pmid42552215,
year = {2026},
author = {Kamba, S and Kuroki, M and Takemura, I and Tabata, H and Minei, R and Shimamoto, M and Ogura, A and Hasegawa, M and Ishikawa, M},
title = {Enrichment of Lysobacter in a long-term organically managed agricultural field with low soilborne disease incidence.},
journal = {Journal of bioscience and bioengineering},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jbiosc.2026.07.002},
pmid = {42552215},
issn = {1347-4421},
abstract = {Disease-suppressive soils, in which soilborne pathogens are naturally suppressed, offer a promising model for sustainable crop protection, particularly in organic farming systems where chemical disease control options are limited. Although disease suppression in these soils is considered to rely on biological control, the underlying mechanisms remain poorly understood. In this study, we investigated soil from a long-term organically managed field in Shiga Prefecture, Japan, where soilborne disease incidence has remained consistently low, to identify bacterial community features potentially associated with this field. The 16S rRNA gene amplicon sequencing indicated that this soil harbored a bacterial community distinct from those of nearby agricultural soils. Following the application of organic compounds, the genus Lysobacter, a taxon with known antagonistic activity against plant pathogens, was markedly enriched in response to proteinaceous organic inputs. This enrichment was consistent across sampling times and specific to certain proteinaceous organic inputs, whereas minimal effects were observed on chitin, N-acetyl-d-glucosamine, or cysteine. Broader soil surveys indicated that Lysobacter enrichment was not strictly associated with whether soils had been managed under organic or conventional farming practices. Stepwise multiple regression analysis identified 10 co-occurring bacterial genera that were strongly associated with Lysobacter abundance. These findings highlight condition-dependent Lysobacter enrichment as a characteristic microbial response to proteinaceous organic amendments in this low-disease-incidence field and provide microbial insights that may inform microbiome-based strategies for sustainable soil management.},
}

@article {pmid42552305,
year = {2026},
author = {Lu, Y and Shao, D and Xiao, Y and Jiang, YZ and Shao, ZM},
title = {Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {42552305},
issn = {2059-3635},
support = {82341003//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Humans ; *Neoplasms/immunology/pathology/therapy/genetics ; *Inflammation/immunology/pathology/therapy/genetics ; *Tumor Microenvironment/immunology/genetics ; *Cell Movement/immunology/genetics ; Animals ; Chemokines/immunology ; },
abstract = {Cancer and inflammatory diseases are critically influenced by dynamic interactions between pathological tissues and the host immune system. The precise migration of immune cells into the local microenvironments of tumors or inflammation is a fundamental prerequisite for them to exert their functions. Immune reservoirs, including tertiary lymphoid structures, secondary lymphoid structures, bone marrow and the intestinal tract, serve as critical mobilization hubs for diverse lymphoid and myeloid populations to infiltrate tumors or inflamed sites. The directional migration of immune cells is orchestrated through complex regulatory networks involving chemokine or cytokine-receptor pairs, adhesion molecule interactions, extracellular vesicle signaling, metabolic reprogramming and microbiota modulation. In both tumors and inflammation, immune cell trafficking shapes the local immune landscape, contributing to either immune protection or pathological progression. Contemporary therapeutic strategies targeting immune cell migration encompass the following axes: precision modulation of chemokine or cytokine networks, architectural reprogramming of lymphatic structures or extracellular matrix, dietary intervention and strategic manipulation of microbiome. Nevertheless, clinical translation remains hindered by microenvironmental heterogeneity, suboptimal migratory efficiency, and technical limitations in longitudinal tracking of cellular dynamics. This review integrates recent findings from oncology and inflammatory diseases to explore the origins, phenotypes and trafficking mechanisms of migratory immune cells, highlighting how advances in understanding immune migration across cancer and inflammation can inform therapeutic innovation and precision immunomodulation.},
}

Humans
*Neoplasms/immunology/pathology/therapy/genetics
*Inflammation/immunology/pathology/therapy/genetics
*Tumor Microenvironment/immunology/genetics
*Cell Movement/immunology/genetics
Animals
Chemokines/immunology

@article {pmid42552537,
year = {2026},
author = {Shi, W and Li, N and Cheng, S and Zhao, Y and Zhang, Y and Ding, H and Li, Y and Bi, R and Lu, X and Li, Z and Wang, Y},
title = {Chemotherapy-driven gut microbiota remodeling in ovarian cancer: a prospective longitudinal study.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {42552537},
issn = {1479-5876},
mesh = {Humans ; Female ; *Ovarian Neoplasms/drug therapy/microbiology ; Longitudinal Studies ; Prospective Studies ; *Gastrointestinal Microbiome/drug effects ; Neoplasm Recurrence, Local/microbiology/pathology ; *Antineoplastic Agents/therapeutic use/pharmacology ; Middle Aged ; RNA, Ribosomal, 16S/genetics ; },
abstract = {BACKGROUND: The gut microbiome shapes chemotherapy efficacy and outcomes in several cancers, but evidence in ovarian cancer (OC) remains limited and largely cross-sectional. Despite high initial response rates, long-term relapse in OC remains frequent, while conventional markers capture only short-term therapeutic sensitivity. Whether longitudinal gut-microbiome trajectories during chemotherapy are associated with long-term recurrence remains unknown.

METHODS: Within the prospective SOCFCP cohort (N = 91; 13 recurrences), 100 serial fecal samples from a 33-patient sub-cohort were analyzed by 16S rRNA sequencing across the early, middle and late chemotherapy phases. Microbial successional trajectories and their association with recurrence were assessed by linear mixed-effects modeling, multivariable MaAsLin3 and repeated-measures correlation (rmcorr) networks, alongside stratified and covariate-adjusted sensitivity analyses and patient-level bootstrap assessment. The cumulative severe-toxicity-recurrence relationship was estimated by Firth penalized-likelihood regression, suited to sparse, separation-prone events.

RESULTS: Microbial α-diversity rose progressively across the chemotherapy course (Shannon time effect p = 0.002), consistent with ecological succession, with higher turnover among peripheral than in core taxa (p = 0.005). Cumulative severe toxicity was not associated with recurrence (Firth OR = 0.99, 95% CI 0.68-1.39). Crucially, recurrent patients exhibited a progressive depletion of Fusicatenibacter (recurrence × time coefficient = -5.35, q < 0.001) that persisted across all sensitivity analyses-stratified, medication-adjusted, antibiotic-depleted and clinically-adjusted models (coefficient -4.60 to -5.66, all q < 0.001). PICRUSt2-based functional inference identified recurrence-associated differences in predicted de novo nucleotide-biosynthesis and cell-wall-assembly pathway abundance (q < 0.05). A bootstrap-supported co-variation network further linked specific taxa, notably Escherichia-Shigella and Roseburia, to these recurrence-associated pathways.

CONCLUSION: Chemotherapy-driven gut-microbiome remodeling, in particular the recurrence-associated depletion of Fusicatenibacter, was associated with long-term OC relapse, whereas cumulative severe toxicity showed no significant association with recurrence. These longitudinal microbial dynamics support a candidate non-invasive marker that warrants external validation, and provide a hypothesis-generating rationale for testing whether targeting specific predicted bacterial functional pathways can modulate the host anti-tumor milieu.},
}

Humans
Female
*Ovarian Neoplasms/drug therapy/microbiology
Longitudinal Studies
Prospective Studies
*Gastrointestinal Microbiome/drug effects
Neoplasm Recurrence, Local/microbiology/pathology
*Antineoplastic Agents/therapeutic use/pharmacology
Middle Aged
RNA, Ribosomal, 16S/genetics

@article {pmid42553012,
year = {2026},
author = {AlRamadneh, TN and S, RJ and Nayak, PP and Nanda, A and Hasnaawei, SA and Bhatt, A and Chauhan, AS and Singla, S and Nourizadeh, M},
title = {Microbiota-Neuroinflammation Crosstalk in Primary Brain Tumors: Focus on Glioblastoma.},
journal = {Brain and behavior},
volume = {16},
number = {8},
pages = {e71648},
doi = {10.1002/brb3.71648},
pmid = {42553012},
issn = {2162-3279},
mesh = {Humans ; *Glioblastoma/microbiology/immunology/metabolism ; *Brain Neoplasms/microbiology/immunology/metabolism ; Animals ; *Gastrointestinal Microbiome/physiology/immunology ; *Neuroinflammatory Diseases/immunology/metabolism/microbiology ; Tumor Microenvironment/immunology ; Blood-Brain Barrier/metabolism ; Inflammation ; },
abstract = {PURPOSE: Glioblastoma (GBM) is the most aggressive primary brain tumor in adults and remains difficult to treat because of diffuse invasion, immunosuppression, metabolic adaptability, and therapy resistance. This review evaluates how gut microbiota and microbiota-associated neuroinflammatory signaling may contribute to GBM biology and therapeutic response.

METHOD: We synthesized mechanistic, preclinical, translational, and emerging clinical evidence on microbiota-neuroinflammation interactions in GBM. The review focused on gut-brain axis pathways, microbial metabolites, blood-brain barrier (BBB) regulation, glial and myeloid immune activity, tumor-associated microbial signatures, microbial peptide-HLA presentation, and microbiome-informed biomarker or therapeutic strategies.

FINDING: Current evidence suggests that microbiota-related signals may influence GBM through systemic immune modulation, short-chain fatty acids, tryptophan-derived metabolites, polyamines, BBB effects, and altered microglial and tumor-associated myeloid cell function. Polyamine metabolism may sustain myeloid-cell-mediated immunosuppression in the acidic GBM tumor microenvironment, whereas microglial GLUT5-dependent fructose metabolism may limit inflammatory antigen presentation and adaptive antitumor immunity. Sequencing-based studies have reported bacterial and fungal nucleic acid signatures in brain tumor specimens, but these findings require careful interpretation because of low biomass, contamination risk, and methodological variability. Preclinical models further indicate that microbiome modulation can alter inflammatory tone, tumor growth, immune-cell infiltration, and response to immune checkpoint blockade.

CONCLUSION: Microbiota-regulated neuroinflammation is a biologically plausible contributor to GBM progression, immune suppression, and treatment resistance. However, most evidence remains preclinical or early translational. Well-controlled, spatially resolved, multi-omic studies are required before microbiome-based biomarkers or interventions can be clinically implemented for patient stratification and future precision clinical neuro-oncology applications.},
}

Humans
*Glioblastoma/microbiology/immunology/metabolism
*Brain Neoplasms/microbiology/immunology/metabolism
Animals
*Gastrointestinal Microbiome/physiology/immunology
*Neuroinflammatory Diseases/immunology/metabolism/microbiology
Tumor Microenvironment/immunology
Blood-Brain Barrier/metabolism
Inflammation

@article {pmid42553056,
year = {2026},
author = {Elias, AE and El-Chami, C and Bagnall, J and McBain, AJ and O'Neill, CA},
title = {Lacticaseibacillus rhamnosus GG lysate inhibits Staphylococcus aureus biofilm formation in human skin explants.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1885754},
pmid = {42553056},
issn = {2235-2988},
mesh = {Humans ; *Biofilms/drug effects/growth & development ; *Staphylococcus aureus/drug effects/physiology/growth & development ; *Skin/microbiology ; *Lacticaseibacillus rhamnosus ; Skin Microbiome ; Bacterial Lysates ; Keratinocytes/microbiology ; Organ Culture Techniques ; *Probiotics/pharmacology ; },
abstract = {Staphylococcus aureus is a leading cause of skin and soft tissue infections and a major nosocomial pathogen, with biofilm formation contributing to significantly higher morbidity and mortality. In atopic dermatitis (AD), where skin barrier dysfunction and microbial dysbiosis are common features, S. aureus abundance and biofilm formation are associated with disease severity and flare recurrence. We previously demonstrated that a lysate of Lacticaseibacillus rhamnosus GG (LGG)- a common human commensal and widely used probiotic strain- can inhibit S. aureus attachment to human keratinocytes by mechanisms including displacement and competitive exclusion. In this study, we extended these findings utilizing organ-cultured human skin to evaluate the protective effects of LGG lysate against S. aureus challenge in a physiologically relevant model. LGG lysate preserved skin integrity by preventing S. aureus penetration, proliferation, eDNA release and biofilm maturation. These effects were dose-dependent and effective when the lysate was applied from 24 hours pre-S. aureus inoculation to up to 3 hours post inoculation. Together, these data provide mechanistic insight into microbiome- pathogen interactions at the skin surface which could be exploited for therapeutic potential, particularly in the prevention of nosocomial S. aureus skin infections and mitigating S. aureus-driven flares in AD.},
}

Humans
*Biofilms/drug effects/growth & development
*Staphylococcus aureus/drug effects/physiology/growth & development
*Skin/microbiology
*Lacticaseibacillus rhamnosus
Skin Microbiome
Bacterial Lysates
Keratinocytes/microbiology
Organ Culture Techniques
*Probiotics/pharmacology

@article {pmid42553057,
year = {2026},
author = {Huang, P and Cai, Z},
title = {Identifying epigenetic and microbial biomarkers for preterm birth using DNA methylation and gut microbiome data.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1743283},
pmid = {42553057},
issn = {2235-2988},
mesh = {Humans ; Female ; *DNA Methylation ; *Premature Birth/diagnosis/genetics/microbiology ; Pregnancy ; *Biomarkers/blood ; Case-Control Studies ; *Epigenesis, Genetic ; *Gastrointestinal Microbiome/genetics ; RNA, Ribosomal, 16S/genetics ; Adult ; Feces/microbiology ; },
abstract = {BACKGROUND: Preterm birth (PTB), defined as delivery before 37 weeks, is a major cause of neonatal morbidity and mortality worldwide. Evidence suggests that both epigenetic dysregulation and gut microbial imbalance contribute to the inflammatory and metabolic disturbances associated with PTB; however, few studies have examined these factors in conjunction to identify integrated predictive biomarkers.

OBJECTIVES: This study aimed to identify epigenetic and microbial signatures associated with PTB by integrating maternal second-trimester genome-wide DNA methylation profiles with gut microbiome composition.

METHODS: A case-control study was conducted with 120 pregnant women, grouped into two categories: preterm (≤37 weeks, n = 60) and full-term (>37 weeks, n = 60). Maternal blood and fecal samples were collected simultaneously. DNA methylation was profiled using the Illumina MethylationEPIC array, and gut microbiota were characterized through 16S rRNA sequencing. Differentially methylated regions (DMRs) and differentially abundant taxa were identified using FDR < 0.05. Sparse canonical correlation analysis and network modeling were applied to integrate the datasets and identify linked epigenetic-microbial features predictive of PTB.

RESULTS: Women with PTB showed distinct methylation changes in immune and inflammation-related genes, including IL6, CXCL10, TNFAIP3, and PPARGC1A. Gut microbiome analysis revealed significantly reduced α-diversity (Shannon index: 2.81 ± 0.31 vs. 3.42 ± 0.36, p = 0.002), enrichment of pro-inflammatory taxa (Prevotella, Sutterella, Veillonella), and depletion of beneficial genera, including Lachnospiraceae, Faecalibacterium, and Bifidobacterium. Integrated analysis showed strong cross-domain associations (r = 0.68, p < 0.001), linking immune-gene hypomethylation with enrichment of inflammatory taxa. The combined biomarker panel achieved high predictive performance (AUC = 0.87; sensitivity = 82%; specificity = 84%), outperforming methylation-only and microbiome-only models. Functional enrichment highlighted convergence on NF-κB signaling, cytokine interactions, and butyrate metabolism.

CONCLUSIONS: The study shows that coordinated epigenetic alterations and gut microbial dysbiosis contribute to PTB. These biomarkers are detectable during the second trimester (18-24 weeks), supporting their potential for mid-pregnancy risk stratification. The integrated methylation-microbiome signature offers strong potential for early, non-invasive prediction and supports development of targeted maternal interventions.},
}

Humans
Female
*DNA Methylation
*Premature Birth/diagnosis/genetics/microbiology
Pregnancy
*Biomarkers/blood
Case-Control Studies
*Epigenesis, Genetic
*Gastrointestinal Microbiome/genetics
RNA, Ribosomal, 16S/genetics
Adult
Feces/microbiology

@article {pmid42553064,
year = {2026},
author = {Skupa, SA and Hernandez, JB and Smith, AL and Drengler, EM and Rai, J and Pan, J and Seth, AK and Rai, SN and Clayton, JB and D'Angelo, CR and El-Gamal, D},
title = {Impact of high-fat Western diet on chronic lymphocytic leukemia disease progression and gut microbiome profile in Eµ-TCL1 mice.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1842275},
pmid = {42553064},
issn = {2234-943X},
abstract = {BACKGROUND: The composition and function of the gut microbiome have been shown to contribute to both health and disease. One of the most powerful modulators of microbial composition and function is diet.

MATERIALS AND METHODS: Using the Eµ-TCL1 murine model of B-cell chronic lymphocytic leukemia (CLL), we assigned male and female mice to a high-fat, high-carbohydrate Western diet (HF) or standard chow (CH) diet.

RESULTS: Mice consuming a HF diet had significantly shorter survival than those consuming a CH diet, irrespective of sex. We also observed a significant increase in splenic involvement by CLL in the HF diet-fed mice at time of sacrifice. Mice receiving the HF diet demonstrated immediate and profound effects on the gut microbiome, marked by reduced alpha diversity and significantly different community composition as measured by beta diversity. A larger change in alpha diversity between the pre-CLL engraftment (F1) and 4-weeks post-engraftment (F3) assessment significantly correlated with higher disease burden at week 4 (p = 0.009, r = 0.406) and worse survival (p = 0.001, r = -0.492). Notably, there was a sustained increase in Akkermansia muciniphila and Bacteroidetes thetaiotaomicron in HF diet-fed mice, coupled with a corresponding increase in microbiome functional pathways related to arginine and histidine biosynthesis, chitin degradation, and nucleotide biosynthesis.

DISCUSSION: Collectively our data provides evidence of the profound and sustained impact of a high-fat Western diet on the gut microbiome community and CLL pathogenesis in the Eµ-TCL1 murine model of CLL.},
}

@article {pmid42553088,
year = {2026},
author = {Huang, Y and Zhao, Y and Xin, X and Lin, S},
title = {Molecular insights into lower respiratory tract microbiota reveal disease-specific biomarkers and shared microbial networks in asthma and COPD.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1840378},
pmid = {42553088},
issn = {2235-2988},
mesh = {Humans ; *Pulmonary Disease, Chronic Obstructive/microbiology ; *Asthma/microbiology ; *Biomarkers/analysis ; *Microbiota/genetics ; Bronchoalveolar Lavage Fluid/microbiology ; *Respiratory Tract Infections/microbiology ; Female ; Male ; Middle Aged ; Aged ; Bacteria/classification/genetics/isolation & purification ; High-Throughput Nucleotide Sequencing ; Adult ; },
abstract = {BACKGROUND: Lower respiratory tract infections (LRTIs) exacerbate chronic airway diseases, yet phenotype-specific microbial signatures are poorly defined. We applied broncho-alveolar lavage fluid (BALF) genomic sequencing to identify biomarkers for asthma and chronic obstructive pulmonary disease (COPD).

METHODS: Between December 2023 and February 2025, 1-146 adults with suspected LRTI enrolled from the First Hospital of Jilin University underwent BALF next-generation sequencing. Patients were stratified by lung function, with the impaired pulmonary function group further divided into asthma, COPD-mild-moderate, and COPD-severe subgroups. Disease-specific key biomarkers were identified using machine learning algorithms and analyzed for co-occurrence.

RESULTS: Impaired pulmonary function was not only associated with pathogenic microorganisms and its higher microbial burden, but also associated with a distinct community structure. Random forest models revealed disease-specific biomarkers, with Prevotella intermedia, Finegoldia magna, and Human parvovirus enriched in asthma, Veillonella parvula, Human respiratory syncytial virus, and Haemophilus influenzae enriched in COPD-mild-moderate, and Human respiratory syncytial virus, Human coronavirus, and Human parainfluenza virus enriched in COPD-severe. Co-occurrence network identified hubs linking asthma-centric (Haemophilus parainfluenzae and Schaalia odontolytica) and COPD-centric (Klebsiella pneumoniae, Veillonella parvula, and Streptococcus constellatus) clusters, suggesting potential cross-phenotype microbial crosstalk.

CONCLUSIONS: Genomic sequencing profiling delineates distinct yet overlapping airway microbiota across separate pulmonary dysfunctional diseases - asthma and COPD. Compact biomarker panels classify each condition accurately and reveal shared microbial hubs that may drive chronic inflammation and exacerbations, supporting microbiome-guided precision diagnostics and therapy.},
}

Humans
*Pulmonary Disease, Chronic Obstructive/microbiology
*Asthma/microbiology
*Biomarkers/analysis
*Microbiota/genetics
Bronchoalveolar Lavage Fluid/microbiology
*Respiratory Tract Infections/microbiology
Female
Male
Middle Aged
Aged
Bacteria/classification/genetics/isolation & purification
High-Throughput Nucleotide Sequencing
Adult

@article {pmid42553090,
year = {2026},
author = {Yunusbaeva, M and Sabirova, D and Borodina, L and Khasanova, K and Yunusbayeva, A and Altinbaev, R and Ganiev, I and Yunusbayev, B},
title = {Bifidobacterium- and Escherichia-dominant ecological guilds shape altered microbial metabolic capacity of the gut microbiome in tuberculosis patients.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1751447},
pmid = {42553090},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome ; Female ; *Tuberculosis/microbiology ; *Bifidobacterium/metabolism/isolation & purification ; Adult ; Metabolic Networks and Pathways ; Male ; Middle Aged ; },
abstract = {INTRODUCTION: The gut microbial community plays a key role in maintaining the host immune homeostasis. However, current analytical approaches analyze individual taxa rather than gut communities, thereby missing community-level functions performed by units, such as ecological guilds. Delineating ecological units is a promising approach for summarizing the functional output of microbes and their impact on the host.

METHODS: In this study, we investigated gut bacteria in 33 tuberculosis patients and 47 healthy controls using enterosignatures (ESs), ecological units of co-occurring bacteria related by function. We focused on detecting enterosignatures enriched in the gut communities of tuberculosis (TB) patients. For each patient-enriched enterosignature, we counted the metabolic pathways encoded by its member species. In this manner, we characterized the functional potential of ecological guilds enriched in TB patients. Finally, we tested whether ecological guilds correlate more closely with disease and host biomarkers.

RESULTS AND DISCUSSION: We show that inferred ESs represent reproducible units that facilitate proper comparison of identified ecological guilds to those observed in worldwide donor populations. Namely, dominant enterosignatures in the analyzed healthy donors reproduced the same ecological guilds observed among healthy individuals worldwide. In contrast, most TB patients carried two enterosignatures (ES-Bifi and ES-Esch) that were hallmarks of disturbed gut communities and atypical for healthy adults. We estimated the abundance of metabolic pathways encoded by member species of these patient-enriched ESs. We found that an increase in bacterial species comprising ES-Bifi and ES-Esch harbor an increased number of pathways for fermenting simple sugars, with end products such as acetate and lactate. A greater number of ecological guilds that ferment glucose to lactate might indicate an altered gut environment in patients, including increased acidity and disturbed carbohydrate flux. Taken together, our analyses suggest that ESs represent a biologically meaningful unit for reducing the complexity of the human gut microbiome and a tool for recognizing sharper patterns behind noisy taxonomic and functional diversity.},
}

Humans
*Gastrointestinal Microbiome
Female
*Tuberculosis/microbiology
*Bifidobacterium/metabolism/isolation & purification
Adult
Metabolic Networks and Pathways
Male
Middle Aged

@article {pmid42553157,
year = {2026},
author = {Wang, S and Liu, J and Zheng, J and Hu, M and Tian, C},
title = {Beyond desalinization: root interactions with halophyte Suaeda salsa reshape soybean rhizosphere metabolite-microbiome networks.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1847720},
pmid = {42553157},
issn = {1664-462X},
abstract = {INTRODUCTION: Halophyte-based intercropping may involve root interactions beyond desalinization in alleviating salt stress in glycophytes.

METHODS: To elucidate the mechanisms of root interactions enhancing soybean (Glycine max) salt tolerance intercropping with Suaeda salsa, we analyzed rhizosphere metabolomes and bacterial communities under two salt treatments (no additional NaCl, S1; 3 g kg[-1] NaCl, S3) and three root interaction modes: (1) plastic barrier (no root interactions), (2) nylon mesh barrier (root interactions only), and (3) no barrier (root interactions with potential salt redistribution).

RESULTS: Both NL and NS significantly increased soybean biomass compared with PL under both salt treatments, with no significant difference between NL and NS. Under S3, NL increased soybean biomass by 80% relative to PL without significantly changing soil electrical conductivity, accompanied by increases in rhizosphere carbohydrates, organic acids, betaine, flavonoids, and putative plant growth-promoting bacteria (PGPB). Although soybean rhizosphere Na[+] decreased under NS compared with PL and NL, this was accompanied by reduced putative PGPB abundance and no further biomass increase compared with NL. Coumestrol, trehalose-6-phosphate, and isopentenyl pyrophosphate (IPP) were identified as hub metabolites associated with soybean rhizosphere microbial community structure, with the IPP-related module representing a potential component of the salt-response network. Intercropping also increased available phosphorus (AP) in both species' rhizospheres, with increases in soybean associated with organic acids and those in S. salsa associated with rhizosphere pH shifts and putative PGPB changes.

