@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.},
}

@article {pmid42544462,
year = {2026},
author = {Rizaludin, MS and Dickschat, JS and Raaijmakers, JM and Garbeva, P},
title = {Volatile dialogues between plants and microorganisms.},
journal = {Natural product reports},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6np00045b},
pmid = {42544462},
issn = {1460-4752},
abstract = {Covering: up to 2026Volatile organic compounds (VOCs) are key mediators of long-distance communication in biological systems. While their roles in plant-insect interactions are well established, emerging evidence highlights their importance in plant-microbe interactions. In this highlight, we discuss the biosynthesis and ecological functions of plant VOCs (pVOCs) and their impact on microbiome assembly and function. We examine how constitutive and stress-induced pVOCs shape microbial community composition and how microbial VOCs (mVOCs) influence plant growth and defense by modulating hormonal and metabolic pathways. We further address the bidirectional nature of volatile-mediated interactions and the challenges associated with studying complex VOC blends in natural environments. Understanding these dynamic volatile dialogues provides new opportunities for microbiome engineering and sustainable crop production.},
}

@article {pmid42544994,
year = {2026},
author = {Long, S and Yang, Z and Zeng, C and Yang, H and Cao, L and Wang, D and Liu, Y and Lin, Q and Zheng, Y},
title = {Nonlinear response mechanisms of microbial communities to coral reef biogeomorphy in the South China Sea.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0116926},
doi = {10.1128/aem.01169-26},
pmid = {42544994},
issn = {1098-5336},
abstract = {UNLABELLED: To resolve how planktonic microbial composition, assembly mechanisms, and interaction architectures vary across coral reef biogeomorphic states, we sought to identify process-relevant indicators of reef resilience. We analyzed size-fractionated microbiomes from 57 stations in the South China Sea using 16S/18S rRNA amplicon sequencing. A distance-decay model defined a near-coral reef influence zone within 588 m, and reefs were classified into Poor, Moderate, and Good states based on coral density metrics. Results showed that microbial composition diverged significantly between near-coral reefs and off-coral reef zones. Although alpha diversity remained relatively stable, characteristic coral reef amplicon sequence variants (ASVs) showed clear state-associated variation across reef biogeomorphic states. The assembly of coral reef characteristic ASVs was predominantly stochastic, yet deterministic processes strengthened under intermediate conditions, indicating a transitional restructuring phase. Network complexity displayed a hump-shaped pattern, peaking in moderate states, whereas networks in good-condition reefs were sparser but more stable due to cross-kingdom interactions and increased module hubs. Ultimately, embedding microbiome analyses within a biogeomorphic framework reveals nonlinear, state-dependent microbial reorganization missed by standard richness metrics. These responsive taxa and interaction architectures jointly provide mechanistic indicators for diagnosing coral reef health in rapidly changing tropical seas.

IMPORTANCE: Microbial composition, assembly processes, and interaction architecture jointly provide process-relevant indicators of reef condition and resilience across coral-reef biogeomorphic states. Although alpha diversity remained broadly stable across space and biogeomorphic grades, substantial microbial turnover, pronounced state responsiveness of characteristic taxa, and marked shifts in network organization revealed strong state dependence in microbial reorganization. Responsive taxa and interaction-architecture metrics jointly provide mechanistic, process-relevant indicators for diagnosing reef condition and resilience in rapidly changing tropical seas.},
}

@article {pmid42545008,
year = {2026},
author = {Boyaci, I and Delice, B and Koc, F and Yildirim, S},
title = {Ramadan fasting induces temporal gut microbiome remodeling without metabolic improvement in adults with prediabetes.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0074226},
doi = {10.1128/spectrum.00742-26},
pmid = {42545008},
issn = {2165-0497},
abstract = {UNLABELLED: Ramadan fasting is a naturally occurring, time-restricted dietary pattern involving daily abstinence from food and drink from dawn to sunset. In this longitudinal study, we investigated the impact of Ramadan fasting on gut microbiome dynamics and metabolic outcomes in prediabetic individuals, whose responses to fasting can be uniquely altered due to decreased metabolic plasticity. Seventeen adults diagnosed with prediabetes were sampled pre-Ramadan (baseline), end of Ramadan (1-month), and 3 months post-fasting. Gut microbiome was profiled using 16S rRNA gene sequencing, and metabolic and anthropometric measurements were performed. Time-dependent coordinated changes were investigated using network-based approaches. Ramadan fasting was associated with distinct, time-dependent shifts in the gut microbiome. Genus-level richness did not change significantly across time points, while alpha diversity (Shannon and Simpson indices) increased significantly at the end of Ramadan and partially reverted by 3 months post-fasting. Beta diversity analyses showed the greatest compositional separation between baseline and 1-month, followed by partial reversion at 3 months. End-of-Ramadan samples showed the enrichment of facultative anaerobes and selected short-chain fatty acid (SCFA)-associated taxa, whereas several butyrate-producing genera increased by 3 months post-fasting, consistent with temporally phased dynamics among SCFA-associated lineages. Despite these microbial and predicted functional changes, glycemic and lipid markers remained largely unchanged, while insulin resistance and adiposity indices increased over time, and microbiome-metabolic relationships did not translate into consistent metabolic improvement.

IMPORTANCE: This study shows that Ramadan fasting is associated with temporal remodeling of gut microbial composition and predicted function in individuals with prediabetes although these changes were not accompanied by clear short-term metabolic improvement. We observed coordinated shifts in bacteria linked to short-chain fatty acid production and changes in overall community balance. However, these microbial changes did not translate into measurable improvements in blood glucose or lipid levels. These findings suggest that microbiome-associated changes occurring during Ramadan fasting may not be sufficient, within the context of prediabetes, to yield measurable short-term metabolic improvement. Behavioral and metabolic restrictions may influence the extent to which microbiome-associated changes correspond with metabolic outcomes, highlighting the need for larger, diet-controlled longitudinal studies.},
}

@article {pmid42545010,
year = {2026},
author = {Li, C and Mitchell, A},
title = {Nonantibiotic-driven evolution reveals rare but predictable routes to broad antibiotic resistance.},
journal = {mBio},
volume = {},
number = {},
pages = {e0116826},
doi = {10.1128/mbio.01168-26},
pmid = {42545010},
issn = {2150-7511},
abstract = {Many medications not prescribed to treat infectious diseases have antibacterial activity at physiologically relevant concentrations, raising the risk that chronic administration of such nonantibiotics may inadvertently select for resistance in the host microbiome. However, how frequently such exposures select for adaptations that impact broad drug resistance, including to antibiotics, remains unclear. Here, we systematically evolved Escherichia coli under exposure to 40 antibiotics and nonantibiotics and profiled the cross-resistance of the drug-adapted strains to 21 antibiotics representing all major classes. Our measurements revealed that most drug-adapted strains did not become multidrug resistant. However, five nonantibiotics and three antibiotics emerged as exceptions and were repeatedly selected for broad antibiotic resistance. Whole-genome sequencing of all 168 evolved strains revealed that changes in the regulation of efflux pumps repeatedly underlay broad drug resistance and converged into two key regulatory genes, acrR and lon. Our work suggests that although inadvertent antibiotic cross-resistance is rare, specific nonantibiotics can still potentially pose a risk for the emergence of multidrug resistance.IMPORTANCEMany medications not typically prescribed to treat infectious diseases have potent antimicrobial activity at physiological concentrations. This anti-bacterial activity raises concern that long-term administration of such nonantibiotics might unintentionally select for multidrug resistance, including resistance to antibiotics. Using Escherichia coli, we show that in most cases, these nonantibiotics do not broadly select for resistance to antibiotics in vitro. However, we identified five nonantibiotics that repeatedly selected for resistance to multiple antibiotics through a shared mechanism of action-upregulation of the multidrug efflux pump AcrAB-TolC. These findings highlight that while the overall risk is low, certain nonantibiotics may still contribute to the emergence of multidrug resistance. Identifying these high-risk drugs can help guide safer prescribing practices and inform strategies to limit the spread of antibiotic resistance.},
}

@article {pmid42545016,
year = {2026},
author = {Seo, Y and Kim, J and Yeom, M and Park, S-Y and Lee, S and Ahn, S and Hahm, D-H and Kim, K and Kwon, S-K and Park, H-J},
title = {Gut microbiota contributes to the therapeutic effect of acupuncture in atopic dermatitis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0391225},
doi = {10.1128/spectrum.03912-25},
pmid = {42545016},
issn = {2165-0497},
abstract = {UNLABELLED: The gut microbiome is increasingly recognized as a central regulator of immune homeostasis, metabolic balance, and therapeutic outcomes. Atopic dermatitis (AD), a chronic inflammatory skin disease, is closely linked to gut microbial dysbiosis. Traditionally regarded as a neurostimulatory therapy, acupuncture (Acu) has demonstrated increasing efficacy in alleviating AD symptoms and improving gastrointestinal function. These observations suggest that the therapeutic effects of Acu in AD may be mediated, in part, by modulation of the gut microbiome. In this study, AD patients were stratified into responder (R) and non-responder (NR) groups based on clinical improvement. Gut microbiome profiling revealed that R patients exhibited greater microbial diversity and compositional stability, indicative of a more balanced gut ecosystem. Specific taxa, including Alistipes ihumii and Odoribacter splanchnicus, were enriched in R individuals and may serve as microbial predictors of treatment responsiveness. Importantly, fecal microbiota transplantation (FMT) from R donors restored Acu efficacy in a mouse model of AD, whereas FMT from NR donors did not. These findings support the gut-skin axis and highlight the integral role of the gut microbiome in mediating the therapeutic effects of Acu for AD, suggesting potential for microbiome-based personalized treatment.

