@article {pmid42684938,
year = {2026},
author = {Petry, B and Boggiatto, PM and Buckley, A and Cassmann, ED and Sarlo Davila, K and Olsen, SC and Fernandes, LGV and Tibbs-Cortes, B and Rahic-Seggerman, FM and Palmer, MV and Putz, EJ},
title = {Temporal transcriptomic and microbiome changes in American bison during experimental SARS-CoV-2 challenge.},
journal = {G3 (Bethesda, Md.)},
volume = {},
number = {},
pages = {},
doi = {10.1093/g3journal/jkag231},
pmid = {42684938},
issn = {2160-1836},
support = {//U.S. Department of Agriculture/ ; //American Rescue Plan (ARP)/ ; #3625-32000-232-00D//Agricultural Research Service (ARS)/ ; //Animal and Plant Health Inspection Service (APHIS)/ ; //Wildlife Services (WS)/ ; //ARS Research Participation Program/ ; //Oak Ridge Institute for Science and Education (ORISE)/ ; //U.S. Department of Energy (DOE)/ ; //ORAU/ ; DE-SC0014664//DOE/ ; },
abstract = {Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to pose a threat to humans as well as domestic and wild animals. The variability in severity of clinical signs, the zoonotic potential, and the host-specific response to infection contribute to the persistence of circulation of disease. In wildlife species, white-tailed deer have been shown to be more permissive to infection than bovids. However, among bovids, American bison have shown a greater susceptibility than cattle. In this study, we investigate the transcriptomic response to experimental SARS-CoV-2 infection in bison over time. Substantial numbers of differentially expressed genes were identified between pre- and 2, 5, 7, 14, and 21 days post-inoculation. Kyoto Encyclopedia of Genes and Genomes and Gene Ontology term analysis identified associations with immune response, inflammatory response, and viral infection including COVID-19. Ingenuity Pathway Analysis of the coronavirus pathway highlighted differences in signaling at days 2 versus 21 post-inoculation. We additionally examined changes in the nasal microbiome of bison over the course of experimental infection, which suggested an increase in opportunity for secondary infection causing pathogens such as Mannheimia. Collectively, this study presents a profile of bison transcriptomic response to SARS-CoV-2 infection and continues to expand our understanding of variation in host response.},
}

@article {pmid42685157,
year = {2026},
author = {Abedi, AA and Pourbozorg, G and Abdou, M and Hoveidaei, AH and Parvizi, J and Citak, M},
title = {Changes in the Management of Periprosthetic Joint Infection Over the Past 50 Years.},
journal = {The Journal of bone and joint surgery. American volume},
volume = {},
number = {},
pages = {},
doi = {10.2106/JBJS.26.00650},
pmid = {42685157},
issn = {1535-1386},
abstract = {➢ Periprosthetic joint infection (PJI) remains a major complication of joint arthroplasty, associated with morbidity and health-care burden. Although room for progress remains, the management of PJI has evolved over the past 50 years from empiric, procedure-centered approaches to structured, evidence-based, and biologically informed strategies.➢ This article summarizes key developments in the prevention, diagnosis, and treatment of PJI, driven by advances across multiple clinical and scientific subspecialties.➢ Diagnostic approaches have advanced from reliance on clinical findings and culture to a multimodal framework integrating validated criteria, serological and synovial biomarkers, and molecular techniques. Surgical management has similarly evolved toward individualized strategies, including debridement with implant retention, 1-stage or 2-stage revision, and salvage surgery tailored to host, pathogen, and disease characteristics.➢ Advances in microbiology, particularly the recognition of biofilm and the emerging role of the human microbiome, have further reshaped the understanding of PJI. Overall, this article examines how developments in prevention, diagnosis, surgical treatment, and microbiology have driven a transition toward precision-based, biology-informed, and individualized management of PJI.},
}

@article {pmid42685222,
year = {2026},
author = {Feng, C and Gao, G and He, Q and Kwok, LY and Liu, C and Li, C and Dong, L and Sun, Z and Zhang, H},
title = {Bifidobacterium animalis subsp. lactis V9 overcomes CYFRA 21-1-linked immunochemotherapy resistance in NSCLC via microbial metabolites.},
journal = {Science advances},
volume = {12},
number = {36},
pages = {eaeg8202},
pmid = {42685222},
issn = {2375-2548},
mesh = {Humans ; *Carcinoma, Non-Small-Cell Lung/therapy/immunology/metabolism/drug therapy ; Animals ; *Lung Neoplasms/therapy/immunology/metabolism/drug therapy/microbiology ; *Bifidobacterium animalis/metabolism ; *Antigens, Neoplasm/blood/metabolism ; Mice ; *Keratin-19/blood/metabolism ; *Drug Resistance, Neoplasm ; Female ; Immunotherapy ; Male ; },
abstract = {Gut dysbiosis drives therapeutic resistance, yet the relationships among typical tumor markers, gut microbiota, and treatment efficacy remain poorly defined. Here, elevated serum CYFRA 21-1 in advanced non-small cell lung cancer (NSCLC) correlates with gut dysbiosis, including Bifidobacterium animalis depletion and reduced immunomodulatory metabolites. Fecal supernatant from patients with high-CYFRA attenuated immunochemotherapy efficacy in tumor-bearing mice, linked to disrupted tryptophan and phenylalanine metabolism. Adjuvant B. animalis subsp. lactis V9 enhanced tumor control and antitumor immunity, coinciding with elevated quinaldic acid and catechol, metabolites associated with caspase-dependent apoptosis and ferroptosis. Cell-free fecal supernatant transferred antitumor effects, independent of bacterial colonization. In a randomized, double-blind, placebo-controlled pilot trial (n = 30), adjunctive B. lactis V9 associated with a higher objective response rate (47% versus 33%), disease control rate (87% versus 67%), and prolonged progression-free survival in responders, who exhibited enriched B. animalis and elevated quinaldic acid/catechol (area under the curve = 0.73/0.82). These findings suggest CYFRA 21-1 may identify a modifiable, microbiome-linked state of treatment resistance.},
}

Humans
*Carcinoma, Non-Small-Cell Lung/therapy/immunology/metabolism/drug therapy
Animals
*Lung Neoplasms/therapy/immunology/metabolism/drug therapy/microbiology
*Bifidobacterium animalis/metabolism
*Antigens, Neoplasm/blood/metabolism
Mice
*Keratin-19/blood/metabolism
*Drug Resistance, Neoplasm
Female
Immunotherapy
Male

@article {pmid42685246,
year = {2026},
author = {Lei, S and Qiu, X and Wang, Z and Zhang, Z and Zha, A and Zhou, Y and Chen, H and Huang, J and Yu, Z},
title = {Gut microbial H2S promotes metabolic dysfunction in mice via hepatic PPARα suppression.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag226},
pmid = {42685246},
issn = {1751-7370},
abstract = {This study investigates the role of gut microbiota-derived hydrogen sulfide (H2S) in obesity and glucose metabolism disorders. By integrating human gut metagenomic data, intervention experiments in mouse models, and in vitro cellular assays, we identified a signature of microbial sulfur metabolism in human cohorts and provided experimental evidence for its causal role and underlying metabolic mechanisms in mice. In clinical cohorts with obesity and glucose metabolism disorders, we observed a notable enrichment of genes involved in sulfur transport and H2S production. In mouse models, administration of H2S-producing Desulfovibrio desulfuricans, engineered Escherichia coli expressing phsABC, and the H2S donor NaHS consistently induced body weight gain and impaired glucose tolerance. Transcriptome analysis and cellular experiments indicated that H2S was associated with downregulation of the PPAR signaling pathway and lipid metabolism pathways in the liver, which may contribute to the abnormal accumulation of lipids and glycogen. Furthermore, rescue experiments using a PPAR agonist and an H2S adsorbent partially reversed these metabolic abnormalities. Collectively, our work provides experimental evidence in mouse models demonstrating that gut microbial H2S promotes metabolic dysfunction through hepatic PPARα suppression, providing potential targets for microbiome-based therapeutic interventions.},
}

@article {pmid42685265,
year = {2026},
author = {Ren, J and Yang, Z and Liu, W and Tat Alexander Ng, M},
title = {AResKGLM: a graph-grounded language-model framework for interpretable multi-hop antimicrobial resistance reasoning.},
journal = {Briefings in bioinformatics},
volume = {27},
number = {5},
pages = {},
doi = {10.1093/bib/bbag456},
pmid = {42685265},
issn = {1477-4054},
support = {//Tencent AI for Life Sciences Lab/ ; },
mesh = {*Computational Biology/methods ; Large Language Models ; *Drug Resistance, Microbial ; Humans ; },
abstract = {Antimicrobial resistance (AMR) threatens microbiology and microbiome bioinformatics because resistance phenotypes are shaped by interactions among genes, mobile genetic elements, and functional environments across microbial communities. Prioritizing resistance determinants requires models that reason across knowledge graphs (KGs) linking genes, proteins, pathways, drugs, and microbial phenotypes. Existing graph-based methods compress this evidence into scalar scores, whereas large language models can produce explanations not grounded in structured evidence. We developed AResKGLM (Antimicrobial Resistance Knowledge Graph Language Model), a graph-grounded language-model framework for interpretable microbial AMR bioinformatics that serializes breadth-first-search-retrieved multi-hop paths and per-entity biomedical descriptions into a structured Context-Path-Question prompt. Llama-3-8B and DeepSeek-R1-7B are adapted with QLoRA to produce binary link predictions and concise reasoning traces. On the KIDs benchmark, AResKGLM (Llama-3-8B) achieved F1 = 0.8482, outperforming KG-BERT (0.7213), NBFNet (0.5260), and ULTRA (0.2541) (paired Wilcoxon $p = 1.2 \times 10^{-7}$
). Its advantage increased with reasoning depth: F1 decreased from 0.9197 at 2 hops to 0.8148 at 6 hops, whereas KG-BERT dropped from 0.8110 to 0.6716. Counterfactual path corruption produced an apparent F1 of 0.000, mechanically forced by the probe label assignment; the operative diagnostic is the per-sample flip rate (0.04-0.16), consistent with sensitivity to supplied biological evidence rather than reliance on pretrained priors alone. Cross-species evaluation yielded F1 = 0.81-0.88 with Matthews correlation coefficient (MCC) = 0.35-0.54 on Mycobacterium tuberculosis, Pseudomonas aeruginosa, and Staphylococcus aureus. Temporal ranking of 81 post-2022 gene-drug associations achieved Precision@20 = 100% and AUC-PR = 0.855. AResKGLM offers an interpretable, reproducible framework for multi-hop AMR reasoning, linking candidate prioritization with mechanism-oriented hypothesis generation.},
}

*Computational Biology/methods
Large Language Models
*Drug Resistance, Microbial
Humans