DISCUSSION: These findings indicate that root interactions enrich salt-tolerance-related metabolites in the soybean rhizosphere and suggest potential metabolic-microbial coupling underlying intercropping-induced salt tolerance.},
}

@article {pmid42553192,
year = {2026},
author = {Huang, M and Jackson, PPJ and Chatzifragkou, A and Rastall, RA},
title = {Exploring the prebiotic potential of commercial cellobiose: a randomized, controlled trial.},
journal = {Gut microbiome (Cambridge, England)},
volume = {7},
number = {},
pages = {e13},
pmid = {42553192},
issn = {2632-2897},
abstract = {Cellobiose, a β-(1 → 4)-linked disaccharide indigestible by humans, is a novel candidate prebiotic. Evidence from controlled human trials on its effects on the gut microbiota and metabolites remains limited. We conducted an exploratory randomised, double-blind, placebo-controlled trial in 37 healthy adults. Participants were allocated to three arms for 4 weeks, received 5 g/day and 10 g/day for cellobiose, oligofructose P95, or maltodextrin placebo. The primary endpoint was change in absolute abundance of Bifidobacterium and Lactobacillus (measured by 16S rRNA gene sequencing). Secondary endpoints included other taxa, diversity, faecal short-chain fatty acids (SCFAs) measured by gas chromatography-mass spectrometry and gastrointestinal (GI) tolerability. Cellobiose did not significantly change Bifidobacterium or Lactobacillus versus baseline or placebo (P > 0.05). Oligofructose P95 induced a borderline increase in Bifidobacterium (P = 0.049). Overall community composition remained unchanged. However, network analyses under cellobiose revealed tighter positive correlations among key genera. Faecal SCFA levels were not altered. GI symptom rates were low and similar across all arms. Cellobiose, at doses up to 10 g/day, is safe and well tolerated but did not enrich classic beneficial taxa. The findings suggest cellobiose drives subtle community shifts towards butyrate-producing bacteria.},
}

@article {pmid42553207,
year = {2026},
author = {Zhao, R and Xiao, Y and Fan, X},
title = {Circadian rhythms in the tumor microenvironment: spatiotemporal immune regulation and chronotherapeutic opportunities.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1878388},
pmid = {42553207},
issn = {1664-3224},
mesh = {Humans ; *Tumor Microenvironment/immunology ; *Circadian Rhythm/immunology ; Animals ; *Neoplasms/immunology/therapy ; *Chronotherapy ; Circadian Clocks ; },
abstract = {The tumor microenvironment (TME) is increasingly recognized as a temporally organized ecosystem rather than a static structural niche. Circadian rhythms, generated by transcriptional-translational feedback loops involving CLOCK, BMAL1, PER, CRY, REV-ERB, and ROR, coordinate systemic physiology and local cellular programs that are directly relevant to tumor initiation, progression, and therapeutic response. In this review, we summarized how circadian regulation shapes tumor rhythmicity across multiple biological scales, from central clock-mediated synchronization to peripheral clocks within epithelial cells, stromal cells, adipocytes, and immune populations. Emphasis is placed on the spatiotemporal regulation of antitumor immunity within the TME. At the same time, dendritic cell migration, antigen presentation, CD8[+] T cell infiltration, and T cell exhaustion display time-dependent features that influence the efficacy of immune surveillance and immunotherapy. These findings supported a four-dimensional view of the TME, in which biological timing is a critical determinant of immune competence. We further discussed emerging therapeutic strategies that exploit circadian biology, including small-molecule clock modulators, rhythm-responsive nanomedicine, chronologically optimized CAR-T cell therapy, and time-of-day-dependent immune checkpoint blockade. Although most mechanistic evidence remains preclinical, and many clinical observations are retrospective, current data suggest that treatment timing may be a modifiable, low-cost parameter for improving anti-tumor efficacy while reducing toxicity. Finally, we highlighted future opportunities in microbiome-informed chronotherapy, multi-omics profiling, and digital twin modeling. Integrating temporal information into oncology may shift precision medicine from a static biomarker-driven framework toward a dynamic, time-resolved therapeutic paradigm.},
}

Humans
*Tumor Microenvironment/immunology
*Circadian Rhythm/immunology
Animals
*Neoplasms/immunology/therapy
*Chronotherapy
Circadian Clocks

@article {pmid42553212,
year = {2026},
author = {Bajguz, A and Żeruń, J},
title = {Brassinosteroids as phytohormonal shields against micro- and nanoplastic stress in plants.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1920456},
pmid = {42553212},
issn = {1664-462X},
abstract = {Microplastics (MPs) and nanoplastics (NPs) are biologically active stressors in agricultural soils, where they alter soil physical structure, disrupt rhizosphere processes, impair water and nutrient acquisition, and provoke oxidative and hormonal disequilibrium in plants. Brassinosteroids (BRs), particularly brassinolide and 24-epibrassinolide, have recently emerged as modulators of plant responses to plastic-particle stress. Current evidence indicates that BRs do not detoxify plastics directly. Instead, they reorganize plant performance across interconnected layers: aquaporin-linked NP transport, antioxidant and ascorbate-glutathione metabolism, photosystem II function, hormone crosstalk, secondary metabolism, and rhizosphere feedbacks. In tomato, BRs reduced polystyrene-NP accumulation in edible tissues by suppressing aquaporin genes. In Pinellia ternata and rice, BRs attenuated MP/NP-induced growth inhibition by restoring photosynthetic efficiency and redox control. This mini review synthesizes these findings and frames BRs as eco-hormonal regulators of the plant-plastic-soil interface, while highlighting priorities for field-realistic validation.},
}

@article {pmid42553649,
year = {2026},
author = {Canonaco, F and Acerbi, E and Stella, F},
title = {Correction: Improving DirectLiNGAM for high-dimensional microbiome data: roots screening and eBIC based model selection.},
journal = {Frontiers in systems biology},
volume = {6},
number = {},
pages = {1929002},
doi = {10.3389/fsysb.2026.1929002},
pmid = {42553649},
issn = {2674-0702},
abstract = {[This corrects the article DOI: 10.3389/fsysb.2026.1835323.].},
}

@article {pmid42553678,
year = {2026},
author = {Hu, R and Wu, J and Chen, N and Ma, W and Hu, Q},
title = {Gut-testis axis: how microbiota influence male reproductive health.},
journal = {Asian biomedicine : research, reviews and news},
volume = {20},
number = {3},
pages = {149-154},
pmid = {42553678},
issn = {1875-855X},
abstract = {The intestinal flora forms a complex ecosystem that interacts with the host, influencing health and fitness through mechanisms that connect with distant organs like the brain, liver, muscles, and testes. The gut microbiota plays a vital role in regulating androgen production and metabolism, and can cross the blood-testis barrier to influence spermatogenesis. This review highlights the significance of the gut-testis axis in male reproductive and sexual health, based on extensive studies exploring how gut microbes impact testicular function. Gaining this understanding deepens our knowledge of the gut-testis axis and its role in male reproductive health.},
}

@article {pmid42553701,
year = {2026},
author = {Balardin, RR and Nora, DD and Figueroa Rosado, YZ and Hardy, ICW and Godoy-Vitorino, F and Verle Rodrigues, JC},
title = {Behavioral and Microbial Profiling of the Bethylid Wasp Cephalonomia stephanoderis for Biocontrol of the Coffee Berry Borer.},
journal = {Biological control : theory and applications in pest management},
volume = {219},
number = {},
pages = {},
pmid = {42553701},
issn = {1049-9644},
abstract = {The coffee berry borer (CBB, Hypothenemus hampei) is the most destructive pest of coffee, causing significant economic consequences in an array of coffee-producing regions, including Puerto Rico. Following the implementation of biological control programs using the parasitoid wasp Cephalonomia stephanoderis, key questions remain regarding how laboratory-reared wasps compare to field wasps in retaining beneficial traits, such as foraging, host attack, and offspring production. It is also of interest whether laboratory and field populations differ in the microbiota they harbor, as microbial communities can directly influence insect performance. Making these comparisons, we find that core natural-enemy functions remain largely intact in laboratory-reared wasps, but that small differences exist between these and field-collected wasps in terms of host-stage preference and oviposition timing. We also find substantial differences in microbial composition between field-collected wasps and those reared in the laboratory. Field-collected parasitoids harbored a simple microbial profile dominated by the Actinomycetota, a diverse phylum of Gram-positive bacteria, particularly in the family Corynebacterium, while laboratory-reared wasps exhibited higher diversity involving a broader range of bacterial phyla. These microbiome differences, confirmed by alpha and beta diversity analyses, suggest that laboratory rearing restructures parasitoid-associated microbial communities. While behavioral performance remained largely comparable, differences in microbial community composition suggest that microbiota should be considered when evaluating laboratory-reared agents for pest management programs. Further studies are needed to better understand microbial shifts and their potential links to parasitoid behavior and performance.},
}

@article {pmid42553733,
year = {2026},
author = {Deng, J and Chen, FH and Wu, WJ and Huang, TY and Cui, GZ and Hong, W},
title = {Pleiotropic roles of the MATE transporter CD20030 in Clostridioides difficile: linking multidrug resistance to oxidative stress defense and virulence regulation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1865850},
pmid = {42553733},
issn = {1664-302X},
abstract = {BACKGROUND: The multidrug-resistant pathogen Clostridioides difficile (C. difficile) presents a persistent clinical threat. While Multidrug and Toxic Compound Extrusion (MATE) transporters are recognized as xenobiotic efflux pumps, their pleiotropic roles in pathogen physiology, particularly in stress adaptation and virulence regulation, remain largely unexplored. Understanding how C. difficile adapts and thrives in the face of host defenses and antimicrobial pressures, potentially influencing gut microbiome dynamics, is crucial for combating C. difficile infection.

METHODS: We functionally characterized the MATE transporter gene CD20030 (mate) in C. difficile 630. A markerless deletion mutant (Δmate) and a complemented strain were constructed using a CRISPR-Cas9 system. Phenotypic assays determining antimicrobial susceptibility, oxidative stress tolerance, autolysis, and cytotoxicity were integrated with comparative proteomic profiling to assess the physiological changes.

RESULTS: The Δmate mutant demonstrated broad-spectrum hypersensitivity to antibiotics and hydrogen peroxide, indicating the involvement of this transporter in intrinsic resistance and oxidative defense. The mutant exhibited reduced autolysis; however, toxin production (tcdA and tcdB) and cytotoxicity were significantly upregulated. In soft agar assays, the mutant showed expanded surface spreading. Proteomic data identified a >10,000-fold downregulation of flagellar structural proteins (FliC, FlgC) and a concurrent upregulation of the surface adhesin CwpV. This molecular evidence indicates a "swimming-to-sliding transition" driven by metabolic stress, rather than active swimming motility. These phenotypic and proteomic shifts present a resource reallocation strategy, where the bacterium sacrifices energy-consuming flagellar assembly to prioritize survival and virulence, potentially altering its interaction with the gut epithelial surface and resident microbiota.

CONCLUSION: The MATE transporter (CD20030) operates as a pleiotropic regulatory hub and metabolic sentinel in C. difficile. Its absence induces metabolic reprogramming that orchestrates a motility-virulence trade-off, linking multidrug resistance directly to bacterial pathogenesis. These physiological adaptations likely dictate the pathogen's colonization and persistence strategies within the gut niche, potentially perturbing the host-microbiome equilibrium during infection.},
}

@article {pmid42553854,
year = {2026},
author = {Ferrini, A and Del Monaco, A and Zampogna, B and Bosso, A and Zampoli, A and Parisi, FR and Capperucci, C and Diaz Balzani, LA and Papalia, R},
title = {Hip Osteoarthritis and the Human Microbiome: Current Concepts, Biological Insights and Future Directions.},
journal = {Orthopedic reviews},
volume = {18},
number = {},
pages = {164467},
pmid = {42553854},
issn = {2035-8164},
abstract = {Osteoarthritis (OA) is among the leading causes of disability worldwide, yet its pathogenesis remains incompletely understood. Once considered a "non-inflammatory" degenerative disorder, OA is now recognized as a condition driven by chronic low-grade inflammation. Emerging evidence implicates gut dysbiosis as a modifiable risk factor, promoting systemic inflammation through impaired gut permeability and translocation of microbial components. These immune-modulating molecules can trigger pro-inflammatory cascades and pathological bone remodeling. This review summarizes current knowledge linking gut dysbiosis and knee osteoarthritis and extends these insights to hip osteoarthritis (HOA). Observational and genetic studies support a causal role for the microbiota, identifying specific taxa associated with either increased or reduced HOA risk. Preclinical and clinical data describe a mechanistic axis linking intestinal dysbiosis, synovial inflammation, and cartilage degeneration. In animal models, particularly under high-fat/high-sucrose diets, visceral adiposity emerges as a major driver of joint damage. While microbial metabolites such as short-chain fatty acids appear protective, the detection of microbial DNA within joint tissues remains controversial, suggesting possible joint-specific microbial ecosystems. Based on these findings, microbiota-targeted strategies are under investigation as potential interventions to influence OA progression and relieve hip pain. However, longitudinal cohorts and randomized clinical trials in HOA are needed to clarify causal mechanisms and therapeutic efficacy in HOA.},
}

@article {pmid42553918,
year = {2026},
author = {Chen, H and Zhang, B and Zhu, B and Zhou, P and Xu, C and Li, Q and Chen, W},
title = {Comparison of the effects of stent-based diversion technique versus prophylactic double-lumen ileostomy on intestinal flora in postoperative patients with rectal cancer.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1791364},
pmid = {42553918},
issn = {1664-302X},
abstract = {BACKGROUND: The stent-based diversion technique (SDT), as a novel surgical approach for reducing anastomotic leakage (AL) following low anterior resection (LAR), achieving effective intestinal diversion while avoiding ileostomy and subsequent stoma reversal surgery. Although multicenter randomized controlled trials have demonstrated the safety of SDT, the alterations in postoperative intestinal microbiota following SDT remain inadequately characterized.

METHODS: This study enrolled 40 patients with mid-low rectal cancer (21 SDT, 19 PDI). Rectal swab samples were collected preoperatively and at 3 weeks and 3 months postoperatively (n = 120) for metagenomic sequencing. α- and β-diversity analyses were performed to compare microbial community characteristics. LEfSe was used for differential analysis of species and KEGG functional pathways. Postoperative clinical outcomes including AL and anastomotic stricture (AS) were assessed.

RESULTS: The SDT group showed a significantly lower incidence of AS compared with the PDI group (4.76% vs. 31.58%, p < 0.05). Preoperative α- and β-diversity were comparable between groups. Postoperatively, the SDT group exhibited higher microbial richness at both 3 weeks and 3 months (both p < 0.05). In the PDI group, the α-diversity showed a continuous decline from 3 weeks to 3 months postoperatively compared with the preoperative baseline (p < 0.05). However, the SDT group demonstrated no significant decrease in α-diversity at 3 weeks (p > 0.05), but did at 3 months (p < 0.05). Significant intergroup β-diversity divergence emerged from 3 weeks onward (both p < 0.05). The SDT group showed significant structural changes from 3 weeks to 3 months (p < 0.05), whereas the PDI group remained stable. At 3 weeks, opportunistic pathogens (e.g., Parvimonas micra) were enriched in the PDI group, while the SDT group enriched beneficial taxa (e.g., Akkermansia). By 3 months, the PDI group exhibited enrichment of oral/genitourinary-derived bacteria (Prevotellaceae, Porphyromonas, Fusobacterium), whereas the SDT group showed higher abundance of beneficial Bacteroidota (e.g., Phocaeicola vulgatus). Functionally, the SDT group enriched amino acid and carbohydrate metabolism pathways, while the PDI group enriched translation and energy metabolism pathways.

CONCLUSION: We found that SDT better preserves postoperative gut microbiota diversity, promotes the restoration of beneficial bacteria, and influences microbial functional pathways, thereby establishing a more favorable microbiome environment for patients.},
}

@article {pmid42554126,
year = {2026},
author = {Reggiardo, B and Saad, J and Travers, MA and Labreuche, Y and Goudenège, D and Toulza, E and Broquard, C and Andree, KB and Mougin, J and Argenta, N and Courtay, G and Pouzadoux, J and Romatif, O and Caro, A and Furones, D and Vezzulli, L and Corno, G and Di Cesare, A and Gairin, I and Petton, B and Wegner, KM and Montagnani, C and Boulo, V and Destoumieux-Garzón, D},
title = {Vibrio Community Structure Shapes the Diversity of Carbenicillin-Hydrolysing Class A β-Lactamase Circulating in European Coastal Environments.},
journal = {Environmental microbiology},
volume = {28},
number = {8},
pages = {e70383},
doi = {10.1111/1462-2920.70383},
pmid = {42554126},
issn = {1462-2920},
support = {869178-AquaticPollutants//European Union's Horizon 2020 research and innovation programme/ ; //Institut Français de Recherche pour l'Exploitation de la Mer/ ; ANR-21-EXES-0005//Agence Nationale de la Recherche/ ; ANR-10-LABX-41//Agence Nationale de la Recherche/ ; 88881.987362/2024-01//Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)/ ; Sv1064/25//Comité Français d'Evaluation et la Coopération Universitaire et Scientifique avec le Brésil/ ; //Centre National de la Recherche Scientifique/ ; },
mesh = {Animals ; *Vibrio/enzymology/genetics/classification/isolation & purification/drug effects ; Europe ; *beta-Lactamases/genetics/metabolism ; *Carbenicillin/metabolism ; *Seawater/microbiology ; Ostreidae/microbiology ; Phylogeny ; Anti-Bacterial Agents/pharmacology ; },
abstract = {Coastal environments are increasingly recognised as reservoirs of known antibiotic resistance genes (ARGs), but are less frequently identified as sources of novel ARGs. Here, we investigated class A β-lactamases circulating in European coastal environments used for oyster farming. We examined their diversity, function, and the ecological factors associated with their geographic distribution and environmental dynamics. A high diversity of carbenicillinases was detected in the culturable microbiome of European oysters. The Harveyi and Splendidus clades were key Vibrio lineages structuring the geography of carbenicillinase diversity. The Harveyi clade was primarily associated with the circulation of known carbenicillinases in Mediterranean samples, whereas the Splendidus clade contributed previously uncharacterized carbenicillinase sequences across all Europe. A one-year seasonal monitoring revealed that Vibrio alginolyticus drives the circulation of blaCARB-42 in the Mediterranean Thau lagoon, with dynamics strongly associated with seawater temperature. blaCARB-42 conferred intrinsic resistance to both carboxypenicillins and aminopenicillins in V. alginolyticus, which was found in most other species of the Harveyi clade with additional resistances to aztreonam, third-generation cephalosporins and aminoglycosides. Since the Harveyi clade includes major human pathogens, these findings have direct implication for environmental and One Health surveillance, as rising seawater temperatures may increase coastal exposure to antibiotic-resistant Harveyi clade Vibrio.},
}

Animals
*Vibrio/enzymology/genetics/classification/isolation & purification/drug effects
Europe
*beta-Lactamases/genetics/metabolism
*Carbenicillin/metabolism
*Seawater/microbiology
Ostreidae/microbiology
Phylogeny
Anti-Bacterial Agents/pharmacology

@article {pmid42554132,
year = {2026},
author = {Masum, MHU and Nayem, MR and Mahdeen, AA and Sultana, S and Barua, A},
title = {Characterizing the Milk Microbiome in Subclinical Mastitis: A Pilot 16S rRNA-Based Study in Cattle and Water Buffalo.},
journal = {Veterinary medicine and science},
volume = {12},
number = {5},
pages = {e71154},
doi = {10.1002/vms3.71154},
pmid = {42554132},
issn = {2053-1095},
mesh = {Animals ; *Buffaloes ; *Milk/microbiology ; Cattle ; *Microbiota ; Pilot Projects ; Female ; *Mastitis, Bovine/microbiology ; RNA, Ribosomal, 16S/analysis ; Bangladesh ; *Bacteria/classification/isolation & purification ; RNA, Bacterial/analysis ; },
abstract = {BACKGROUND: In the dairy sector of Bangladesh, subclinical mastitis (SCM) is a substantial and frequently undiagnosed challenge, with reported prevalence rates of 60%-77% in cattle and approximately 52% in buffaloes. Due to its complex characteristics and progressive development, efficient diagnosis and management are essential for enhancing dairy productivity.

OBJECTIVES: This pilot study employed 16S rRNA amplicon sequencing using Oxford Nanopore's MinION to investigate the milk microbiota of healthy and mastitic cattle and buffalo.

RESULTS: A total of 423 clustered nucleotide sequences were identified in the samples, indicating significant taxonomic diversity: 11 phyla, 26 classes, 58 orders, 120 families and 272 genera. Distinct phylum-level patterns were observed, with Firmicutes predominating in healthy milk and a relative increase in Proteobacteria and Actinobacteriota in mastitic samples. At the genus level, Streptococcus and Lactococcus were predominant in mastitic samples, whereas Staphylococcus and Lactococcus were more prevalent in healthy milk. The results indicate that although overall microbial diversity was relatively consistent across groups, mastitis correlated with alterations in bacterial community composition, with notable differences between cattle and buffalo.

CONCLUSION: This study suggests a potential association between SCM and microbial shifts; however, microbiome profiling cannot yet be recommended for diagnostic application. Clinical applicability requires validation in large-scale studies with individual-level sampling.},
}

Animals
*Buffaloes
*Milk/microbiology
Cattle
*Microbiota
Pilot Projects
Female
*Mastitis, Bovine/microbiology
RNA, Ribosomal, 16S/analysis
Bangladesh
*Bacteria/classification/isolation & purification
RNA, Bacterial/analysis

@article {pmid42554290,
year = {2026},
author = {Sulaiman, I and Maher, TM},
title = {The Gut Speaks to the Lung: Fecal Microbiota and Survival in Idiopathic Pulmonary Fibrosis.},
journal = {American journal of respiratory and critical care medicine},
volume = {},
number = {},
pages = {},
doi = {10.1093/ajrccm/aamag410},
pmid = {42554290},
issn = {1535-4970},
}

@article {pmid42554585,
year = {2026},
author = {Yang, Y and Olah, P and Salava, A and Barker, J and Lauerma, A and Andersson, B and Fyhrquist, N and Homey, B and Alenius, H},
title = {Multi-omics analyses reveal host-microbe interactions in atopic dermatitis and psoriasis.},
journal = {Journal of the European Academy of Dermatology and Venereology : JEADV},
volume = {},
number = {},
pages = {},
doi = {10.1111/jdv.70654},
pmid = {42554585},
issn = {1468-3083},
support = {261366//FP7 Health/ ; 821511//Innovative Medicines Initiative 2 Joint Undertaking/ ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) and psoriasis (PSO) are chronic inflammatory skin diseases that impose substantial physical and psychological burdens. Although fungal-bacterial balance is important for skin immune homeostasis, the role of the skin mycobiome and its interaction with bacterial communities and host immunity in these diseases remains poorly understood.

OBJECTIVES: To characterize alterations in the skin mycobiome and its interactions with bacterial communities and host immune responses in AD and PSO.

METHODS: Adult patients with chronic AD, plaque-type PSO and healthy volunteers were included in this study. Skin microbiota samples and biopsies were collected from lesional and non-lesional skin areas, including the posterior thigh for AD and the lower back for PSO. Whole-metagenome shotgun sequencing was used to profile microbial communities. SparCC was used to construct fungal-bacterial co-occurrence networks, and integration of host transcriptomic and microbial features was performed using O2PLS.

RESULTS: Both AD and PSO showed disease-associated restructuring of Malassezia species and reduced fungal-bacterial ecological connectivity in lesional skin. In AD, Malassezia arunalokei was inversely associated with Staphylococcus aureus and linked to antimicrobial peptide-centred host gene modules enriched for IL-17 signalling. Its abundance decreased with increasing disease severity and inversely correlated with inflammatory immune cell signatures. In PSO, altered Malassezia composition was associated with IL-17-driven transcriptional programmes and lipid metabolic pathways, suggesting interactions between fungal imbalance and inflammatory-metabolic processes.