IMPORTANCE: Increasing evidence supports the gut microbiome's role in modulating treatment responses in atopic dermatitis (AD), but direct evidence linking acupuncture efficacy with microbiome composition has been lacking. Previous studies did not assess causal relationships via fecal microbiota transplantation (FMT) or functional metagenomics. This study identifies specific gut microbes associated with acupuncture response in AD and confirms their causal role using FMT. It also links functional metabolic pathways to therapeutic efficacy, offering a mechanism-based insight. Our findings support microbiome-informed personalized acupuncture approaches for AD and suggest gut microbiota as a therapeutic modulator in neuroimmune regulation.

CLINICAL TRIALS: This study was registered in the Korean Clinical Trial Registry (CRIS, registration number: KCT0005422).},
}

@article {pmid42545019,
year = {2026},
author = {Kulosa, M and Belisário-Ferrari, MR and Semmler, F and Büttner, M and Duck, C and Namazi, Z and Jehmlich, N and von Bergen, M and Bonitz, T and Kaysser, L},
title = {Establishment of an in vitro aerobic bacterial community as a model of the human lung microbiome.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0049126},
doi = {10.1128/msystems.00491-26},
pmid = {42545019},
issn = {2379-5077},
abstract = {The human lung microbiome is increasingly recognized as a key player in drug metabolism, yet it remains largely understudied. To replicate this complex physiological environment in a controlled setting, we developed a simplified artificial lung microbiome model composed of four representative bacterial species: Pseudomonas koreensis, Rothia aeria, Neisseria cinerea, and Streptococcus downei. We successfully established a stable 10-day co-culture at 34°C using brain heart infusion medium, as validated by quantitative PCR, viability PCR, and conventional microbiological methodologies. Integrated bioinformatic analyses revealed a variety of potential microbe-microbe interactions, which were supported by metaproteomic analysis using mass spectrometry. Our model provides a foundation for in-depth studies, such as, for example, the effects of pulmonary drugs on the lung microbiome, and how, in turn, the microbiome may influence therapeutic outcomes.IMPORTANCEOnce thought to be sterile, the lung microbiome is now understood to host a dynamic microbiome capable of influencing respiratory health and disease. Understanding interactions among the microbes within this community is essential, as these relationships may drive disease progression or foster resilience in both acute and chronic inflammatory conditions. We developed a reproducible lung microbiome model comprising Pseudomonas koreensis, Rothia aeria, Streptococcus downei, and Neisseria cinerea. Simplified models enable controlled studies to dissect specific microbial interactions, laying the foundation for insights into lung microbial ecology. In the future, more complex models will enhance our understanding of microbial roles in disease outcomes, with our platform serving as a basis for testing therapeutic strategies.},
}

@article {pmid42545021,
year = {2026},
author = {Khan, MQN and Xiang, W-Q and Ren, M-X},
title = {Diversity and sources of floral microbial communities.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0032326},
doi = {10.1128/aem.00323-26},
pmid = {42545021},
issn = {1098-5336},
abstract = {Flowers serve as a key ecological interface where microorganisms, plants, and pollinators interact, yet the processes shaping flower microbiota remain insufficiently synthesized. In this review, we summarize the current literature on the assembly and distribution of floral microbiota across floral organs through three major transmission pathways: insect vectors, bird visitation, and aerial deposition. We assess the organ-specific distribution and transmission pathways of microbial taxa across nectar, stigma, petals, pollen, and anthers, and estimate the relative importance of each of these vectors in microbial dispersal. Our analysis reveals a strong research bias toward nectar and stigma, which collectively dominate the studies of floral microbiota. Based on the currently available literature, insect pollinators, especially the honeybees and bumblebees, emerge as the most frequently reported agents of microbial transfer by repeated deposition of microbes onto floral organs. Bird-mediated transmission, despite its geographic restriction, plays a key role in ornithophilous systems, whereas aerial deposition appears to have a comparatively limited influence. We also emphasize the effect of floral microbes on flower attractiveness, phenotypic changes, and the systemic microbial movement within plants. This review incorporates flower ecology, microbiology, and pollination biology, and points out how flowers act as microbial gateways between the aboveground and belowground parts of plants, and how flowers remain underappreciated for their role in systemic interaction between plants and microbes.},
}

@article {pmid42545022,
year = {2026},
author = {Bull, J and Durham, PL and Mirza, BS},
title = {Effects of liraglutide on gut bacterial community dynamics.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0034326},
doi = {10.1128/spectrum.00343-26},
pmid = {42545022},
issn = {2165-0497},
abstract = {Liraglutide, a GLP-1 receptor agonist, is used to induce weight loss. However, limited information exists on liraglutide's effects on the gut bacterial community and their restoration after washout. We investigated liraglutide's effect on the gut bacterial community in diet-induced obese (DIO) mice and whether these changes persist after washout. Twenty-four male C57BL/6J mice on high-fat (HFC) or low-fat (LFC) diets were monitored for 21 days. A subgroup of high-fat mice received daily liraglutide for 14 days (HFL), followed by a 7-day washout. Liraglutide induced significant weight loss by Day 4, which persisted during treatment and partially reversed post-treatment. For bacterial community analysis, 7.1 million 16S rRNA gene sequences were retrieved using Illumina paired-end sequencing. We observed distinct shifts in the gut bacterial community structure during liraglutide treatment, which mostly returned to baseline after the 7-day washout. Using Similarity Percentages analysis, 21 amplicon sequence variants (ASVs) were identified as major contributors. Nine ASVs, related to Lactobacillus gasseri, L. paragasseri, L. johnsonii, and Leptogranulimonas caecicola, significantly increased during treatment and declined post-washout. The remaining 12 ASVs, associated with protein- and carbohydrate-fermenting bacteria (Romboutsia, Faecalicatena, and Oscillibacter), decreased during treatment. Comparison across all groups identified 29 ASVs, clustering into seven phylogenetic groups, highlighting liraglutide's enrichment of bile acid- and mucin-associated taxa and suppression of carbohydrate-fermentative genera. These findings demonstrate that liraglutide induces rapid, diet-dependent, yet reversible shifts in the gut microbiome, favoring lactic acid-producing bacteria while reducing fermentative taxa. Such microbial changes may contribute to liraglutide's metabolic effects and provide insight into host-microbiome interactions in obesity treatment.IMPORTANCEObesity and overweight states are intricately linked to the gut bacterial community; however, the effects of common obesity treatments such as GLP-1 receptor agonists on gut bacteria remain unclear. Here, we show that liraglutide, a GLP-1 analog, reshapes the gut bacterial community in diet-induced obese mice relative to untreated obese and lean controls. By including baseline samples when mice were at a normal weight, we distinguished bacterial changes due to the drug from those due to obesity progression, as well as how the community structure is affected during a washout period. Liraglutide treatment selectively increased beneficial gut bacteria (e.g., Lactobacillaceae) under high-fat conditions. These bacterial shifts during GLP-1 therapy may contribute to its metabolic benefits and broaden our understanding of host bacterial interactions in the context of diet and weight management.},
}

@article {pmid42545024,
year = {2026},
author = {Carlson-Jones, JAP and Goddard, TR and Papudeshi, B and Mallawaarachchi, V and Whiteson, KL and Warner, MS and Morton, JM and Jersmann, HPA and Edwards, RA},
title = {DNA sequencing for microbial surveillance in cystic fibrosis airways: advances, challenges, and clinical translation.},
journal = {Clinical microbiology reviews},
volume = {},
number = {},
pages = {e0035225},
doi = {10.1128/cmr.00352-25},
pmid = {42545024},
issn = {1098-6618},
abstract = {SUMMARYDNA sequencing has revolutionized microbial surveillance in cystic fibrosis (CF), transforming pathogen identification from culture-dependent to total microbial community identification using molecular-based approaches. Techniques such as 16S rRNA gene sequencing have uncovered the complexity of the CF airway microbiome, while shotgun metagenomics, metatranscriptomics, and viromics now provide strain-level, functional, and viral insights beyond bacterial identification. Despite these advances, key technical and logistical challenges remain, including the processing of high-viscosity sputum samples, overwhelming host DNA contamination, managing large data sets, and the integration of complex bioinformatic outputs into clinical workflows. Emerging innovations such as host DNA depletion protocols, targeted enrichment panels, and adaptive sampling on Oxford Nanopore platforms are helping to overcome these barriers, improving microbial recovery and sequencing efficiency. As cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapies are changing the lives of people with cystic fibrosis (pwCF), sequencing offers an unprecedented opportunity to track potential microbial adaptation in response. This review investigates current advances, limitations, and translational opportunities in DNA sequencing for CF airway microbiome surveillance, highlighting how these technologies can help reshape research and clinical microbiology in the post-modulator era.},
}