@article {pmid42685266,
year = {2026},
author = {Colajanni, A and Uricaru, R and Darko, S and Subramanian, R and Douek, DC and Thiébaut, R and Thebault, P},
title = {Benchmarking methods for extracting microbial signal from host-dominated metatranscriptomes.},
journal = {Briefings in bioinformatics},
volume = {27},
number = {5},
pages = {},
doi = {10.1093/bib/bbag454},
pmid = {42685266},
issn = {1477-4054},
mesh = {Humans ; *Microbiota/genetics ; Benchmarking ; *Transcriptome ; *Gene Expression Profiling/methods ; Sequence Analysis, RNA/methods ; *Computational Biology/methods ; },
abstract = {Human RNA sequencing (RNA-seq) data originally generated for human transcriptome profiling are overwhelmingly dominated by host sequences, yet they often contain a small fraction of non-human reads that can be exploited for microbial detection. When such datasets are repurposed for secondary microbiome-oriented analyses, extracting and accurately classifying this weak microbial signal becomes technically challenging, and no ready-to-use pipeline currently exists. In this study, we evaluate computational strategies for filtering host reads and classifying microbial transcripts in host-dominated RNA sequencing data. We compare assembly-based approaches similar to those used in a previous study focusing on microbial translocation with state-of-the-art assembly-free methods, and assess their respective strengths and limitations using simulated datasets reflecting low microbial abundance. Our results show that assembly-based methods yield accurate taxonomic predictions but struggle at low read depth, whereas assembly-free methods are more robust in sparse settings at the cost of reduced precision. To leverage the complementarity of both approaches, we propose a hybrid pipeline that integrates assembly-based and assembly-free classification. On simulated data, this hybrid strategy improves microbial classification performance compared with either approach alone. Application to a real human metatranscriptomic dataset analyzed in a microbial translocation context illustrates the broader microbial signal captured by the hybrid approach, despite intrinsic challenges related to the absence of reliable ground truth and the risk of host read misclassification. Our work provides a framework for extracting microbial signals from host-dominated human metatranscriptomes, enabling the reuse of existing transcriptomic datasets for microbiome-related analyses, including but not limited to microbial translocation studies.},
}

Humans
*Microbiota/genetics
Benchmarking
*Transcriptome
*Gene Expression Profiling/methods
Sequence Analysis, RNA/methods
*Computational Biology/methods

@article {pmid42685372,
year = {2026},
author = {Kim, C and Kim, C and Choi, IG and Kalčíková, G and Laforsch, C and Jung, J},
title = {Contrasting effects of conventional PET and biodegradable PHB microplastics on population dynamics and gut microbiome responses in Daphnia magna.},
journal = {Aquatic toxicology (Amsterdam, Netherlands)},
volume = {300},
number = {},
pages = {107982},
doi = {10.1016/j.aquatox.2026.107982},
pmid = {42685372},
issn = {1879-1514},
abstract = {Research on the ecotoxicity of biodegradable microplastics (MPs) in Daphnia magna is rapidly growing, while their population-level effects remain unclear. This study compared the population-level effects of conventional MPs (polyethylene terephthalate, PET) and biodegradable MPs (polyhydroxybutyrate, PHB) on D. magna over 45 days. Gut microbiome and transcriptomic analyses were also conducted to elucidate the underlying mechanisms of the observed responses. PET MPs significantly (p < 0.05) decreased D. magna population biomass relative to control, whereas PHB MPs showed no significant effects. Both types of MPs altered the gut microbial community structure of D. magna, with PHB inducing a selective increase in potential degraders. Transcriptomic data showed that PET MPs significantly (p < 0.05) increased the expression of genes related to stress and defense responses. In contrast, PHB MPs significantly (p < 0.05) upregulated genes associated with metabolic processes. Further research incorporating direct assessment of PHB degradation, host energy assimilation, and wider range of exposure concentrations is required to clarify the mechanisms underlying the distinct responses to biodegradable and conventional MPs. This study highlights the importance of considering polymer types in MP environmental risk assessments and underscores the need of integrating multiple endpoints for a comprehensive evaluation.},
}

@article {pmid42685478,
year = {2026},
author = {Wang, Y and Zhang, Y and Gao, F and Liu, J and He, Y and He, J and Xu, G},
title = {Self-sustaining microbial reductive debromination of brominated flame retardants driven by sewage sludge-derived endogenous organics amid competing electron acceptors.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143412},
doi = {10.1016/j.jhazmat.2026.143412},
pmid = {42685478},
issn = {1873-3336},
abstract = {Polybrominated diphenyl ethers (PBDEs) and tetrabromobisphenol A (TBBPA) are prevalent brominated flame retardants in wastewater and sewage sludge, yet the sustainability and robustness of their microbial reductive debromination remain poorly understood, particularly in the presence of co-existing electron acceptors (e.g., nitrate and sulfate). Here we revealed that sewage sludge-derived endogenous organic matter sustained efficient microbial reductive debromination of both TBBPA and PBDEs without external organics amendment. Over 99% TBBPA was transformed to bisphenol A within 30 days, whereas PBDE debromination occurred sequentially after TBBPA depletion, producing lower-brominated congeners (33.9%) and diphenyl ether (17.9%) after 120 days. Unexpectedly, amendment of external organic carbons (formate, acetate, pyruvate, and lactate) did not enhance debromination and instead stimulated methanogenesis, indicating diversion of electron flow towards competing reduction pathways. Reductive debromination remained highly active in the presence of 0.5-10 mM nitrate and sulfate, and similar debromination extent of both pollutants was achieved as the controls, although high nitrate and sulfate concentrations decreased TBBPA debromination rates by 42.8-67.4%. Notably, active debromination persisted even at sulfide concentrations exceeding 6 mM generated from sulfate reduction, revealing exceptional sulfide tolerance of sludge-associated organohalide-respiring bacteria (OHRB). Dehalococcoides and Dehalobacter were identified as obligate OHRB involved in debromination, with Dehalococcoides exhibiting high tolerance to nitrate-, sulfate-, and sulfide-associated stress. Moreover, the sludge microbiome was resilient and metabolically integrated despite redox perturbations. Collectively, these findings reveal sewage sludge as a self-sustaining and resilient platform for reductive debromination and provide a low-cost strategy for remediation of brominated pollutants in wastewater, sludge and other anaerobic environments.},
}

@article {pmid42685797,
year = {2026},
author = {Spencer, S and Valenzuela, KN and Cheng, Z and Leung, B},
title = {Spatially controlled polymicrobial human airway model recapitulates complex interactions between Pseudomonas aeruginosa and lung commensals.},
journal = {Biomedical materials (Bristol, England)},
volume = {},
number = {},
pages = {},
doi = {10.1088/1748-605X/aea1cc},
pmid = {42685797},
issn = {1748-605X},
abstract = {Airway barrier dysfunction is a hallmark of chronic lung diseases including cystic fibrosis, asthma, and chronic obstructive pulmonary disease, and is often shaped by polymicrobial rather than single-species interactions with the host tissue. However, extended host-microbe co-culture with rapid-colonizing airway pathogens such as Pseudomonas aeruginosa is difficult to sustain in accessible in vitro systems, limiting mechanistic study of polymicrobial barrier and inflammatory dynamics. Here we developed and validated an aqueous two-phase system (ATPS) that spatially confines bacterial communities over a human bronchial epithelial-endothelial transwell co-culture, extending the stable co-culture window to 24 h while preserving assayable barrier and cytokine readouts. Using a validation-by-recapitulation approach, the platform reproduced established in vivo phenomena: P. aeruginosa-driven barrier disruption, attenuation of pathogenic effects by the commensals R. mucilaginosa and L. casei with preserved junctional architecture, and S. pneumoniae exacerbation of barrier permeability accompanied by elevated IL-8 despite apparent junctional preservation. This accessible ATPS-based biomaterials platform requires no microfluidic or iPSC-derived components and provides a tractable foundation for mechanistic studies of polymicrobial interactions at the airway epithelial barrier.},
}

@article {pmid42685805,
year = {2026},
author = {Arena, L and Prescott, MP},
title = {Parental Factors Associated with US Youth Ultra-Processed Food Outcomes: A Systematic Review.},
journal = {Appetite},
volume = {},
number = {},
pages = {108774},
doi = {10.1016/j.appet.2026.108774},
pmid = {42685805},
issn = {1095-8304},
abstract = {Ultra-processed food (UPF) comprises 67% of the average US youth diet, among the highest rates globally. Health burdens associated with youth UPF intake include overweight/obesity, glucose dysregulation, poor cardiovascular health, liver disease, microbiome disruption, dental problems, DNA damage, mental health concerns, and lower cognitive and academic performance. This systematic review investigates parental factors associated with US youth UPF intake, preference, selection, or access. A comprehensive literature review was conducted using PRISMA guidelines. PubMed, CINAHL, Scopus, and Web of Science databases were searched. Inclusion criteria required studies to examine youth (aged 0-19) UPF outcomes and parental factors. The Mixed Methods Appraisal Tool assessed study bias and quality. PROSPERO registration number: CRD420251248701. The search yielded 1727 articles, 888 after duplicates removed. Full text review resulted in 11 extracted articles: 9 quantitative and 2 qualitative. Parental factors associated with child UPF outcomes included education level, gender (female), UPF intake, more frequent soda and fast-food intake, belief in food advertising, reward-based eating drive, allowing youth to watch greater hours of TV, and the home food environment. Mixed findings were found with parental substance use, depending on prenatal, maternal, and paternal use, cigarette, alcohol, or illicit drugs, and child age. Notable null findings included parent age, living with a partner, household income, shared family meals, human milk exposure, and parent motivation, attitude, and self-efficacy to limit junk food and eat more fruits/vegetables. Further research around parental factors and US youth UPF intake is warranted. Intervening in identified target areas may help mitigate youth UPF outcomes.},
}

@article {pmid42685867,
year = {2026},
author = {Zhang, L and Chun, Y and Valeiron, S and Grishina, G and Lo, T and Wang, J and Sicherer, S and Bunyavanich, S},
title = {Coordinated changes in oral propionate, oral microbiota, and peripheral blood inflammatory processes during peanut oral immunotherapy.},
journal = {The Journal of allergy and clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaci.2026.08.015},
pmid = {42685867},
issn = {1097-6825},
abstract = {BACKGROUND: Peanut allergy is an increasingly prevalent condition without curative treatment. Oral immunotherapy (OIT) can induce desensitization, but its mechanisms are not fully understood. Administration of oral short-chain fatty acids (SCFAs) in murine models induces favorable immunomodulation that overlaps with processes observed in OIT. We hypothesized that in human populations, oral SCFA levels change during OIT and are associated with systemic downregulation of Type 2 processes.

METHODS: Within a clinical trial of children age 4-14 years with high-threshold peanut allergy randomized to OIT or avoidance, we profiled oral SCFA levels, the oral microbiome, and peripheral blood transcriptome over the course of OIT or avoidance. Statistical and network analyses were carried out to test our hypotheses.