CONCLUSIONS: Our findings expand current models of skin dysbiosis beyond bacteria and suggest that disrupted fungal-bacterial interactions are linked to immune activation in AD and PSO and, in AD, to disease severity. Although further validation is required, skin microbiome features may provide clinically relevant information for disease monitoring, patient stratification and future microbiome-informed therapeutic strategies. Our study lays the groundwork for microbiome modulation as a potential therapeutic strategy for AD and PSO.},
}

@article {pmid42554630,
year = {2026},
author = {Tandon, A and Bais, AK and Shrinet, J and Tripathi, V and Gupta, D},
title = {Effect of alcohol and smoking on methamphetamine users' oral microbiome and metabolome.},
journal = {The American journal of drug and alcohol abuse},
volume = {},
number = {},
pages = {1-13},
doi = {10.1080/00952990.2026.2697752},
pmid = {42554630},
issn = {1097-9891},
abstract = {Background: The oral microbiome comprises the microbial communities inhabiting the oral cavity, whereas the oral metabolome reflects the small molecules generated by host and microbial metabolic activity. These systems may provide insight into substance-related physiological disruption, including altered inflammation, immune signaling, and host - microbial interactions. Although the individual effects of methamphetamine, alcohol, and smoking have been explored, their combined impact on these systems remains largely unexplored.Objectives: To investigate the metabolic and microbiome alterations associated with chronic methamphetamine use in individuals with alcohol and tobacco use.Methods: High-throughput metabolomic and microbiome datasets from methamphetamine users (Males:168, Females: 50), stratified by self-reported tobacco smoking and alcohol use, were analyzed using integrative bioinformatics approaches, including multivariate and pathway enrichment analyses, to identify dysregulated metabolic pathways and microbial alterations across defined subgroups.Results: The study revealed significant upregulation in metabolites like prostaglandin E2 (log-2-fold-change: 2.63, Cohen's D: |~0.881|, p-val: 7.1 × 10[-10]) and glutamylisoleucine (log-2-fold-change: 1.42, Cohen's D: |~0.88|, p-val: 2.5 × 10[-2]). Microbes such as Bacteroides (log-2-fold-change: -4.91, Cohen's D: |~1.95|, p-val: 1.3 × 10[-4]) and Brachymonas (log-2-fold-change: -2.47, Cohen's D: |~1.09|, p-val: 5.8 × 10[-3]) were significantly downregulated. This suggests that long-term concurrent methamphetamine use, alcohol consumption, and smoking are associated with alterations in microbial and metabolic pathways related to oxidative stress, glutathione metabolism, and neuroactive signaling.Conclusions: The oral microbiome and metabolomic profiles may serve as accessible indicators of substance-related biological disruption. They may also help identify clinically relevant targets for monitoring risk, guiding personalized interventions, and developing informed strategies to support recovery.},
}

@article {pmid42554875,
year = {2026},
author = {Zhang, H and Zhang, Y and Zhang, C and Yang, Y and Hu, B and He, T and Zhang, J and Song, X and Su, Y},
title = {Microbial architects of cigar fermentation: a critical review of beneficial roles in quality enhancement and detrimental potential for mould spoilage.},
journal = {Archives of microbiology},
volume = {208},
number = {11},
pages = {},
pmid = {42554875},
issn = {1432-072X},
support = {2023530000241002//the Science and Technology Plan Project of the China National Tobacco Corporation, Yunnan Provincial Company/ ; yxyc2023007//General Project of the Science and Technology Program of Yuxi Company, Yunnan Provincial Tobacco Company/ ; },
mesh = {*Fermentation ; *Fungi/metabolism/growth & development ; *Nicotiana/microbiology/metabolism ; *Food Microbiology ; *Bacteria/metabolism/classification/isolation & purification ; },
abstract = {Cigar tobacco fermentation is a microbially driven process that transforms raw tobacco leaves into a product with distinctive sensory attributes, yet the current understanding of the microbial roles in this process remains fragmented between descriptive community surveys and isolated mechanistic studies, with beneficial and detrimental microbial functions rarely integrated into a unified risk-benefit assessment. This review critically examines the microbiology of cigar fermentation through a dual-axis framework organized around beneficial metabolic functions and detrimental spoilage potential, each resolved into microbial identity, biochemical mechanism, and environmental modulation dimensions. We synthesize evidence from culture-dependent and culture-independent studies on microbial community assembly and succession, where Bacillus, Staphylococcus, and Aspergillus emerge as core fermentation genera, and evaluate the complementary three-pathway system - macromolecular enzymatic degradation, targeted biotransformation of tobacco alkaloids and polyphenols, and de novo biosynthesis of aroma-active volatiles - that drives flavor and quality enhancement. We further analyze the contrastive microbial balance governing tobacco-specific nitrosamine (TSNA) formation, where nitrate-reducing bacteria compete with nitrate-assimilating and nitrite-scavenging microorganisms to determine the net TSNA load. In parallel, we critically examine the mould spoilage microbiology of cigar fermentation, identifying the environmental thresholds - humidity above 80% RH, water activity above 0.85, and inadequate aeration - that select for mycotoxigenic Aspergillus and Penicillium species producing aflatoxins and ochratoxin A at levels that persist into the finished product. We survey emerging biotechnological strategies spanning bioaugmentation with defined starter cultures, biostimulation through environmental optimization, and biocontrol of spoilage fungi, and identify five critical research gaps - including the absence of gnotobiotic fermentation models and the predominance of correlative over causal studies - that must be addressed to translate microbial ecology into predictable fermentation biotechnology. By integrating microbial ecology, fermentation biochemistry, spoilage prevention, and applied biotechnology, this review is intended for researchers in tobacco microbiology and fermentation science, as well as cigar manufacturers, quality-control practitioners, and biotechnologists seeking microbiome-based strategies for quality improvement and risk mitigation.},
}

*Fermentation
*Fungi/metabolism/growth & development
*Nicotiana/microbiology/metabolism
*Food Microbiology
*Bacteria/metabolism/classification/isolation & purification

@article {pmid42546842,
year = {2026},
author = {Su, Y and Qin, X and Guo, L and Zhao, H},
title = {Distinguishing true from false idiopathic pulmonary fibrosis: Progress in biomarkers for early identification of rheumatoid arthritis.},
journal = {Biomedical journal},
volume = {},
number = {},
pages = {101021},
doi = {10.1016/j.bj.2026.101021},
pmid = {42546842},
issn = {2320-2890},
abstract = {BACKGROUND: Patients initially diagnosed with idiopathic pulmonary fibrosis (IPF) have an underlying risk of being in a preclinical phase of rheumatoid arthritis (RA), but effective biomarkers for early identification of this transition are lacking.

OBJECTIVE: This review aims to comprehensively summarize predictive markers for future RA in patients meeting IPF diagnostic criteria, supporting early risk stratification and pre-arthritic intervention.

METHODS: Using "idiopathic pulmonary fibrosis", "rheumatoid arthritis", "predictive markers", "markers", "clinical research", "in vitro experiments", "mechanism", and their combinations as keywords, a structured literature search was conducted in the PubMed database for relevant literature from 2001 to 2025.

RESULTS: The propensity for RA to develop in patients initially meeting IPF diagnostic criteria has a multi-dimensional basis: genetic susceptibility provides the background; immune dysregulation mediates the dissemination of autoimmunity from a pulmonary origin to systemic involvement; inflammatory markers reflect disease activity; environmental exposure acts as an external trigger. Based on these mechanisms, four predictive marker types were identified: genetic susceptibility, immune activation, inflammatory injury, and environmental exposure. However, current studies are mainly cross-sectional and retrospective, lacking prospective validation of predictive efficacy; combined application strategies, clinical value and microbiome-based indicators all require further clinical verification.

CONCLUSION: This review identified four early-warning markers-genetic susceptibility, immune activation, inflammatory injury, and environmental exposure-that may signal future RA in patients initially presenting with IPF. These findings support shifting from passive diagnosis to active screening for earlier intervention. Future research should focus on multi-dimensional prediction models, prospective cohort studies, and ultimately achieving early identification and intervention for this hidden RA-prone population.},
}

@article {pmid42547019,
year = {2026},
author = {Wu, YZ and Yu, JC and Li, J and Yang, CJ and Mao, SY},
title = {Integrated multi-omics analysis reveals the co-adaptive mechanisms between ruminal microbiota and host epithelium in water buffaloes under chronic heat stress.},
journal = {Journal of dairy science},
volume = {},
number = {},
pages = {},
doi = {10.3168/jds.2026-28742},
pmid = {42547019},
issn = {1525-3198},
abstract = {Chronic heat stress is a major environmental challenge constraining water buffalo (Bubalus bubalis) production, yet its mechanistic impacts on the ruminal ecosystem remain unclear. This study aims to systematically elucidate the coordinated changes in ruminal microbial structure and function, metabolome, and epithelial transcriptional responses in water buffaloes under chronic heat stress. Ten cannulated buffaloes (Nili-Ravi × Murrah) were used as experimental subjects and randomly assigned to 2 groups: one receiving fan and sprinkler cooling (NHS) and the other exposed to the natural environment (HS). This study aimed to analyze their apparent digestibility, ruminal fermentation parameters, and ruminal microbial community structure and function along with their metabolic characteristics, as well as to dissect the transcriptional responses of the rumen epithelium to chronic heat stress. Results showed that chronic heat stress did not significantly affect feed intake or apparent nutrient digestibility, but markedly altered ruminal fermentation and nitrogen metabolism, manifested as a reduced ammonia nitrogen (NH3-N) concentration (HS vs. NHS, 4.44 vs. 7.86 mg/dL), an increased proportion of acetate (HS vs. NHS, 68.86 vs. 66.74%), and a decreased proportion of propionate(HS vs. NHS, 20.40 vs. 22.14%). Chronic heat stress imposed selective pressure on the ruminal microbial community, driving functional changes at the microbial level. The overall abundance of multiple CAZyme families increased, enhancing the potential for structural carbohydrate degradation; concurrently, the abundance of genes encoding key enzymes for pyruvate-to-acetyl-CoA conversion rose, consistent with elevated acetate synthesis potential; enrichment of nitrogen metabolism-related genes suggested enhanced microbial ammonia assimilation capacity. At the metabolic level, chronic heat stress induced specific metabolite dynamics, including decreased phosphatidylcholine PC(16:0/18:1(9Z)) content and accumulation of the flavonoid metabolite naringenin, indicating co-activation of phospholipid hydrolysis and flavonoid metabolic pathways. At the host level, transcriptional changes in rumen epithelium were primarily reflected in reduced ion transport capacity and enhanced cellular stress protection. In summary, the adaptive response of water buffaloes to chronic heat stress is primarily driven by the functional plasticity of the ruminal microbiome, which maintains energy supply and metabolic homeostasis to some extent by altering carbon and nitrogen metabolic fluxes; meanwhile, transcriptional regulation in the host rumen epithelium contributes to co-adaptation, though certain absorption-related functions may be compromised due to stress. These findings provide a biological basis for maintaining ruminal functional homeostasis and health in water buffaloes under high-temperature conditions through nutritional interventions.},
}

@article {pmid42547063,
year = {2026},
author = {Starr, ME and Taylor, MD and Su, L and Murao, A and Schwulst, SJ and Lederer, JA and Brenner, M},
title = {New Approach Methodologies (NAMs) Complement but Cannot Replace Animal Models in Critical Care Medicine Research.},
journal = {Journal of leukocyte biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jleuko/qiag108},
pmid = {42547063},
issn = {1938-3673},
abstract = {Critical care research focuses on life-threatening conditions such as sepsis, trauma, hemorrhage, and burn injury, which account for millions of hospitalizations and hundreds of thousands of deaths annually in the United States alone. Recent policy initiatives by the U.S. Food and Drug Administration (FDA) and the National Institutes of Health (NIH) have promoted New Approach Methodologies (NAMs), including organoids, organ-on-chip platforms, and computational models, as alternatives to animal research. While NAMs offer valuable tools for mechanistic investigation and screening applications, this review examines whether current NAM technologies can adequately replace animal models in critical care research. Critical illness involves the whole organism, including dynamic organ-organ interactions, immune-microbiome crosstalk, and adaptive systemic feedback loops. By examining major domains in critical care research and targeted organ injuries, it becomes clear that while NAMs excel at interrogating isolated subsystems, they cannot currently replicate integrated physiological responses. Animal models remain essential for questions requiring assessment of multi-organ dysfunction, therapeutic safety evaluation, and clinically relevant disease trajectories. Premature policy shifts away from animal research will impede advances in critical care medicine. This review proposes a "methodological pluralism" approach that integrates NAMs with appropriately designed animal studies through harmonized endpoints and reverse-translation frameworks. Recommendations include continued refinement of animal models to better represent the heterogeneity of human populations, adoption of quality standards for preclinical research, and strategic deployment of both NAMs and animal models based on fit-for-purpose criteria. We believe this approach will satisfy ethical considerations, scientific rigor, and public health needs in critical care research.},
}

@article {pmid42547359,
year = {2026},
author = {Binda, C and Gibiino, G and Perini, B and Coluccio, C and Fabbri, S and Giuffrida, P and Cucchetti, A and Casadei, A and Lucchi, G and Cristini, F and Raumer, L and Savarino, E and Cricca, M and Benech, N and Sambri, V and Fabbri, C},
title = {Microbiological assessment of bile in patients after endoscopic retrograde cholangio-pancreatography (ERCP): The "MICROBILE" registry.},
journal = {Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.dld.2026.06.015},
pmid = {42547359},
issn = {1878-3562},
abstract = {BACKGROUND: Microbial communities were recently revealed in the biliary tract of pancreaticobiliary disorders. However, evidence is limited and comparative data are lacking.

AIMS: We aimed to characterize the biliary microbiota in patients with naïve papilla affected by obstructive jaundice eligible for endoscopic treatment.

METHODS: 222 consecutive patients undergoing ERCP were prospectively enrolled from July 2022 to August 2023. Bile was sampled before and after sphincterotomy,then stored for cultures and resistance profiles.

RESULTS: Pre-sphincterotomy (66,6%) and post-sphincterotomy samples (67,5%) revealed bacterial growth, with similar components. Gram-positive bacteria, as Enterococcus spp, were mainly identified. Age ≥60 years, Charlson Comorbidity Index (CCI) ≥4, fever, ongoing antimicrobial therapy and positive blood cultures were associated with positive bile cultures. Positive C-reactive protein was independently related to positive cultures. Multidrug Resistand (MDR) strains, according to international standardized definition, were detected (18%), with a higher prevalence of ESBL bacteria and E. faecium VRE. Antimicrobial therapy was an independent risk factor for MDR biliary bacteria in the multivariate analysis. Positive cultures, polymicrobial flora, and MDR bacteria were similar in malignant and benign disease.

CONCLUSION: Multiple clusters and MDR bacteria were detected in patients with obstructive jaundice. We identified clinical and biochemical risk factors for bacteriobilia and MDR commensals.},
}

@article {pmid42547409,
year = {2026},
author = {Burow, C and Shenderey, R and Chowdhury, F and Shah, N and Pai, N},
title = {Nutritional and environmental determinants of maturation and disruption of the early life gut microbiome: A narrative review.},
journal = {JPEN. Journal of parenteral and enteral nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpen.70127},
pmid = {42547409},
issn = {1941-2444},
abstract = {The first 1000 days of life represent a critical window for gut microbiome assembly, with lifelong implications for child growth, immune development, and disease risk. This review synthesizes evidence on maternal, perinatal, and especially nutritional factors that influence early-life intestinal colonization and highlights the consequences of microbial disruptions during this period. In utero exposures and birth-associated factors can profoundly shape microbial development, reducing diversity and beneficial taxa. Nutrition exerts a particularly dominant and modifiable influence: breastfeeding supports Bifidobacterium-rich communities, while formula use and early complementary feeding shape microbiota diversity and metabolic function. Dietary quality, fiber intake, and food diversity are key determinants of microbial maturation and resilience. Undernutrition and inadequate diets contribute to microbial dysbiosis, creating a self-reinforcing cycle of malabsorption, growth failure, and long-term metabolic consequences. Early microbial perturbations are associated with a range of acute and chronic diseases, including necrotizing enterocolitis, obesity, type 1 diabetes, inflammatory bowel disease, and atopic disorders. Strategies to restore microbial balance require further validation, particularly in nutritionally vulnerable populations. The absence of a universal definition for a "healthy" pediatric microbiome limits the development of targeted interventions. Emerging metrics, such as microbiota-for-age z-scores and functional microbiome profiling, may help define microbiota maturity and therapeutic efficacy.},
}

@article {pmid42547464,
year = {2026},
author = {Kim, HB and Park, J and Lim, CS and Um, JY and Chung, BY and Park, CW and Lee, DK and Kim, HO},
title = {Skin Lipid Dysregulation in Atopic Dermatitis and Related Inflammatory Skin Diseases.},
journal = {Allergy, asthma & immunology research},
volume = {18},
number = {4},
pages = {485-506},
doi = {10.4168/aair.2026.18.4.485},
pmid = {42547464},
issn = {2092-7355},
support = {RS-2022-NR070251/NRF/National Research Foundation of Korea/Korea ; RS-2023-KH141546/MOHW/Ministry of Health and Welfare/Korea ; /Hallym/Hallym University/Korea ; },
abstract = {Epidermal lipids are essential for skin barrier function and actively influence cutaneous immune homeostasis. Recent advances have transformed our understanding of skin lipid dysregulation in allergic diseases, revealing complex bidirectional relationships between barrier dysfunction and immune activation. This review provides a comprehensive analysis of the 2020-2025 literature on skin lipid metabolism in allergic and inflammatory diseases, with a particular focus on molecular mechanisms, diagnostic biomarkers, therapeutic advances, and implications for precision medicine. Key discoveries include the finding that sphingomyelin deacylase, long linked to ceramide (CER) deficiency, is actually the β-subunit of acid ceramidase. In atopic dermatitis, this enzyme shifts its substrate specificity to sphingomyelin, depleting the barrier lipid pool. Type 2 cytokines, particularly interleukin (IL)-4 and IL-13, suppress lipid biosynthesis through Janus kinase (JAK)/Signal Transducer and Activator of Transcription 6-mediated downregulation of fatty acid (FA) elongases. This suppression, particularly affecting elongation of very long-chain fatty acid (ELOVL) enzymes, such as ELOVL1, ELOVL3, and ELOVL6, disrupts the synthesis of ultra-long-chain CERs essential for barrier function. JAK inhibitors effectively reverse T helper 2 (Th2)-mediated lipid suppression, while optimized topical lipid ratios (3:1:1 CER: cholesterol: FA) enhance barrier repair. Innovations, such as lipid nanoparticles and microbiome-modulating therapies, further support personalized treatment strategies. The integration of barrier repair with targeted immunomodulation-guided by lipidomic and genomic profiling-marks a paradigm shift toward predictive and preventive approaches in allergic skin diseases. Early intervention strategies that simultaneously address immune dysregulation and lipid metabolism hold promise for preventing the atopic march and sustaining long-term remission.},
}

@article {pmid42547472,
year = {2026},
author = {Kang, J and Yim, Y and Lee, H and Kang, SM and Lee, DG and Heo, YM and Jo, H and Kang, S and Kim, HJ and Yon, DK and Nehs, CJ},
title = {Subtype-Specific Efficacy of Topical Streptococcus Postbiotic Emollient in Adolescents and Adults With Atopic Dermatitis and Comorbid Allergies: A Post-hoc Analysis of a Randomized, Double-Blind, Vehicle-Controlled Trial.},
journal = {Allergy, asthma & immunology research},
volume = {18},
number = {4},
pages = {611-619},
doi = {10.4168/aair.2026.18.4.611},
pmid = {42547472},
issn = {2092-7355},
support = {RS-2025-02220492/MOHW/Ministry of Health and Welfare/Korea ; },
abstract = {Topical Streptococcus postbiotic emollient (Strain CX) has shown efficacy for mild-to-moderate atopic dermatitis (AD) in a previous study; however, treatment responses according to allergic comorbidity status have not yet been explored. We conducted a post hoc analysis to evaluate the differential therapeutic effects of Strain CX in patients with AD stratified by the presence or absence of allergic comorbidities. This post hoc analysis was derived from a randomized, double-blind, vehicle-controlled trial (Clinical Research Information Service of South Korea, KCT0007876). A total of 98 patients with mild-to-moderate AD were stratified into placebo (n = 33), AD without allergic comorbidities (n = 29), and AD with allergic comorbidities (n = 36) groups. The primary outcomes were the Investigator's Global Assessment (IGA) score and the proportions of participants achieving 25% or 50% improvement in the Eczema Area and Severity Index (EASI), assessed at weeks 4 and 8. The secondary outcomes included a range of skin-related clinical and molecular measures, along with additional evaluations of serum inflammatory and allergic biomarkers as laboratory measures in the per-protocol analysis set. At week 8, 55.2% (16/29) of participants in the AD without allergic comorbidities group achieved an IGA score of 0 or 1 with ≥ 1 point reduction, compared to 30.6% (11/36) in the AD with allergic comorbidities group (P = 0.0272). Both Strain CX intervention groups showed significant improvements in skin parameters, including EASI, skin moisture, and transepidermal water loss. Notably, the AD with allergic comorbidities group solely exhibited significant reductions in systemic inflammatory markers, including sIL-2R (mean, -231.19; 95% confidence interval [CI], -378.82 to -83.57 pg/mL), CCL17 (-127.05; 95% CI, -251.80 to -2.31 pg/mL), and CCL22 (-578.40; 95% CI, -939.31 to -217.49 pg/mL). Clinical skin responses improved more in patients with AD without allergic comorbidities, while immunomodulatory benefits were observed in those with allergic comorbidities. These findings support patient stratification based on allergic comorbidity status for personalized Strain CX treatment strategies. Trial Registration: Clinical Research Information Service Identifier: KCT0007876.},
}

@article {pmid42547723,
year = {2026},
author = {Fong, SB and Boyer, E and Marie-Cousin, A and Le Gall-David, S and Sixou, JL and Bonnaure-Mallet, M and Desclos-Theveniau, M and Meuric, V},
title = {Does permanent tooth eruption introduce periodontal pathogens? A preliminary study.},
journal = {Odontology},
volume = {},
number = {},
pages = {},
pmid = {42547723},
issn = {1618-1255},
abstract = {The colonization of the periodontal sulcus by pathogenic oral bacteria may be promoted by the eruption of permanent teeth. To analyse the evolution of the oral microbiota during teeth eruption. Sub-gingival microbiome analyses (16S) of primary teeth and eruption permanent teeth sulci (case-matched) were carried out with periodontitis sample controls. A number of disease-associated bacteria including Tannerella forsythia, Treponema denticola and Fretibacterium sp. HMT 360 have been detected in erupting teeth samples but were absent in primary teeth. The formation of deeper sulcus during permanent teeth eruption may create an early colonization niche for periodontal pathogens in older children or young adults which may be implicated later in periodontal diseases.},
}

@article {pmid42547810,
year = {2026},
author = {Volkmann, ER and Herzog, EL and Feghali-Bostwick, C},
title = {Sex-dependent mechanisms in rheumatic diseases.},
journal = {Nature reviews. Rheumatology},
volume = {},
number = {},
pages = {},
pmid = {42547810},
issn = {1759-4804},
abstract = {Sex differences in the prevalence, clinical phenotypes and therapeutic responses of rheumatic diseases have been recognized for decades, but the underlying mechanisms remain largely unknown. Accumulating evidence highlights the critical roles of both immune and non-immune cells in disease pathogenesis and the influence of sex hormones on cellular function. In addition, factors such as sex chromosomes, hormonal regulation, antiviral immune response, the gut microbiome and genetic and epigenetic variation probably contribute to the divergent features of rheumatic diseases between women and men. A deeper understanding of these intersecting pathways might uncover novel therapeutic targets. Thus far, treatment strategies for rheumatic diseases largely focus on immunomodulation; however, elucidating the biological basis of sex differences could enable the development of preventative therapies that target hormonal pathways and the gut microbiome, with the potential to avert both the onset and progression of these debilitating diseases to improve health for all patients.},
}

@article {pmid42547826,
year = {2026},
author = {Schierwagen, R and Carraturo, F and Iyappan, A and Brol, MJ and Druart, C and Israelsen, M and Hassani, Z and Legent, K and Godoy, Y and Vecchi, C and Rodriguez, J and Villesen, IF and Jarde, A and Arumugam, M and Krag, A and Maguin, E and Bork, P and , and Doré, J and Trebicka, J and Fasano, A},
title = {Multidisciplinary Delphi consensus statement on minimal standards for clinical metadata and end points in microbiome studies.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {42547826},
issn = {1759-5053},
abstract = {The lack of harmonization for microbiome-based clinical studies represents a critical issue for microbiome researchers and stakeholders, although microbiome research and clinical studies on the gut microbiome have been intensively conducted for more than a decade. The selection of a minimum metadata set to be analysed and reported during clinical studies with microbiome outcomes, the identification of reference materials, the definition of standardized sampling procedures and data analysis protocols, and the choice of unified clinical end points are still lacking. The two-round Delphi survey, conducted within the framework of the Horizon Europe Human Microbiome Action (HMA) consortium, aimed to standardize metadata collection, sampling procedures, data generation and sharing, and standard operating procedures for aspects of gut microbiome-based clinical studies beyond outcomes. The process involved 72 scientists and experts worldwide in the first round and 61 experts in the second round, with an 85% participation rate from the first to the second round. On the basis of the outcome of the Delphi survey, the HMA consortium provided 15 recommendations that might be taken up by the community at large to promote coherence and harmonization in the way microbiome clinical research is and will be performed. The recommendations mainly focus on the gut microbiome and diseases associated with the gastrointestinal tract and gut-organ axes.},
}

@article {pmid42547877,
year = {2026},
author = {Luo, X and Shan, H and Wang, B and Qi, L and Ding, M and Qi, Y and Zhou, J and Fan, J and Han, G and Cheng, B and Chen, J and Li, X},
title = {ZmHPATR1 orchestrates phyllosphere organic acid flux to recruit Sphingomonas and enhance resistance of maize to Curvularia leaf spot.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71485},
pmid = {42547877},
issn = {1469-8137},
support = {2022YFD201005//National Key Research and Development Program of China/ ; 2025SWYZ0200//Bio-breeding Laboratory of Anhui Province/ ; NELCOF20240104//National Engineering Laboratory of Crop Stress Resistance Breeding/ ; },
abstract = {Leaf spots caused by Curvularia lunata infection pose a significant threat to global maize production. Although resistance gene breeding faces challenges due to pathogen evolution, the plant microbiome has emerged as a key modulator of disease resistance. However, the mechanisms via which plant genes regulate phyllosphere metabolites to recruit beneficial microbes remain poorly understood. Here, we combined gene mapping, metabolomics, microbiome analyses, cytological analysis, and in vitro and in vivo experiments to investigate the disease resistance mechanism of ZmHPATR1. We first identified that the loss-of-function mutation in ZmHPATR1 significantly increased the levels of fumaric acid, folic acid, and tetrahydrofolic acid in the leaves, leading to the enrichment of the genus Sphingomonas. We further demonstrated that the extracellular polysaccharide, welan gum, biosynthesized by Sphingomonas, effectively inhibited C. lunata growth and disrupted its cell structure. These results enable us to comprehensively understand the complicated mechanisms of plant resistance to disease through a four-level regulatory network that links plant genes, metabolites, microbes, and pathogens. Our findings provide new strategies for targeted microbiome-based disease-resistant breeding and the development of novel biopesticides for maize.},
}