@article {pmid42545083,
year = {2026},
author = {Nyoni, NF and Duarte-Coimbra, S and Forcina, G and Pérez-Pardal, L and Beja-Pereira, A},
title = {Characterization of the Genital Microbiota in Portuguese Native Goats.},
journal = {Reproduction in domestic animals = Zuchthygiene},
volume = {61},
number = {8},
pages = {e70297},
doi = {10.1111/rda.70297},
pmid = {42545083},
issn = {1439-0531},
support = {PTDC/BAA-AGR/28575/2017//Fundação para a Ciência e a Tecnologia/ ; PTDC/BAA-AGR/28866/2017//Fundação para a Ciência e a Tecnologia/ ; POCI-01-0145-FEDER-028575//FEDER funds through COMPETE2020 - Programa Operacional Competividade e Internacionalização (POCI)/ ; POCI-01-0145-FEDER-028866//FEDER funds through COMPETE2020 - Programa Operacional Competividade e Internacionalização (POCI)/ ; },
mesh = {Animals ; *Goats/microbiology ; Female ; *Microbiota ; Male ; RNA, Ribosomal, 16S/genetics ; Portugal ; Bacteria/classification/isolation & purification/genetics ; Vagina/microbiology ; *Genitalia, Female/microbiology ; Sheep/microbiology ; },
abstract = {Evaluating the reproductive microbiome in small ruminant livestock, such as goats and sheep, is crucial for improving breeding performance, promoting animal health, and optimizing pregnancy outcomes. A healthy microbiome in the reproductive tract inhibits infections, regulates immune activity, and reduces the risk of microbial imbalances that negatively affect pregnancy. Understanding this microbiome also supports better disease control, informs advanced animal husbandry practices for goats and sheep, and contributes to global food security. This study aimed to characterize the genital microbiome of three local Portuguese goat breeds-Preta de Montesinho, Serrana, and Serpentina-using 16S rRNA metabarcoding. Samples were collected from 39 goats and, for comparison, seven sheep from a local breed-Serra da Estrela. Microbiome differences were obtained when integrating breed and sex factors in goats. The predominant genera in both vaginal and preputial samples included Fusobacterium, Aerococcus, Corynebacterium, Sediminibacterium, Campylobacter, and Ralstonia. Significant compositional differences were observed across breed, sex, and species as indicated by Bray-Curtis dissimilarity. By characterizing the caprine reproductive microbiota through metabarcoding, this study fills an important knowledge gap and establishes a baseline for future research on disease-associated changes in the male and female urogenital tract microbiota of small ruminants.},
}

Animals
*Goats/microbiology
Female
*Microbiota
Male
RNA, Ribosomal, 16S/genetics
Portugal
Bacteria/classification/isolation & purification/genetics
Vagina/microbiology
*Genitalia, Female/microbiology
Sheep/microbiology

@article {pmid42545096,
year = {2026},
author = {Garey, KW and Hurdle, JG},
title = {Case Commentary: Emergence of clinically relevant fidaxomicin-resistant Clostridioides difficile strains.},
journal = {Antimicrobial agents and chemotherapy},
volume = {},
number = {},
pages = {e0048226},
doi = {10.1128/aac.00482-26},
pmid = {42545096},
issn = {1098-6596},
abstract = {Clostridioides difficile infection (CDI) has limited antibiotic treatment options, with fidaxomicin being the guideline-preferred antibiotic. C. E. Kaple, S. N. Redmond, J. L. Cadum, B. Hausman, et al. (Antimicrob Agents Chemother 0:e00130-26, 2026, https://doi.org/10.1128/aac.00130-26) describe a case of clinical failure in an elderly patient with CDI treated with a pulsed-taper fidaxomicin regimen, in which the MIC increased from 0.05 μg/mL at baseline to 32 μg/mL in isolates recovered during relapse. Relapsing symptoms were eventually resolved only after switching to oral vancomycin. This case, together with other recent clinical reports, may be the tip of the iceberg, signaling that fidaxomicin-resistant C. difficile can arise during treatment and contribute to clinical failure. It further challenges the assumption that high colonic drug concentrations mitigate resistance and underscores the need for improved surveillance and the development of clinically applicable molecular diagnostics to detect fidaxomicin resistance in CDI patient samples.},
}

@article {pmid42545324,
year = {2026},
author = {Ahmed, A and Rodini, S and Alrubyea, F and Akl, M},
title = {Semaglutide-Induced Sarcopenia via GLP-1R-mTOR-Satellite Cells Axis and Muscle-Glucose Feedback Loop Potentially Leading to Refractory Hyperglycemia in Type 2 Diabetes: A Case-Driven Hypothesis.},
journal = {Problemy endokrinologii},
volume = {72},
number = {3},
pages = {60-65},
doi = {10.14341/probl13660},
pmid = {42545324},
issn = {2308-1430},
mesh = {Semaglutide ; Humans ; Male ; *Diabetes Mellitus, Type 2/drug therapy/metabolism ; Middle Aged ; *Glucagon-Like Peptides/adverse effects ; TOR Serine-Threonine Kinases/metabolism ; *Sarcopenia/chemically induced/metabolism ; *Hyperglycemia/metabolism/chemically induced ; Glucagon-Like Peptide-1 Receptor/metabolism ; *Hypoglycemic Agents/adverse effects ; Satellite Cells, Skeletal Muscle/metabolism/drug effects ; Muscle, Skeletal/metabolism ; Glucose/metabolism ; },
abstract = {Glucagon-like peptide-1 receptor agonists (GLP-1RAs) like semaglutide have transformed type 2 diabetes mellitus (T2DM) management, yet emerging concerns highlight potential risks of accelerated sarcopenia and subsequent metabolic disruptions. This case-driven hypothesis explores a 53-year-old male with T2DM diagnosed in 2014, who experienced progressive glycemic failure despite standard therapies, including metformin, glipizide, sitagliptin, and empagliflozin. Transition to dulaglutide 1.5 mg for 1.5 years followed by semaglutide (titrated from 0.25 to 1 mg weekly starting September 2024) resulted in weight loss from 84 kg to 70 kg by September 2025, accompanied by sarcopenic symptoms (muscle weakness, reduced mobility) and refractory hyperglycemia (fasting glucose 300 mg/dL, HbA1c 9%), persisting post-discontinuation on September 1, 2025, despite metformin and empagliflozin. We posit that semaglutide may precipitate acute sarcopenia via unexpected GLP-1R-mTOR-satellite cells axis crosstalk, disrupting AMPK-mTOR balance to suppress anabolic mTORC1/IGF-1 signaling (potentially by 25-35%) while enhancing catabolic FOXO/ubiquitin-proteasome and excessive autophagy pathways. This could extend to myokine reprogramming (elevated myostatin/GDF15, reduced irisin/IL-15), glucagon/α-cell compensation inducing hyperglucagonemia (15-25% rise), microbiome-bile acid shifts fostering low-grade inflammation (IL-6/TNF-α upregulation by 10-15%), mitochondrial mass reduction (20-25% via AMPK), and NMJ disassembly, collectively impairing muscle as the primary glucose sink (reducing GLUT4-mediated uptake by 35-45%) and initiating a «muscle-glucose feedback loop» with hepatic gluconeogenesis amplification, yielding treatment-resistant hyperglycemia.Supporting evidence from cohorts (e.g., 24-month study showing ASMI/grip strength declines in 432 patients), longitudinal analyses (NMJ degradation with CAF22/NfL elevations in 141 men), secondary trials (9.3% psoas volume loss in 51 MASLD cases), and case reports (fatigue in a 74-year-old, rhabdomyolysis in a 47-year-old) aligns with this framework, as does in vitro data linking GLP-1 excess to kinesin-1/GLUT4 inhibition and ATP depletion (20-30%). This novel hypothesis underscores sarcopenia's role in GLP-1RA-induced metabolic paradoxes, urging prospective studies on muscle-preserving interventions like resistance training or GLP-1R modulators to refine T2DM paradigms and inspire multidisciplinary research into endocrine-muscle interactions.},
}

Semaglutide
Humans
Male
*Diabetes Mellitus, Type 2/drug therapy/metabolism
Middle Aged
*Glucagon-Like Peptides/adverse effects
TOR Serine-Threonine Kinases/metabolism
*Sarcopenia/chemically induced/metabolism
*Hyperglycemia/metabolism/chemically induced
Glucagon-Like Peptide-1 Receptor/metabolism
*Hypoglycemic Agents/adverse effects
Satellite Cells, Skeletal Muscle/metabolism/drug effects
Muscle, Skeletal/metabolism
Glucose/metabolism