RESULTS: Among the 56 children in the clinical trial with complete multi-omic profiles over the trial duration, 29 were randomized to OIT and 27 to avoidance. 100% of the participants in the OIT group achieved desensitization compared to 18.5% in the avoidance group. Oral levels of the SCFA propionate increased with OIT but not avoidance (FDR=0.042) and remained elevated with sustained unresponsiveness. Oral propionate levels positively correlated with the relative abundances of several oral microbes, including known propionate producers Prevotella spp. (r=0.47, FDR 3.75x 10-3) and Veillonella (r=0.39, FDR 1.45x10-2). Oral propionate levels negatively correlated with peripheral blood transcript expression of OIT-associated Fcγ receptors (FDR≤ 0.05), IL-4 & IL-13 signaling (FDR≤ 0.05), and neutrophil degranulation pathways (FDR≤ 0.05).

CONCLUSIONS: This study raises the intriguing possibility of oral propionate serving as an important immunoregulatory bridge between local and systemic processes in peanut OIT.

TRIAL REGISTRATION: ClinicalTrials.gov NCT03907397.},
}

@article {pmid42685930,
year = {2026},
author = {Babenkova, PI and Golovina, NA and Reprintseva, VN and Karaulova, SO and Vostrikova, AD and Burakova, IY and Pogorelova, SV and Smirnova, YD and Morozova, PD and Shutikov, VA and Mikhailov, EV and Kozin, SV and Dzhimak, SS and Gureev, AP and Syromyatnikov, MY},
title = {Comenic acid as a modulator of the gut-testis axis in pyridaben-induced toxicity.},
journal = {Reproductive toxicology (Elmsford, N.Y.)},
volume = {},
number = {},
pages = {109342},
doi = {10.1016/j.reprotox.2026.109342},
pmid = {42685930},
issn = {1873-1708},
abstract = {Pyridaben is an acaricide that inhibits mitochondrial complex I, which disrupts mitochondrial viability and causes oxidative stress. Pyridaben administration was associated with significant damage to mitochondrial DNA (mtDNA) in mice. The oxidative stress related to pyridaben exposure also co-occurred with alterations in the morphology of the testes and intestines, leading to the activation of the Nrf2-dependent protective pathway in testicular tissue, reduction of the seminiferous tubule lumen accompanied by interstitial tissue swelling, and adaptive changes in the intestinal epithelial tissue. Comenic acid (CA) exhibits active antioxidant properties; in the group receiving CA, the mtDNA copy number increased. Functionally, pyridaben considerably reduced the alpha diversity of the intestinal microbiome, while CA administration appeared to normalize this indicator, also mitigating shifts in beta diversity. Taxonomic analysis revealed that pyridaben elevated the abundance of the families Bacteroidaceae and Muribaculaceae, which aligned with a functional upregulation of endotoxic dTDP-β-L-rhamnose and L-lysine biosynthesis pathways. Conversely, CA treatment attenuated these shifts, reducing opportunistic taxa while concurrently upregulating protective pathways, including folate transformations and CDP-diacylglycerol biosynthesis. These findings suggest that CA, potentially due to its antioxidant properties and modulation of the intestinal microbial and functional profiles, may exert a compensatory effect against pyridaben-induced toxicity via the gut-testis axis.},
}

@article {pmid42686068,
year = {2026},
author = {Zhou, J and Gu, T and Li, S},
title = {A bioinformatics framework using public 16S rRNA gene amplicon data to assess the presence of target bacteria in bat and rodent samples.},
journal = {Journal of microbiological methods},
volume = {},
number = {},
pages = {107684},
doi = {10.1016/j.mimet.2026.107684},
pmid = {42686068},
issn = {1872-8359},
abstract = {Validating the ecological distribution of a newly isolated bacterial species in natural hosts remains challenging due to the lack of specific detection assays and the cost of large-scale screening. Here, we describe a dual-strategy bioinformatics pipeline that leverages publicly available 16S rRNA gene amplicon sequencing data to reliably and inexpensively confirm target bacterial presence. The method first extracts hypervariable regions from the target bacterium's full-length 16S rRNA gene and evaluates their specificity by calculating an A-value-defined as the highest sequence similarity to any non-target strain in reference databases. Regions with an A-value below the 98.7% species threshold are selected. These are then aligned against Amplicon Sequence Variants (ASVs) from public datasets to compute a B-value (highest similarity to ASVs within a sample). A novel classification logic (B > A) is applied to designate samples as positive or negative, reducing false positives. The pipeline incorporates multi-level controls, including process/biological negatives and positives. Testing with novel species (Clostridium sp. nov.) and a formally described species (Streptococcus lishijunsis), along with common commensal species demonstrated that region-specific performance varies, highlighting the need for pre-validation. The framework successfully distinguished target-positive from negative samples, with phylogenetic support for specificity. This approach provides a rigorous, cost-effective, and accessible workflow that links in vitro isolation to in vivo ecological validation using existing public data.},
}

@article {pmid42686295,
year = {2026},
author = {Schouten, D and Wiersinga, WJ and van Vught, L},
title = {Post-Sepsis Syndrome: From Pathogenesis Toward Novel Management Strategies.},
journal = {Critical care clinics},
volume = {42},
number = {4},
pages = {745-761},
doi = {10.1016/j.ccc.2026.05.003},
pmid = {42686295},
issn = {1557-8232},
mesh = {Humans ; *Sepsis/complications/therapy/physiopathology ; Post-Infectious Disorders ; Patient Readmission/statistics & numerical data ; },
abstract = {Sepsis survivorship is increasing, but many survivors develop post-sepsis syndrome, marked by high early readmission rates and new-onset conditions, notably recurrent infections, cardiovascular, psychiatric, and kidney disease. Persistent physical, cognitive, and psychological sequelae may further impair daily functioning. Emerging evidence suggests lasting immune dysregulation, likely interacting with mitochondrial dysfunction, immunosuppression, endothelial injury, low-grade inflammation, and microbiome disruption. While evidence for targeted postdischarge interventions remains limited and yields mixed results, much can still be done. Several strategies can begin during hospitalization, and after discharge a primary-care-centered, risk-stratified follow-up pathway may support recovery and reduce readmissions and complications.},
}

Humans
*Sepsis/complications/therapy/physiopathology
Post-Infectious Disorders
Patient Readmission/statistics & numerical data

@article {pmid42686665,
year = {2026},
author = {Morris, MJ and Jaggernath, KC and Martin, AD and Ramdass, RS},
title = {The Puerperium in the Modern Dairy Cow: A Review.},
journal = {Reproduction in domestic animals = Zuchthygiene},
volume = {61 Suppl 2},
number = {},
pages = {e70303},
doi = {10.1111/rda.70303},
pmid = {42686665},
issn = {1439-0531},
mesh = {Animals ; Female ; Cattle/physiology ; *Postpartum Period/physiology ; Uterus/physiology ; Pregnancy ; Cattle Diseases/physiopathology ; Uterine Diseases/veterinary ; Fertility/physiology ; },
abstract = {The puerperium represents a critical physiological period during which the bovine reproductive tract transitions from pregnancy to renewed fertility. In the modern high-producing dairy cow, this transition is challenged by profound metabolic, endocrine, immunological, and structural demands that collectively influence uterine health, ovarian function, and subsequent reproductive performance. This review examines current understanding of the physiology of the puerperium in dairy cattle, with particular emphasis on uterine involution, immune clearance of postpartum contamination, endocrine regulation, and resumption of ovarian cyclicity. Further, it contrasts high-yielding Holsteins with fertility selected dairy populations. Normal uterine involution involves coordinated myometrial contraction, tissue remodelling, endometrial regeneration, and tightly regulated inflammatory responses. Failure of these processes predisposes cows to postpartum uterine disorders, including retained fetal membranes, metritis, endometritis (purulent vaginal discharge with cytological confirmation), and pyometra, which remain major contributors to subfertility and economic loss. Central to the pathophysiology of puerperal disease is negative energy balance, which disrupts immune competence, alters hepatic steroid metabolism, impairs ovarian signalling, and compromises oocyte and embryo quality. Emerging evidence highlights the complex interplay between metabolism, immunity, and the uterine microbiome, shifting current perspectives away from pathogen-centric models toward host resilience. Advances in biomarkers, genomic selection, and precision monitoring offer new opportunities for targeted reproductive management. Ultimately, optimisation of transition period management remains the cornerstone of supporting physiological puerperal recovery and sustaining reproductive efficiency in modern dairy systems.},
}

Animals
Female
Cattle/physiology
*Postpartum Period/physiology
Uterus/physiology
Pregnancy
Cattle Diseases/physiopathology
Uterine Diseases/veterinary
Fertility/physiology

@article {pmid42686848,
year = {2026},
author = {Wu, Y and Liu, F and Liu, Y and Zheng, M and Sun, J and Shi, X and Wu, J and Du, Y and Deng, H and Zhou, X},
title = {Dynamic biomass micro-nanofibre framework for entrapment and clearance of gastrointestinal microplastics.},
journal = {Nature nanotechnology},
volume = {},
number = {},
pages = {},
pmid = {42686848},
issn = {1748-3395},
support = {52373062//National Natural Science Foundation of China (National Science Foundation of China)/ ; 52173061//National Natural Science Foundation of China (National Science Foundation of China)/ ; 52573122//National Natural Science Foundation of China (National Science Foundation of China)/ ; 52203069//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Microplastics (MPs) are infiltrating global food systems, where they disseminate systemically, posing unmet health risks as current strategies fail to prevent bioaccumulation. We have engineered an oral alginate-chitin micro-nanofibre framework (Alg-Ch) as a pH-responsive scavenger, which was formed via lyophilization-induced hydrogen bonding and physical entanglement between alginate microfibres and chitin nanofibrous sheets (1:10 ratio). Alg-Ch captured MPs predominantly through two mechanisms: electrostatic adsorption onto a protonated chitin nanonetwork in gastric acid, and physical entrapment by swollen alginate at intestinal pH. It captured 500-nm spherical MPs of varying surface chemistry (polystyrene (PS), PS-COOH, PS-NH2) and composition (polyethylene terephthalate, polymethyl methacrylate), and irregular fragments including PS fibres, polypropylene, and polyethylene, achieving capacities of 816.6 mg g[-1] (stomach) and 1114.5 mg g[-1] (intestine), and retained >47% efficacy with food. In mice, Alg-Ch reduced colonic MP fluorescence by ∼50% within 2 h and accelerated faecal elimination. A 13-week Alg-Ch intervention restored tight-junction proteins ZO-1, occludin and claudin-5, decreased serum levels of interleukin-6, lipopolysaccharide, tumour necrosis factor and interleukin-1β, and promoted recovery of short-chain fatty acid-producing genera, with no evidence of body-weight loss, organ toxicity or histopathological lesions. This biocompatible platform unifies mechanical sequestration, barrier repair and microbiome rehabilitation, offering a scalable strategy to mitigate the risks of ingested MPs and the global health burden of plastic pollution.},
}