@article {pmid42547881,
year = {2026},
author = {Schuck, LK and Ernetti, JR and Buttimer, S and de Assis, AB and Martins, RA and Pontes, MR and Zanatta, AC and Tosta, MB and Toledo, LF and Becker, CG},
title = {Differential skin-bacteriome-mediated defense against chytridiomycosis in two neotropical frog species.},
journal = {Animal microbiome},
volume = {8},
number = {1},
pages = {},
pmid = {42547881},
issn = {2524-4671},
support = {FAPESP #2022/11096-8; #2020/02994-7; #2022/07125-2//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; CNPq #302834/2020-6//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; DBI-2120084//The National Science Foundation/ ; },
abstract = {Symbiotic microbial communities have been implicated in host resistance to pathogens, but their effects are rarely demonstrated experimentally in wildlife. This study tested how skin-associated bacterial communities (i.e., bacteriomes) influence infection by the chytrid fungus Batrachochytrium dendrobatidis (Bd) in two tropical frog species, Haddadus binotatus and Ischnocnema henselii, which differ in susceptibility to Bd. Using a 2x2 factorial experimental design, frogs of both species were assigned to treatments crossing Bd exposure and antibiotic-mediated bacteriome suppression. In parallel, we cultured 786 bacterial isolates from frog skin and assayed their ability to inhibit Bd in vitro, generating a functional database of Bd-inhibitory symbionts. Haddadus binotatus with an unsuppressed skin bacteriome and exposed to Bd showed no reduction in survival relative to Bd-unexposed controls, consistent with the lack of Bd infection previously observed in wild populations. In contrast, bacteriome suppression increased mortality and infection intensity under Bd exposure. Bd infection intensity in H. binotatus also decreased with the proportion of Bd-inhibitory sequence reads in the bacteriome, and a significant interaction between antibiotic treatment and Bd exposure affecting survival was detected, consistent with bacteriome-mediated protection in this species. In contrast, I. henselii experienced lower survival under Bd exposure in general. Species-specific log-rank tests revealed that bacteriome suppression significantly increased mortality under Bd exposure in H. binotatus but not in I. henselii, where survival was reduced under Bd exposure regardless of bacteriome state, suggesting fundamentally different defense strategies between species. Functional attributes of microbial communities, rather than diversity alone, appear to be key to disease outcomes. This work advances understanding of host-microbe-pathogen interactions and highlights microbiome function as a critical axis of wildlife disease defense.},
}

@article {pmid42547909,
year = {2026},
author = {McGregor, K and Parsons, T and Simons, E and Scott, J and Kozyrskyj, A and Quince, C},
title = {Microbial Diversity Estimation and Hill Number Calculation Using the Hierarchical Pitman-Yor Process.},
journal = {Statistics in medicine},
volume = {45},
number = {18-19},
pages = {e70689},
doi = {10.1002/sim.70689},
pmid = {42547909},
issn = {1097-0258},
support = {RGPIN-2021-03634//Natural Sciences and Engineering Research Council of Canada/ ; /BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BBX011089/1//Earlham Institute Strategic Programme/ ; BBS/E/ER/230002C//Earlham Institute Strategic Programme/ ; BB/CSP1720/1//UK's Biotechnology and Biological Sciences Research Council/ ; BBS/E/T/000PR9818//UK's Biotechnology and Biological Sciences Research Council/ ; BBS/E/T/000PR9817//UK's Biotechnology and Biological Sciences Research Council/ ; },
mesh = {Humans ; *Microbiota ; *Models, Statistical ; Computer Simulation ; *Biodiversity ; },
abstract = {BACKGROUND: The human microbiome comprises the microorganisms that inhabit the various locales of the human body and plays a vital role in human health. The composition of a microbial population is often quantified through measures of species diversity, which summarize the number of species along with their relative abundances into a single value. In a finite microbiome sample, there will be species missing from the target population, which will affect the diversity estimates.

METHODS: We employ a model based on the hierarchical Pitman-Yor (HPY) process to model the species abundance distributions over multiple populations. The model parameters are estimated using a Gibbs sampler. We also derive estimates of species diversity, conditional and unconditional on the observed data, as a function of the HPY parameters. Finally, we derive a general formula for the Hill numbers in the HPY context.

RESULTS: We show that the Gibbs sampler for the HPY model performs well in simulations. We also show that the conditional estimates of diversity from the HPY model improve over naïve estimates when species are missing. Similarly, the conditional HPY estimates tend to perform better than the naïve estimates especially when the number of individuals sampled from a population is small. Finally, we illustrate results of applying the HPY model in an infant gut microbiome dataset.},
}

Humans
*Microbiota
*Models, Statistical
Computer Simulation
*Biodiversity

@article {pmid42548006,
year = {2026},
author = {Liu, S and Shi, C and Zhou, Y and Dai, C},
title = {Amino acid homeostasis in the kidney: Physiological roles and pathological dysregulation.},
journal = {Physiological reports},
volume = {14},
number = {15},
pages = {e71029},
doi = {10.14814/phy2.71029},
pmid = {42548006},
issn = {2051-817X},
support = {M2025040//Medical Research Project of Jiangsu Commission of Health/ ; MQ2025008//Medical Research Project of Jiangsu Commission of Health/ ; },
mesh = {Humans ; *Homeostasis/physiology ; Animals ; *Amino Acids/metabolism ; *Kidney/metabolism/physiopathology/pathology ; *Kidney Diseases/metabolism/physiopathology/pathology ; Amino Acids, Branched-Chain/metabolism ; },
abstract = {Amino acids are fundamental to life as protein building blocks and key regulators of metabolism and signaling. The kidney plays a critical, yet underappreciated, role in amino acid homeostasis through three interconnected pillars: selective glomerular filtration, efficient tubular reabsorption, and metabolic processing, which includes de novo synthesis and interconversion of amino acids, as well as their catabolism for energy production and gluconeogenesis. These processes are tightly coupled to systemic acid-base regulation, gluconeogenesis, and whole-body nitrogen clearance. When kidney function declines, the resulting alterations in amino acid profiles are not merely passive markers of reduced filtration but are increasingly recognized as potential mediators that may actively contribute to disease progression, as supported by a growing body of preclinical and clinical evidence. This Review synthesizes current knowledge on renal amino acid homeostasis and proposes four dysregulation patterns in kidney disease: metabolic rewiring, branched-chain amino acids paradox, uremic toxin accumulation, and organelle dysfunction. We further discuss emerging therapeutic strategies aimed at restoring amino acid homeostasis, including dietary modulation, pharmacological targeting of metabolic enzymes and transporters, and microbiome-directed interventions. Finally, we identify key unanswered questions that should guide future research in this rapidly evolving field.},
}

Humans
*Homeostasis/physiology
Animals
*Amino Acids/metabolism
*Kidney/metabolism/physiopathology/pathology
*Kidney Diseases/metabolism/physiopathology/pathology
Amino Acids, Branched-Chain/metabolism

@article {pmid42548192,
year = {2026},
author = {Feng, J and Wang, Z and Xu, Y and Peng, J and Xu, C and Xie, Q and Li, Y and Chen, W and Chen, J and Wang, X and Gao, WQ and Li, L and Meng, X},
title = {Intestinal epithelial SETD2 maintains gut microbial homeostasis to attenuate colitis.},
journal = {Clinical and translational medicine},
volume = {16},
number = {8},
pages = {e70754},
doi = {10.1002/ctm2.70754},
pmid = {42548192},
issn = {2001-1326},
support = {2022YFA1302704//National Key R&D Program of China/ ; 2023YFC1404101//National Key R&D Program of China/ ; YG2024ZD11//Interdisciplinary Program of Shanghai Jiao Tong University/ ; 32570684//National Natural Science Foundation of China/ ; 82372604//National Natural Science Foundation of China/ ; U23A20441//National Natural Science Foundation of China/ ; W2431055//National Natural Science Foundation of China/ ; },
mesh = {Animals ; Mice ; *Colitis ; *Histone-Lysine N-Methyltransferase/metabolism/genetics ; *Homeostasis ; *Gastrointestinal Microbiome/physiology/drug effects/genetics ; Mice, Knockout ; *Intestinal Mucosa/metabolism ; Male ; },
abstract = {BACKGROUND: Disruption of host-microbiota homeostasis is a fundamental hallmark of inflammatory bowel disease (IBD) pathogenesis. Host epigenetic modifications and corresponding alterations in gene expression levels can impact the composition of gut microbes. SET domain containing 2 (SETD2) is a critical epigenetic regulator with established tumor-suppressive roles, but its function in intestinal microbial ecology and colitis progression remains unexplored. We aimed to investigate the specific role of SETD2 in maintaining gut microbial homeostasis and modulating colitis progression.

METHODS: RNA sequencing (RNA-seq), assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and cleavage under targets and tagmentation sequencing (CUT&Tag-seq) were conducted on colonic epithelial cells from intestinal epithelial cell-specific SETD2 knockout (Setd2[vil-ko]) mice to identify key mediators contributing to colitis development. Faecal samples underwent 16S rRNA sequencing and non-targeted metabolomics analysis to characterise microbial dysbiosis and metabolic perturbations. Molecular experiments and faecal microbiome transplantation experiment were conducted to explore and validate the role of SETD2 in colitis development.

RESULTS: SETD2 deficiency induced overproduction of Reg3 lectins and disrupted gut microbiota composition. Beneficial commensal bacteria were depleted and dysregulated metabolites were accumulated in Setd2[vil-ko] mice. Supplementation with healthy-like gut microbiota significantly ameliorated the exacerbated colitis induced by SETD2 deficiency.

CONCLUSIONS: Our findings uncover a previously unrecognised role for SETD2 in maintaining microbial homeostasis, offering new mechanistic insights into how epigenetic regulation preserves intestinal homeostasis and suggesting novel therapeutic avenues for IBD.},
}

Animals
Mice
*Colitis
*Histone-Lysine N-Methyltransferase/metabolism/genetics
*Homeostasis
*Gastrointestinal Microbiome/physiology/drug effects/genetics
Mice, Knockout
*Intestinal Mucosa/metabolism
Male

@article {pmid42548196,
year = {2026},
author = {Santorelli, G and Pembrey, L and da Cunha, SS and Petherick, ES and Badrick, E and Goodwin, L and Oddie, S and Pearce, N and Wright, J},
title = {The Effect of Intrapartum Antibiotic Prophylaxis at Caesarean Section on Childhood Obesity: A Quasi-Experimental Study in Two Bi-Ethnic UK Cohorts.},
journal = {Paediatric and perinatal epidemiology},
volume = {},
number = {},
pages = {},
doi = {10.1111/ppe.70179},
pmid = {42548196},
issn = {1365-3016},
support = {223601/WT_/Wellcome Trust/United Kingdom ; NIHR200166//National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care Yorkshire and Humber/ ; 16/150/06//Health Technology Assessment Programme/ ; },
abstract = {BACKGROUND: Clinical guidelines now recommend administering intrapartum antibiotic prophylaxis (IAP) before skin incision at caesarean section to prevent maternal infection. However, this practice exposes the fetus to antibiotics, raising concerns about potential long-term effects on the infant microbiome and the risk of childhood obesity.

OBJECTIVES: To assess whether the timing of IAP at caesarean section-before skin incision versus after umbilical cord clamping-is associated with childhood obesity at age 4-5 years.

METHODS: We conducted a quasi-experimental study of a hospital-wide policy change in clinical practice using data from two birth cohorts (Born in Bradford [BiB] and Born in Bradford's Better Start [BiBBS]). The study included 1985 children of White British or Pakistani heritage born by caesarean section between 2007 and 2019. Children exposed to pre-incision IAP (n = 324) were compared with those unexposed (post-cord clamping IAP; n = 1661). The primary outcome was obesity (BMI z-score > 95th percentile) at age 4-5 years. Adjusted Risk Ratios (aRR) were estimated using multivariable Poisson regression stratified by ethnicity.

RESULTS: The prevalence of obesity was 11.9%. Adjusted risk ratios for obesity were 1.25 (95% CI 0.53 to 2.98) for White British children and 1.25 (95% CI 0.64 to 2.43) for Pakistani children. Similarly, estimates for BMI z-score had wide confidence intervals indicating, limited precision.

CONCLUSIONS: We did not observe a clear difference in childhood obesity at 4-5 years between pre-incision and post-cord clamping prophylactic antibiotics at caesarean section. Confidence intervals were wide, and modest clinically relevant effects cannot be excluded. Findings are compatible with no large adverse effect and may provide reassurance regarding the metabolic safety of current clinical practice.},
}

@article {pmid42548232,
year = {2026},
author = {Li, X and Wei, Y and Cheng, Q and Xiao, S and Yao, S and Yang, D and Wang, J and Chen, L and Li, Q and Zhan, T},
title = {Total flavonoids of litchi seed attenuates cellular senescence by inhibiting the production of SASP through p65 suppression and ameliorates pulmonary fibrosis.},
journal = {Acta biochimica et biophysica Sinica},
volume = {58},
number = {7},
pages = {1637-1652},
doi = {10.3724/abbs.2025206},
pmid = {42548232},
issn = {1745-7270},
mesh = {Animals ; *Litchi/chemistry ; *Flavonoids/pharmacology ; *Cellular Senescence/drug effects ; *Seeds/chemistry ; *Pulmonary Fibrosis/metabolism/drug therapy/pathology/chemically induced ; Mice ; *Senescence-Associated Secretory Phenotype/drug effects ; Bleomycin ; DNA Damage/drug effects ; Mice, Inbred C57BL ; },
abstract = {Anti-aging foods not only benefit elderly individuals but also drive the development of safe and effective natural drugs. Here, we report that the addition of total flavonoids of litchi seed (TFL) delays replicative senescence and stress-induced senescence. TFL alleviates the senescence-associated secretory phenotype (SASP) and reduces the degree of DNA damage caused by bleomycin (BLM). TFL also counteracts stress-induced pulmonary senescence and fibrosis. TFL reduces the protein level of p21 in mouse lung and alleviates pulmonary fibrosis. Transcriptome profiling further reveals that TFL plays a key role in its anti-aging mechanism by inhibiting the SASP. Mechanistically, TFL suppresses p65 protein expression, thereby inhibiting IL-1α and IL-1β and delaying cellular senescence. Gut microbiome analysis reveals that the abundance and functions of the mouse gut microbiome change after BLM exposure and that TFL treatment reverses these changes. Overall, we provide a theoretical basis for the future application of TFL as a potential anti-aging product.},
}

Animals
*Litchi/chemistry
*Flavonoids/pharmacology
*Cellular Senescence/drug effects
*Seeds/chemistry
*Pulmonary Fibrosis/metabolism/drug therapy/pathology/chemically induced
Mice
*Senescence-Associated Secretory Phenotype/drug effects
Bleomycin
DNA Damage/drug effects
Mice, Inbred C57BL

@article {pmid42548287,
year = {2026},
author = {Kolodyazhna, A and Wiersinga, WJ},
title = {Protecting the gut microbiome when treating bloodstream infections: the price of anaerobic coverage.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciag461},
pmid = {42548287},
issn = {1537-6591},
}

@article {pmid42548466,
year = {2026},
author = {Yang, L and Tao, Y and He, Y and Liu, S and Gan, L and Dai, A and Ni, Q and Wang, Y and Li, F and Liu, Q and Hu, Y and Wang, Y and Lu, W},
title = {Metagenomic and metabolomic profiling in primary aldosteronism with coexisting obstructive sleep apnea.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1858100},
pmid = {42548466},
issn = {1664-2392},
mesh = {Humans ; *Sleep Apnea, Obstructive/metabolism/complications/microbiology/genetics ; Female ; *Hyperaldosteronism/metabolism/complications/genetics/microbiology ; Male ; *Metagenomics/methods ; *Metabolomics/methods ; Prospective Studies ; Middle Aged ; *Gastrointestinal Microbiome/genetics ; *Metabolome ; Adult ; Feces/microbiology ; Polysomnography ; },
abstract = {BACKGROUND: Primary aldosteronism (PA) frequently coexists with obstructive sleep apnea (OSA), and this comorbidity is associated with increased cardiometabolic risk. Although both PA and OSA have been individually linked to gut microbiome alterations, it remains unclear which layer of gut microbiome-associated variation best reflects clinical heterogeneity in PA with coexisting OSA.

METHODS: In this prospective observational study, we performed shotgun metagenomic sequencing and untargeted fecal metabolomic profiling in 29 adults with clinically confirmed PA, who were stratified according to OSA severity (G1-G4) based on overnight polysomnography. Microbial gene richness, taxonomic composition, functional potential based on KEGG annotation, and antibiotic resistance gene profiles were analyzed using standardized bioinformatic workflows. Metabolomic variation was assessed using multivariate analysis, pathway enrichment, and additional exploratory analyses incorporating apnea-hypopnea index (AHI) as a continuous variable. Multiple-testing correction was applied to metabolite-level comparisons.

RESULTS: Global gut microbial gene richness, alpha diversity, beta diversity, and broad functional profiles did not show strong group-level separation across OSA severity strata. Additional analyses using AHI as a continuous variable similarly showed no significant association between AHI and overall gene richness or alpha diversity indices. Nevertheless, selective genera showed exploratory associations with AHI, suggesting that localized taxonomic signals may occur despite relative stability of global community structure. Antibiotic resistance gene profiles showed marked inter-individual variability without clear group-level separation, although ARO richness showed an exploratory inverse association with AHI. In contrast, fecal metabolomic profiling revealed nominal phenotype-associated differences, including trehalose-related metabolites and FAHFA species that showed inverse exploratory associations with AHI. However, no individual metabolite remained significant after global Benjamini-Hochberg false discovery rate correction.

CONCLUSIONS: In PA with coexisting OSA, gut microbiome-associated heterogeneity appears to be more readily reflected by selected taxonomic and metabolic signals than by global microbial diversity or broad functional potential. However, given the small sample size, limited control of clinical and lifestyle confounders, and lack of metabolite-level significance after global FDR correction, these findings should be interpreted as exploratory and hypothesis-generating. Larger controlled cohorts incorporating PA subtype, medication exposure, dietary assessment, and longitudinal validation are needed.},
}

Humans
*Sleep Apnea, Obstructive/metabolism/complications/microbiology/genetics
Female
*Hyperaldosteronism/metabolism/complications/genetics/microbiology
Male
*Metagenomics/methods
*Metabolomics/methods
Prospective Studies
Middle Aged
*Gastrointestinal Microbiome/genetics
*Metabolome
Adult
Feces/microbiology
Polysomnography

@article {pmid42548549,
year = {2026},
author = {Chen, Y and Duan, W and Du, M and Guo, M and Sun, Y},
title = {Gut microbiota and constipation: from causal evidence to therapeutic strategies-a state-of-the-art narrative review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1817279},
pmid = {42548549},
issn = {1664-302X},
abstract = {Constipation is a common functional disorder of the gastrointestinal tract with a global prevalence of approximately 10-20%, which seriously affects patients' quality of life and imposes a heavy socioeconomic burden. In recent years, the role of the gut microbiota in the pathogenesis of constipation has received increasing attention, particularly in the context of the brain-gut axis theory. In this narrative review, we critically examine the research literature on constipation and intestinal microecology published over the past decade, focusing on four aspects: (1) the characteristics of the gut microbiota in patients with constipation, including changes in microbial diversity, alterations in the abundance of specific taxa, and differences across constipation subtypes; (2) Mendelian randomization studies that provide genetic-level evidence consistent with the hypothesis that certain microbiota alterations may precede constipation rather than merely result from it; (3) mechanisms of microbiota-host interactions mediated by the brain-gut axis, with an emphasis on neural, metabolic and immune pathways; and (4) microbiota-based intervention strategies (probiotics, prebiotics, synbiotics, postbiotics and fecal microbiota transplantation) and their clinical evidence. Our findings suggest that specific microbiota alterations may contribute to constipation pathophysiology and the promise of personalized, microbiome-based therapies. Although microbiota-based interventions show potential therapeutic value in selected patients, current evidence is limited by substantial heterogeneity in study design, small sample sizes, inconsistent microbiome signatures, and limited long-term safety data. High-quality evidence from large, well-designed RCTs is lacking for most interventions, and findings from low-certainty studies (e.g., conference abstracts, animal experiments, small uncontrolled trials) should be interpreted as preliminary and hypothesis-generating rather than conclusive. Therefore, microbiota-targeted therapies should currently be considered exploratory or adjunctive rather than established standard treatments for constipation. Future progress will require standardized methodologies, mechanistic validation studies, and phenotype-stratified clinical trials to support translation toward precision microbiome-based medicine.},
}

@article {pmid42548609,
year = {2026},
author = {Mukherjee, A and Yılmaz, B and Bartkiene, E and Rocha, JM},
title = {Editorial: Mechanisms of fermented foods and interactions with the gut microbiome.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1923421},
doi = {10.3389/fmicb.2026.1923421},
pmid = {42548609},
issn = {1664-302X},
}

@article {pmid42548690,
year = {2026},
author = {Wagner, A and Kuljukka, A and Kumstat, M and Ihalainen, JK},
title = {Low energy availability, the gut microbiome, and bone health in athletes: a mechanistic narrative review based on athlete evidence and clinical analogues.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1901299},
pmid = {42548690},
issn = {2296-861X},
abstract = {Low energy availability (LEA) is a central aetiological factor in Relative Energy Deficiency in Sport (REDs) and is frequently associated with impaired skeletal health in athletic populations, although skeletal responses can be heterogeneous. However, athletes with apparently similar energetic and training exposures can differ in bone mineral density, bone turnover and bone stress injury risk, indicating that additional physiological mediators may modify the skeletal response to under-fuelling. The gut microbiome has emerged as a plausible candidate because microbial metabolites, intestinal barrier integrity, immune signalling and endocrine pathways can influence bone remodelling. Direct studies integrating energy availability, gut microbiome profiling and bone outcomes in athletes are currently lacking. This narrative review therefore synthesises athlete evidence for the LEA-bone relationship and uses clinical and preclinical analogues of chronic energy deficiency to develop a testable gut-bone framework for sport. The accumulated evidence from athletes primarily supports the direct LEA-bone relationship, whereas the candidate gut-bone microbiome component remains a biologically plausible hypothesis based on clinical and preclinical models. Specifically, evidence from athletes supports LEA and REDs risk as contributors to lower bone mineral density, altered bone microarchitecture, suppressed bone formation markers and bone stress injury risk, although findings vary by sex, sport type, skeletal loading, assessment method and timing. Evidence from anorexia nervosa and other undernutrition models suggests that energy deficiency can be accompanied by altered microbial diversity, depletion of short-chain fatty acid-producing taxa, lower short-chain fatty acid availability, impaired barrier function and low-grade inflammation. Mechanistically, short-chain fatty acids, endotoxin-mediated inflammation, insulin-osteocalcin signalling, bile acid pathways and amino acid metabolites may intersect with canonical REDs endocrine disturbances to influence bone remodelling. The available evidence does not establish a causal gut-mediated pathway in athletes, but it supports a biologically plausible model that should be tested in prospective athlete cohorts using integrated assessments of energy availability, diet, training load, microbiome composition and function, endocrine status, bone turnover and bone structure.},
}

@article {pmid42548700,
year = {2026},
author = {Masenya, K and Ledwaba, MB and Khumalo, N and Makgabo, SM and Mokgokong, SP and Chaisi, M},
title = {A snapshot of the microbiome of blood and ticks of captive cheetahs (Acinonyx jubatus) from selected conservation facilities in South Africa.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1882746},
pmid = {42548700},
issn = {1664-302X},
abstract = {Cheetahs (Acinonyx jubatus) are listed as vulnerable on the IUCN Red List, with populations declining across their native range due to anthropogenic pressures. To support conservation, breeding programs have been established in South Africa and globally. However, captivity introduces new ecological challenges, including increased exposure to ticks and tick-borne pathogens (TBPs). Translocation of cheetahs may further facilitate the spread of pathogens, potentially affecting animal health and introducing infections into new environments. Despite these risks, little is known about the blood and tick microbial communities of captive and free-ranging cheetahs in South Africa. This study investigated the composition, abundance, taxonomic classification, of bacteria detected in captive cheetahs and associated ticks in South Africa. Full-length 16S rRNA gene sequencing was performed on samples originating from 10 adult cheetahs and 20 tick specimens representing 8 tick species from the genera Amblyomma, Haemaphysalis, Hyalomma, and Rhipicephalus across five provinces of South Africa. Sequencing was conducted using the PacBio platform, and reads were classified to genus level using the SILVA microbial database at a 99% confidence threshold. Amplicon Sequence Variant (ASV) analysis identified both known and unknown bacterial taxa, including genera harboring potential zoonotic pathogens. Proteobacteria was the dominating bacterial phylum in both the host and tick microbiota, however ticks had a larger proportion of Proteobacteria than hosts. At the genus level, the tick bacterial microbiomes were dominated by the genus Coxiella, while host microbiomes were dominated by Bacillus and Stenotrophomonas. The compositions of dominant genera in female ticks constituted a higher abundance of Coxiella and Methylobacterium-Methylorubrum compared to males. Accounting for the low-biomass nature and contamination risks of blood, resulted in the Shannon and Simpson diversity indices being significantly higher for host samples, while ticks maintained significantly higher observed ASV richness. Beta-diversity analysis further revealed significant differences in microbial community structure between hosts and ticks (p < 0.05), making sample type to be the primary factor shaping bacterial composition. In contrast, sex, province, and tick species did not significantly influence Beta-diversity. Overall, these findings highlight distinct bacterial community patterns between hosts and ticks and emphasize the importance of sample type in structuring tick-associated microbiomes and the importance of continuous surveillance and monitoring of TBPs during wildlife translocation to reduce risks to wildlife, livestock, and human health.},
}