@article {pmid42545553,
year = {2026},
author = {Li, YM and Shao, QZ and Ko, CY and Chen, Y and Haley, DR and Hamadi, HY and Zhao, M},
title = {Gut microbial dysbiosis in a Southern Chinese cohort of patients with Parkinson's disease.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {9},
pages = {},
pmid = {42545553},
issn = {1572-9699},
mesh = {Humans ; *Parkinson Disease/microbiology/drug therapy/complications ; *Dysbiosis/microbiology ; *Gastrointestinal Microbiome ; Aged ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Female ; Male ; Middle Aged ; *Bacteria/classification/genetics/isolation & purification ; China ; Fatty Acids, Volatile/metabolism ; East Asian People ; },
abstract = {Parkinson's disease (PD) is the second most common neurodegenerative disorder, affecting approximately 10 million people worldwide. Growing evidence suggests that gut microbial dysbiosis may be crucial in PD pathogenesis through the gut-brain axis. However, bacterial profiles can vary based on factors like diet, age, and medication use. This study explores gut microbial dysbiosis in patients with Parkinson's disease (PD), considering disease severity, age, and medication use.Faecal samples were collected from PD patients (n = 42) and age-matched controls (n = 25) and analysed using 16S rRNA gene pyrosequencing targeting the V3-V4 hypervariable regions. Taxonomic distinctions were assessed with particular focus on short-chain fatty acid (SCFA)-producing bacteria. Significant differences in faecal microbiome composition were observed between PD patients and controls. Anticholinergic and dopaminergic agents altered the abundance of SCFA-producing bacteria (Ruminococcaceae, Clostridiales, Blautia). Alistipes abundance was not significantly altered across medication groups in exploratory analyses. The faecal microbiota in PD patients showed modifications related to disease severity, age, and medication use. These changes appeared early and were influenced by medical interventions. This study highlights the intricate gut microbiome-PD relationship, suggesting potential therapeutic avenues and further research directions.},
}

Humans
*Parkinson Disease/microbiology/drug therapy/complications
*Dysbiosis/microbiology
*Gastrointestinal Microbiome
Aged
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Female
Male
Middle Aged
*Bacteria/classification/genetics/isolation & purification
China
Fatty Acids, Volatile/metabolism
East Asian People

@article {pmid42545567,
year = {2026},
author = {Volz Gonzalez, I and Pérez Lleó, A and Almenar Llorens, P and Pedro Monzonís, M and Douterelo, I},
title = {Biofilms and disinfection by-products in Mediterranean drinking water networks: effect of temperature on disinfection strategies.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {8},
pages = {},
pmid = {42545567},
issn = {1573-0972},
support = {INNCAD/2020/44//Agencia Valenciana de la Innovación/ ; },
mesh = {*Biofilms/growth & development ; *Drinking Water/microbiology/chemistry ; *Disinfection/methods ; RNA, Ribosomal, 16S/genetics ; Temperature ; *Bacteria/genetics/classification/isolation & purification/drug effects ; Spain ; *Disinfectants/analysis ; Seasons ; Water Microbiology ; Chlorine/analysis ; Water Purification/methods ; Water Quality ; DNA, Bacterial/genetics ; Microbiota ; Water Supply ; },
abstract = {Biofilms inhabiting drinking water networks can degrade water quality, leading to disinfectant depletion, pipe corrosion and organoleptic issues. In this study, the use of in situ biofilm sampling devices, which enabled sample collection without interrupting the supply, provided insights into physicochemical and biological interactions within a network in Valencia (Spain). The devices were installed in an operational chlorinated network and monitored over a year to assess biofilm dynamics. Water quality was evaluated using standard methods for faecal indicator bacteria (FIB) and pathogens, alongside physicochemical parameters including disinfection by-products (DBPs), geosmin, and metals. Biofilms devices were sampled every 3 months to examine development and biofilm regrowth under seasonal conditions. Bacterial communities were characterised using 16S rRNA gene amplicon sequencing and analysed in relation to environmental factors. No FIB or pathogens were detected in any water sample, yet DNA analysis in biofilms (particularly in 6- and 9-month-old biofilms) showed the presence of sequences related with potential opportunistic pathogens including Legionella spp. and Staphylococcus spp. DBPs, increased during warmer months coinciding with higher chlorine dosages and iron and manganese concentrations. A core microbiome formed mainly by species of Pseudomonas spp. and Acidovorax spp. was found in water and biofilm samples. A clear temporal succession in biofilm composition was observed, with diversity peaking at mid-developmental stages, yet regrowth was seasonally independent. The installation of biofilm sampling devices in real networks was effective at monitoring microbial dynamics, providing key information for distribution infrastructure management including optimisation of cleaning and disinfection strategies.},
}

*Biofilms/growth & development
*Drinking Water/microbiology/chemistry
*Disinfection/methods
RNA, Ribosomal, 16S/genetics
Temperature
*Bacteria/genetics/classification/isolation & purification/drug effects
Spain
*Disinfectants/analysis
Seasons
Water Microbiology
Chlorine/analysis
Water Purification/methods
Water Quality
DNA, Bacterial/genetics
Microbiota
Water Supply

@article {pmid42545598,
year = {2026},
author = {Buitrago, SP and Garzón-Ospina, D and Largo-Latorre, LS and Hernandez-Zambrano, LJ and Espinosa-Ramirez, AJ},
title = {Site-specific bacterial microbiome patterns across contrasting anthropogenic settings in the upper Chicamocha River, Colombia: a full-length 16S rRNA gene pilot survey.},
journal = {Environmental monitoring and assessment},
volume = {198},
number = {9},
pages = {},
pmid = {42545598},
issn = {1573-2959},
mesh = {Colombia ; *Rivers/microbiology ; *Environmental Monitoring ; RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; *Bacteria/classification/genetics ; Pilot Projects ; *Water Microbiology ; },
abstract = {High-mountain urban rivers in tropical South America remain underrepresented in molecular monitoring studies, limiting the identification of bacterial assemblages associated with local anthropogenic pressures. This study characterized bacterial microbiome composition, diversity, and 16S rRNA gene-based predicted functional profiles at five sites in the upper Chicamocha River, Colombia, representing contrasting settings, including a wastewater treatment plant (WWTP)-influenced reach, a thermoelectric cooling pond, agrolivestock influence, and a downstream municipal-industrial reach. Full-length 16S rRNA gene amplicon sequencing using PacBio HiFi generated 737,344 high-quality reads and 4921 amplicon sequence variants. Bacterial assemblages showed site-specific patterns, with high multisite Sørensen dissimilarity mainly attributable to taxon turnover. Ammonium was the only physicochemical variable significantly associated with community ordination. The WWTP-influenced site showed high relative abundance of the phyla Bacillota and Campylobacterota, particularly of the genus Arcobacter, whereas the cooling pond showed increased representation of the genus Sphingorhabdus. Flavobacterium was most abundant at agrolivestock-influenced sites, while the genera Limnohabitans and Polynucleobacter dominated the downstream site. Functional inference suggested site-associated KEGG profiles, including predicted xenobiotic-biodegradation pathways and categories annotated to membrane transport, motility, and antimicrobial drug resistance. These findings provide a preliminary molecular monitoring baseline and identify candidate taxa and pathways for targeted validation in future watershed surveillance, supporting the development of molecular monitoring strategies for undersampled Andean high-mountain urban rivers.},
}

Colombia
*Rivers/microbiology
*Environmental Monitoring
RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
*Bacteria/classification/genetics
Pilot Projects
*Water Microbiology

@article {pmid42545731,
year = {2026},
author = {Maiese, K},
title = {Oxidative stress, aging, metabolism, SIRT1, and the gut microbiota: the neurocardiac basis of cognitive loss.},
journal = {Medical gas research},
volume = {},
number = {},
pages = {},
pmid = {42545731},
issn = {2045-9912},
abstract = {FactsCardiovascular disease, Alzheimer's disease, and multiple sclerosis share a neurocardiac basis linked by cellular metabolism and diabetes, indicating the presence of common pathological pathways.Current care remains symptomatic and prevention focused, and interventions targeting shared pathways such as oxidative stress, senescence, and autophagy are lacking.Apolipoprotein E (APOE), glucagon-like peptide-1 (GLP-1) agonism, silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), mitochondrial dynamics, and the gut microbiome are key modulators of the neurocardiac axis and are highly interdependent.Understanding the interactions among ferroptosis, pyroptosis, and apoptosis under comorbid conditions is essential for clinical translation.Open questionsIs oxidative stress a primary driver or a consequence of autophagy dysregulation that links cardiac dysfunction to cognitive decline?Are GLP-1 receptor agonists neuroprotective independent of glycemic control, and what is the optimal timing and disease stage?Which microbial metabolites influence mitochondrial dynamics and senescence, and can microbiome targeting improve both cardiac and cognitive outcomes?Is combined inhibition of ferroptosis and pyroptosis superior to single-pathway blockade, and how can strategies for different comorbidity profiles be chosen?How can APOE genotypes and individual metabolic states guide personalized therapies that simultaneously reduce cardiovascular risk and neurodegeneration? Cardiovascular disease and cognitive loss have a neurocardiac basis. Poor vascular perfusion can impair cognitive function in both Alzheimer's disease and multiple sclerosis. However, a treatment gap exists because current approaches do not adequately address the shared underlying cellular mechanisms responsible for cognitive dysfunction in these conditions. Current treatments for cognitive impairment in diseases such as cardiovascular disease, Alzheimer's disease, multiple sclerosis, and diabetes often fail to fully address the shared underlying cellular mechanisms. Consequently, the prevailing precision treatment strategy, which focuses on managing symptoms and preventing disease progression, is insufficient. This highlights the urgent need for innovative approaches capable of targeting these common cellular pathways across these diverse conditions. Novel investigations into oxidative stress, cellular senescence, programmed cell death with apoptosis, ferroptosis, pyroptosis, and autophagy, cellular metabolism with apolipoprotein E and glucagon-like peptide-1 receptor agonism, silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae), mitochondrial dynamics, and the gut microbiome offer the potential to address the risk factors and clinical treatments for cardiovascular disease and cognitive loss. These pathways are exquisitely dependent upon one another and require in-depth knowledge of the modulatory cellular mechanisms for effective translation to clinical care.},
}