@article {pmid42687109,
year = {2026},
author = {Capparotto, A and Ciampanelli, A and Salvucci, P and Chesneau, G and Herpell, J and Sello, S and Sudiro, C and Clauw, P and Altissimo, A and Hacquard, S and Vuolo, F and Giovannetti, M},
title = {Plant genetic and root-associated microbial diversity modulate Lactuca sativa responsiveness to a soil inoculum under phosphate deficiency.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71529},
pmid = {42687109},
issn = {1469-8137},
support = {//NextGenerationEU/ ; //Ministero dell'Università e della Ricerca/ ; //Università degli Studi di Torino - Dipartimento di Scienze della Vita e Biologia dei Sistemi/ ; },
abstract = {Microbial-based approaches offer a promising strategy to decrease the use of chemical fertilizers in agriculture. Among them, arbuscular mycorrhizal fungi (AMF), which extend root surface area and enhance phosphate uptake, and phosphate-solubilizing bacteria (PSB) are particularly relevant. However, their effectiveness depends strongly on plant genetic diversity. To identify genetic markers underlying plant responses to beneficial soil microbes, we studied a panel of 128 fully sequenced Lactuca sativa varieties under controlled phosphate-starvation conditions and treated with AMF and PSB. Lettuce genetic variation showed a strong effect on physiological and morphological responses to microbial inoculation. Genome-wide association studies identified specific genomic regions associated with changes in leaf phosphate content and shoot biomass following treatment. Beyond genetic factors, we observed shifts in fungal β-diversity and increased bacterial α-diversity associated with phenotypic variation. We also identified 44 amplicon sequence variants associated with agriculturally relevant traits. Among these, six bacterial strains were experimentally validated through in vitro and pot experiments for their effects on leaf phosphate concentration and shoot biomass. Overall, we highlighted key genetic, microbial, and physiological mechanisms that may enhance microbial treatments for improved plant phosphate management in lettuce.},
}

@article {pmid42687557,
year = {2026},
author = {Vorobev V, A and Gadzhieva Z, K and Malov S, I and Syrova A, I and Su-Yanz K, M and Syrova A, I},
title = {[Microbiome as a Novel Player in the Development and Treatment of Renal Cancer: A Systematic Review and Meta-Analysis].},
journal = {Urologiia (Moscow, Russia : 1999)},
volume = {},
number = {1},
pages = {143-153},
pmid = {42687557},
issn = {1728-2985},
mesh = {Humans ; *Kidney Neoplasms/microbiology/therapy ; *Carcinoma, Renal Cell/microbiology/therapy ; *Microbiota ; Gastrointestinal Microbiome ; },
abstract = {RELEVANCE: Growing evidence highlights the significant role of the human microbiota and microbiome in the pathogenesis of malignant tumors, including renal cell carcinoma (RCC). This systematic review evaluates studies addressing the associations between the microbiota/microbiome and the development and progression of RCC, as well as the influence of the microbiota on therapeutic efficacy in this malignancy.

MATERIALS AND METHODS: The review was conducted in accordance with PRISMA guidelines. A systematic search of bibliographic databases (PubMed, Scopus, etc.) using the keywords ("renal cell carcinoma"/"kidney cancer"/"renal cancer" and "microbiota"/"microbiome") identified 12,547 publications. After removal of duplicates and screening for eligibility, 33 studies directly examining the relationship between the microbiota and RCC were included in the analysis. Studies not relevant to the topic or focusing on tumor growth without specific reference to kidney cancer were excluded.

RESULTS: The review summarizes the composition and alterations of the microbiota in RCC: (1) the intratumoral microbiota of renal tumors differs from that of adjacent healthy kidney tissue, showing reduced diversity and distinct bacterial profiles; (2) the gut microbiota of RCC patients is dysbiotic compared with healthy controls, characterized by enrichment of potentially pro-carcinogenic taxa and depletion of protective bacteria; (3) the urinary microbiome also undergoes changes in RCC, though data remain limited. Potential mechanisms have been proposed: microbiota-derived metabolites (e.g., tryptophan-kynurenine pathway intermediates, short-chain fatty acids, trimethylamine N-oxide [TMAO]) may influence the tumor microenvironment, immune response, and metastatic potential. Importantly, gut microbiota composition has been shown to modulate response to immunotherapy in RCC: higher microbial diversity and the presence of specific taxa (e.g., Akkermansia muciniphila) are associated with improved response to immune checkpoint inhibitors, whereas dysbiosis and antibiotic exposure correlate with diminished efficacy. Several studies have demonstrated that modulation of the microbiome (via probiotics, prebiotics, or fecal microbiota transplantation) can enhance antitumor immunity and improve treatment outcomes in RCC, although clinical data specifically addressing RCC onset and progression remain limited.

CONCLUSIONS: The microbiota and microbiome are increasingly recognized as key factors in the development and progression of renal cell carcinoma, also influencing the effectiveness of contemporary therapeutic strategies. Further research is required to establish causal relationships and to develop microbiome-oriented approaches for the prevention and treatment of RCC.},
}

Humans
*Kidney Neoplasms/microbiology/therapy
*Carcinoma, Renal Cell/microbiology/therapy
*Microbiota
Gastrointestinal Microbiome

@article {pmid42687641,
year = {2026},
author = {Lee, M},
title = {From resistance mechanisms to therapy: Antimicrobial resistance in Gram-negative bacteria.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {64},
number = {8},
pages = {e2604017},
doi = {10.71150/jm.2604017},
pmid = {42687641},
issn = {1976-3794},
support = {//National Research Foundation of Korea/ ; RS-2023-00210754//Ministry of Science and ICT/ ; },
mesh = {*Gram-Negative Bacteria/drug effects/genetics ; Humans ; *Anti-Bacterial Agents/pharmacology/therapeutic use ; *Gram-Negative Bacterial Infections/microbiology/drug therapy ; *Drug Resistance, Multiple, Bacterial ; beta-Lactamases/metabolism/genetics ; *Drug Resistance, Bacterial ; Bacterial Proteins/metabolism/genetics ; },
abstract = {Antimicrobial resistance poses a major global health challenge, and infections caused by multidrug-resistant Gram-negative bacteria are associated with substantial morbidity and mortality. In contrast to many Gram-positive pathogens, Gram-negative bacteria combine intrinsic barriers with acquired determinants, including enzymatic drug inactivation, reduced outer membrane permeability, active efflux, and target modifications, which collectively compromise the efficacy of multiple antibiotic classes. Previous reviews have largely catalogued resistant pathogens or antimicrobial agents. This review provides a mechanism-focused overview of antimicrobial resistance in clinically important Gram-negative bacteria and explains how dominant resistance determinants translate into clinically relevant failure modes, such as delayed effective therapy, limited treatment options, and increased reliance on toxic last-line agents. Current and emerging therapeutic strategies are discussed through a mechanism-based lens, emphasizing newer β-lactam/β-lactamase inhibitor combinations and nontraditional approaches, including phages, antivirulence, and microbiome-based interventions. This review highlights the conceptual links between resistance mechanisms, clinical impact, and rational therapeutic choices and identifies priorities for future research aimed at mitigating antimicrobial-resistant Gram-negative infections.},
}

*Gram-Negative Bacteria/drug effects/genetics
Humans
*Anti-Bacterial Agents/pharmacology/therapeutic use
*Gram-Negative Bacterial Infections/microbiology/drug therapy
*Drug Resistance, Multiple, Bacterial
beta-Lactamases/metabolism/genetics
*Drug Resistance, Bacterial
Bacterial Proteins/metabolism/genetics

@article {pmid42687714,
year = {2026},
author = {Velsko, IM and Hübner, A and Fagernäs, Z and Yates, JAF and Mann, AE and Hofman, CA and Ozga, AT and Lewis, CM and Speller, C and Fiddyment, S and Francken, M and Wahl, J and Krause, J and Radini, A and King, T and Warinner, C},
title = {The Oral Microbiome of King Richard III of England.},
journal = {American journal of biological anthropology},
volume = {191},
number = {1},
pages = {e70350},
pmid = {42687714},
issn = {2692-7691},
support = {//Werner Siemens Stiftung/ ; //Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany's Excellence Strategy/ ; //Max Planck Harvard Research Center for the Archaeoscience of the Ancient Mediterranean (MHAAM)/ ; //Max Planck Society/ ; },
mesh = {Humans ; *Microbiota/genetics ; England ; *Dental Calculus/microbiology/history ; DNA, Ancient/analysis ; History, 15th Century ; *Mouth/microbiology ; History, Medieval ; History, Ancient ; Phylogeny ; Metagenome/genetics ; },
abstract = {OBJECTIVES: Metagenomic investigations of ancient dental calculus provide insights into oral health, disease, and diet. Here, we analyze the dental calculus metagenome of King Richard III of England (1452-1485).

MATERIALS AND METHODS: Dental calculus DNA was extracted from three teeth of King Richard III and shotgun sequenced to a depth of nearly 400 million reads. The metagenomic data were taxonomically profiled and compared to new and previously published dental calculus metagenomes from England, Ireland, the Netherlands, and Germany spanning the Neolithic to the present. Sequencing data were de novo assembled, and metagenome-assembled genomes assigned to the genus Tannerella were investigated for phylogenetic relatedness and virulence. Putative dietary DNA was assessed for authenticity.

RESULTS: The dental calculus of King Richard III was well-preserved and yielded an exceptionally high quantity of DNA. Oral microbiome species diversity fell within the range previously observed among other northern European populations, suggesting that a royal lifestyle and a rich diet did not substantially impact his oral microbiota. The reconstructed Tannerella genomes contained many virulence factors found today among oral Tannerella species. No putative dietary DNA could be authenticated.

DISCUSSION: The dental calculus of King Richard III produced one of the richest ancient oral metagenomes published to date, yet the species diversity was indistinguishable from that of commoners living in northern Europe over the last 7000 years. Insufficient plant and animal DNA were recovered to investigate diet, suggesting that dental calculus may not be a sufficient source of dietary DNA even when exceptionally well-preserved.},
}

Humans
*Microbiota/genetics
England
*Dental Calculus/microbiology/history
DNA, Ancient/analysis
History, 15th Century
*Mouth/microbiology
History, Medieval
History, Ancient
Phylogeny
Metagenome/genetics

@article {pmid42687847,
year = {2026},
author = {Dichter, J},
title = {Bile Acid Metabolism as a Unifying Readout for Diet, Microbiome Function, and Gastrointestinal Disease.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {17},
pages = {e72273},
pmid = {42687847},
issn = {1530-6860},
mesh = {Humans ; *Bile Acids and Salts/metabolism ; Animals ; *Gastrointestinal Diseases/metabolism/microbiology ; *Diet ; *Gastrointestinal Microbiome/physiology ; Receptors, Cytoplasmic and Nuclear/metabolism ; },
abstract = {Bile acid biology has advanced through significant conceptual shifts. Once understood primarily as biological detergents, bile acids are now recognized as signaling molecules and, more recently, as a chemically diverse set of host- and microbe-derived metabolites. The 2020 discovery of microbially conjugated bile acids (MCBAs) and the expansion of the recognized catalog from approximately 20 species to more than 200 mark a new phase in this trajectory. Clinical translation has not kept up. Direct farnesoid X receptor (FXR) agonism failed twice in trials for non-alcoholic steatohepatitis, later received a serious liver injury safety communication from the U.S. Food and Drug Administration, and was voluntarily withdrawn from the United States market. The standard of care for bile acid diarrhea and post-cholecystectomy diarrhea still relies largely on chemical binding with drugs introduced in the 1960s and 1970s. This Perspective argues that the gap between bile acid biology and bile acid medicine persists in part because the field has not been organized around the bile acid pool as a shared measurable output. Researchers studying dietary modulators of the gut microbiome have worked in separate communities around fiber, fermented foods, polyphenols, protein, and dietary fat. Each of these inputs can shape bile acid metabolism, yet many intervention studies do not measure it. The most immediately implementable bile acid-targeted strategy is specified dietary intervention designed with measurable bile acid outcomes and evaluated with the precision of pharmacological therapy. Four recommendations follow: intervention studies should routinely measure bile acid outcomes; clinicians should test bile acid metabolism in conditions involving dysregulation; regulators should develop a framework for multicomponent dietary therapies; and researchers should build infrastructure for population-scale longitudinal monitoring.},
}