@article {pmid42548799,
year = {2026},
author = {Miller, AJ and Jo, MC and Hui, CK and Petereit, J and Woodhams, DC and Voyles, J},
title = {Effects of Timing of Microbial Exposure on Microbiome Assembly and Amphibian Immune Development.},
journal = {Ecology and evolution},
volume = {16},
number = {8},
pages = {e74063},
pmid = {42548799},
issn = {2045-7758},
abstract = {Critical periods of development are time points that are especially sensitive to disruptions. Critical periods are important for microbiome assembly and the development of an effective immune system and, therefore, can have large and lasting impacts on host health, even through later life stages. Here, we investigated how a disruption to the microbiome of amphibians (treatment with a cocktail of six antibiotics and one antifungal compound) during early life and subsequent introduction to microbes at different developmental stages influences microbiome assembly and the development of the immune system (lymphoid tissues thymus and spleen). We found that antimicrobial treatments and introduction to microbes altered microbiome assembly (total microbial richness, antifungal microbial richness, composition, and relative abundances) and these changes were dependent on the timing of microbial introduction. Tadpoles treated with antimicrobials and then introduced to microbes at different developmental stages also had higher scaled abundances of bacteria in the phylum Actinobacteriota. However, after 7.5 weeks of tadpole development, we found no effects of treatment on lymphoid organ (thymus and spleen) size or on lymphoid cell counts. Overall, these results suggest that a disruption to the microbiome during early development, and more specifically, the length of the disruption and timing of reintroduction to microbes, can have significant impacts on microbiome assembly, potentially leading to long term impacts on host health.},
}

@article {pmid42548903,
year = {2026},
author = {Wei, M and Lian, T and Chen, L and Wang, L and Ye, J and Yao, X and Duan, S and Lu, Z and Tu, J and Li, H and Xu, XY and Zhou, J and He, J and Zhu, F and Bonfante, P and Tran, LP and Pang, Z and Zhou, X and Xu, Z and Zhang, L and Wang, M and Wang, X and Tian, CF and Liu, YX and Sun, K and Wang, E and Xie, X},
title = {The plant microbiome: From ecological foundations to precision microbial engineering for sustainable agriculture.},
journal = {iMeta},
volume = {},
number = {},
pages = {e70152},
pmid = {42548903},
issn = {2770-596X},
abstract = {Plants are best understood as evolutionary holobionts, in which the host and its associated microbiomes operate as an integrated unit to influence growth, health, and stress resilience. This comprehensive review synthesizes the most current knowledge of plant-associated microbiomes across key ecological compartments, including the rhizosphere, endosphere, phyllosphere, and seeds, highlighting their assembly drivers, functional mechanisms, and translational potential. We dissect the molecular foundations of rhizobial and arbuscular mycorrhizal (AM) symbioses, the plant-AM fungus-bacterium continuum, alongside emerging concepts including the aerial root mucilagesphere, phyllosphere homeostasis, and the pathobiome. We further explore host genetic, metabolic, and environmental determinants of microbiome assembly, and present cutting-edge methodologies ranging from quantitative profiling to artificial intelligence-driven synthetic community design. Finally, we outline a strategic blueprint for harnessing standardized synthetic microbiomes and precision microbiome engineering to advance sustainable agriculture. This integrative framework bridges fundamental ecology with practical applications, delineating a path toward climate-resilient crop production.},
}

@article {pmid42549006,
year = {2026},
author = {Ji, Z and Kang, L and Liu, S and Jiang, Q and Wei, W},
title = {The Bacteria-Fungi-Phage Interplay in Periodontitis and Peri-Implantitis.},
journal = {International journal of dentistry},
volume = {2026},
number = {},
pages = {7239600},
pmid = {42549006},
issn = {1687-8728},
abstract = {OBJECTIVE: This review aims to summarize current evidence on the interactions among bacteria, fungi, and bacteriophages in periodontitis and peri-implantitis, and to discuss their ecological significance, pathogenic mechanisms, and potential clinical implications.

SUBJECTS AND METHODS: This review synthesizes current insights into the roles of the oral microbiome in these diseases, with a focus on the critical interplay between bacteria, fungi, and bacteriophages.

RESULTS: Our analysis demonstrates that disease progression is marked by a shift toward polymicrobial synergy. Keystone pathogens and opportunistic fungi engage in intricate interactions within biofilms, including physical coadhesion and metabolic cross-feeding, which enhance microbial resilience and virulence. Bacteriophages, acting as natural modulators of bacterial populations, emerge as a promising therapeutic approach to disrupt these pathogenic communities. This bacteria-fungi-phage consortium synergistically modulates host immune responses, fostering chronic inflammation and tissue destruction.

CONCLUSION: An integrated, multikingdom perspective on the oral ecosystem is critical for clinical advancement. Future strategies should prioritize personalized interventions that combine multiomics biomarker analysis with targeted therapies to effectively disrupt polymicrobial biofilms, restore homeostasis, and overcome antimicrobial resistance.},
}

@article {pmid42549049,
year = {2026},
author = {Farsi, F and Sarvi, DG and Abbasi, M and Hasani-Ranjbar, S},
title = {Empagliflozin in the Absence of Diabetes: A Systematic Review of Its Anthropometric and Metabolic Effects in Humans and Animals.},
journal = {International journal of endocrinology},
volume = {2026},
number = {},
pages = {5558442},
pmid = {42549049},
issn = {1687-8337},
abstract = {PURPOSE: Obesity raises metabolic and cardiovascular risk and represents a major public health challenge. The sodium-glucose cotransport-2 inhibitor empagliflozin (EMPA) may improve metabolic parameters beyond glycemic control. This systematic review critically evaluated the effects of EMPA on anthropometric and metabolic outcomes in overweight or obese subjects without diabetes and identified key areas for future research.

METHODS: This systematic review included studies identified through searches of five databases (Scopus, Web of Science, PubMed, Google Scholar, and the Cochrane Library) from January 2023 to May 2026. Following duplicate removal and PRISMA-guided screening, 27 studies were included (7 randomized controlled trials and 20 animal studies). Studies were excluded if they involved diabetic populations, lacked appropriate comparator groups, or did not meet predefined eligibility criteria. The Cochrane and SYRCLE tools were used to assess the quality of human and animal evidence, respectively.

RESULTS: Animal studies primarily used EMPA doses of 8-30 mg/kg/day, whereas human trials employed fixed clinical doses of 10-12.5 mg daily. In human investigations, EMPA significantly lowered body weight with notable improvements in fasting glucose. Preclinical studies largely supported these findings and additionally demonstrated improvements in hepatic steatosis, lipid metabolism, and inflammatory markers. Proposed mechanisms included modulation of FGF21 signaling, hepatic PDK4 expression, hypothalamic neuropeptides, NF-κB activity, mitochondrial function, and gut microbiome composition.

CONCLUSION: Even in the absence of diabetes, EMPA shows potential for improving anthropometric and metabolic indices. However, clinical evidence remains limited and further human trials are needed to confirm its long-term safety, efficacy, and underlying molecular mechanisms.},
}

@article {pmid42549219,
year = {2026},
author = {Liu, X and Wang, Y},
title = {JAK1-preferential inhibition in refractory inflammatory bowel disease: reframing upadacitinib as a strategy for rapid immune recalibration.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1893892},
pmid = {42549219},
issn = {1664-3224},
mesh = {Humans ; *Janus Kinase 1/antagonists & inhibitors/metabolism ; *Inflammatory Bowel Diseases/drug therapy/immunology ; *Heterocyclic Compounds, 3-Ring/therapeutic use/pharmacology ; Animals ; *Janus Kinase Inhibitors/therapeutic use ; Signal Transduction/drug effects ; Cytokines/metabolism ; },
abstract = {Inflammatory bowel disease (IBD) management has moved from symptom control toward treat-to-target strategies, yet many patients with ulcerative colitis or Crohn's disease remain difficult to treat after primary non-response, secondary loss of response, or intolerance to advanced therapy. Upadacitinib, an oral Janus kinase 1 (JAK1)-preferential inhibitor, has shown clinically meaningful efficacy in both ulcerative colitis and Crohn's disease, including biologic-experienced populations. In this Perspective, we propose rapid immune recalibration as a hypothesis-generating clinical model for interpreting rapid inflammatory control following JAK1-preferential inhibition in selected patients with inflammation-dominant refractory IBD, rather than as an established biological mechanism or evidence of a durable immune reset. Recalibration is defined here as an early pharmacologically induced shift in the intensity and balance of convergent cytokine signaling, not as immune homeostasis restoration, mucosal healing, transmural repair, fibrosis reversal, or proven disease modification. We distinguish established clinical evidence from mechanistic rationale and from unvalidated downstream hypotheses, including barrier stabilization, microbiome change, anti-fibrotic potential, and biomarker-guided positioning. We also outline measurable clinical criteria, feasible biomarkers, exploratory translational endpoints, and safety boundaries that should guide future testing of this framework. This more bounded interpretation may help inform future efforts to move refractory IBD treatment from empirical drug switching toward mechanism-informed therapeutic choice without overstating the current evidence.},
}

Humans
*Janus Kinase 1/antagonists & inhibitors/metabolism
*Inflammatory Bowel Diseases/drug therapy/immunology
*Heterocyclic Compounds, 3-Ring/therapeutic use/pharmacology
Animals
*Janus Kinase Inhibitors/therapeutic use
Signal Transduction/drug effects
Cytokines/metabolism

@article {pmid42549306,
year = {2026},
author = {Zhang, G and Zhang, Y and Huang, S and McGrath, C and Yang, Y and Shan, Z},
title = {PBM's effects on plaque microbiome for periodontal-orthodontic patients during retention.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2693412},
pmid = {42549306},
issn = {2000-2297},
abstract = {OBJECTIVES: This pilot study aimed to determine whether adjunctive photobiomodulation (PBM) alters dental plaque microbiota and clinical parameters in periodontitis patients during orthodontic retention.

METHODS: Six stage IV, grade C periodontitis patients entering orthodontic retention were enrolled in this split-mouth study. One arch side received monthly PBM therapy (GaAlAs diode laser) for six months; the contralateral side received sham irradiation. Periodontal examinations were performed. Supragingival and subgingival plaque samples were evaluated at appliance removal (Ti), 6 months (Tii) and 12 months (Tiii) using 16S rRNA sequencing.

RESULTS: No significant differences were observed in periodontal clinical parameters between PBM and placebo sites at any time point (P > 0.05). Microbiome analysis showed similar alpha and beta diversity in supragingival and subgingival microbiota between the groups (P > 0.05). Exploratory genus-level differences were limited, with Treponema enriched in placebo supragingival plaque and Aggregatibacter in placebo subgingival plaque at Tii, while Catonella differed in time-pooled supragingival comparisons. No headline differential genera were detected at Ti and Tiii.

CONCLUSION: Adjunctive PBM did not significantly alter overall plaque microbial community structure or clinical periodontal parameters. However, a few periodontitis-associated genera showed nominal, exploratory differences. These hypothesis-generating signals warrant confirmation in adequately powered trials.},
}

@article {pmid42549413,
year = {2026},
author = {Feng, S and Si, X and Lu, C and Gao, Z and Wang, J and Yang, Q and Lu, S and Su, T and Yang, J and He, X and Wu, L},
title = {Washed microbiota transplantation improves clinical symptoms, gut microbiota, and metabolic profiles in autism spectrum disorder in a twin cohort.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1885281},
pmid = {42549413},
issn = {1664-302X},
abstract = {OBJECTIVE: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by impaired social communication, repetitive behaviors, and restricted interests. Dysregulation of the microbiota-gut-brain axis is closely associated with the pathogenesis of ASD. Washed microbiota transplantation (WMT) has emerged as a promising intervention for ASD, but existing cohort studies lack genetically identical controls, making it difficult to distinguish intervention-related changes from genetic and environmental confounding factors. This twin-paired controlled study adopted a study design that minimizes the influence of genetics and shared environment, to explore the associations of WMT with clinical symptoms, gut microbiota, and metabolic profiles in children with ASD.

METHODS: Three pairs of age- and environment-matched twins (one ASD-affected, one typically developing sibling) were enrolled. WMT was administered to the ASD participant in each pair. Fecal samples were collected at baseline and post-intervention. Gut microbiota and metabolic profiles were analyzed using metagenomic sequencing and targeted metabolomics, respectively. Clinical outcomes were evaluated using the Childhood Autism Rating Scale (CARS), Autism Behavior Checklist (ABC), Sleep Disturbance Scale for Children (SDSC), and Bristol Stool Form Scale (BSFS). Relevant observations were carried out to explore potential changing trends.

RESULTS: After WMT, CARS, ABC, SDSC, and BSFS exhibited small numerical directional shifts toward healthier values, but none reached statistical significance. Gut microbial structure and function presented a shifting trend toward the profile of their typically developing twin siblings. Abnormal lipid and energy metabolism indicators showed partial ameliorative trends, and the number of differential metabolites between ASD patients and healthy siblings was markedly reduced. Tyrosine and phenylalanine metabolic pathways, together with Segatella, Negativibacillus, and Sangeribacter, may be associated with incomplete phenotypic changes in this cohort.

LIMITATIONS: Although the twin-pair design has high internal validity and can provide strong causal inference evidence for the effect of microbiota transplantation in treating ASD, this study has limitations such as a small sample size, a single-center non-randomized observational design. All findings in this pilot study are merely descriptive trends, and the relevant mechanism analysis only provides correlational clues. A single session of microbiota transplantation failed to fully adjust aromatic amino acid metabolism in ASD children. No definitive causal relationship can be concluded based on the findings of this small-sample pilot study.

CONCLUSION: Under tightly controlled genetic and environmental conditions, gut microbial dysbiosis presents correlational characteristics with ASD-related phenotypes. WMT was associated with consistent remodeling of gut microbial ecology and partial resolution of metabolic dysregulation in ASD children, with multi-omic signatures converging toward healthy twins. Clinical rating scales only displayed non-significant minor numerical shifts, which cannot be interpreted as evidence of clinical symptom improvement. These initial findings provide exploratory mechanistic clues and phenotypic data supporting WMT as a targeted microbiome intervention approach for ASD, and await further validation through large-scale randomized controlled trials.

CLINICAL TRIAL REGISTRATION: Identifier ChiCTR2400091105.},
}

@article {pmid42549425,
year = {2026},
author = {Maynez-Perez, AO and Cahyo, HN and Niu, P and Aho, VTE and Pope, PB and Schwarm, A},
title = {Intricate microbiome differences observed in lactating cows across methane intensity phenotypes.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag155},
pmid = {42549425},
issn = {2730-6151},
abstract = {Methane emissions from ruminants can be expressed through several metrics as total production, yield, or intensity, each reflecting distinct aspects of energy utilisation. Among these, methane intensity defined as grams of methane emitted per kilograms of energy-corrected milk, directly links emissions to productive efficiency; however, the microbial mechanisms underlying variation in this trait remain unclear. Here, we applied genome-resolved metagenomics and metatranscriptomics to characterise rumen microbial identity, functional potential, and transcriptional activity in lactating cows differing in methane intensity while sharing breed and diet. Microbial community composition and diversity were comparable across phenotypes. However, rumen microbial gene expression revealed marked functional divergence. The rumen content of low-methane-intensity cows showed enriched transcription of fructan-degrading carbohydrate-active enzymes and butyrate-forming pathways, primarily encoded by RUG440 (Atopobiaceae) metagenome-assembled genomes. These functions suggest a fructan-butyrate metabolic axis supported by potential cross-feeding between primary degraders and butyrate producers. Conversely, the high-methane intensity rumen exhibited greater transcription of pectin-degrading carbohydrate-active enzymes, mainly carried by Prevotella metagenome-assembled genomes, suggesting methyl-ester hydrolysis and methanol release. Despite higher methanogenesis transcript levels in high-methane intensity cows, total methane production did not differ between groups. Together, these findings reveal two contrasting functional configurations of the rumen microbiome in Norwegian Red dairy cattle: a fructan-butyrate-oriented metabolism in low-methane-intensity cows and a pectin-methanol-oriented metabolism in high-methane-intensity counterparts. This study provides genome-resolved, multi-omic evidence that microbial carbohydrate specialization and fermentation routing contribute to methane intensity phenotypes in dairy cows, offering mechanistic insights for improving ruminant climate efficiency.},
}

@article {pmid42549467,
year = {2026},
author = {Tellez-Corral, MA and Barrientos-Sánchez, S and Ruiz-Gómez, JA and Rodrìguez-Ciodaro, A and Espriella, CM and Díez-Ortega, H},
title = {Gram-positive oral bacteria as reservoirs of transferable antimicrobial resistance genes in dentistry.},
journal = {Journal of conservative dentistry and endodontics},
volume = {29},
number = {7},
pages = {779-784},
pmid = {42549467},
issn = {2950-4708},
abstract = {BACKGROUND: The oral cavity is a complex microbial ecosystem that acts as a reservoir of antimicrobial resistance genes associated with antibiotics used in dental practice, particularly in Gram-positive bacteria.

AIMS: This study aimed to analyze antimicrobial resistance genes in oral isolates of Streptococcus, Staphylococcus, and Enterococcus.

MATERIALS AND METHODS: Two hundred and fifty isolates were analyzed. Microbiological identification and antimicrobial susceptibility tests were performed using MicroScan in accordance with the Clinical and Laboratory Standards Institute guidelines. Polymerase chain reaction was used to detect resistance genes; blaZ, erm, mef, msrA, lnu, and aac (6')-aph (2").

STATISTICAL ANALYSIS: Descriptive statistics were applied to assess phenotypic resistance, co[-]resistance and multidrug resistance (MDR). Gene co-occurrence patterns were evaluated using heatmap analysis in Python (Seaborn).

RESULTS: Resistance was primarily associated with blaZ (n = 70). Co-resistance occurred in 15 isolates, most commonly blaZ + aac (6')-aph (2") (4 cases). MDR occurred in 7 isolates, with mecA + mef + lnu + aac (6')-aph (2") as the most frequent pattern (n = 2). The co-occurrence of genes revealed recurrent associations between β-lactam, macrolide-lincosamide-streptogramin and aminoglycoside resistance determinants.

CONCLUSIONS: The oral cavity acts as a reservoir of transferable antimicrobial resistance genes in Gram-positive bacteria, with co-resistance and MDR patterns relevant to dental practice.},
}

@article {pmid42549478,
year = {2026},
author = {Armstrong, E and Pinto, R and Kulikova, M and Yee, NR and Rishu, A and Muscedere, J and Sibley, S and Maslove, DM and Boyd, JG and Evans, GA and Detsky, M and Marshall, JC and Taggart, LR and Friedrich, JO and Tsang, JLY and Duan, E and Ali, KF and McCullagh, D and Findlater, A and Daley, P and Ramendra, R and Lother, S and Lamontagne, F and Fowler, R and Daneman, N and Coburn, B},
title = {Association of anti-anaerobic antibiotics with mortality and the gut microbiome: a sub-study of the BALANCE randomized clinical trial.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciag460},
pmid = {42549478},
issn = {1537-6591},
abstract = {BACKGROUND: Patients with suspected bloodstream infection often receive broad-spectrum antibiotics with anaerobic activity in the absence of clinical indication for anaerobic coverage. Anti-anaerobic antibiotics have been linked to adverse clinical outcomes in other populations, potentially by depleting intestinal anaerobes.

METHODS: We conducted a planned sub-study of the multisite BALANCE randomized controlled trial of antibiotic duration for bloodstream infection to assess the impact of anti-anaerobic antibiotics (receipt from three days pre-index culture to seven days post-index) on mortality and gut microbiome composition with metagenomic sequencing in patients without clinical indication for anaerobic coverage who survived to seven days post-index culture. The primary exposure was receipt of anti-anaerobic antibiotics from three days prior to the index culture to seven days post-index culture.

RESULTS: Among the 2851 eligible patients included in our primary analysis, 2106 (74%) received anti-anaerobic antibiotics and 745 (26%) did not. After balancing measured potential confounders through inverse probability of treatment weighting, anti-anaerobic antibiotics were associated with higher 90-day mortality (OR = 1.41, 95% CI 1.03 to 1.92, p = 0.03) and depletion of gut anaerobe relative abundance (fixed effect estimate = -16.59, 95% CI -30.67 to -2.52, p = 0.02). Increased duration of anti-anaerobic antibiotics was associated with greater mortality risk and additional gut anaerobe depletion.

CONCLUSIONS: Anti-anaerobic antibiotics are associated with increased mortality and gut microbiome disruption in patients with bloodstream infection. Minimizing exposure to anti-anaerobic antibiotics for bloodstream infection should be further explored in clinical trials as a potential treatment strategy to improve patient outcomes.},
}

@article {pmid42549638,
year = {2026},
author = {Hsu, SH and Chua, HH and Liou, BY and Cheng, YY and Lin, CR and Chen, YH and Yang, TH and Wu, SH and Tsuei, DJ and Chen, HL and Chang, MH and Ni, YH and Chen, HL},
title = {Vancomycin enriches Parabacteroides goldsteinii in the gut and promotes reconstruction of the hepatobiliary system in cholestasis.},
journal = {The Journal of pathology},
volume = {},
number = {},
pages = {},
doi = {10.1002/path.70101},
pmid = {42549638},
issn = {1096-9896},
support = {109-2314-B-002-161-MY3//National Science and Technology Council, Taiwan/ ; 110-2634-F-002-044//Ministry of Education in Taiwan/ ; 111-2634-F-002-017//Ministry of Education in Taiwan/ ; },
abstract = {Impaired bile secretion disrupts the gut microbiome and perpetuates cholestatic liver injury. Vancomycin (VCM) has been shown to improve cholestasis in human patients, but its biological effects remain unclear. This study aimed to investigate the therapeutic effects of VCM on microbiome modulation and the restoration of liver function. VCM was administered in a modified Abcb11 knockout (KO) mice model with pre-existing cholestasis to examine its therapeutic effects and microbiome changes. After 2 weeks of treatment, VCM significantly decreased serum bilirubin while maintaining stable transaminase in the KO mice. Three-dimensional imaging of pan-CK expression by immunofluorescence revealed improvement of the disrupted biliary epithelium and interconnected bile duct network, as evidenced by increased coverage and cumulative duct length in the liver. Gene expression and hepatic bile acid profiling demonstrated that VCM enhanced canalicular/sinusoidal bile acid export while repressing bile acid synthesis, with a reduction in tauro-β-muricholic acid, the predominant bile acid in mice, in KO livers. Fecal microbial analysis using next-generation sequencing identified Parabacteroides goldsteinii (PG) as the predominant species after VCM treatment. KO mice fed PG demonstrated improved cholestasis, with significantly reduced direct bilirubin, alkaline phosphatase, total bile acids in serum, as well as fewer reactive ductules in the liver. In vitro culture of ductal organoids suggested that PG directly promoted the growth of cholangiocytes. RNA sequencing results suggested that PG suppressed pro-inflammatory Lyz1 (mouse orthologous gene of human LYZ) and Aqp4 and increased pro-proliferative Muc6 and Chrm3. This study highlights the therapeutic potential of VCM in cholestasis by enriching PG in the gut and improving biliary structures in the liver, identifying PG as a potential probiotic with beneficial effects in cholestasis. © 2026 The Pathological Society of Great Britain and Ireland.},
}

@article {pmid42549688,
year = {2026},
author = {Jia, Q and Wang, H and Yin, W and Zhang, C and Xu, X and Liang, S and Pan, W and Tang, B and Xiao, W and Liu, S and Lü, M},
title = {Sex differences in fecal microbiota transplantation for mitigating radiation-induced thrombocytopenia in mice: efficacy amplified by inulin.},
journal = {Platelets},
volume = {},
number = {},
pages = {2701022},
doi = {10.1080/09537104.2026.2701022},
pmid = {42549688},
issn = {1369-1635},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) shows potential in promoting hematopoiesis, with efficacy influenced by donor sex. However, its role in radiation-induced thrombocytopenia (RIT) and its sex-specific effects remain unclear. While inulin may enhance FMT efficacy, this has not been explored in the context of RIT.

METHODS: We established an irradiation-induced thrombocytopenia (RIT) model in male and female mice via 4 Gy X-rays exposure. FMT was administered orally as a fecal suspension. Platelet recovery was monitored via hematology analyzer, megakaryopoiesis was assessed by flow cytometry and H&E staining; gut microbiota changes were evaluated by 16S rRNA sequencing.

RESULTS: Sex-matched FMT accelerated platelet recovery and promoted megakaryocyte production in the bone marrow and spleen only in female mice, accompanied by an increase in Akkermansia abundance. Furthermore, transplanting feces from female donors also accelerated platelet recovery in irradiated male mice, whereas feces from male donors does not. INU selectively enriched probiotic colonization, thereby fostering a favorable microbial structure that enhanced FMT efficacy.