@article {pmid42545757,
year = {2026},
author = {Huang, Z and Ng, SC and Sokol, H and Rolhion, N},
title = {Precision microbiome medicine and therapeutics: the enabling role of in vitro gut models.},
journal = {FEMS microbiology reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsre/fuag038},
pmid = {42545757},
issn = {1574-6976},
abstract = {The human gut microbiome exhibits profound interindividual variability, challenging the efficacy of generalized interventions and underscoring the need for precision approaches to microbiome-associated diseases. Such strategies require comprehensive, individualized assessment of microbial ecosystems and their functional responses, an objective that remains difficult to achieve in vivo. In vitro gut models offer a promising alternative, maintaining personalized microbial communities in controlled environments and enabling detailed investigation of microbiome dynamics. Complementary microbe-host co-culture systems incorporating human cells further permit mechanistic interrogation of host responses to microbial stimuli. Together, these integrated platforms offer a translational framework for developing tailored therapeutics. In this Perspective, we examine how in vitro gut models can advance microbiome-based personalized medicine, discuss key determinants of therapeutic variability, and outline the relevance, limitations, and future directions of these systems in designing targeted, more effective interventions.},
}

@article {pmid42545829,
year = {2026},
author = {Tjo, H and Jiang, V and Jeffrey, PD and Zhu, A and Link, AJ and Joseph, JA and Conway, JM},
title = {Structural insights into xyloglucan recognition by an ABC transporter from a Gram-positive, thermophilic bacterium.},
journal = {The FEBS journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/febs.70667},
pmid = {42545829},
issn = {1742-4658},
support = {//Techint Group Roberto Rocca Graduate Fellowship/ ; DGE-2039656//National Science Foundation Graduate Research Fellowship Program/ ; //Tau Beta Pi Graduate Fellowship/ ; //Princeton University/ ; //Omenn-Darling Bioengineering Institute at Princeton University/ ; //High Meadows Environmental Institute, Princeton University William Clay Ford, Jr. '79 and Lisa Vanderzee Ford '82 Graduate Fellowship Fund/ ; },
abstract = {Xyloglucan (an α-1,6-xylosyl-substituted β-1,4-glucan) is a major hemicellulose of the primary cell wall of many plants and an important growth substrate for biomass-degrading bacteria in diverse ecological niches, including the gut microbiome and hot springs. In Gram-positive bacteria, xyloglucan is deconstructed into soluble oligosaccharides in the extracytoplasmic space before import by ATP-Binding Cassette (ABC) transporters, but the structural basis for this process remains poorly understood. Here, we identified an ABC transporter for xyloglucan uptake (Athe_2052-2054) in the Gram-positive, plant biomass-degrading thermophile Anaerocellum bescii, which is conserved across the Anaerocellum genus. We solved the apo crystal structure of its extracellular substrate-binding protein (SBP), Athe_2052, revealing a unique tertiary fold found only in a small subset of SBPs that bind complex oligosaccharides. To our knowledge, Athe_2052 is the first structurally characterized ABC SBP known to recognize xyloglucan oligosaccharides. Biophysical analysis showed that while Athe_2052 binds unsubstituted β-glucan chains, recognition of xyloglucan side chains in the binding pocket markedly increases affinity (Kd = 14 nm) for xyloglucan heptasaccharide (XXXG), the principal oligosaccharide released during xyloglucan deconstruction. Molecular modeling revealed that xyloglucan heptasaccharide, owing to its branched substitutions, is bound in a distinct conformation compared to unsubstituted β-glucans. This represents a unique mode of xyloglucan recognition driven by α-linked side chain interactions rather than β-glucan backbone recognition alone. Together, these findings provide the first structural basis for xyloglucan oligosaccharide recognition by an ABC transporter in Gram-positive bacteria.},
}

@article {pmid42545901,
year = {2026},
author = {K, SR and Y, LA},
title = {A Scoping Review of Machine Learning and Deep Learning Methods for Autism Spectrum Disorder Diagnosis and Analysis.},
journal = {Journal of visualized experiments : JoVE},
volume = {},
number = {233},
pages = {},
doi = {10.3791/71972},
pmid = {42545901},
issn = {1940-087X},
mesh = {Humans ; *Autism Spectrum Disorder/diagnosis ; *Deep Learning ; *Machine Learning ; },
abstract = {Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by diverse behavioral, cognitive, sensory, and communication profiles, making early diagnosis and personalized intervention challenging. Recent advances in machine learning (ML) and deep learning (DL) have enabled the development of computational tools for ASD screening, classification, severity assessment, and intervention monitoring. This review synthesizes findings from 50 recent studies that applied ML and DL techniques to ASD-related datasets, including electroencephalography (EEG), eye-tracking, behavioral video, microbiome, voice acoustic, demographic, and multimodal data. The review addresses three key questions: (i) which data modalities and computational approaches are most frequently used, (ii) how diagnostic performance is evaluated across different study designs, and (iii) what methodological challenges limit clinical translation. The literature is organized according to data modality, algorithmic approach, and clinical readiness. Approaches examined include conventional ML methods, convolutional neural networks, graph neural networks, hybrid deep learning architectures, federated learning, explainable artificial intelligence, topological data analysis, and multimodal fusion. The findings suggest that multimodal and graph-based approaches provide a more comprehensive representation of ASD phenotypes than single-modality methods. Explainability and privacy-preserving learning have also emerged as important considerations for clinical deployment. However, many reported high-performance models are based on small sample sizes, repeated use of the ABIDE dataset, class imbalance, single-site validation, or limited external testing, raising concerns regarding generalizability. Beyond diagnostic accuracy, this review evaluates model interpretability, calibration, scalability, validation rigor, and clinical applicability. Overall, the analysis highlights the need for standardized benchmarks, externally validated multimodal datasets, clinically relevant evaluation metrics, and decision-support systems that complement rather than replace expert clinical assessment in ASD diagnosis and management.},
}

Humans
*Autism Spectrum Disorder/diagnosis
*Deep Learning
*Machine Learning

@article {pmid42546570,
year = {2026},
author = {Li, H and Wu, C and Song, X and Sun, X and Qu, X and Xiong, B and Du, H and He, X and Ma, M and Mao, Q},
title = {Concentration-dependent alleviation of lead toxicity in rapeseed by elevated CO2 is associated with rhizosphere microbiome remodeling.},
journal = {Ecotoxicology and environmental safety},
volume = {323},
number = {},
pages = {120535},
doi = {10.1016/j.ecoenv.2026.120535},
pmid = {42546570},
issn = {1090-2414},
abstract = {Interactive effects of elevated CO2 (eCO2) and heavy metal pollution on plant-microbe systems are critical for predicting ecosystem responses under future climate scenarios. We investigated how eCO2 modulates lead (Pb) toxicity in rapeseed (Brassica napus) and its rhizosphere microbiome using a two-factor experiment with three CO2 concentrations (400, 550, and 700 ppm) and three Pb levels (0, 70, and 400 mg·kg[-1)]. The alleviating effect of eCO2 on Pb toxicity was strongly concentration-dependent. Moderate eCO2 (550 ppm) significantly increased biomass, photosynthetic rate, nutrient uptake, and non-enzymatic antioxidant capacity (glutathione and ascorbate), thereby mitigating Pb-induced oxidative damage. Conversely, 700 ppm eCO2 induced photosynthetic acclimation and provided limited protection. Concurrently, eCO2 reshaped rhizosphere bacterial community in a concentration-dependent manner, enriching stress-tolerant taxa including Proteobacteria and Paenibacillus, and enhancing predicted functional pathways related to carbon and energy metabolism. Mantel analysis revealed strong positive correlations between plant nutrient status and microbial functional potential. We propose a "plant-microbe interaction framework" in which moderate eCO2 increases photosynthetic carbon inputs, fostering beneficial microbial communities that in turn support plant tolerance to Pb stress. These findings highlight the non-linear nature of CO2-heavy metal interactions and provide new insights for microbe-assisted phytoremediation strategies under future climate conditions.},
}