Humans
*Bile Acids and Salts/metabolism
Animals
*Gastrointestinal Diseases/metabolism/microbiology
*Diet
*Gastrointestinal Microbiome/physiology
Receptors, Cytoplasmic and Nuclear/metabolism

@article {pmid42687886,
year = {2026},
author = {Youngblood, V and Armstrong, TD and Nguyen-Alley, K and Green, AE and Kelly, ME and Johnson, B and Stanley, A and Gilbreth, P and Cook, M and Coxe, T and Bradshaw, JL and Azad, RK and Cunningham, RL and Lund, AK},
title = {Sex-specific gut microbial and metabolic responses to inhaled diesel exhaust particle exposure are modified by probiotic treatment in C57BL/6 mice.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-10713368/v1},
pmid = {42687886},
issn = {2693-5015},
abstract = {Background Epidemiological and experimental studies indicate that susceptibility to traffic-generated particulate matter (PM)-induced metabolic dysfunction varies by sex, with females frequently exhibiting greater vulnerability. Recent evidence suggests that disruption of the lung-gut axis and subsequent gut-derived inflammatory signaling may contribute to these outcomes. However, the effects of inhaled PM on gut microbiome signaling and the metabolic milieu across sexes remain inadequately characterized. This study examined whether diesel exhaust particulate (DEP) exposure induces sex-specific metabolic and inflammatory responses and whether probiotic supplementation differentially modifies these effects in males and females. Methods Male and female C57BL/6 mice were exposed to 35 µg DEP (1 mg/mL, SRM-2975) or saline control via oropharyngeal aspiration twice weekly for 50 days, with or without probiotic supplementation (Winclove Ecologic® Barrier probiotics). Systemic metabolic outcomes in plasma were assessed using a multiplex hormone panel. Gut microbiome composition was characterized using 16S rRNA sequencing, and gut-derived signaling was evaluated through plasma lipopolysaccharide (LPS) quantification and short-chain fatty acid (SCFA) analysis. Three-way ANOVAs with sex as a biological variable were conducted to determine differential responses to DEP exposure and probiotic intervention. Results DEP exposure induced sex-dependent alterations in gut microbial composition, circulating metabolites, and endotoxemia. In females, DEP exposure resulted in taxonomic shifts and reduced microbial diversity, whereas probiotic treatment produced the most pronounced community-level expansion in DEP-exposed males. Beta-diversity analyses confirmed significant treatment-associated differences in community composition, identifying probiotic treatment as the primary driver, with stronger community-level effects in females and more limited effects in males. These changes corresponded with alterations in circulating SCFA and LPS levels, with more pronounced effects observed in females. Conclusions Biological sex is a major determinant of susceptibility to DEP-induced metabolic and inflammatory dysregulation. Females demonstrated heightened systemic and gut-derived responses to DEP exposure. Probiotic supplementation modified several of these functions, with effects varying by sex. Notably, probiotic supplementation produced opposing effects on glucagon in DEP-exposed animals depending on sex, underscoring the importance of biological sex in determining both the direction and magnitude of microbiome-targeted intervention outcomes. These findings support the inclusion of sex as a biological variable in environmental health research and suggest that microbiome-targeted interventions may provide sex-specific protective effects against PM-induced metabolic dysfunction.},
}

@article {pmid42687904,
year = {2026},
author = {Sharma, S and Zhang, T and McElderry, J and Lee, O and Hoang, P and Zeng, L and Webster, N and Alexandrov, L and Raz, E and Landi, MT and Bertin, S},
title = {Detection of House Dust Mite-derived DNA in Human Lung Tumors by Whole-Genome Sequencing.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-10438367/v1},
pmid = {42687904},
issn = {2693-5015},
abstract = {Lung cancer in never-smokers (LCINS) accounts for an increasing proportion of lung cancer cases, yet its risk factors remain poorly understood. House dust mites (HDM) are common aeroallergens that induce airway inflammation, but their potential contribution to lung cancer is unknown. We analyzed unmapped whole-genome sequencing reads from 783 lung cancers from the Sherlock- Lung (n = 621 never-smokers) and EAGLE (n = 162 smokers) cohorts, including 328 matched adjacent normal lung tissues. After removal of human sequences, reads were aligned to reference genomes from the two major HDM species and confirmed by BLAST. Samples with top BLAST matches were classified as HDM-detected. Associations between HDM detection and genomic, microbiome, and bulk RNA-seq-derived immune features were evaluated. HDM-derived DNA was detected at low abundance in a subset of tumors and adjacent normal tissues, with higher detection frequencies in tumors than matched normal tissues and in smokers than never-smokers. In LCINS tumors, HDM detection was not associated with tumor mutational burden or recurrent driver alterations but was associated with modest differences in immune cell composition and a limited but reproducible bacterial co-detection pattern. These findings provide a foundation for investigating aeroallergen-derived DNA signatures and their potential relationship to the lung tumor microenvironment.},
}

@article {pmid42688031,
year = {2026},
author = {Lu, L and Li, J and Yao, X},
title = {Probiotic mediated modulation of neonatal health: a meta-analysis of prematurity-related morbidity, jaundice, and respiratory distress.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1866590},
pmid = {42688031},
issn = {2235-2988},
mesh = {Humans ; *Probiotics/therapeutic use/administration & dosage ; Infant, Newborn ; *Respiratory Distress Syndrome, Newborn/prevention & control/epidemiology ; Infant, Premature ; *Jaundice, Neonatal/prevention & control/epidemiology ; *Infant Health ; Gastrointestinal Microbiome ; Dietary Supplements ; },
abstract = {INTRODUCTION: Prematurity remains a major contributor to neonatal morbidity and mortality worldwide, with neonatal jaundice and respiratory distress syndrome (RDS) representing two of the most common complications associated with immature hepatic and pulmonary development. Increasing evidence suggests that probiotic supplementation may improve neonatal outcomes through modulation of the gut microbiome, gut-liver axis, and gut-lung axis; however, published findings remain inconsistent. The meta-analysis evaluated the effects of probiotic supplementation on prematurity-related morbidity, with particular emphasis on neonatal jaundice and RDS.

METHODS: The study was conducted according to PRISMA 2020 guidelines, and a comprehensive literature search of PubMed, Scopus, Web of Science, and the Cochrane Library identified 18 eligible studies comprising 2,587 preterm infants. Methodological quality was assessed using the Cochrane Risk of Bias 2 tool and Newcastle-Ottawa Scale, and pooled effect estimates were calculated using random-effects models.

RESULTS: Probiotic supplementation significantly reduced the incidence of neonatal jaundice (RR = 0.72, 95% CI: 0.61-0.84; p < 0.001), peak total serum bilirubin levels (MD = -1.84 mg/dL, 95% CI: -2.47 to -1.21), and phototherapy requirements (RR = 0.68, 95% CI: 0.55-0.82; p < 0.001). The incidence of RDS was significantly reduced (RR = 0.79, 95% CI: 0.66-0.95; p = 0.012), accompanied by a shorter duration of respiratory support (MD = -1.9 days, 95% CI: -2.8 to -1.0). Moderate heterogeneity was observed across pooled analyses (I² = 42-57%). Exploratory meta-regression suggested that probiotic formulation, early initiation (<72 h), and gestational age contributed to between-study variability.

DISCUSSION: Probiotic supplementation was associated with favorable clinical outcomes in preterm infants. The moderate between-study heterogeneity, variability in probiotic strains, formulations, dosages, and treatment protocols, together with limited long-term safety data, warrant cautious interpretation. Future adequately powered multicenter randomized controlled trials, standardized probiotic interventions, individual-patient-data meta-analyses, and long-term follow-up studies are required before routine clinical implementation and standardized probiotic treatment recommendations can be established.},
}

Humans
*Probiotics/therapeutic use/administration & dosage
Infant, Newborn
*Respiratory Distress Syndrome, Newborn/prevention & control/epidemiology
Infant, Premature
*Jaundice, Neonatal/prevention & control/epidemiology
*Infant Health
Gastrointestinal Microbiome
Dietary Supplements

@article {pmid42688076,
year = {2026},
author = {Gao, G and Zhao, X and Lu, X and Yu, S and Chen, L},
title = {IBD-related inflammatory memory and colorectal cancer: epigenetic mechanisms and microbiome interventions.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1912351},
pmid = {42688076},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Epigenesis, Genetic ; *Colorectal Neoplasms/immunology/genetics/etiology/microbiology ; *Gastrointestinal Microbiome/immunology ; Trained Immunity ; *Inflammatory Bowel Diseases/immunology/microbiology/genetics/complications ; Epigenetic Memory ; *Colitis-Associated Neoplasms/immunology/microbiology/genetics ; Intestinal Mucosa/immunology/microbiology ; DNA Methylation ; *Immunologic Memory ; },
abstract = {Colitis-associated cancer (CAC) develops within chronically inflamed mucosa and differs from sporadic colorectal cancer in its field effects, multifocality, and sequence of molecular events. In addition to ongoing inflammation and mutation, experimental studies indicate that epithelial, immune, and stromal compartments can retain altered states after an initiating inflammatory stimulus has subsided. In this review, inflammatory memory is used operationally for a persistent molecular, cellular, tissue, or microbial state that changes the response to a later challenge. This definition distinguishes epithelial epigenetic memory from trained innate immunity, adaptive lymphocyte memory or exhaustion, and chronic signaling that depends on continued stimulation. We synthesize evidence for persistent chromatin accessibility, histone modification, DNA methylation, enhancer activity and three-dimensional organization, epithelial plasticity, immune-stromal circuits, and microbiota-derived metabolites. These responses can support mucosal repair, but repeated activation within a genetically altered field may facilitate clonal expansion and tumor development. We also assess emerging methylation, circulating tumor DNA, stool DNA, single-cell, and spatial biomarkers and grade proposed interventions according to evidence from cell culture, organoids, animal models, human tissues, and clinical studies. Because chromatin- and microbiome-directed interventions remain largely preclinical, selective modulation of pathological persistence-not complete "memory erasure"-is the appropriate translational objective.},
}