CONCLUSIONS: The sexually dimorphic gut microbiota contributes to sex-specific FMT efficacy in alleviating radiation-induced thrombocytopenia, which can be further amplified by inulin. This study offers sex-specific microbial therapy for radiation-induced thrombocytopenia and a prebiotic-based strategy to boost FMT efficacy.},
}

@article {pmid42549889,
year = {2026},
author = {Liu, J and Yue, H and Li, J and Fang, Z and Bi, T and Li, C and Yi, H and Zhao, Y and Feng, Y and Zhao, S and Hu, Y},
title = {Probiotic Clostridium butyricum CB-a alleviates intestinal inflammation through targeted modulation of the microbiome metabolome axis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0135126},
doi = {10.1128/spectrum.01351-26},
pmid = {42549889},
issn = {2165-0497},
abstract = {This study investigated the capacity of Clostridium butyricum CB-a, a novel environmental isolate with unique ecological adaptability, to restore host-microbiome homeostasis in a dextran sodium sulfate (DSS)-induced murine model of intestinal dysbiosis. Integrated 16S rRNA gene sequencing and untargeted LC-MS/MS metabolomics revealed that CB-a (1 × 10[8] CFU/mL, administered orally) fundamentally restructured the colonic microbial architecture. Specifically, it enriched beneficial, short-chain fatty acid (SCFA)-producing consortia (e.g., Lactobacillus, Bacteroides, and Alloprevotella) while suppressing opportunistic pathobionts (Escherichia-Shigella) and mitigating excessive mucin-degrading bacteria (Akkermansia). This ecological shift was accompanied by a pronounced metabolic reconfiguration, highlighted by the significant restoration of fecal SCFA pools, predominantly butyrate (P < 0.05). Mechanistically, multi-omics correlation potential that the CB-a-driven microbial remodeling alleviates mucosal inflammation through SCFA-linked host-microbe signaling. This pathway explicitly involves the upregulation of G-protein-coupled receptors (GPR41, GPR43, and GPR109A), the inhibition of histone deacetylases (HDAC1/2), and the subsequent reinforcement of epithelial tight junction proteins (ZO-1, Occludin). Furthermore, CB-a significantly attenuated systemic pro-inflammatory cytokine expression while restoring superoxide dismutase (SOD) antioxidant capacity. These findings provide mechanistic insights into how this specific environmental isolate modulates the intestinal microenvironment, offering a robust theoretical basis for deploying C. butyricum in functional interventions targeting microbiota-associated inflammatory disruptions.IMPORTANCESevere gut inflammation, such as inflammatory bowel disease, is often driven by a breakdown in our natural gut bacteria. Although probiotics are popular treatments, how they actually repair the gut remains largely unknown. Our study highlights the remarkable healing ability of Clostridium butyricum CB-a, a natural bacterium isolated from the environment. We discovered that this microbe acts as an ecological engineer for the digestive system. It actively rescues the damaged gut by promoting the growth of beneficial bacteria and suppressing harmful ones. This positive shift triggers the release of natural, healing molecules that calm the immune system and rebuild the protective gut lining. By uncovering the exact steps this bacterium takes to restore digestive harmony, our work provides a powerful blueprint for designing highly targeted, natural probiotic therapies to combat severe intestinal diseases.},
}

@article {pmid42549904,
year = {2026},
author = {Bywater, A and Seffrin, AN and Bisanz, JE and Di Gioia, F and Kovac, J},
title = {Soilless farming system design impacts the diversity and composition of microbiota.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0116726},
doi = {10.1128/aem.01167-26},
pmid = {42549904},
issn = {1098-5336},
abstract = {Controlled environment agriculture (CEA), including soilless farming systems, is expanding to improve food security and resource efficiency. However, little is known about how different soilless farming system designs influence microbial populations that may be relevant to plant health and food safety. This study investigated the effects of soilless system type on microbial load and bacterial community composition in nutrient solution and on bok choy leaves over two growing cycles. Soilless systems, including deep water culture (DWC), Kratky (KR), nutrient film technique (NFT), ebb and flow (EF), and drip irrigation (DI), were evaluated. Significant differences in aerobic plate count (APC) in nutrient solution were observed among system types, with the DI system exhibiting the highest counts across both cycles. Increased nutrient solution pH was negatively associated with APC, whereas temperature did not significantly affect microbial concentrations. APC on bok choy leaves at harvesting was not significantly different by system type. Bacterial community composition in nutrient solution significantly varied by system type, temperature, growing cycles, and sampling day. Microbial alpha diversity also varied significantly by system type. Core microbiota analysis identified Acidovorax, Legionella, and Caulobacter as both core and hub taxa, with Acidovorax being the only genus detected across all samples. These findings indicate that microbial dynamics differ among soilless system designs and across growing cycles, suggesting that factors not monitored in this study strongly influence microbial community composition. Furthermore, we identified core and hub bacterial genera warranting further investigation of their function in CEA and their impact on plant health and food safety.IMPORTANCEThis study demonstrated that microbial load and community composition in hydroponic production varied by soilless system type and between growing cycles. We found that system design had a significant effect on community composition. Furthermore, the community compositions differed between growing cycles, suggesting that factors not measured in this study significantly shaped the community structure. Drip irrigation systems exhibited higher microbial loads compared to other systems. Leaf-associated microbial load showed insignificant differences across systems and growing cycles, likely due to limited contact with nutrient solutions. Acidovorax was detected across all samples, warranting further investigation of its role in hydroponic systems.},
}

@article {pmid42549911,
year = {2026},
author = {Lai, W and Zhang, Y and Huang, S and Lai, S and Lin, F and Wang, Z and Sun, S and Yang, F},
title = {The FERM guild: a differentially correlated microbial module drives hypertension via metabolic flux perturbations.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0035826},
doi = {10.1128/msystems.00358-26},
pmid = {42549911},
issn = {2379-5077},
abstract = {UNLABELLED: Hypertension is a major risk factor for cardiovascular diseases, with changes in gut microbiota composition and function being closely associated with its onset and progression. However, the high inter-individual variability in gut microbiota complicates the identification of pathogenic mechanisms using traditional methods. In contrast, the smaller variability in gut microbial metabolites offers a more reliable and consistent basis for cross-individual comparisons. Parsimonious flux balance analysis (pFBA), integrated with double machine learning (DoubleML), identified 17 metabolites significantly associated with hypertension (P < 0.05, robustness value [RV] >0.1). These included meso-2,6-diaminoheptanedioate, p-hydroxyphenylacetic acid, cellobiose, dextran 40 (1,6-α-D-glucan), L-glutamic acid, and kestopentaose, among others. Differential microbial correlation network analysis identified a key microbial subnetwork, termed the FERM guild, consisting of 19 species, with prominent genera including Faecalibacterium, Enterobacter, Roseburia, and Methanobrevibacter. Using Gene Set Enrichment Analysis (GSEA), the dysregulation of this guild was found to be strongly associated with a set of 17 hypertension-related metabolites (P = 0.017). Further analysis revealed that the contribution of FERM genera to key metabolites is significantly associated with blood pressure (P < 0.05), even without significant differences in their abundance; additionally, an imbalance exists between FERM genera and other species. Our findings reveal that hypertension is associated with a disruption of gut microbial diversity, structure, and metabolic function. Seventeen key metabolites related to blood pressure regulation were identified, exhibiting pro- or anti-hypertensive potential and linked to functional microbial modules. These results highlight the gut microbiota and its metabolites as promising targets for therapeutic intervention in hypertension.

IMPORTANCE: Hypertension remains a major global public health burden; however, most studies on its relationship with the gut microbiota rely on traditional species-abundance analyses, which are limited by substantial inter-individual variability. In contrast, microbial metabolites show greater stability across individuals and thus offer a more reliable entry point for mechanistic research. By integrating metabolic modeling, causal inference, and network analysis, this study identified 17 key metabolites significantly associated with blood pressure and uncovered a functionally coordinated microbial community (FERM) whose contribution to critical metabolic fluxes (rather than its taxonomic abundance) was closely linked to hypertension. These findings reveal a metabolite-centered mechanism connecting microbial functions to host blood pressure regulation and provide new potential targets for microbiome-based interventions.},
}

@article {pmid42549995,
year = {2026},
author = {Bollinger, E and Feckler, A and Filker, S and Bourassi, H and Maccagnan, A and McArdell, CS and Bundschuh, M},
title = {Antiviral agent modulates freshwater methanogenesis at the nanotrace level.},
journal = {Environmental toxicology and chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1093/etojnl/vgag195},
pmid = {42549995},
issn = {1552-8618},
support = {//NanoKat/ ; //Rhineland-Palatinate/ ; },
abstract = {Antiviral drugs (ATVs), such as oseltamivir carboxylate (OTC), are widely used to treat viral infections. Although environmental levels are in the ng/L to µg/L range, knowledge on risks posed by this substance class is hindered by limited assessments. Evidence on effects on microbially-driven ecosystem processes is especially scarce, which is concerning because viruses are omnipresent in the microbiome and likely to influence microbial functioning. We assessed the influence of OTC on anaerobic methane production, a greenhouse gas largely emitted from natural systems and responsible for around one third of greenhouse gas-driven warming, as a proxy for microbial ecosystem function. Oseltamivir carboxylate inhibited initial methanogenesis between 15% and 40% even at nanotrace levels (i.e., 0.006-600 µg/L). Given that in most treatments methane levels returned to those of the control, the initial inhibition is potentially attributed to a temporally limited OTC-induced shift from a neutral/temperate viral infection of prokaryotes toward a lytic viral replication. Mostly unaffected 16S rRNA metabarcoding community data indicate that this effect might be uniform throughout the community. This study points to ecosystem-level effects at the ng/L range of ATVs, suggesting a significant knowledge gap, which warrants further attention to this group of chemicals.},
}

@article {pmid42550055,
year = {2026},
author = {Xu, X and Zhou, M and Zhang, R and Liu, W and Liu, M and He, J and Wen, Y and Zhou, Y and Fang, H and Lu, L and Wang, X and Li, D and Qin, G and Li, D and Liu, F and Sun, H and He, F},
title = {Combined administration of fructooligosaccharides and Clostridium butyricum attenuates bowel cleansing-induced dysbiosis and safeguards mucosal defense in a murine model.},
journal = {Clinical science (London, England : 1979)},
volume = {},
number = {},
pages = {},
doi = {10.1042/CS20261277},
pmid = {42550055},
issn = {1470-8736},
abstract = {Bowel preparation with polyethylene glycol electrolyte solution (PEG-ELS) is indispensable for gastrointestinal endoscopy and related procedures. However, it disrupts gut microbial homeostasis and increases host vulnerability to ensuing infection. In a murine model, we optimized a synbiotic intervention consisting of fructooligosaccharides (FOS) and Clostridium butyricum (C. butyricum) to improve post-cleansing microbiome resilience and mucosal defense. We evaluated its efficacy and longitudinally monitored the dynamics of gut microbiota in response to bowel cleaning and concurrent bacterial challenge infection. Our data show that the bowel preparation induced a persistent microbial perturbation, resulting in an incomplete spontaneous recovery 15 days after the procedure. A 12-day symbiotic intervention significantly enriched alpha diversity and restored the dysbiosis induced by the cleaning. The intervention also increased Firmicutes/Bacteroidota ratio and the abundance of several key beneficial bacteria in the genera Lactobacillus, Mucispirillum, and Butyricicoccus. Under infectious stress, bowel cleansing markedly aggravated colitis phenotypes, while the intervention alleviated crypt hyperplasia and attenuated inflammatory injury in mice infected with Citrobacter rodentium, resulting in a significant improvement in several colitis indicators. The synbiotic was accompanied by enhanced IL-12/IFN-γ-related antimicrobial responses, increased expression of Muc2 and sIgA, and reshaped bacterial interaction networks disrupted by challenge infection. Our findings demonstrate that the combined administration of FOS and C. butyricum promotes gut microbial homeostasis and host defense. This approach may provide insights into potential dietary strategies for mitigating bowel cleansing-induced microbial disturbances.},
}

@article {pmid42550158,
year = {2026},
author = {Fan, X and Zhou, C and Zhang, P and Ming, Y},
title = {Effects of Different Living Environments on Intestinal Flora in Patients With Schistosoma Japonicum-Induced Liver Fibrosis.},
journal = {MicrobiologyOpen},
volume = {15},
number = {4},
pages = {e70366},
doi = {10.1002/mbo3.70366},
pmid = {42550158},
issn = {2045-8827},
support = {81771722//National Natural Science Foundation of China/ ; 2021SK2032//Key Research and Development Plan of Hunan Province/ ; },
mesh = {Humans ; *Schistosomiasis japonica/complications/microbiology ; *Liver Cirrhosis/parasitology/microbiology/etiology ; Animals ; *Schistosoma japonicum ; RNA, Ribosomal, 16S/genetics ; *Gastrointestinal Microbiome ; China ; Feces/microbiology ; Female ; *Bacteria/classification/genetics/isolation & purification ; Male ; Sequence Analysis, DNA ; Adult ; DNA, Bacterial/genetics/chemistry ; DNA, Ribosomal/genetics/chemistry ; Middle Aged ; },
abstract = {Schistosomiasis japonica is a parasitic disease leading to liver cirrhosis. China's "fishermen going ashore" policy divides patients with schistosomiasis liver fibrosis into two groups: those near the infected waters and those inland far from the infected water. This study aims to compare the differences in intestinal flora between two groups from the perspective of intestinal flora, and provide a basis for future prevention and control priorities. This study collected feces and basic information of patients with Schistosoma japonicum cirrhosis living near infected water and living on land. The characteristics of intestinal flora of the two types of patients were compared by 16sRNA sequencing technology. The infected water contact group and the terrestrial living group showed significant differences in intestinal flora characteristics: the former showed dominance of Firmicutes, high α-diversity, enrichment of butyrate-producing bacteria (such as Blautia), and enhanced environmental adaptability; the latter showed an imbalanced state with increased Proteobacteria and reduced α-diversity, accompanied by abnormal lipid metabolism and barrier function damage.},
}

Humans
*Schistosomiasis japonica/complications/microbiology
*Liver Cirrhosis/parasitology/microbiology/etiology
Animals
*Schistosoma japonicum
RNA, Ribosomal, 16S/genetics
*Gastrointestinal Microbiome
China
Feces/microbiology
Female
*Bacteria/classification/genetics/isolation & purification
Male
Sequence Analysis, DNA
Adult
DNA, Bacterial/genetics/chemistry
DNA, Ribosomal/genetics/chemistry
Middle Aged

@article {pmid42550351,
year = {2026},
author = {Wu, J and Ye, X and Hua, W and Yao, Y and Sun, L and Ma, H and Yu, C and Cheng, Y and Mi, S},
title = {The microbiome-mitochondria axis: the context-dependent role of urolithin A in aging and cancer via mitophagy.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42550351},
issn = {1573-4978},
mesh = {Humans ; *Mitophagy ; *Coumarins/metabolism/pharmacology ; *Neoplasms/metabolism/pathology/microbiology ; *Aging/metabolism ; *Mitochondria/metabolism ; Animals ; *Gastrointestinal Microbiome/physiology ; Signal Transduction ; Microbiota ; },
abstract = {Urolithin A (UA) is a gut microbiota-derived metabolite formed from dietary ellagitannins and ellagic acid. It has drawn sustained interest because it can influence mitochondrial quality control, but the evidence does not support a simple anti-aging or anticancer label. In this review, UA is examined across microbial metabolism, urolithin metabotypes, pharmacokinetic exposure, mitophagy biology, aging-related phenotypes, and cancer. The emphasis is placed on what has been shown, what remains model-dependent, and where translational claims are still premature. Preclinical work links UA to PINK1/Parkin-, TFEB-, AMPK-, sirtuin-, and Nrf2-associated pathways, with reported improvements in mitochondrial turnover and inflammatory signaling. Human data are narrower: most trials have been short and have focused on safety, muscle performance, mitochondrial signatures, and circulating biomarkers. Evidence for cancer prevention or cancer therapy still comes mainly from cell and animal studies. Because mitophagy can limit early mitochondrial damage but may also help established tumors survive hypoxia, nutrient restriction, dormancy, and therapy-induced stress, UA is better regarded as a microbiome-dependent mitochondrial modulator whose effects depend on biological setting. The next step is to define direct molecular targets, test native and conjugated UA at human-relevant exposure ranges, account for UM-A, UM-B, and UM-0 metabotypes, and evaluate cancer-specific endpoints before making therapeutic claims.},
}

Humans
*Mitophagy
*Coumarins/metabolism/pharmacology
*Neoplasms/metabolism/pathology/microbiology
*Aging/metabolism
*Mitochondria/metabolism
Animals
*Gastrointestinal Microbiome/physiology
Signal Transduction
Microbiota

@article {pmid42550428,
year = {2026},
author = {Nami, S and Abbasi, A and Aghebati-Maleki, A and HosseinYari, A and Aghebati-Maleki, L},
title = {Postbiotics: a promising tool in personalized medicine approach for the inflammatory disorders.},
journal = {Molecular and cellular biochemistry},
volume = {},
number = {},
pages = {},
pmid = {42550428},
issn = {1573-4919},
abstract = {Epidemiological studies indicate that modern lifestyle choices are closely linked to the global rise in chronic inflammatory diseases. While considerable research has explored the role of the microbiome in inflammation, a definitive causal relationship has yet to be established. Intestinal epithelial cells (IECs) play a critical role in maintaining a protective barrier that prevents the translocation of harmful molecules and pathogens. Any disruption or compromise to the integrity of these cells can impair this barrier function, facilitating the entry of potentially harmful substances and microorganisms, which subsequently triggers acute inflammatory responses. Microbial dysbiosis is one of the most prominent outcomes of inflammation in the gut, and various therapeutic strategies are currently under investigation to address this imbalance. Among these, probiotics have demonstrated potential in modulating immune and inflammatory responses by altering the composition of the gut microbiota. However, findings from preclinical and clinical studies suggest that probiotics may interfere with the re-establishment of native microbial communities and, in some vulnerable individuals, may even aggravate inflammation. In contrast, postbiotics bioactive compounds produced during the fermentation process by probiotics are emerging as a promising and safer alternative. Increasing scientific evidence supports their beneficial biological effects. In this review, we aim to discuss the most recent findings regarding the anti-inflammatory and immunomodulatory properties of postbiotics, with particular emphasis on key parental probiotic strains.},
}

@article {pmid42550453,
year = {2026},
author = {Li, S and Zhang, Y and Li, Y and Lei, Y and Wu, H and Liu, P and Xi, W and Zhuo, X and Huang, P and Yang, T and Bai, T and Li, J and Cheng, L and Wang, Y and Li, T and Wu, Y},
title = {The maternal gut microbiota influences myocardial maturation and diastolic function of offspring in mice.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {42550453},
issn = {1869-1889},
abstract = {Although the maternal microbiome is recognized as a critical regulator of offspring physiology, its role in heart development and the pathogenesis of heart failure remains largely unclear. Using a germ-free (GF) mouse model, we demonstrated that maternal microbiota depletion leads to spontaneous heart failure with preserved ejection fraction (HFpEF) in adult female offspring, recapitulating the phenotypes of human diastolic dysfunction. Integrated transcriptomic and proteomic profiling of fetal hearts revealed impaired structural cardiomyocyte maturation in GF offspring, characterized by suppressed sarcomere assembly. Metabolomic analysis revealed that acetate was concurrently downregulated in maternal serum and fetal cardiomyocytes. Importantly, prenatal acetate supplementation and fecal microbiota transplantation rescued fetal cardiomyocyte maturation defects and prevented the onset of HFpEF in adult female offspring. Mechanistically, maternal microbe-derived acetate regulates fetal cardiomyocyte maturation by enhancing the levels of H3K9ac and H3K27ac in the MYL2 promoter region, thereby promoting the transcriptional enhancement of MYL2. This developmental reprogramming provides lifelong protection against diastolic dysfunction. In addition, the concentration of acetate in pregnant women's serum was positively correlated with myocardial thickness in the left ventricle of the fetus. Our findings establish maternal microbial metabolites as determinants of cardiac maturation and suggest prenatal acetate supplementation as a novel preventive intervention for developmental diastolic dysfunction.},
}

@article {pmid42550469,
year = {2026},
author = {Chen, Z and Liu, Y and Shi, T and Sun, H and Hu, W and Wei, G and Chen, C},
title = {Surface Charge Dependent Foliar Applied Silicon Quantum Dots Enhance Soybean Salt Tolerance Through Leaf-Root-Microbial Responses.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70787},
pmid = {42550469},
issn = {1365-3040},
support = {2023YFD1900900//National Key Research and Development Program of China/ ; 42277118//National Natural Science Foundation of China/ ; "111Center," B23036//Overseas Expertise Introduction Project for Discipline Innovation on Soil Microbiome & Soil Health in Arid Regions/ ; },
abstract = {Here, we evaluated foliar-applied silicon quantum dots (SiQDs) with different surface charges on soybean salt tolerance. Positively charged SiQDs (P-SiQDs) exhibited stronger foliar retention and penetration than negatively charged SiQDs (N-SiQDs), resulting in a 35.3% higher silicon accumulation in leaves. Under 200 mM NaCl stress, foliar application of P-SiQDs increased shoot dry weight and reduced the Na[+]/K[+] ratio. Compared with N-SiQDs, P-SiQDs more effectively alleviated salt-induced damage to thylakoid ultrastructure and improved photosynthetic performance. A life cycle field pot trial further showed that SiQDs increased the 100-seed weight by 20.1%-25.9% under salt stress. Leaf metabolomics showed significant alterations in lipid metabolite pathways associated with redox homeostasis, accompanied by shifts in the phyllosphere microbiome. P-SiQDs increased the abundance of Chloroflexota, Actinomycetota, and genera such as Paenarthrobacter, Variovorax, and Xanthobacter. Meanwhile, the phyllosphere microbiome shifted toward life-history strategies related to growth, resource acquisition, and salt stress tolerance. In addition, P-SiQDs promoted root growth, nodulation, and nitrogenase activity, leghemoglobin content, and total nitrogen accumulation, together with changes in root exudate composition and the enrichment of salt-tolerant rhizosphere bacteria, including Sphingomonas and Novosphingobium. These findings indicate that surface charge modification is an effective strategy to enhance the efficiency of foliar nano-fertilizer application.},
}

@article {pmid42550502,
year = {2026},
author = {Mukhopadhyay, B},
title = {Nitro- and nitrooxy-organic inhibitors of methanogenesis: revealing knowledge gaps and alternate ways in bovine rumen microbiome metabolism.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0244225},
doi = {10.1128/aem.02442-25},
pmid = {42550502},
issn = {1098-5336},
abstract = {In the rumen, methanogens consume H2, generating methane and thermodynamically facilitating the production of short-chain fatty acids (SCFAs), ruminants' main energy source. Yet in animal trials, inhibiting methanogenesis by 27%-90% with 3-nitrooxypropanol minimally perturbs ruminal SCFA levels, sparing disproportionately low amount of H2. An Applied and Environmental Microbiology article (A. Castaneda, N. Indugu, K. Challa, K. Narayan, et al., Appl Environ Microbiol e01033-25, 2025, https://journals.asm.org/doi/10.1128/aem.01033-25) reports similar outcomes in an in vitro rumen experiment where ethyl-nitroacetate and ethyl-2-nitropropionate inhibited methanogenesis 100%. Hence, the rumen has fallback ways, perhaps evolved through exposures to plant metabolites. The nitroorganics offer an opportunity to determine the consequences of 100% inhibition of ruminal methanogenesis in live animals.},
}

@article {pmid42550534,
year = {2026},
author = {Celik, G and Yanik, E and Inan, N and Yalinay, AM},
title = {Absence of a Consistent Gut or Oral Microbial Signature in Fibromyalgia Under Strictly Controlled Clinical Conditions: A Multi-Compartment 16S rRNA Analysis.},
journal = {Pain physician},
volume = {29},
number = {5},
pages = {E407-E416},
pmid = {42550534},
issn = {2150-1149},
mesh = {Humans ; Female ; *Fibromyalgia/microbiology ; *RNA, Ribosomal, 16S/genetics ; Case-Control Studies ; Adult ; *Mouth/microbiology ; Middle Aged ; Prospective Studies ; *Microbiota ; *Gastrointestinal Microbiome/genetics ; Feces/microbiology ; },
abstract = {BACKGROUND: Fibromyalgia (FM) has been increasingly studied in the context of gut-brain-immune interactions, and several reports have suggested an association between FM and alterations in gut or oral microbial communities. However, prior studies have often suffered from heterogeneous comorbidities, inconsistent sampling procedures, and limited control for environmental factors, making it unclear whether FM is associated with a reproducible, site-independent microbial signature.

OBJECTIVES: To determine whether women with FM exhibit consistent alterations in gut or oral microbiota when evaluated under strictly standardized physiological, clinical, and environmental conditions.

STUDY DESIGN: A prospective, observational, case-control study.

SETTING: The Department of Pain Medicine and Department of Medical Microbiology at Gazi University, Türkiye.

METHODS: The patient selection comprised 31 women (16 with FM; 15 healthy controls) who met rigorous inclusion and exclusion criteria, minimizing confounding from diet, metabolic disease, medications, hormonal status, and recent infections. No therapeutic intervention was performed; all patients provided paired oral mucosal and fecal samples during the follicular phase of the menstrual cycle. Sequencing of 16S rRNA V3-V4was performed on DNA extracted from all samples. Alpha and beta diversity metrics, taxonomic profiles, and differential abundance analyses (including LEfSe with FDR correction) were compared between groups. The clinical severity of FM was assessed using scores on the visual analog scale (VAS), Widespread Pain Index (WPI), and Symptom Severity Scale (SSS).