@article {pmid42546687,
year = {2026},
author = {Howard, DR and Rashid, RB and Ahmed, T and Namubiru, P and Sohel Rana, M and Wilkins, T and Morrow, J and Creek, DJ and Franco, RA and Allenby, MC and Turner, DL and Werder, RB and Manna, S and Satzke, C and Lim, Y and Sun, J and Dennis, PG and Yadav, A and Kueh, AJ and Chung, CK and Forbes-Blom, E and Noti, M and O'Regan, J and Coelho, LP and Brown, CC and Morrison, M and Phipps, S},
title = {Milk osteopontin alters the infant microbiome to drive DC hematopoiesis and disease tolerance.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2026.07.022},
pmid = {42546687},
issn = {1097-4172},
abstract = {Breastfeeding reduces the risk of severe lower respiratory infections (sLRIs), a leading cause of infant mortality; however, the protective mechanisms remain elusive. Here, we demonstrated that the absence of milk-derived osteopontin (OPN), highly expressed in colostrum, predisposes neonatal mice to viral and bacterial sLRI, consequent to disrupted dendritic cell (DC) hematopoiesis in the developing liver and lung. Amelioration of disease severity by oral OPN supplementation was associated with increased enteric abundance of Lactobacillaceae and elevated levels of serum 3-phenyllactic acid (PLA), a peroxisome proliferator-activated receptor gamma (PPARγ) agonist. Supplementation with PLA or the PPARγ agonist rosiglitazone restored lung DC hematopoiesis via airway epithelium-derived chemokine ligand 25 (CCL25)-mediated recruitment of lymphoid-myeloid primed progenitors and induction of a supportive lung niche. PLA-induced DC hematopoiesis and disease tolerance were attenuated by plasmacytoid DC depletion, immunoneutralization of stem cell factor, or genetic deletion of airway epithelial Flt3L. Our findings elucidate a microbiome-host interaction by which milk OPN confers protection against sLRI.},
}

@article {pmid42546815,
year = {2026},
author = {Reyes-Martínez, S and Zapata-Martín Del Campo, CM and Tesoro-Cruz, E and Baldi, S and Aguirre-García, MM and Amedei, A},
title = {Neuropsychiatric disorders and gut dysbiosis: what is the real impact of the kynurenine pathway?.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2026.08.001},
pmid = {42546815},
issn = {1873-7544},
abstract = {The human gut microbiome (GM) influences host physiology through the production of bioactive metabolites. Increasing evidence links GM dysbiosis to neuropsychiatric disorders (NPDs), including anxiety disorders, major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ), via bidirectional signaling along the gut-brain axis (GBA). Among the pathways connecting gut and brain, the tryptophan-kynurenine pathway (TKP) has emerged as a central inflammatory and neuromodulatory mechanism. During immune activation and dysbiosis, tryptophan metabolism shifts toward kynurenine production, generating metabolites with distinct biological effects. Kynurenic acid (KYNA) exerts neuroprotective actions through NMDA receptor antagonism and reduced oxidative stress, whereas quinolinic acid (QUIN) and 3-hydroxykynurenine (3-HK) promote excitotoxicity, mitochondrial dysfunction, and neurodegeneration. Altered KYNA/QUIN balance appears to represent a transdiagnostic feature across NPDs, with preferential QUIN accumulation in mood disorders and pathological KYNA elevation in SCZ, suggesting potential potentially therapeutic relevance. In parallel, the aryl hydrocarbon receptor (AhR), activated by tryptophan-derived microbial metabolites, regulates intestinal barrier integrity, immune responses, and neuroimmunometabolic signaling, functioning as a molecular link between the GM, immune system, and brain. This review explores the interactions among GM dysbiosis, TKP alterations, mitochondrial dysfunction, and AhR signaling in anxiety disorders, MDD, BD, and SCZ, highlighting their potential as biomarkers and targets for personalized therapies.},
}

@article {pmid42541272,
year = {2026},
author = {Duru, VC and Mustafa, BE and Beveridge, I and Gauci, C and Elati, K and Ghafar, A and Nijhof, AM and Jabbar, A},
title = {First in vitro feeding of the Australian marsupial tick, Ixodes hirsti Hassall, 1931, with preliminary microbiome profiling and observations on the nymphal morphology.},
journal = {Current research in parasitology & vector-borne diseases},
volume = {10},
number = {},
pages = {100413},
pmid = {42541272},
issn = {2667-114X},
abstract = {Artificial tick feeding systems (ATFS) provide a valuable alternative to animal-based models for studying tick biology. Ixodes hirsti, an Australian tick species that parasitises marsupials, remains understudied due to challenges in laboratory maintenance. Here, we report the first successful in vitro feeding of I. hirsti larvae, provide preliminary microbiome profiles of unfed larvae and larvae recovered after artificial feeding and present the first molecularly confirmed morphological description of the nymphal stage. Field-collected engorged females of I. hirsti were allowed to oviposit under laboratory conditions. Hatched larvae were artificially fed on blood using silicone membranes supplemented with kangaroo hair and/or kangaroo hair extract. Microbiomes were characterised by 16S rRNA amplicon sequencing, while scanning electron microscopy (SEM) and sequencing of 16S rRNA and cox1 genes were used for morphological and molecular characterisation of nymphs. Membranes treated with hair extract alone yielded the highest attachment rate (71%), whereas kangaroo hair-treated membranes produced superior feeding performance, with shorter time to engorgement (9.26 ± 1.00 days) and a higher engorgement weight (0.91 ± 0.01 mg). Exploratory microbiome profiling showed that fed larval pools had numerically lower microbial richness and evenness than unfed larval pools, although these differences were not significant. A total of 80 microbial taxa were shared between groups, whereas seven and 17 taxa were unique to fed and unfed larvae, respectively. Stenotrophomonas was more abundant in fed larval pools, while Coxiella-like and Rickettsia-like endosymbionts were detected in both fed and unfed larvae. These findings demonstrate that ATFS can be adapted for wildlife-associated ticks with specialised host preferences and provide a practical framework for investigating the biology and microbial ecology of ticks.},
}

@article {pmid42541365,
year = {2026},
author = {Zammar, K and AbuAlrob, MA and Ali, M and Lattanzi, S and Mesraoua, B},
title = {The gut microbiome and drug-resistant epilepsy: Microbiome-antiseizure medication interactions and implications for pharmacoresistance.},
journal = {Epilepsia open},
volume = {},
number = {},
pages = {},
pmid = {42541365},
issn = {2470-9239},
abstract = {Drug-resistant epilepsy (DRE) affects approximately one-third of patients with epilepsy and represents a major unmet clinical need. While traditional hypotheses of pharmacoresistance have focused on alterations in drug targets, efflux transporter overexpression, and intrinsic disease severity, the gut microbiome has recently emerged as a potentially modifiable factor that may function as a systems-level modifier of these established mechanisms rather than a standalone pathway. The gut microbiome harbors a vast repertoire of drug-metabolizing enzymes capable of directly biotransforming orally administered antiseizure medications (ASMs)-including valproic acid, lamotrigine, carbamazepine, and oxcarbazepine-thereby altering their pharmacokinetics, bioavailability, and therapeutic efficacy. Additionally, microbial metabolites modulate host cytochrome P450 enzymes, nuclear receptors, and efflux transporters such as P-glycoprotein, while bacterial β-glucuronidases influence the enterohepatic recirculation of glucuronidated ASMs. Conversely, chronic ASM exposure reshapes the gut microbial ecosystem, creating a self-perpetuating cycle of dysbiosis and pharmacoresistance. This narrative review synthesizes current evidence on microbiome-ASM interactions in DRE, proposes a concrete experimental pipeline for characterizing ASM-specific microbial biotransformation, and outlines a framework for integrating physiologically based pharmacokinetic modeling with microbiome data. We discuss clinical implications for epileptologists-including the role of therapeutic drug monitoring in detecting microbiome-mediated pharmacokinetic variability, the concept of microbiome-neutral ASM selection, and earlier deployment of the ketogenic diet as a microbiome-targeted intervention. We highlight the translational potential of pharmacomicrobiomics-the study of how microbiome variation influences drug disposition and response-and identify critical knowledge gaps that warrant future investigation. PLAIN LANGUAGE SUMMARY: About one in three people with epilepsy continue to have seizures despite treatment. This review summarizes growing evidence that the gut microbiome-the community of bacteria living in the intestines-can influence how seizure medications work by altering their absorption, metabolism, and clearance. The medications themselves can reshape the microbiome in return, creating a cycle that may sustain treatment failure. Understanding this gut-drug relationship may open new paths to personalized epilepsy care through diet, probiotics, and microbiome-guided prescribing.},
}