Humans
Animals
*Epigenesis, Genetic
*Colorectal Neoplasms/immunology/genetics/etiology/microbiology
*Gastrointestinal Microbiome/immunology
Trained Immunity
*Inflammatory Bowel Diseases/immunology/microbiology/genetics/complications
Epigenetic Memory
*Colitis-Associated Neoplasms/immunology/microbiology/genetics
Intestinal Mucosa/immunology/microbiology
DNA Methylation
*Immunologic Memory

@article {pmid42688171,
year = {2026},
author = {Zhang, J and Zhou, H and Zhang, G and Wang, HM},
title = {When the carcinogenic window opens before the screening window: the age-threshold blind spot in early-onset colorectal cancer.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1912787},
pmid = {42688171},
issn = {2234-943X},
abstract = {Early-onset colorectal cancer (EOCRC) screening is constrained by a structural blind spot concealed by age-threshold-based eligibility. This limitation does not primarily reflect insufficient screening resources, but rather a fundamental temporal mismatch between screening logic and carcinogenic exposure. High-risk states may be established decades earlier through accumulated early-life "exposure memory," whereas screening triggered by chronological age can intervene only after risk has already been formed. Consequently, individuals younger than 45 years-the population with one of the fastest increases in EOCRC incidence-remain systematically overlooked even after the initiation age for average-risk screening has been lowered to 45 years. This article outlines two parallel pathways: the metabolic-inflammatory axis, including hyperinsulinemia, IGF-1 signaling, and chronic low-grade inflammation; and the gut microbiome axis, including microbial genotoxicity and mucosal immune dysregulation. We clarify how these pathways may encode risk early in life and jointly shift the carcinogenic window forward, making further reductions in age thresholds insufficient for timely identification of truly high-risk young individuals. Accordingly, we argue that EOCRC screening should move from "age-triggered detection" toward "risk-memory recognition." We propose three strategies stratified by clinical readiness: symptom-triggered colonoscopy triage as diagnostic evaluation rather than screening, earlier assessment of exposure memory, and microbiome-informed risk stratification as a research direction. These approaches may help identify high-risk individuals before the conventional screening age and reduce missed diagnoses and diagnostic delays.},
}

@article {pmid42688227,
year = {2026},
author = {Sclabassi, E and Hur, J and Ling, J and Gao, Y},
title = {The gut microbiome as a modifiable contributor to autism spectrum disorder: a precision gut-immune-brain perspective.},
journal = {Frontiers in child and adolescent psychiatry},
volume = {5},
number = {},
pages = {1900538},
pmid = {42688227},
issn = {2813-4540},
}

@article {pmid42688244,
year = {2026},
author = {Cerckel, K and Frooninckx, L and Van Miert, S and De Smet, J and IJdema, F},
title = {Impact of nursery-to-fattening dietary transitions on gut microbiome composition and growth performance in black soldier fly larvae.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1901348},
pmid = {42688244},
issn = {1664-302X},
abstract = {Black soldier fly (BSF) (Hermetia illucens) larvae are used in large-scale bioconversion due to their capacity to convert diverse organic substrates into high-quality biomass. To improve circularity, rearing practices must be optimized, especially when nutritionally poor, low-cost substrates are used. Production systems often adopt a two-phase feeding strategy in which larvae first receive a nutrient-rich nursery diet before transitioning to a fattening diet. The effects of such a diet shift on the gut microbiome and larval performance remain unclear. This study explores how a diet shift between the nursery stage (0-7 days after egg harvest; DAH) and the fattening stage (DAH 8-15) influences larval performance and microbiome composition. Chicken feed (CF) and artificial supermarket food waste (SFW) were used as contrasting diets across four conditions: continuous feeding (CF to CF and SFW to SFW) and diet shifts (CF to SFW and SFW to CF). At the end of the nursery phase, there was no significant difference in larval weight between the two diets. Immediately after the diet shift (DAH 8-9), CF-nursed larvae were heavier than SFW-nursed larvae, but SFW-nursed larvae gradually reached comparable weights over time. This convergence occurred more rapidly when larvae were maintained on SFW. Notably, survival within both fattening diets was lower for SFW-nursed larvae than for CF-nursed larvae, which may have reduced larval density and feed competition during the fattening phase. Microbiome profiling through 16S rRNA gene amplicon sequencing revealed distinct bacterial communities associated with CF- and SFW-based rearing: CF-reared larvae maintained a consistently diverse community, whereas SFW-reared larvae exhibited low diversity. Following a diet transition, microbial composition shifted toward a fattening-driven profile. However, the rate and extent of this shift depended on the fattening substrate. Under SFW fattening, microbiome differences between nursery treatments disappeared by the end of the experiment, whereas several biomarkers persisted under CF fattening, suggesting a stronger legacy effect of the nursery diet. Overall, these findings demonstrate that interactions between diet, microbiome, and larval physiology shape performance in two-phase rearing systems, highlighting that early-life nutrition can influence microbiome trajectories and affect responses to subsequent feeds, an important consideration for optimizing BSFL production.},
}

@article {pmid42688450,
year = {2026},
author = {Chandrakar, R and Sarkar, S and Panchaxarimath, AV and Paikra, V and Pandey, AK and Rajwade, S},
title = {Ayurveda in Contemporary Clinical Practice: Integrating Traditional Principles With Preventive, Metabolic, and Mind-Body Medicine.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e113836},
pmid = {42688450},
issn = {2168-8184},
abstract = {The increasing burden of chronic, metabolic, and stress-related disorders has created a need for clinical models that emphasize prevention, lifestyle modification, individualized care, and long-term risk reduction. Ayurveda offers a structured framework for diet, behavior, metabolic regulation, constitutional assessment, and mind-body balance; however, its integration into contemporary clinical practice remains constrained by fragmented evidence, heterogeneous interventions, and variable methodological quality. This review examines the relevance of Ayurveda in preventive, metabolic, and mind-body medicine and evaluates how traditional principles may be aligned with evidence-based clinical care. A structured narrative review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar to identify primarily English-language literature published between January 2015 and June 2026. Original clinical studies, randomized trials, observational and translational studies, systematic reviews, methodological studies, and relevant policy documents were selected according to their relevance to preventive, metabolic, mind-body, personalized, safety, and regulatory aspects of Ayurveda. The review was intended as an illustrative narrative synthesis rather than a comprehensive systematic review. The evidence suggests that Ayurveda is most appropriately positioned as an adjunctive framework for cardiometabolic risk reduction, diabetes and metabolic syndrome management, mood and sleep regulation, chronic pain care, and personalized prevention. Emerging fields such as Ayurgenomics, Ayurinformatics, microbiome research, and systems biology may support the translation of traditional constructs such as Prakriti into testable biomedical models. Responsible integration requires rigorous trial design, standardized formulations, transparent reporting, pharmacovigilance, and regulatory oversight. Overall, Ayurveda may contribute to patient-centered preventive and integrative care when applied through evidence-informed, safety-conscious, and clinically accountable models.},
}

@article {pmid42688480,
year = {2026},
author = {Feng, H and Huang, X and Zhuang, Y and Pu, L and Dong, R and Ren, P},
title = {Enterococcus and cancer: from mechanistic insights to clinical translation.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1882184},
pmid = {42688480},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Enterococcus/immunology ; *Neoplasms/therapy/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; Immunotherapy/methods ; Tumor Microenvironment/immunology ; Host-Pathogen Interactions/immunology ; },
abstract = {Despite advances in traditional therapies, the global burden of malignant tumors remains substantial. Although immunotherapy has achieved remarkable breakthroughs by activating the host immune system, its clinical benefits are limited to a subset of patientsowing to low response rates and drug resistance. Emerging evidence highlights the pivotal role of the gut microbiota in determining immunotherapy outcomes. Within this ecosystem, the genus Enterococcus acts as a "double-edged sword": whereas certain strains can enhance antitumor immunity, other species notably Enterococcus faecalis, drive tumor progression by inducing DNA damage and inflammatory cascades. Therefore, elucidating the intricate interactions between Enterococcus and the host immune system is imperative for optimizing immunotherapeutic strategies and developing novel microbiome-based therapies.},
}

Humans
Animals
*Enterococcus/immunology
*Neoplasms/therapy/immunology/microbiology
*Gastrointestinal Microbiome/immunology
Immunotherapy/methods
Tumor Microenvironment/immunology
Host-Pathogen Interactions/immunology

@article {pmid42688507,
year = {2026},
author = {Qixiu, C and Chen, H and Hu, S and Dai, Y and Cui, Y and Zhang, Y and Ping, M and Li, X and Chen, J},
title = {Phenology-dependent assembly and functional potential of the Artemisia lavandulifolia rhizosphere microbiome.},
journal = {3 Biotech},
volume = {16},
number = {9},
pages = {402},
pmid = {42688507},
issn = {2190-572X},
abstract = {UNLABELLED: Plant developmental stages represent important endogenous drivers shaping rhizosphere microbiome assembly and functional potential. However, how rhizosphere microbial communities of Artemisia lavandulifolia shift across distinct phenological stages remains largely unexplored. To address this knowledge gap, we employed high-throughput sequencing to comprehensively characterize the rhizosphere bacterial and fungal communities of A. lavandulifolia during the early vegetative stage (EVS) and late vegetative stage (LVS). Additionally, quantitative PCR was used to determine the absolute abundance of bacterial 16S rRNA, fungal ITS genes, and key functional genes related to carbon, nitrogen, and phosphorus cycling. The results revealed significantly higher α-diversity in both bacterial and fungal communities at LVS compared to EVS (p < 0.05). Co-occurrence network analysis revealed that microbial co-occurrence patterns became increasingly complex with plant development, as evidenced by greater numbers of nodes and edges in both bacterial (1189 vs. 1049 nodes; 98,550 vs. 76,390 edges) and fungal (373 vs. 230 nodes; 6932 vs. 4509 edges) networks during LVS. Notably, absolute abundances of functional genes mediating carbon fixation (cbbLR), nitrogen cycling (amoA), and phosphorus mineralization (phoD) were significantly elevated at LVS relative to EVS (p < 0.05). Collectively, these findings demonstrate that plant ontogeny is associated with stage-dependent shifts in the functional potential of the A. lavandulifolia rhizosphere microbiome, suggesting adaptive adjustments in microbially mediated nutrient cycling to meet heightened host metabolic demands during late vegetative growth.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at https://doi.org/10.1007/s13205-026-05024-2.},
}