RESULTS: No statistically significant differences were observed between FM patients and controls in fecal or oral alpha diversity (Shannon, Simpson, Chao1, Observed OTU indices, all P > 0.05). Beta diversity analyses (Bray-Curtis PERMANOVA) revealed no between-group separation in either compartment (fecal R² = 0.032, P = 0.529; oral R² = 0.032, P = 0.464). Both groups displayed preserved core microbial communities in the gut, dominated by Firmicutes and Bacteroidota and, in the oral cavity, Streptococcus-enriched profiles. Minor genus-level variations were detected, but none remained significant after FDR correction. Cross-site analyses confirmed the expected ecological divergence between oral and fecal habitats but identified no FM-specific microbial pattern. Post hoc sensitivity analysis indicated that the study was powered to detect only moderate effect sizes (R² ≥ 0.11), suggesting that subtle differences might have remained undetected.

LIMITATIONS: A modest sample size, a lack of quantitative dietary assessment, and reliance on 16S rRNA sequencing limited the detection of subtle or functional microbial alterations. Additionally, the cross-sectional design precludes causal inference.

CONCLUSIONS: Under highly controlled sampling and exclusion conditions, FM was not associated with detectable alterations in the diversity or composition of gut or oral microbes. These findings suggest that previously reported dysbiosis may reflect comorbidity-driven or phenotype-specific variation rather than a universal microbial hallmark. Larger, multi-omic and phenotype-stratified studies are needed to clarify functional host-microbiome interactions in FM.},
}

Humans
Female
*Fibromyalgia/microbiology
*RNA, Ribosomal, 16S/genetics
Case-Control Studies
Adult
*Mouth/microbiology
Middle Aged
Prospective Studies
*Microbiota
*Gastrointestinal Microbiome/genetics
Feces/microbiology

@article {pmid42550818,
year = {2026},
author = {Bari, S},
title = {The microbiome in kidney cancer.},
journal = {Clinical advances in hematology & oncology : H&O},
volume = {24},
number = {5},
pages = {328-331},
pmid = {42550818},
issn = {1543-0790},
}

@article {pmid42550883,
year = {2026},
author = {Hern, KE and Phillips, AM and Mageeney, CM and Williams, KP and Sinha, A and Carlson, HK and Poorey, K and Collette, NM and Branda, SS and Arkin, AP},
title = {Niche exclusion of a lung pathogen in mice with designed probiotic communities.},
journal = {eLife},
volume = {14},
number = {},
pages = {},
doi = {10.7554/eLife.108304},
pmid = {42550883},
issn = {2050-084X},
support = {DE-NA0003525//U.S. Department of Energy's National Nuclear Security Administration, Sandia National Laboratories/ ; DE-AC52-07NA27344//U.S. Department of Energy's National Nuclear Security Administration, Lawrence Livermore National Laboratory/ ; },
mesh = {Animals ; *Probiotics/administration & dosage ; Mice ; *Microbiota ; *Burkholderia/physiology ; *Lung/microbiology ; *Burkholderia Infections/prevention & control/microbiology ; },
abstract = {For years, the airway microbiota have been theorized to be gatekeepers of respiratory health, as pathogens entering the airway make contact with resident microbes prior to or coincident with their interaction with host cells. Thus, modification of the native airway community may serve as a means of altering the local environment in favor of health. In this work, we hypothesize that synthetic bacterial communities introduced into the airway can serve as prophylactic countermeasures against infection by Burkholderia thailandensis in mice. We demonstrate that understanding of antagonistic interactions between a pathogen and airway microbiota in vitro can guide identification of probiotics with protective capabilities in vivo. Specifically, we show that niche overlap between the probiotic and pathogen is indicative of probiotic performance in vivo. This work serves as a foundation for the rational design of probiotic communities for protection against and treatment of respiratory infections.},
}

Animals
*Probiotics/administration & dosage
Mice
*Microbiota
*Burkholderia/physiology
*Lung/microbiology
*Burkholderia Infections/prevention & control/microbiology

@article {pmid42551103,
year = {2026},
author = {Esener, N and Kırbaş, M and Kal, Y and Aladağ, F},
title = {Microbial signatures of the vaginal microbiome associated with pregnancy outcome in central Anatolian Merino sheep.},
journal = {Theriogenology},
volume = {265},
number = {},
pages = {118119},
doi = {10.1016/j.theriogenology.2026.118119},
pmid = {42551103},
issn = {1879-3231},
abstract = {Reproductive efficiency is a key determinant of sustainability and profitability in sheep farming systems; however, the role of the vaginal microbiome in shaping pregnancy outcomes remains insufficiently understood. This study aimed to characterise the vaginal microbial communities of Central Anatolian Merino sheep using 16S rRNA gene amplicon sequencing and to explore their potential association with reproductive success. Vaginal samples were collected from 20 healthy ewes (10 non-pregnant (G1), that failed to conceive and returned to oestrus and 10 pregnant (G2), conceived at first service) with comparable physiological characteristics before breeding, followed by high-throughput amplicon sequencing to comprehensively profile the bacterial community structure. Comparative analyses were conducted between pregnant and non-pregnant animals to identify microbial patterns linked to pregnancy outcomes. The vaginal microbiome exhibited a diverse yet structured taxonomic composition across both groups, dominated by members of Bacillota (44.8% in G1 and 45.6% in G2), Actinomycetota (12.0% in G1 and 9.3% in G2), Pseudomonadota (6.6% in G1 and 6.2% in G2) and Bacteroidota (5.6% in G1 and 5.9% in G2). Alpha diversity did not differ significantly between groups (Wilcoxon rank-sum test, p > 0.05 across all indices), and beta diversity showed no significant separation (PERMANOVA, R[2] = 0.055, p = 0.38), indicating substantial community overlap. Differential abundance analysis (edgeR) identified 23 taxa that differed between groups (FDR < 0.05), suggesting that reproductive outcomes may be influenced by subtle ecological shifts rather than large-scale microbial restructuring. Collectively, these findings provide novel insights into the vaginal microbial ecology of Central Anatolian Merino sheep and identify candidate microbial signatures that may warrant further investigation as potential correlates of fertility. Given the observational design and limited sample size, these associations should be interpreted as preliminary and hypothesis-generating. By advancing our understanding of host-microbiome interactions within the reproductive tract, this study establishes a foundation for microbiome-informed strategies aimed at improving reproductive performance and supporting sustainable sheep production.},
}

@article {pmid42551220,
year = {2026},
author = {Horvath, M and Imitola, J},
title = {How the microbiome shapes epigenetic trained memory in neuroinflammation: Implications for neurodegenerative diseases.},
journal = {Journal of neuroimmunology},
volume = {420},
number = {},
pages = {579049},
doi = {10.1016/j.jneuroim.2026.579049},
pmid = {42551220},
issn = {1872-8421},
abstract = {Neurodegenerative diseases are increasingly recognized as disorders involving immune dysregulation. However, the mechanisms underlying this dysfunction remain poorly characterized. Trained immunity has recently emerged as a potential contributor to immune dysregulation, particularly in neuroinflammation and neurodegenerative diseases, where trained immunity is the epigenetic reprogramming of innate immune responses following an initial inflammatory stimulus, which increases responses to subsequent exposures. In parallel, although the brain has traditionally been viewed as an immune-privileged organ, growing evidence indicates that peripheral immune activity exerts significant influence on neuroinflammation in the brain. A major driver of peripheral immunity is the microbiome. Therefore, this perspective aims to present a conceptual framework for a relationship between the microbiome, trained immunity, and neurodegenerative diseases. We first summarize evidence of trained immunity in the brain and its role in neurodegeneration. Next, we highlight the role of the microbiome in peripheral immune modulation and in trained immunity. Finally, we propose potential mechanisms through which the microbiome may induce or modulate trained immunity in the brain. These include: 1) immunogenic microbial metabolites that cross the blood-brain barrier and alter host cell epigenetics; 2) migration of peripherally trained myeloid cells into the brain; 3) viral infection-induced trained immunity that may predispose to neurodegeneration. Together, this perspective suggests that microbiome-induced trained immunity offers a novel mechanism linking peripheral immune regulation with neuroinflammation and neurodegeneration with implications for therapeutic targeting of epigenetic modification as a molecular prevention strategy for progression of neurodegeneration.},
}

@article {pmid42551232,
year = {2026},
author = {Liu, S and Lu, T and Wang, X and Li, J and Dong, H and Liu, W},
title = {Stachyose alleviates alcohol liver injury in mice associated with modulation of TGF-β signaling pathway and gut microbiota.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158656},
doi = {10.1016/j.phymed.2026.158656},
pmid = {42551232},
issn = {1618-095X},
abstract = {BACKGROUND: Alcoholic liver disease (ALD) is a widespread chronic disease that seriously affects physical and mental health. Stachyose (STA), a dietary supplement, has been demonstrated to be a potential active oligosaccharide for alleviating ALD, while its mechanism has not been fully revealed.

PURPOSE: This study aims to explore the effects of STA on ALD and its underlying mechanism.

METHODS: The efficacy of STA on ALD was evaluated using an ALD mouse model. The changes in the lipid profile were investigated through lipidomics. The potential mechanism was explored using transcriptomics, and the expression of key pathways was validated by Western blotting. The impact of STA on gut microbiota and SCFAs was analyzed. Finally, the fecal microbiota transplantation method was used to verify the importance of gut microbiota in the treatment of ALD with STA.

RESULTS: Our findings illustrated that STA alleviated liver injury, as evidenced by decreased levels of ALT and AST. Liver lipidomics analysis showed that STA down-regulated the levels of TG, PC, PI, PS, and DG. STA also restored the dynamic balance of the inflammatory response and oxidative stress. Mechanistically, STA treatment was predominantly associated with inhibiting the activation of the TGF-β signaling pathway in the liver. Furthermore, STA restored the intestinal homeostasis by increasing the abundance of Faecalibaculum and Muribaculum as well as decreasing the abundance of Butyricimonas, Clostridium, and Parabacteroides. Interestingly, administration of an STA-derived microbiome could also alleviate ALD.

CONCLUSION: These findings identify STA as a key bioactive ingredient capable of improving ALD, and emphasize the gut microbiota-dependent mechanism underlying its therapeutic effects.},
}

@article {pmid42551547,
year = {2026},
author = {Yang, R and He, K and Yang, Y and Teng, L},
title = {Microbial influence on tryptophan metabolism in tumors:Mechanisms and potential clinical applications.},
journal = {Biochimica et biophysica acta. Molecular basis of disease},
volume = {},
number = {},
pages = {168395},
doi = {10.1016/j.bbadis.2026.168395},
pmid = {42551547},
issn = {1879-260X},
abstract = {Tryptophan (Trp) metabolism represents a major biochemical interface between the gut microbiota, host immunity, and tumor biology. Trp is metabolized through three interconnected routes: the kynurenine (Kyn) pathway, mainly regulated by indoleamine 2,3-dioxygenase 1 (IDO1) and tryptophan 2,3-dioxygenase 2 (TDO2); the serotonin/5-hydroxytryptamine (5-HT) pathway; and the microbial indole derivative pathway. These metabolites regulate tumor development through multiple mechanisms, including aryl hydrocarbon receptor (AhR) activation, epithelial barrier modulation, immune checkpoint regulation, tumor-associated macrophage polarization, cytotoxic T-cell dysfunction, and treatment response. Importantly, Trp metabolites may exert either tumor-promoting or tumor-suppressive effects depending on microbial composition, metabolite concentration, receptor usage, immune contexture, tumor type, and therapeutic setting. In this review, we summarize recent advances in host- and microbiota-derived Trp metabolism, discuss mechanistic differences between Kyn-AhR and indole-AhR signaling, and critically evaluate therapeutic strategies targeting IDO1/TDO2, microbial metabolites, probiotics, diet, chemotherapy, and immune checkpoint blockade. We also highlight unresolved issues, including causality in microbiome studies, gut versus intratumoral microbiota, biomarker-guided patient selection, and the context-dependent nature of AhR signaling. Collectively, these findings support the concept that tryptophan metabolism functions as a context-dependent host-microbiota co-regulated network, and that its precise modulation may provide novel opportunities for biomarker-guided and mechanism-based cancer therapy.},
}

@article {pmid42551623,
year = {2026},
author = {Shahid, M and Raj, A and Shafi, Z and Ali, S},
title = {Nanopesticides-rhizo-microbiome interactions: Biochemical mechanisms, ecotoxicological effects and implications for pesticide fate and transformation.},
journal = {Comparative biochemistry and physiology. Toxicology & pharmacology : CBP},
volume = {},
number = {},
pages = {110651},
doi = {10.1016/j.cbpc.2026.110651},
pmid = {42551623},
issn = {1532-0456},
abstract = {Nano-enabled pesticides (NanoPs) formulations have emerged as promising alternative to conventional pesticides by improving ingredient stability, delivery, and controlled release. However, their unique physicochemical properties also influence interactions with soil microorganisms, raising concerns regarding ecological safety and long-term impacts on soil ecosystem functions. This review has critically synthesized the current knowledge about NanoPs-microbiome interactions with a focus on biochemical mechanisms underlying microbial responses and implications for pesticide fate and transformation. We review how the properties of NPs (e.g., particle size, surface charge, coatings, dissolution, and eco-corona formation) influence mobility, bioavailability, and microbial exposure. Mechanistic evidence of oxidative stress, membrane damage, enzyme inhibition, metal-ion-mediated toxicity and quorum sensing interference is critically synthesized to elucidate biochemical basis of NanoPs-induced microbial responses. Recent advances in high throughput sequencing and multi-omics technologies are also used to assess changes in microbial diversity, community composition, functional redundancy, microbial interaction networks and ecosystem resilience. The review further compares conventional and nano-formulated pesticides, highlighting differences in microbial toxicity, degradation kinetics, transformation pathways, and metabolite profiles. Current challenges associated with environmental fate assessment, standardized ecotoxicological testing, and microbiome-informed risk evaluation are critically discussed. Emerging opportunities for integrating metagenomics, artificial intelligence, and predictive modelling into environmental risk assessment are also highlighted. Finally, we propose a future research framework centered on microbiome-informed safe-by-design NanoPs, standardized testing protocols, and long-term field validation to support development of environmentally responsible nano-enabled crop protection technologies while preserving soil biodiversity and ecosystem functions.},
}

@article {pmid42543003,
year = {2026},
author = {Kim, M and Del Duca, E and Correa Da Rosa, J and Pulsinelli, J and Estrada, Y and Xu, D and Chan, G and Chen, A and Güler, E and Page, K and Guttman-Yassky, E},
title = {Effect of Abrocitinib on the Skin Microbiome in Patients With Moderate-to-Severe Atopic Dermatitis.},
journal = {Allergy},
volume = {},
number = {},
pages = {},
doi = {10.1111/all.70467},
pmid = {42543003},
issn = {1398-9995},
support = {//Pfizer/ ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) is characterized by microbial dysbiosis, notably an overabundance of Staphylococcus species. This study aimed to evaluate the effects of abrocitinib, a Janus kinase 1-selective inhibitor, on the skin microbiome and clinical outcomes in patients with moderate-to-severe AD.

METHODS: Patients enrolled in JADE MOA (NCT03915496) were randomly assigned to receive once-daily abrocitinib (100 or 200 mg) or placebo for 12 weeks. Skin swabs collected at baseline and Weeks 2, 4, and 12 underwent 16S rRNA gene amplicon sequencing to determine microbial composition. Disease severity was assessed at the same time points using established clinical metrics. Associations between microbial abundance and clinical metrics, as well as inflammatory and skin barrier markers, were investigated.

RESULTS: Data from 43 patients were included. Alpha diversity increased significantly at Week 12 of treatment with abrocitinib 200 mg. Beta diversity analysis revealed clustering of the abrocitinib groups away from placebo as early as Week 2; divergence continued through Week 12. Staphylococcus and S. aureus relative abundance decreased in a dose-dependent manner from Week 2 through Week 12 of abrocitinib treatment. Changes in skin microbial composition corresponded with improvements in clinical metrics of disease severity as well as immune markers of AD.

CONCLUSIONS: Abrocitinib treatment is associated with beneficial changes in the skin microbiome, notably a reduction in S. aureus and increased microbial diversity. These findings provide insight into the mechanism of action of abrocitinib and the interplay of immunomodulation and the skin microbiome in AD.

TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT03915496.},
}

@article {pmid42543158,
year = {2026},
author = {Jiao, Y and Li, L and Ji, X and Cheng, H},
title = {The Role of Gut Microbiota Interventions in the Management of Frailty Syndrome: A Scoping Review and Bibliometric Analysis.},
journal = {Geriatrics & gerontology international},
volume = {26},
number = {8},
pages = {e70734},
doi = {10.1111/ggi.70734},
pmid = {42543158},
issn = {1447-0594},
support = {82301786//National Natural Science Foundation of China (Youth Science Fund Project)/ ; },
mesh = {Humans ; *Frailty/therapy ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; Bibliometrics ; Probiotics/therapeutic use ; Prebiotics ; Frail Elderly ; Aged ; },
abstract = {AIM: The primary aim of this scoping review is to synthesize fragmented evidence on gut microbiota-targeted interventions for frailty. As a complementary objective, we conducted a bibliometric analysis to map the evolving knowledge landscape of this interdisciplinary field, thereby informing the development of future personalized therapeutic strategies and research priorities.

METHODS: We searched nine databases (PubMed, Embase, Web of Science, Scopus, Cochrane Library, CNKI, Wanfang, SinoMed, and VIP) from inception to July 2025 for the scoping review. A dedicated search of the Web of Science Core Collection (up to September 2025) was conducted for the bibliometric analysis to ensure data consistency. Two reviewers independently screened and extracted data. Bibliometric analyses (collaboration networks, keyword co-occurrence, and research trends) and visualizations were performed using CiteSpace (v6.3.R1).

RESULTS: The scoping review screened 3216 records and included 10 studies. Interventions-probiotics, prebiotics, synbiotics, and fecal microbiota transplantation-lasted 4 weeks to 6 months. Frailty was mainly assessed using Fried's phenotype, with outcomes covering frailty severity, physical function, gut microbiota composition, and inflammatory/metabolic markers. Bibliometric analysis identified 358 publications, revealing a sharp rise after 2016. China produced the most studies, and the University of Parma was the top institution. Key themes included gut microbiota, frailty, aging, inflammation, and sarcopenia.

CONCLUSIONS: Given the rapidly growing interest, gut microbiota-targeted interventions represent a promising strategy to slow frailty progression. Future efforts should therefore focus on establishing standardized, multidisciplinary assessment frameworks and elucidating the underlying mechanisms to advance precision nutrition for healthy aging.},
}

Humans
*Frailty/therapy
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
Bibliometrics
Probiotics/therapeutic use
Prebiotics
Frail Elderly
Aged

@article {pmid42543182,
year = {2026},
author = {Liu, Q and Chen, X and Liu, X and Liu, L and Chen, C and Li, L and Liang, W and Xu, P and Pu, J},
title = {Rhizosphere microbiome differentiation and soil environmental drivers in two Monotropastrum species.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {64},
number = {7},
pages = {e2602009},
doi = {10.71150/jm.2602009},
pmid = {42543182},
issn = {1976-3794},
support = {2024-XK-06//Zhejiang Key Discipline in Traditional Chinese Medicine for Pharmaceutical Botony/ ; KJTYSZX2025//Zhejiang Provincial Department of Science and Technology Research Institute Support Program/ ; },
mesh = {*Rhizosphere ; *Soil Microbiology ; *Bacteria/classification/genetics/isolation & purification ; *Fungi/classification/genetics/isolation & purification ; *Soil/chemistry ; *Microbiota ; China ; Phylogeny ; High-Throughput Nucleotide Sequencing ; Hydrogen-Ion Concentration ; },
abstract = {This study compared the rhizosphere microbial communities of two closely related Monotropastrum species (M. humile, Mh; and M. humile var. glaberrima, Mhg) and identified key soil factors associated with their assembly. Bacterial and fungal communities were profiled by Illumina high-throughput sequencing, and soil physicochemical properties were assessed across multiple sites in Zhejiang Province, China. The bacterial communities of both species were dominated by Proteobacteria and Acidobacteriota at the phylum level, while the dominant fungal groups belonged to Ascomycota and Basidiomycota. The two plants shared several dominant bacterial genera, including Serratia, Burkholderia-Caballeronia-Paraburkholderia, and Bradyrhizobium, as well as common dominant fungal genera such as Saitozyma and Podila. Despite these similarities, species-specific enrichment patterns were observed. The rhizosphere of Mhg contained higher abundances of Acidothermus and Lactarius, whereas Mh preferentially enriched Cedecea, Klebsiella, and Russula. Bacterial communities were shaped by pH, soil organic matter (SOM), available potassium (AK), and available phosphorus (AP), whereas fungal communities were primarily influenced by pH, alkali-hydrolyzable nitrogen (AN), and SOM (p < 0.05). These results suggest that both host identity and soil properties contribute to rhizosphere microbial assembly, with clear host-associated differentiation in microbial communities. Notably, the identified host-associated microbial taxa, particularly key mycorrhizal fungi, may serve as potential microbial inoculants, providing new opportunities for the conservation and cultivation of mycoheterotrophic plants.},
}

*Rhizosphere
*Soil Microbiology
*Bacteria/classification/genetics/isolation & purification
*Fungi/classification/genetics/isolation & purification
*Soil/chemistry
*Microbiota
China
Phylogeny
High-Throughput Nucleotide Sequencing
Hydrogen-Ion Concentration

@article {pmid42543263,
year = {2026},
author = {Han, XJ and Jiao, TQ and Gao, CX and Li, DF and Li, XY and Niu, Y},
title = {[Effect of Maxing Kugan Decoction on intestinal flora in bleomycin-induced idiopathic pulmonary fibrosis rats].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {51},
number = {11},
pages = {3017-3027},
doi = {10.19540/j.cnki.cjcmm.20260126.401},
pmid = {42543263},
issn = {1001-5302},
mesh = {Animals ; Male ; *Drugs, Chinese Herbal/administration & dosage ; Rats ; Rats, Sprague-Dawley ; Bleomycin/adverse effects ; *Gastrointestinal Microbiome/drug effects ; *Idiopathic Pulmonary Fibrosis/drug therapy/chemically induced/microbiology/genetics/metabolism ; Humans ; Occludin/genetics/metabolism ; Zonula Occludens-1 Protein/genetics/metabolism ; Interleukin-6/genetics/metabolism ; Interleukin-1beta/genetics ; Lung/drug effects/pathology ; Tumor Necrosis Factor-alpha/genetics/metabolism ; Disease Models, Animal ; },
abstract = {Based on the "lung-gut axis" theory, this study explored the effects of Maxing Kugan Decoction(Mxd) on inflammation and intestinal barrier and flora in rats with bleomycin-induced idiopathic pulmonary fibrosis(IPF). A total of 24 male SD rats were randomly divided into four groups: a control group, a model group, a positive control group and an Mxd treatment group, with 6 rats in each group. After 5 days of quarantine and adaptive feeding, the IPF pathological model was induced by intratracheal instillation of bleomycin under laryngoscopic assistance in the model group, positive control group, and Mxd treatment group. Gastric gavage was initiated after successful modeling, and all SD rats were sacrificed on the 15th day post gavage. HE staining and Masson staining were used to observe histopathological changes of lung tissue, while HE staining was adopted to evaluate jejunal pathological changes. Enzyme-linked immunosorbent assay(ELISA) was performed to detect the serum levels of interleukin-1β(IL-1β), interleukin-6(IL-6), and tumor necrosis factor-α(TNF-α) in rats. AB-PAS staining was employed to determine the number of goblet cells in jejunal mucosal tissue. Immunofluorescence assay was used to detect the expression of zonula occludens-1(ZO-1) and occludin in rat jejunum, and 16S rDNA sequencing was conducted to analyze the intestinal microbiome of all rats. The results showed that the model group exhibited severe damage to jejunal mucosa and lung tissue accompanied by massive inflammatory cell infiltration, while the two treatment groups demonstrated partial structural defects with a small amount of inflammatory cell infiltration in the lungs and jejuna of rats. Compared with the control group, the model group showed significantly decreased body weight, number of goblet cells, and expression of ZO-1 and occludin proteins(P<0.01), while these indicators were notably increased after intervention in the two treatment groups(P<0.05 or P<0.01). According to 16S rDNA sequencing results, Mxd could regulate the richness and diversity of intestinal flora in rats. KEGG pathway analysis indicated that Mxd regulated pathways such as oxidative phosphorylation, amino sugar, and nucleotide sugar metabolism of intestinal flora in rats. In conclusion, the alteration of intestinal microbiome may be one of the potential mechanisms underlying the therapeutic effect of Mxd on IPF. Mxd can regulate the structure of intestinal microbiome, increase the abundance of beneficial bacteria, and reduce the number of harmful bacteria, as well as protect intestinal barrier and inhibit inflammatory response.},
}

Animals
Male
*Drugs, Chinese Herbal/administration & dosage
Rats
Rats, Sprague-Dawley
Bleomycin/adverse effects
*Gastrointestinal Microbiome/drug effects
*Idiopathic Pulmonary Fibrosis/drug therapy/chemically induced/microbiology/genetics/metabolism
Humans
Occludin/genetics/metabolism
Zonula Occludens-1 Protein/genetics/metabolism
Interleukin-6/genetics/metabolism
Interleukin-1beta/genetics
Lung/drug effects/pathology
Tumor Necrosis Factor-alpha/genetics/metabolism
Disease Models, Animal