@article {pmid42541589,
year = {2026},
author = {Gao, Y and Jin, Z},
title = {Seed-borne bacteria-mediated seedling microbiome assembly: genetic and metabolic mechanisms of salt tolerance.},
journal = {Archives of microbiology},
volume = {208},
number = {10},
pages = {},
pmid = {42541589},
issn = {1432-072X},
mesh = {*Salt Tolerance/genetics ; *Seedlings/microbiology ; *Microbiota/genetics ; *Bacteria/genetics/metabolism/classification/isolation & purification ; Rhizosphere ; *Seeds/microbiology ; Soil Microbiology ; },
abstract = {Seed-borne bacteria (SbRB) are the initial colonizers of the seedling microbiome, yet their priority effects and community-shaping functions under salt stress have been underexplored. This review synthesizes recent advances in three interconnected areas: vertical transmission and genetic conservation of SbRB; ecological assembly mechanisms driven by priority effects, including niche preemption, environmental modification, and niche differentiation between rhizosphere and phyllosphere; and molecular pathways that confer salt tolerance, with a focus on the potential "pre‑adaptation" and "immune window" mechanisms of SbRB over common rhizosphere plant growth‑promoting rhizobacteria. We further discuss how SbRB recruit and modulate downstream microbiota through metabolic complementation, siderophore‑mediated competition, and host immune reprogramming. Key challenges (low culturability, agricultural disruption, inconsistent field performance) and future directions (flower‑inoculation, synthetic communities, multi‑omics integration) are highlighted. Harnessing seed‑borne bacteria offers a promising strategy for salt‑tolerant microbiome breeding and green agriculture in saline soils.},
}

*Salt Tolerance/genetics
*Seedlings/microbiology
*Microbiota/genetics
*Bacteria/genetics/metabolism/classification/isolation & purification
Rhizosphere
*Seeds/microbiology
Soil Microbiology

@article {pmid42541648,
year = {2026},
author = {Lancaster, E and Ai, Y and Lee, J},
title = {Exploring community-level gut health amidst COVID-19 pandemic: a proposed application of longitudinal wastewater surveillance.},
journal = {Environmental science and pollution research international},
volume = {},
number = {},
pages = {},
pmid = {42541648},
issn = {1614-7499},
abstract = {Wastewater-based epidemiology (WBE) offers a unique, scalable method to monitor disease burden at a community level by capturing all individuals within a sewershed. While emerging evidence suggests that SARS-CoV-2 may influence the human gut microbiota, which is essential for health and disease outcomes, most microbiome studies remain limited to the individual scale. Given wastewater's sensitivity to fluctuations in human fecal composition, we propose leveraging WBE as a cost-effective tool to characterize longitudinal microbial shifts in community-level gut microbiota throughout the COVID-19 pandemic. In this exploratory study, we analyze wastewater from two central Ohio, USA, cities, Columbus and Newark, which differ in socioeconomic and demographic characteristics. Monthly influent samples (n = 69) were collected from August 2020 through June 2022. Clinical COVID-19 cases were collected from within each sewershed, and SARS-CoV-2 gene concentrations were quantified from wastewater samples. 16S rRNA gene sequencing was conducted to characterize human-gut-associated bacterial communities. We report that wastewater influent exhibits distinct genus-level bacterial signatures reflective of each catchment population. Significant temporal changes in bacterial structure and diversity were observed across both cities, indicating community gut health shifts throughout the pandemic. Several taxa, including but not limited to Collinsella, Megasphaera, and Actinobacteriota, showed notable relative abundance fluctuations that may be linked to infection and warrant further investigation as potential microbial biomarkers. This study demonstrates that urban population-level gut microbiome patterns can be robustly characterized through wastewater influent. Most notably, this 23-month study represents the first effort to examine community gut microbiota structural changes across two cities during the COVID-19 pandemic. Our findings highlight sewage as a population-level proxy for public health status and disease burden while offering a novel framework for integrating microbiome science into WBE. This study underscores the potential of wastewater surveillance to advance global infectious disease preparedness and population-scale microbiome research.},
}

@article {pmid42541861,
year = {2026},
author = {Hao, Y and Huang, Y and Cai, H and Chen, R and Liang, X and Huang, X},
title = {Association Between cnm-Positive Streptococci and Cerebral Small Vessel Disease: Insights From Oral Health and Microbiome Status.},
journal = {International dental journal},
volume = {76},
number = {5},
pages = {109787},
doi = {10.1016/j.identj.2026.109787},
pmid = {42541861},
issn = {1875-595X},
abstract = {INTRODUCTION AND AIMS: Cerebral small vessel disease (CSVD) is associated with various severe neurological outcomes; while oral cnm-positive streptococci are suggested to be involved in cerebrovascular lesions, the specific associative features between these bacteria and CSVD have not yet been systematically investigated. This study aims to investigate the prevalence of cnm-positive streptococci in patients with CSVD and explore the correlation between infection and CSVD severity. By integrating oral health indices and microbiome sequencing, we evaluate the oral hygiene status and microbial dysbiosis characteristics of cnm-positive streptococci carriers. Furthermore, cnm-positive streptococci derived from CSVD patients will be isolated, identified, and subjected to whole-genome sequencing to provide a foundation for future research.

METHODS: To explore cnm-positive streptococci prevalence and its association with CSVD, we conducted a case-control study comparing their oral detection rates between healthy controls and CSVD patients. We also performed 16S rRNA gene high-throughput sequencing of oral plaque microbiota and assessed oral health, including the simplified oral hygiene index (OHI-S), the decayed, missing, and filled teeth (DMFT) index, oral hygiene practices, gingival status, and saliva scores.

RESULTS: cnm-positive streptococci were more prevalent in CSVD patients, correlating with higher OHI-S and microbial dysbiosis. Multivariable regression models (adjusted for demographic/vascular risk factors) linked cnm positivity to periventricular hyperintensities (PVH), deep white matter hyperintensities (DWMH), Fazekas score, and total CSVD burden (not cerebral microbleeds (CMBs)/lacunes).

CONCLUSION: Oral cnm-positive streptococci are independently associated with CSVD phenotypes, particularly those characterized by white matter injury. These findings presents a potential oral-cerebrovascular interaction and imply that managing specific virulent oral strains may be a noteworthy consideration in future clinical research.},
}

@article {pmid42542265,
year = {2026},
author = {Liao, G and Zhu, M and Zhang, Y and Zhai, S and Chen, C and Yan, Z and Fu, L and Zheng, L and Song, C and Yu, Y and Tang, H},
title = {Mechanism and Active ingredients of Gancao Qinlian Granules in ameliorating ulcerative colitis:integrated in vivo, in vitro, network pharmacology and untargeted metabolomics investigation.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {122263},
doi = {10.1016/j.jep.2026.122263},
pmid = {42542265},
issn = {1872-7573},
abstract = {Gancao Qinlian Granules (GQG) are a granulated formulation of the classical prescription Gancao Xiexin Tang, originally documented by Zhang Zhongjing in the Treatise on Febrile and Miscellaneous Diseases (Shang Han Za Bing Lun, c. 220 CE). This formula comprises six medicinal components: Glycyrrhiza glabra L. (Gancao), the radix of Scutellaria baicalensis Georgi (Huangqin), Ziziphus jujuba Mill. (Dazao), the rhizomes of Zingiber officinale Roscoe (Ganjiang), the dried tuber of Pinellia ternata (Thunb.) Breit (Banxia) , and the rhizoma of Coptis chinensis Franch (Huanglian). GQG has been extensively employed in traditional and contemporary clinical practice for the treatment of ulcerative colitis (UC). Nevertheless, its candidate bioactive constituents and underlying mechanisms of action remain incompletely elucidated.

AIM OF THE STUDY: To comprehensively characterize the chemical composition of GQG and elucidate its therapeutic mechanisms against UC through an integrated strategy combining network pharmacology prediction, serum/colon/fecal multi-omics profiling (metabolomics and microbiome), and experimental validation.

MATERIALS AND METHODS: Initially, GQG was analyzed by UHPLC-Q-Exactive Orbitrap MS under negative/positive ion modes, with compound identification via mzCloud, HMDB, and literature matching. C57BL/6 mice (n=8/group) were induced with UC using 3% dextran sulfate sodium (DSS) for 15 days. UC-related targets from GeneCard, PharmGkb, TTD, and OMIM were integrated to construct compound-target-pathway networks (Cytoscape 3.10.1). Secondly, GQG (9g/kg/d, 12g/kg/d, 15g/kg/d) or mesalazine (300 mg/kg) was administered orally for 10 days. Disease severity was assessed daily via Disease Activity Index (DAI: weight loss, stool consistency, bleeding). Post-euthanasia, colon length was measured, and histopathology (H&E, Alcian Blue-Periodic Acid Schiff staining) analyzed mucosal damage and goblet cell depletion. Colon IL-1β levels were quantified by immunohistochemistry (IHC). Then, serum, fecal, and colonic tissue samples underwent UHPLC-Q-Exactive Orbitrap MS-based untargeted metabolomics. Differentially expressed metabolites (DEMs) were identified (VIP >1, p<0.05) and pathways enriched via KEGG. Fecal 16S rDNA sequencing (Illumina NovaSeq) analyzed microbial α/β-diversity and differential taxa (LEfSe, LDA score >3). Subsequently, Integrated component analysis, network pharmacology, and metabolomics data to obtain the mechanism by which GQG improves UC, and verify the related target proteins through IHC and Western blot. Finally, obtain the candidate bioactive constituents in GQG through molecular docking, and verify the efficacy of these bioactive constituents with their targets on a cellular model.