@article {pmid42688516,
year = {2026},
author = {Belenichev, I and Popazova, O and Dmytriieva, O and Chertov, S and Bukhtiyarova, N and Ryzhenko, V and Oliynyk, S and Lee, S and Yi, KH},
title = {Molecular cytokine-dependent mechanisms of periodontitis pathogenesis and the potential for pharmacological IL-1 modulation in disease treatment.},
journal = {Frontiers in dental medicine},
volume = {7},
number = {},
pages = {1849807},
pmid = {42688516},
issn = {2673-4915},
abstract = {Periodontitis (P) is one of the most common human dental diseases, with significant medical and social implications. According to the World Health Organization, more than 45% of the adult population worldwide exhibits clinical signs of periodontitis, with 10%-15% of cases becoming generalized with destruction of the alveolar bone. This review presents the results of modern research demonstrating that the etiopathogenesis of periodontitis is not limited to local microbial factors; systemic, social, and behavioral factors can play a significant role, determining the body's susceptibility to chronic inflammation. In this study, we focus on the role of cytokines in the athogenesis of periodontitis. Based on modern research, we demonstratethe general biological significance of cytokines and their role in initiating periodontal inflammation and systemic diseases associated with periodontitis. The molecular and biochemical cytokine-dependent mechanisms of initiation and progression of oxidative stress in periodontitis are covered in detail. The role of individual cytokines in the pathogenesis of periodontitis is shown: interleukin-1 (IL-1), IL-6, tumor necrosis factor (TNF-α), interferon-gamma, IL-10, IL-23, IL-17, and Th17 cells. The review presents a modern approach to complex drug therapy of periodontitis. The arsenal of antiseptics, antibiotics, and synthetic antimicrobial agents available to dentists is presented. A new approach is demonstrated in the use of probiotics-live microorganisms (probiotics, symbiotics, and bacteriophages) that maintain the balance of the oral microbiome. Beyond standard antimicrobial and anti-inflammatory therapies, host modulators, antioxidants, and bioregulatory agents play a vital role in treating P. They effectively suppress proinflammatory cytokines, mitigate oxidative stress, and improve metabolic activity in affected tissues. We present data on the development of individual regenerative structures using bioactive polymers and 3D printing for the future treatment of chronic periodontitis, as well as the potential use of biomaterials with nanostructured components, collagen matrices with nanoparticles, hydrogels with functional peptides, synthetic polymers with a modest antibacterial effect, and transplantation of mesenchymal stem cells, as well as bioactive scaffolds with stem cells. The most important section of the review is devoted to the clinical and pharmacological properties of cytokine modulators-TNF-α blockers, IL-6 blockers, and IL-1 blockers. Using current research results, including our own, we demonstrate the potential of using an IL-1 receptor antagonist and its new dosage form, such as a dental gel.},
}

@article {pmid42688521,
year = {2026},
author = {Zhou, J and Ye, X and Zou, J and Zou, L and Cheng, L and Zhu, Z and Liao, G and Zhou, X and Ren, B},
title = {[Age-Related Changes in the Oral Microbiota].},
journal = {Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition},
volume = {57},
number = {4},
pages = {941-952},
pmid = {42688521},
issn = {1672-173X},
mesh = {Humans ; *Microbiota/physiology ; *Mouth/microbiology ; *Aging/physiology ; Age Factors ; Infant ; Child ; },
abstract = {The human microbiome consists of microbial communities inhabiting different body sites and their genetic information, and plays an important role in maintaining host health. As an important component of the human microbiome, the oral microbiota contributes to maintaining oral microbial homeostasis, regulating local immune responses, participating in nutrient metabolism, and modulating systemic health. Initial colonization of the oral microbiota in early life lays the foundation for subsequent microbial development and lifelong oral health, and alterations in the oral microbiota are closely associated with various oral and systemic diseases. This review systematically summarizes the age-related succession of the oral microbiota across infancy, childhood and adolescence, adulthood, and old age; analyzes oral diseases associated with microbial dysbiosis at different life stages; discusses host-related, microenvironmental, and exogenous factors influencing age-related changes in the oral microbiota; and summarizes intervention strategies based on microbial ecological regulation. This review aims to provide new insights into age-related changes in the oral microbiota and to support the development of a life-course oral microbial health management model.},
}

Humans
*Microbiota/physiology
*Mouth/microbiology
*Aging/physiology
Age Factors
Infant
Child

@article {pmid42688585,
year = {2026},
author = {Liu, S and Huang, L and Xiao, S and Li, Y and Luo, S and Hou, E and Zhang, Y and Jin, M and Wang, Y and Zong, X},
title = {Astaxanthin Alleviates Intestinal Ferroptosis through Gut Commensal Lepagella muris-Mediated Retinoic Acid Production and SLC7A11 Activation.},
journal = {Research (Washington, D.C.)},
volume = {9},
number = {},
pages = {1421},
pmid = {42688585},
issn = {2639-5274},
abstract = {Intestinal epithelial injury is increasingly linked to ferroptosis, yet how dietary bioactives engage the gut microbiota to restrain this process remains largely unresolved. Here, astaxanthin (ASTA) was identified as a microbiota-engaged regulator of intestinal ferroptosis and lipid peroxidation. ASTA markedly ameliorated dexamethasone-induced intestinal injury, and this protection was closely associated with the attenuation of epithelial ferroptosis. Depletion of the gut microbiota largely abolished the protective effect of ASTA, establishing the gut microbiota as an essential mediator of its intestinal bioactivity. Microbiome and metabolome profiling further revealed that ASTA reshaped the microbial metabolic landscape, with retinol metabolism emerging as a dominant pathway linked to ferroptosis resistance. Among the altered metabolites, retinoic acid was identified as a pivotal ASTA-associated metabolite that connected microbial remodeling with the restoration of epithelial anti-ferroptosis capacity. Metagenomics combined with in vitro bacterial metabolic assays identified Lepagella muris as a candidate ASTA-responsive bacterium capable of contributing to retinoic acid production. Mechanistically, retinoic acid protected intestinal epithelial cells from ferroptosis and barrier disruption through activation of SLC7A11, thereby reinforcing the anti-ferroptosis defense system. This study moves beyond the conventional view of ASTA as a direct antioxidant and reveals a microbiota-enabled redox metabolic mechanism that may be therapeutically exploited for ferroptosis-associated diseases.},
}

@article {pmid42688768,
year = {2026},
author = {Gao, Y and Liu, C and He, X},
title = {The impact of gut microbiota on insulin resistance in polycystic ovary syndrome: mechanisms and therapeutic prospects.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1840605},
pmid = {42688768},
issn = {2235-2988},
mesh = {*Polycystic Ovary Syndrome/microbiology/therapy/physiopathology ; Humans ; *Insulin Resistance ; Female ; *Gastrointestinal Microbiome/physiology ; Dysbiosis ; Animals ; },
abstract = {Polycystic ovary syndrome (PCOS) is a prevalent endocrine and metabolic disorder, with insulin resistance (IR) serving as its core pathophysiological feature and a key driver of long-term metabolic complications. Recent studies have revealed that the gut microbiota, as a critical environmental factor, plays a significant role in the pathogenesis of PCOS. The gut microbiota profoundly engages in the pathophysiology of PCOS-IR through multiple pathways and networked interactions. This review provides a comprehensive narrative synthesis of the latest evidence on gut microbiota dysbiosis in PCOS-IR, with a particular focus on its molecular mechanisms, and evaluates therapeutic strategies based on gut microbiota modulation. It seeks to provide theoretical foundations and forward-looking perspectives for precision microbiome therapies. Importantly, this is a narrative review with a mechanistic focus, rather than a formal systematic review or meta-analysis.},
}

*Polycystic Ovary Syndrome/microbiology/therapy/physiopathology
Humans
*Insulin Resistance
Female
*Gastrointestinal Microbiome/physiology
Dysbiosis
Animals

@article {pmid42688815,
year = {2026},
author = {Chen, Z and Liu, W and Guo, Z and Guo, Y and Hou, J and Rong, M and Zheng, H and Cui, Z},
title = {Research progress and application prospects of multi-omics integration strategies in precision risk stratification of type 1 diabetes mellitus.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1891938},
pmid = {42688815},
issn = {1664-3224},
mesh = {Humans ; *Diabetes Mellitus, Type 1/diagnosis/metabolism/genetics/etiology ; *Multiomics ; Biomarkers ; Risk Assessment ; *Precision Medicine/methods ; Metabolomics ; Genomics/methods ; Genetic Predisposition to Disease ; Proteomics/methods ; Animals ; },
abstract = {Type 1 diabetes (T1D) is a chronic metabolic disease mediated by autoimmunity. Its pathogenesis involves complex interactions between genetic susceptibility and environmental factors. Conventional T1D risk stratification primarily relies on genetic markers, islet autoantibodies, and glycemic indicators. Although these biomarkers remain indispensable in current clinical practice, they are often insufficient when used alone to accurately identify ultra-early high-risk individuals, predict disease progression rates, or support individualized preventive strategies. Consequently, more comprehensive molecular approaches are needed to improve precision risk stratification. In recent years, the rapid development of multi-omics technologies has provided new strategies for precise risk stratification of T1D. This narrative review critically evaluates how multi-omics integration strategies can improve precision risk stratification throughout the T1D disease continuum by integrating complementary molecular information from genomics, transcriptomics, proteomics, metabolomics, epigenomics, and the microbiome. Particular emphasis is placed on stage-specific biomarker discovery, multi-omics data integration frameworks, artificial intelligence-assisted prediction models, biomarker validation, and the opportunities and challenges associated with clinical translation. Current evidence suggests that integrated multi-omics approaches have the potential to improve risk prediction accuracy, distinguish heterogeneous disease trajectories, identify individuals at imminent risk of progression, and provide biologically informed targets for precision intervention. However, important challenges remain, including data harmonization, external validation, model interpretability, cost-effectiveness, and integration into routine clinical screening programs. Future research should prioritize prospective multicenter cohorts, standardized analytical pipelines, externally validated prediction models, and clinically interpretable multi-omics frameworks to facilitate the translation of precision risk stratification into routine T1D prevention and management.},
}

Humans
*Diabetes Mellitus, Type 1/diagnosis/metabolism/genetics/etiology
*Multiomics
Biomarkers
Risk Assessment
*Precision Medicine/methods
Metabolomics
Genomics/methods
Genetic Predisposition to Disease
Proteomics/methods
Animals

@article {pmid42688840,
year = {2026},
author = {Li, J and Liu, Y and Gao, T and Ding, H and Hu, R and Wang, Y and Wu, B},
title = {Progress in interventions for vaginal microecology.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1888581},
pmid = {42688840},
issn = {2235-2988},
mesh = {Humans ; *Vagina/microbiology ; Female ; *Microbiota ; *Probiotics/administration & dosage/therapeutic use ; *Dysbiosis/therapy/microbiology ; Prebiotics/administration & dosage ; Synbiotics/administration & dosage ; },
abstract = {A balanced vaginal microbiome is fundamental to reproductive and gynecologic health, yet dysbiosis is common and clinically consequential. This narrative review synthesizes recent advances in microecological interventions, including probiotic, prebiotic, and synbiotic regimens; combination therapies; and vaginal microbiota transplantation. We place a particular focus on emerging delivery platforms like hydrogel-based carriers, which improve probiotic viability, mucosal adhesion, and controlled release. The review also explores how metagenomic analysis is refining community state typing, identifying pathogenic consortia, and enabling data-driven patient stratification and response monitoring. Despite these advances, key challenges remain, such as strain selection, functional validation, colonization durability, heterogeneous clinical endpoints, and clear regulatory pathways for live biotherapeutics. Future priorities must include developing functionally defined strain consortia, standardizing clinical outcomes, integrating multi-omics with biomaterials engineering, and conducting rigorous multicenter trials to deliver durable, safe, and truly individualized therapies.},
}