@article {pmid42543311,
year = {2026},
author = {Lin, YS and Ma, RZ and Jiang, TY and Zhu, HM and Ni, H and Wang, Y and Zhang, G and Li, JY and Shi, JL},
title = {[Mechanism of Tianma Gouteng Yin in treating early-stage Parkinson's disease based on 16S rRNA sequencing and metabolomics].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {51},
number = {12},
pages = {3522-3531},
doi = {10.19540/j.cnki.cjcmm.20260312.701},
pmid = {42543311},
issn = {1001-5302},
mesh = {Animals ; Rats ; Male ; RNA, Ribosomal, 16S/genetics ; Metabolomics ; *Drugs, Chinese Herbal/administration & dosage ; *Parkinson Disease/drug therapy/metabolism/genetics/microbiology ; Rats, Sprague-Dawley ; Humans ; Gastrointestinal Microbiome/drug effects ; Disease Models, Animal ; alpha-Synuclein/metabolism/genetics ; Tyrosine 3-Monooxygenase/metabolism/genetics ; Bacteria/genetics/classification/isolation & purification ; },
abstract = {Based on an early-stage Parkinson's disease(PD) rat model, this study employed 16S rRNA sequencing and untargeted metabolomics to investigate the action mechanism of Tianma Gouteng Yin(TGY) in treating early-stage PD. The early-stage PD rat models were established by subcutaneous injection of rotenone for seven days and were randomly divided into a control group, a model group, a positive drug group(levodopa, 50 mg·kg~(-1)), and TGY groups with low, medium, and high doses(9.82, 19.64, and 39.28 g·kg~(-1)), with intragastric administration for seven days during modeling. Behavioral indicators of rats(open field, inclined plane, and pole tests) were determined. The pathological morphology of brain tissue and the expressions of tyrosine hydroxylase(TH) and α-synuclein(α-syn) were detected. The levels of neurotransmitters including dopamine(DA), 5-hydroxytryptamine(5-HT), 3,4-dihydroxyphenylacetic acid(DOPAC), levodopa, and homovanillic acid(HVA) were measured. The inflammatory factors including tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), and interleukin-1β(IL-1β) were detected. 16S rRNA sequencing and untargeted metabolomics were conducted on colonic contents to explore the pharmacodynamic effects of TGY and its regulatory mechanisms on gut microbiota and metabolism. RESULTS:: show that TGY can significantly improve motor dysfunction in early-stage PD rats, increase the number of TH-positive cells, inhibit the abnormal aggregation of α-synuclein(α-syn), up-regulate the levels of neurotransmitters, reduce the levels of inflammatory factors in the colon and striatum, thereby exerting a neuroprotective effect. Gut microbiota analysis reveals that TGY can reverse the trends of reduced α-diversity of gut microbiota, increased Firmicutes/Bacteroidetes(F/B) ratio, and increased abundance of pro-inflammatory genera(e.g., Ruminococcus), restore the abundance of beneficial genera(e.g., Bacteroides), and reshape the gut microbiota structure. Metabolomic analysis demonstrates that TGY intervention significantly reverses the differential metabolites in the model group, mainly involving energy and amino acid metabolic pathways such as pyruvate metabolism, β-alanine metabolism, and aminoacyl-tRNA biosynthesis. In conclusion, TGY may exert therapeutic effects on early-stage PD by regulating the axis of microbiota, inflammation, and neuronal injury, with energy and amino acid metabolism as the hub, through these metabolic pathways.},
}

Animals
Rats
Male
RNA, Ribosomal, 16S/genetics
Metabolomics
*Drugs, Chinese Herbal/administration & dosage
*Parkinson Disease/drug therapy/metabolism/genetics/microbiology
Rats, Sprague-Dawley
Humans
Gastrointestinal Microbiome/drug effects
Disease Models, Animal
alpha-Synuclein/metabolism/genetics
Tyrosine 3-Monooxygenase/metabolism/genetics
Bacteria/genetics/classification/isolation & purification

@article {pmid42543381,
year = {2026},
author = {Cheng, X and Xu, M and Wei, J and Cao, C},
title = {Cancer drug response and resistance: molecular mechanisms and combating strategies.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {42543381},
issn = {2059-3635},
support = {2025AFB580//Natural Science Foundation of Hubei Province (Hubei Provincial Natural Science Foundation)/ ; 82573812//National Natural Science Foundation of China (National Science Foundation of China)/ ; 2023YFC2705802//National Key Laboratory of Science and Technology on Communications/ ; },
mesh = {Humans ; *Drug Resistance, Neoplasm/genetics ; *Neoplasms/drug therapy/genetics/pathology ; Animals ; *Antineoplastic Agents/therapeutic use ; },
abstract = {Despite remarkable advances in cancer drug treatment, including chemotherapy, targeted therapy, and immunotherapy, therapeutic resistance remains a formidable clinical barrier, limiting durable responses and long-term survival. Drug resistance can be broadly categorized as intrinsic, where tumors fail to respond to initial treatment, or acquired, which emerges during or after therapy due to adaptive or evolutionary processes. A comprehensive understanding of the multifactorial and dynamic nature of resistance is essential for improving treatment efficacy. In this review, we systematically examine the molecular and cellular determinants of drug response and resistance across 22 cancer types, highlighting key resistance mechanisms such as compensatory pathway activation, phenotypic plasticity, immune evasion, enhanced DNA damage repair, and the survival of drug-tolerant persister cells. These mechanisms are further contextualized across major therapeutic modalities, supported by clinical trials. We also present emerging strategies to overcome resistance, including rational drug combinations, novel agents, microbiome modulation, adaptive and intermittent therapies and advanced drug delivery systems, each illustrated with representative clinical studies. Moreover, we discuss cutting-edge tools that are revolutionizing resistance research, including single-cell and spatial multiomic profiling, patient-derived tumor organoid and xenograft (PDO/PDX) models, and artificial intelligence (AI)-powered predictive analytics. By integrating insights across molecular, cellular, and clinical dimensions, this review offers a strategic framework for understanding and tackling cancer drug resistance, with important translational implications for the future of precision oncology.},
}

Humans
*Drug Resistance, Neoplasm/genetics
*Neoplasms/drug therapy/genetics/pathology
Animals
*Antineoplastic Agents/therapeutic use

@article {pmid42543494,
year = {2026},
author = {Yin, X and Ramirez, L and Lampei, C and Azarbad, H and Greif, D and Martiné, E and Liu, C and Kong, F and Ang, LP and Herrmann, S and Opgenoorth, L and Bader, MY},
title = {Bacterial communities on upper and lower leaf surfaces show distinct seasonal response patterns.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71483},
pmid = {42543494},
issn = {1469-8137},
support = {507084794, grant OP 219-20-1//the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) through Research Unit 5571 "PhytOakmeter"/ ; LOEWE/2/15/519/03/08.001(0002)/88//LOEWE research initiative of the State of Hesse/ ; },
abstract = {Leaf surfaces represent one of the largest microbial habitats on Earth, which can be divided into upper and lower leaf surfaces. Upper and lower leaf surfaces offer contrasting microenvironments that vary through the seasons. This variation has rarely been quantified; however, in spite of it being highly relevant for leaf-microbiome contributions to terrestrial ecosystems, especially forests. To address this gap, we tracked bacterial communities on both surfaces of the same pooled leaves of Quercus robur in situ from spring to autumn, using genetically identical ramets to control host and genotypic variation. We combined 16S rRNA sequencing with analyses of leaf structural and physiological traits to link bacterial taxonomic, phylogenetic, and assembly characteristics. The two surfaces hosted distinct bacterial communities whose divergence intensified through the growing season. Upper-surface bacterial diversity remained relatively stable and was mainly associated with dynamic leaf traits, whereas lower-surface communities showed faster compositional and assembly-related shifts and were associated with both dynamic and stable leaf traits. These contrasting seasonal patterns reveal that within-leaf heterogeneity represents a fundamental axis of variation for bacterial seasonal dynamics, providing new insight into how microhabitat structure and host traits jointly shape phyllosphere functioning.},
}

@article {pmid42543502,
year = {2026},
author = {Guo, Q and Chen, X and Duan, J and Korpelainen, H and Li, C},
title = {Sexual dimorphism in root exudation mediates belowground neighbor recognition and shapes rhizosphere soil microbial assembly.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71486},
pmid = {42543502},
issn = {1469-8137},
support = {2025SZRJJ0048//Hangzhou Normal University/ ; 0022112//Zhejiang University/ ; },
abstract = {Sexual dimorphism in physiological traits is a hallmark of dioecious plants, yet whether these differences extend belowground to mediate neighbor recognition and rhizosphere microbiome assembly remains largely unexplored. Using split-root experiments, [13]C-pulse labeling, and multi-omics with dioecious Populus cathayana, we dissected the interactions between plant sex, root exudation, and microbiome assembly. We demonstrated that male and female plants discriminate neighbor sex by modulating their root exudation. Females perceiving same-sex neighbors upregulated defense-related metabolites, whereas under inter-sexual interactions they shifted toward growth-promoting pathways. Males significantly increased the allocation of newly fixed photosynthetic carbon to the rhizosphere. Specifically, [13]C incorporation into bacterial and fungal phospholipid fatty acids (PLFAs) was markedly higher when males grew in female-conditioned soil compared to male-conditioned soil. This male-driven carbon investment fostered highly interconnected cross-kingdom microbial networks with a significantly higher proportion of positive associations. Consistently, females grown under inter-sexual interactions exhibited greater nitrogen contents and higher photosynthetic rates than those under intra-sexual interactions. Our findings demonstrated that sexual dimorphism in root exudation drives the assembly of more complex and positively connected microbial networks, providing a transformative framework for understanding how belowground sexual recognition enhances the ecological resilience and productivity of mixed-sex plant populations.},
}

@article {pmid42543553,
year = {2026},
author = {Azhar, AA and Zahanuddin, A and Ya'cob, Z and Lau, YL and Mokhtar, AS},
title = {16S rRNA profiling of bacterial communities in the brown dog tick Rhipicephalus linnaei from stray dogs in Perak, Malaysia.},
journal = {Tropical biomedicine},
volume = {43},
number = {2},
pages = {191-197},
doi = {10.47665/tb.43.2.008},
pmid = {42543553},
issn = {2521-9855},
mesh = {Animals ; Malaysia ; *RNA, Ribosomal, 16S/genetics ; Dogs/parasitology ; *Rhipicephalus/microbiology ; Female ; *Bacteria/classification/genetics/isolation & purification ; Male ; DNA, Bacterial/genetics/chemistry ; *Microbiota ; Phylogeny ; *Tick Infestations/veterinary/parasitology ; Sequence Analysis, DNA ; },
abstract = {Rhipicephalus linnaei is a widespread tick species infesting dogs and capable of transmitting pathogens of veterinary and zoonotic concern. However, its associated bacterial communities remain poorly described in Malaysia. This study profiles the bacterial microbiome of R. linnaei collected from stray dogs in Kampar, Perak, using 16S rRNA gene amplicon sequencing targeting the V3-V4 region. A total of 360 ticks were collected from 13 dogs, of which 290 were pooled according to life stages and sex for microbial profiling. Shannon diversity indices indicated the mixed adult/nymph pool exhibited the highest richness and evenness (H'=5.4), whereas engorged adult females displayed the lowest diversity (H'=2.35), dominated by Gammaproteobacteria. Principal coordinate analysis revealed distinct microbial assemblages among pools, explaining 72% of total variance. Among 137 detected genera, Coxiella (0.6-34%), Staphylococcus (0.4-29%), Stenotrophomonas (0.3-5%), and Streptococcus (0.02-6%) were consistently found across all pools. Low-abundance but clinically relevant genera, including Ehrlichia (0.64%) and Nocardia (< 0.01%), were detected in adult males. The consistent presence of Coxiella-like endosymbionts across all stages suggests a likely symbiotic role in nutrient provisioning and reproduction. To our knowledge, this is the first 16S rRNA gene-based profiling of the bacterial communities associated with R. linnaei collected from stray dogs in Malaysia. This study highlights variation across pooled tick categories and contributes to improved understanding of tick-borne pathogen ecology within a One Health framework.},
}

Animals
Malaysia
*RNA, Ribosomal, 16S/genetics
Dogs/parasitology
*Rhipicephalus/microbiology
Female
*Bacteria/classification/genetics/isolation & purification
Male
DNA, Bacterial/genetics/chemistry
*Microbiota
Phylogeny
*Tick Infestations/veterinary/parasitology
Sequence Analysis, DNA

@article {pmid42543745,
year = {2026},
author = {Min, BR and Genovese, G and Spagnuolo, D and Hilaire, M and Ismael, H and Chaudhary, S and Pitta, DW and Indugu, N},
title = {The Potential Role of Two Red Macroalgae (Asparagopsis taxiformis and A. armata) That Promote Anti-Methanogenic Activities in Laboratory Conditions.},
journal = {Animal science journal = Nihon chikusan Gakkaiho},
volume = {97},
number = {1},
pages = {e70225},
doi = {10.1111/asj.70225},
pmid = {42543745},
issn = {1740-0929},
support = {//Cooperative Extension Program for Agricultural Environmental Sciences, Tuskegee University, Tuskegee, AL/ ; ALX-SRS22//USDA National Institute of Food and Agriculture, McIntire-Stennis (M-S) program/ ; NR233A750004G103//USDA/NRCS Climate-Smart Commodities funding/ ; },
mesh = {*Methane/metabolism ; Animals ; *Fermentation ; *Rumen/microbiology/metabolism ; *Rhodophyta ; *Seaweed ; Nitrous Oxide/metabolism ; *Dietary Supplements ; Microbiota ; },
abstract = {The objectives of this study were to evaluate the effects of two red macroalgae species (RMS; Asparagopsis taxiformis and A. armata) on rumen fermentation profiles, greenhouse gas (GHG) emissions, microbiome changes, and anti-methanogenic activities. The two RMSs were included at dietary levels of 0%, 2%, and 4% (as-fed basis) in an in vitro experiment with triplicate incubations (n = 3). Gases were collected using an ANKOM Gas Production system and analyzed for methane (CH4) and nitrous oxide (N2O) via gas chromatography. The RMS supplementation increased total gas, lactate, butyrate, valerate, hexanoate, heptanoate, 4-ethylphenol production, and AGR (non-glucogenic [acetate + butyrate]/glucogenic [propionate]) ratio (p < 0.01), while reducing production of CH4 (mg/g DM), acetate, propionate, iso-butyrate, phenylpropionate, phenylacetate, and acetate/propionate (A/P) ratios (p < 0.01), and in vitro dry matter digestibility (IVDMD; % DM) (p < 0.01) as RMS supplementation increased. With both algal species present, there were decreases in Actinobacteria, Firmicutes (p < 0.001), Firmicutes/Bacteroidetes ratio (F/B), and Methanobrevibacter sp. (p < 0.01), but increases in Spirochetes, Proteobacteria (methanotrophs; p < 0.001), Candidatus methanomethylophilus alvus (CMC), and non-methanogenic archaea Thermoplasma sp. (p < 0.001) at 2% and 4% DM. Therefore, it may be possible to suppress methanogenesis both directly and indirectly by adding RMS.},
}

*Methane/metabolism
Animals
*Fermentation
*Rumen/microbiology/metabolism
*Rhodophyta
*Seaweed
Nitrous Oxide/metabolism
*Dietary Supplements
Microbiota

@article {pmid42543801,
year = {2026},
author = {Sadowska, K and Hart, K},
title = {Gut Microbiome and ADHD: A Narrative Review of Clinical Evidence and Practice Implications.},
journal = {Journal of human nutrition and dietetics : the official journal of the British Dietetic Association},
volume = {39},
number = {4},
pages = {e70327},
doi = {10.1111/jhn.70327},
pmid = {42543801},
issn = {1365-277X},
mesh = {Humans ; *Attention Deficit Disorder with Hyperactivity/microbiology/therapy ; *Probiotics/therapeutic use ; *Gastrointestinal Microbiome/physiology ; Child ; Randomized Controlled Trials as Topic ; Adult ; },
abstract = {OBJECTIVE: This narrative review evaluates the current evidence on the efficacy of probiotic interventions for Attention Deficit Hyperactivity Disorder (ADHD) symptoms in both medicated and drug-naïve paediatric and adult populations and assesses the implications for clinical dietetic practice.

DESIGN: A narrative review synthesizing randomized controlled trials and observational microbiome studies in paediatric and adult populations, specifically distinguishing between probiotic monotherapy and adjunctive protocols.

RESULTS: Observational data confirm gut microbiome alterations in ADHD populations, although specific bacterial signatures vary across studies. Evidence from treatment trials demonstrates that the efficacy of probiotics as monotherapy for core ADHD symptoms remains inconclusive. However, specific adjunctive trials combining probiotics with conventional medication have reported preliminary positive findings on symptom reduction, though results remain heterogeneous. Adult evidence is sparse but indicates potential benefits for emotional dysregulation in specific contexts.

CONCLUSIONS: This review concludes that current data do not support universal probiotic supplementation or routine clinical recommendation. However, when families inquire about complementary approaches, the existing literature enables evidence informed guidance within a shared decision-making framework that acknowledges the preliminary nature of current findings and sets realistic expectations.},
}

Humans
*Attention Deficit Disorder with Hyperactivity/microbiology/therapy
*Probiotics/therapeutic use
*Gastrointestinal Microbiome/physiology
Child
Randomized Controlled Trials as Topic
Adult

@article {pmid42544021,
year = {2026},
author = {Fan, Y and Guo, X and Lyu, J and Wang, X and Xu, F and Yan, J and He, Y},
title = {Hepatotoxicity in the Era of Precision Medicine: Toxicological Mechanisms and Management of Immune and Cell Therapy-Induced Liver Injury.},
journal = {Medicinal research reviews},
volume = {},
number = {},
pages = {},
doi = {10.1002/med.70093},
pmid = {42544021},
issn = {1098-1128},
support = {82474179//National Natural Science Foundation of China/ ; 2024A1515011705//Guangdong Basic and Applied Basic Research Foundation/ ; 2023A1515110677//Guangdong Basic and Applied Basic Research Foundation/ ; JCYJ20240813113552066//Foundation of Shenzhen Science and Technology Innovation Commission/ ; HUUF-MS-202301//Hospital University United Fund of The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen/ ; },
abstract = {Immune checkpoint inhibitors and adoptive cell therapies have revolutionized cancer treatment, yet their success is accompanied by immune-related hepatotoxicity that can range from asymptomatic enzyme elevation to life-threatening liver failure. Unlike conventional drug-induced liver injury, immune-mediated hepatotoxicity arises from complex, therapy-specific mechanisms that remain incompletely understood, creating critical knowledge gaps in risk prediction and prevention. This review incorporates current evidence on the clinical presentation, mechanistic pathways, and risk factors underlying hepatotoxicity across major immune and cell therapy platforms, with emphasis on translating mechanistic insights into actionable management strategies. We systematically examine hepatotoxicity patterns for immune checkpoint inhibitors, CAR-T cell therapies, bispecific T-cell engagers, and tumor-infiltrating lymphocyte therapy, integrating clinical trial data, real-world evidence, and mechanistic studies. Our analysis shows distinct injury mechanisms: T-cell-mediated hepatocyte destruction following checkpoint blockade, cytokine-driven bystander injury during cytokine release syndrome, and emerging on-target/off-tumor toxicity from engineered lymphocytes. Critical risk modifiers include pre-existing liver disease, concomitant hepatotoxic medications, gut microbiome dysbiosis from antibiotic exposure, and host pharmacogenomic variation. We propose three priority research directions: development of predictive biomarkers enabling pretreatment risk stratification, microbiome-directed interventions to preserve hepatic immune tolerance, and implementation of Safety-by-Design engineering strategies that integrate hepatotoxicity prevention into therapeutic design. This review provides a mechanistic framework for transitioning from reactive toxicity management to predictive, personalized prevention, essential for maximizing the therapeutic potential of immune and cell therapies while protecting patient safety in this rapidly expanding treatment landscape.},
}

@article {pmid42544154,
year = {2026},
author = {Li, Y and Wang, J and Zhang, N and Xu, X and Dai, X and Li, Y and Cheng, L and Liu, H and Ren, P and Ma, H},
title = {Causal Relationship Between Gut Microbiome and Infectious Mononucleosis: Bidirectional Mendelian Randomization Reveals Infectious Mononucleosis-Driven Gut Dysbiosis.},
journal = {Cureus},
volume = {18},
number = {7},
pages = {e111983},
pmid = {42544154},
issn = {2168-8184},
abstract = {Background To assess bidirectionality between gut microbiota and Epstein-Barr virus (EBV)-driven infectious mononucleosis (IM), we conducted two-sample Mendelian randomization (MR). Given IM's heterogeneous symptoms and evidence linking microbiota to viral infection, this may inform novel prevention or treatment strategies. Methods We employed a bidirectional two-sample MR framework using summary data from 207 gut microbial taxa and 205 metabolic pathways (Dutch Microbiome Project, n = 7,738) and the FinnGen consortium. Causality was assessed via inverse variance weighting (IVW), MR-Egger, weighted median, and mode-based estimation. Statistical significance was set at P <0.05 (Bonferroni-corrected), with instruments validated by F-statistics >10. Heterogeneity and pleiotropy were evaluated using Cochran's Q, MR-Egger intercepts, and leave-one-out analyses. Results Forward MR: Several bacterial pathways and taxa were positively associated with IM risk. These include the de novo purine nucleotide biosynthesis II superpathway (odds ratio (OR) = 1.246, 95% confidence interval (CI): 1.026-1.514, P = 0.027), anhydromuropeptide recycling (OR = 1.24, 95% CI: 1.014-1.517, P = 0.036), the superpathway of unsaturated fatty acid biosynthesis (Escherichia coli) (OR = 1.194, 95% CI: 1.019-1.4, P = 0.028), Lactobacillaceae (OR = 1.109, 95% CI: 1.02-1.206, P = 0.016), and Lactobacillus (OR = 1.108, 95% CI: 1.017-1.207, P = 0.019). Conversely, several taxa and pathways exhibited protective effects. These include the glucose-1-phosphate degradation pathway (G1P-DP) (OR = 0.852, 95% CI: 0.731-0.994, P = 0.042), heme biosynthesis from glutamate (OR = 0.809, 95% CI: 0.676-0.969, P = 0.032), the superpathway of L-tyrosine biosynthesis (OR = 0.9, 95% CI: 0.811-0.998, P = 0.046), the flavin biosynthesis I pathway (OR = 0.817, 95% CI: 0.672-0.993, P = 0.042), Streptococcaceae (OR = 0.869, 95% CI: 0.779-0.968, P = 0.011), and Streptococcus (OR = 0.844, 95% CI: 0.731-0.937, P = 0.020). Reverse MR: IM was found to causally alter gut microbiome composition. IM was associated with a decrease of beneficial genera such as Roseburia (OR = 0.901, 95% CI: 0.837-0.982, P = 0.016) and Bacteroides ovatus (OR = 0.915, 95% CI: 0.841-0.995, P = 0.038), as well as Streptococcus (OR = 0.876, 95% CI: 0.775-0.991, P = 0.035). Conversely, IM increased the risk of enrichment for Prevotellaceae (OR = 1.107, 95% CI: 1.016-1.210, P = 0.020) and Prevotella copri (OR = 1.096, 95% CI: 1.000-1.200, P = 0.048). Regarding metabolic pathways, IM increased the risk of polyamine biosynthesis II (OR = 1.123, 95% CI: 1.016-1.243, P = 0.024), L-lysine biosynthesis II (OR = 1.094, 95% CI: 1.008-1.118, P = 0.031), and L-lysine biosynthesis VI (OR = 1.083, 95% CI: 1.000-1.172, P = 0.048), while showing a protective association with L-rhamnose degradation I (OR = 0.922, 95% CI: 0.851-0.999, P = 0.046). Conclusion This study provides genetic evidence of a bidirectional causal relationship between the gut microbiome and IM. These findings suggest that IM may influence gut microbial ecosystem structure, characterized by a reduction in beneficial symbionts (e.g., Roseburia) and an enrichment of potentially pro-inflammatory taxa (e.g., P. copri). These findings may inform future microbiota-targeted interventions or risk stratification strategies for EBV-related diseases. Limitations include the European ancestry of study populations and the need for mechanistic validation.},
}

@article {pmid42544167,
year = {2026},
author = {Chang, WL and Chen, CY and Wu, JH and Hou, YC},
title = {Association of Gut Microbiome Shifts With Metabolic Alterations in Prediabetes: A Cross-Sectional Study.},
journal = {Cureus},
volume = {18},
number = {7},
pages = {e111964},
pmid = {42544167},
issn = {2168-8184},
abstract = {Background Early identification and intervention are essential to prevent the progression of prediabetes to type 2 diabetes mellitus (T2DM). The gut microbiota plays a key role in host metabolism, and its dysbiosis may contribute to metabolic disorders. This study aimed to compare gut microbiota profiles between individuals with prediabetes and healthy adults and to explore their potential metabolic associations. Materials and methods A total of 117 adults aged 18-65 years were recruited, including 57 patients with prediabetes and 60 healthy controls. Demographic data and stool samples were collected. Gut microbiota composition was analyzed using 16S rRNA gene sequencing targeting the V3-V4 region. To minimize batch effects, raw sequencing data from both cohorts were processed using a unified bioinformatics pipeline. Results Individuals with prediabetes exhibited significantly lower gut microbial diversity (Simpson index, p < 0.001) and distinct microbial composition (Permutational Multivariate Analysis of Variance (PERMANOVA), p = 0.001) compared with healthy controls. Additionally, several bacterial genera differed significantly between groups, with 11 genera enriched and four genera depleted in the prediabetes group, indicating a shift in gut microbiota structure associated with prediabetes. Conclusion The gut microbiota of individuals with prediabetes differed significantly from that of healthy adults, showing reduced diversity and altered bacterial composition. These findings indicate that gut microbiota dysbiosis is associated with prediabetes-related metabolic alterations, although causal relationships cannot be inferred due to the cross-sectional design.},
}