RESULTS: Chemical profiling revealed 121 constituents in GQG, with 53 flavonoids (43.8%) including core bioactive markers (e.g., licoflavone B, licuroside). In DSS-induced ulcerative colitis mice, GQG (12g/kg/d) exerted potent therapeutic effects: reducing disease activity index, attenuating colon shortening, restoring goblet cells, and suppressing colon IL-1β. Mechanistically, GQG remodeled gut microbiota composition and function, increasing beneficial taxa (Muribaculaceae, Lactobacillus). This microbiota restructuring directly drove metabolic reprogramming. Suppression of pro-inflammatory metabolism: purine degradation (hypoxanthine), tryptophan-derived uremic toxins (kynurenine), pathogenic bile acids (deoxycholic acid). Integrative analysis of the microbiota-metabolite axis reveals that GQG extract can regulate the NF-κB/NLRP3 inflammasome cascade through p-NF-κB p65 expression, NLRP3 assembly (NLRP3, Caspase-1), and ASC speck formation. Combined with molecular docking, six key components in GQG exhibit high affinity for critical targets. In vitro cellular experiments demonstrate that these core candidate bioactive components effectively inhibit key targets within the target pathway.

CONCLUSIONS: GQG ameliorates UC by modulating gut microbiota structure and function, restoring microbial co-metabolism (e.g., SCFA synthesis, bile acid homeostasis), and subsequently inhibiting the NF-κB/NLRP3 inflammasome axis. This integrated approach substantiates the ethnopharmacological application of GQG for UC.},
}

@article {pmid42542278,
year = {2026},
author = {Shukla, A and Rughwani, D and Aditya, AK and Ray, AK},
title = {The Impact of Climatic Extreme Temperatures on Gut Microbiome-mediated Cardio-Metabolic Health.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128877},
doi = {10.1016/j.envpol.2026.128877},
pmid = {42542278},
issn = {1873-6424},
abstract = {Climate change increases extreme temperature events, like heat and cold waves. Temperature stress can cause gut dysbiosis, potentially affecting cardiometabolic health. In temperature stress conditions, beneficial microbes like Lactobacillus and Bifidobacterium, and favourable metabolites like short-chain fatty acids are observed to be downregulated, while features like Proteobacteria and Prevotella were found to be upregulated. These alterations may lead to upregulation of lipopolysaccharides, trimethylamine N-oxide, and dysregulation in bile acid metabolism, highlighting this as a potential biomarker for disease risk. Furthermore, we discussed mechanistic pathways potentially impacted, including endothelial dysfunction, gut barrier integrity, and energy homeostasis, that link microbial perturbations to metabolic dysfunction and increased risk of cardiometabolic diseases. Moreover, this review proposes potential therapeutic strategies like faecal microbiota transplantation, probiotic supplementation, nanomedicine, and dietary modulation that target the gut microbiome to alleviate the cardiometabolic risks exacerbated by temperature stress. This is the first review to comprehensively synthesize recent scientific findings on the impact of temperature stress in gut microbiome across multiple animal models, and its potential implications on cardiometabolic health.},
}

@article {pmid42542528,
year = {2026},
author = {Zhang, X and Ning, Z and Figeys, D},
title = {Enrichment and Metaproteomic Analysis of Lysine Acetylation in Fecal Microbiome Samples.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3018},
number = {},
pages = {155-168},
pmid = {42542528},
issn = {1940-6029},
mesh = {Acetylation ; Humans ; *Lysine/metabolism ; *Proteomics/methods ; *Feces/microbiology ; Protein Processing, Post-Translational ; *Proteome ; *Microbiota ; *Gastrointestinal Microbiome ; },
abstract = {Among the various posttranslational modifications (PTMs) found in microbiome samples, lysine acetylation is known to be abundant and plays an important role in regulating microbial short-chain fatty acid (SCFA) metabolism. The latter is a crucial microbiome function that significantly impacts human intestinal health. This chapter describes a detailed protocol for lysine acetylomic profiling of microbial proteins in human fecal microbiome samples. The protocol consists of stool sample preprocessing, microbiome protein extraction and digestion, immunoaffinity enrichment of lysine acetylated peptides, and high-resolution mass spectrometry analysis for the identification and quantification of lysine-acetylated proteins.},
}

Acetylation
Humans
*Lysine/metabolism
*Proteomics/methods
*Feces/microbiology
Protein Processing, Post-Translational
*Proteome
*Microbiota
*Gastrointestinal Microbiome

@article {pmid42542576,
year = {2026},
author = {Lin, Z and Zhou, D and Jiang, J and Kwan, P and Tian, X},
title = {The potential role of the lung-brain axis in the pathophysiology of epilepsy: A hypothesis-driven perspective.},
journal = {Genes & diseases},
volume = {13},
number = {6},
pages = {102240},
pmid = {42542576},
issn = {2352-3042},
abstract = {The pathophysiology of epilepsy remains poorly understood. One of the less explored areas is the role of the lung-brain axis, a sophisticated and intricate bidirectional connection between these two vital organs. Inhaled air pollutants can disrupt lung microbiome homeostasis. This disruption, analogous to gut dysbiosis implicated in neurological conditions, may contribute to epilepsy pathogenesis. Here, we review the existing evidence and theoretical foundations supporting the hypothesis that dysbiosis within the lung microbiota may play a role in the pathophysiology of epilepsy. This includes the links between environmental factors (particularly air pollution) and epilepsy susceptibility; the associations between lung-intrinsic microbiota dysregulation and neurological dysfunction; and the underlying molecular, immunological, and neural mechanisms that enable the lung-brain axis to modulate epileptogenesis. Furthermore, we outline the possible potential pathogenic mechanisms of epilepsy from the perspective of the microbiota-lung-brain axis, offer fresh perspectives on the pathophysiology of epilepsy, and explore potential new research directions related to the lung-brain axis and epilepsy. We propose that a deeper understanding of the function of the lung-brain axis will provide new insights into the etiology, diagnosis, prognosis, and treatment of epilepsy.},
}

@article {pmid42542867,
year = {2026},
author = {Zhang, E and Yin, X and Lu, Y and Quan, H and Li, L and Wang, Z and Lan, X},
title = {Characterization of the microbiome and polyphenolic compounds in the medicinal plant Dracocephalum tanguticum.},
journal = {PeerJ},
volume = {14},
number = {},
pages = {e21626},
pmid = {42542867},
issn = {2167-8359},
mesh = {*Polyphenols/analysis/metabolism ; *Microbiota ; *Plants, Medicinal/microbiology/chemistry ; Endophytes/classification/isolation & purification/metabolism/genetics ; *Lamiaceae/microbiology/chemistry ; Plant Leaves/microbiology/chemistry ; Bacteria/classification/isolation & purification/genetics ; Ascomycota/isolation & purification ; Plant Stems/microbiology/chemistry ; Plant Roots/microbiology/chemistry ; Metabolomics ; },
abstract = {Dracocephalum tanguticum (Maxim) is rich in various chemical constituents and is widely used in traditional Zang medicine. Endophytes play a direct or indirect role in the biosynthesis of active compounds and plant growth. However, little is known about the characteristics of endophytes and polyphenolic compounds in the various organs of D. tanguticum. In this study, high-throughput sequencing and polyphenol-targeted metabolomics were employed to analyze endophytic community diversity and assembly processes, polyphenolic compound content, and their correlations. The results showed that the endophytic compositions of the leaf and stem organs were similar, and significantly different from that in the root organs; however, the endophytic diversity did not differ significantly across the various organs. Actinobacteriota and Pseudomonadota were the dominant bacterial phyla, Ascomycota and Basidiomycota were the dominant fungal phyla in the various organs, while the dominant endophytic genera were significantly different. The endophytic community assembly was influenced mainly by stochastic processes in the various organs. A total of 75 polyphenolic compounds were identified, and the contents of the polyphenolic compounds in the various organs of D. tanguticum differed significantly. The correlation analysis revealed varying degrees of positive and negative correlation between endophytes and polyphenolic compounds. These findings clarify the characteristics of the endophytes and polyphenolic compounds, and lay a theoretical foundation for the identification and application functional microbiomes in the D. tanguticum.},
}

*Polyphenols/analysis/metabolism
*Microbiota
*Plants, Medicinal/microbiology/chemistry
Endophytes/classification/isolation & purification/metabolism/genetics
*Lamiaceae/microbiology/chemistry
Plant Leaves/microbiology/chemistry
Bacteria/classification/isolation & purification/genetics
Ascomycota/isolation & purification
Plant Stems/microbiology/chemistry
Plant Roots/microbiology/chemistry
Metabolomics