Humans
*Vagina/microbiology
Female
*Microbiota
*Probiotics/administration & dosage/therapeutic use
*Dysbiosis/therapy/microbiology
Prebiotics/administration & dosage
Synbiotics/administration & dosage

@article {pmid42688927,
year = {2026},
author = {Dong, J and Lv, J and Sun, G and Xiao, Z},
title = {Phenotype-Aware Biomarker Discovery in Childhood Asthma: Microbiome-Metabolome Signatures and Translational Readiness.},
journal = {International journal of general medicine},
volume = {19},
number = {},
pages = {615244},
pmid = {42688927},
issn = {1178-7074},
abstract = {Childhood asthma is a common but biologically heterogeneous disease, and this heterogeneity limits the performance of one-size-fits-all biomarkers for diagnosis, risk stratification, and disease monitoring. Microbiome and metabolome profiling are attractive in pediatric asthma because they reflect host-environment interactions at mucosal surfaces and may capture clinically relevant variation not fully explained by conventional markers. However, their translational value in children remains uncertain. This review critically examines the current evidence on microbiome- and metabolome-based biomarkers in childhood asthma from a clinically oriented perspective, with emphasis on four settings of practical relevance: early-life risk and disease development, allergic and non-allergic asthma, severe, uncontrolled, or exacerbation-prone disease, and lung-function or inflammatory phenotypes. Current data suggest that composite and phenotype-linked signatures are more informative than isolated taxa or single metabolites. The most convincing signals arise in early-life microbial maturation trajectories and in unstable disease, where upper-airway microbial patterns and integrated metabolic profiles show the greatest potential for clinical stratification. Allergic burden appears to be reflected more consistently by metabolomic than microbiome findings, whereas lung-function and inflammatory phenotypes currently show stronger metabolite-trait associations than reproducible airway microbial correlates. Across phenotypes, pathway-level convergence is more robust than single-marker reproducibility, with recurring signals involving microbial fermentation and short-chain fatty acid biology, bile acid metabolism, tryptophan and histamine pathways, and lipid remodeling. Nevertheless, most pediatric studies remain cross-sectional, modest in size, and heterogeneous in phenotype definitions, sampling matrices, and analytical platforms. No microbiome- or metabolome-based signature is currently ready for routine pediatric clinical use. The most realistic near-term translational direction is the development of age-contextualized, phenotype-oriented reduced panels that are prospectively validated in multicenter cohorts and shown to provide clinical value beyond existing tools for childhood asthma diagnosis, risk stratification, and monitoring.},
}

@article {pmid42688943,
year = {2026},
author = {Rukonge, PA and Kawuribi, V and Lu, Z and Oluwaseun, AF and Sheng, Y and Yan, K and Zheng, Z and Liu, X and Chu, L and Yu, G},
title = {From granulomas to tumors: post-tuberculosis immune and structural lung remodeling as a driver of carcinogenesis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1889276},
pmid = {42688943},
issn = {1664-3224},
mesh = {Humans ; *Lung Neoplasms/immunology/pathology/etiology ; Animals ; *Tuberculosis, Pulmonary/immunology/complications/pathology ; *Granuloma/immunology/pathology ; *Carcinogenesis/immunology ; T-Cell Exhaustion ; Tumor Microenvironment/immunology ; *Lung/immunology/pathology/microbiology ; },
abstract = {Although antibiotic therapy effectively cures active tuberculosis (TB), many survivors are left with permanent lung damage and long-lasting immune alterations. Growing epidemiological evidence indicates that individuals with prior pulmonary TB have a two- to three-fold increased risk of lung cancer, independent of smoking, suggesting mechanisms beyond shared risk factors. This review advances the concept that TB imprints a durable "memory" within the lung, characterized by persistent structural remodeling and immune reprogramming that together create a tumor-permissive microenvironment. We synthesize evidence showing that TB granulomas act as dynamic immune niches that induce hypoxia, fibrosis, and immune exhaustion, features that frequently persist after microbiological cure. Post-TB sequelae including fibrotic scarring, cavitation, bronchiectasis, and vascular remodeling, promote chronic inflammation, oxidative DNA damage, and mechanotransduction pathways linked to oncogenesis. Concurrently, sustained T-cell exhaustion, macrophage polarization toward tumor-associated phenotypes, and impaired antigen presentation weaken tumor surveillance. We further discuss emerging roles for lung microbiome dysbiosis in sustaining inflammation. Collectively, these processes provide a mechanistic framework linking healed TB to lung carcinogenesis and highlight TB survivors as a distinct population for targeted surveillance and preventive strategies.},
}

Humans
*Lung Neoplasms/immunology/pathology/etiology
Animals
*Tuberculosis, Pulmonary/immunology/complications/pathology
*Granuloma/immunology/pathology
*Carcinogenesis/immunology
T-Cell Exhaustion
Tumor Microenvironment/immunology
*Lung/immunology/pathology/microbiology

@article {pmid42689139,
year = {2026},
author = {Shuixing, Z and Jing, Z and Alshehri, D and Al-Amrah, H and Manzoor, I and Aiying, Y},
title = {Hormone priming and metabolic engineering of phytohormone crosstalk in rice under combined biotic and abiotic stresses: a multi-omics perspective for climate-resilient crop development.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1924558},
pmid = {42689139},
issn = {1664-462X},
abstract = {Rice (Oryza sativa L.) is the caloric backbone for more than half of humanity, yet it remains one of the most vulnerable crops to the simultaneous biotic and abiotic stresses exacerbated by climate change. Phytohormone priming and the complex crosstalk networks governed by transcription factor hubs like WRKY, MYB, and NAC serve as the central adaptive mechanism for stress resilience. This review synthesizes how multi-omics integration, including spatial and single-cell transcriptomics, is resolving the molecular architecture of hormonal priming and epigenetic stress memory. We critically evaluate advanced metabolic engineering and genome-editing strategies such as CRISPR-Cas9, base/prime editing, and synthetic gene circuits that enable precision modifications to decouple stress tolerance from historical yield penalties. Furthermore, we discuss the emerging roles of microbiome-assisted priming via synthetic consortia and the application of artificial intelligence and digital twins (continuously updated computational models of crop physiology) for predictive stress management. By integrating these diverse technological pillars, we propose a systems-level roadmap for developing climate-resilient rice cultivars capable of maintaining yield stability across a volatile combinatorial stress landscape. This synthesis provides a framework for translating mechanistic hormonal insights into field-applicable cultivars to ensure global food security.},
}

@article {pmid42689141,
year = {2026},
author = {Moser, B and Saxby, SM and Lebby, S and Letendre, JD and Lange, S and Mendez, MA and Trus, TL and Honigsberg, E and Billmeier, SE and Gilbert-Diamond, D and Dao, MC and Meijer, JL},
title = {Daily fiber supplementation after bariatric surgery demonstrates tolerability and influence on the fecal gut microbiome.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1912097},
pmid = {42689141},
issn = {2296-861X},
abstract = {INTRODUCTION: This study assessed the feasibility and tolerance of a 30-day resistant potato starch (RPS) supplement in patients who recently underwent bariatric surgery and its effect on microbial production of fecal short-chain fatty acids (SCFA).

METHODS: This clinical trial (ClinicalTrials.gov, identifier: NCT05653648), conducted at Dartmouth Hitchcock Medical Center, provided 30-days of RPS supplement (titration: 24 g for 15 days; 48 g for 15 days) starting 90-days post-op and assessed gastrointestinal symptoms, dietary intake (24 h recall), fecal SCFAs, and fecal gut microbiome (n = 30).

RESULTS: The RPS supplement was well tolerated by participants (77% achieving consumption goal), with modest, but significant increases in self-reported gas (p = 0.004) and abdominal rumbling (p = 0.047). It was associated with an increase in the Bifidobacterium genus (LDA score >4, p < 0.001) and specifically, an enrichment of B. faecale/adolescentis (p = 0.006), one of two known primary degraders of RPS. No changes were observed in the abundance of cross-feeders or in SCFA concentrations. Alpha diversity measures were significantly lower post-RPS, and there was no change in species richness.

DISCUSSION: This study demonstrated that a RPS supplement is tolerable in post-op bariatric patients and that the gut microbiome is responsive to fiber interventions. RPS increased the abundance of SCFA-producing bacteria but did not alter fecal SCFAs, likely due to competition among cross-feeders.},
}

@article {pmid42689286,
year = {2026},
author = {Liu, H and Li, J and Wei, Z and Li, N and Yao, K},
title = {Engineered Nanozymes for Colorectal Cancer Therapy: Catalytic Reprogramming of the Tumor Microenvironment.},
journal = {International journal of nanomedicine},
volume = {21},
number = {},
pages = {640248},
pmid = {42689286},
issn = {1178-2013},
mesh = {*Colorectal Neoplasms/drug therapy/therapy/metabolism ; Humans ; *Tumor Microenvironment/drug effects ; Animals ; Catalysis ; *Nanostructures/chemistry ; Antineoplastic Agents/chemistry ; Nanomedicine ; },
abstract = {Colorectal cancer (CRC) remains difficult to treat because redox adaptation, metabolic plasticity, mucin-associated delivery barriers, immune exclusion, and microbiota-dependent signaling jointly limit conventional therapy. Engineered nanozymes provide a reaction-centered strategy for exploiting these CRC-specific vulnerabilities. This review critically compares metal, metal-oxide, carbon-based, porous-framework, and single-atom nanozymes with respect to catalytic mechanism, enzyme-mimicking activity, substrate dependence, controllability, biosafety, and translational suitability. We examine how acidity, hydrogen peroxide, hypoxia, glutathione enrichment, metabolic dysregulation, mucin barriers, and the gut microbiota influence catalytic performance. We further evaluate evidence for chemotherapy sensitization, chemodynamic, photothermal, photodynamic, sonodynamic, immunotherapeutic, and multimodal treatment, emphasizing both mechanistic synergy and limitations of the available preclinical models. Major translational barriers include non-standardized catalytic assays, heterogeneous intratumoral substrates, off-target reactive oxygen species toxicity, uncertain degradation and long-term fate, microbiome disruption, manufacturing reproducibility, and limited validation in orthotopic, immunocompetent, organoid, and patient-derived systems. We therefore position CRC nanozyme therapy as a disease-oriented catalytic medicine platform whose clinical value will depend on biomarker-guided selection, programmable activation, and degradable, locally controllable designs.},
}

*Colorectal Neoplasms/drug therapy/therapy/metabolism
Humans
*Tumor Microenvironment/drug effects
Animals
Catalysis
*Nanostructures/chemistry
Antineoplastic Agents/chemistry
Nanomedicine

@article {pmid42689363,
year = {2026},
author = {Monika, P and Sadanandan, B and Tejashree, HR and Darbha, M and Gupta, K and Reneeka, S},
title = {Catechins and Their Effect on the Gut Microbiome in Health and Cancer.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.70435},
pmid = {42689363},
issn = {1099-1573},
abstract = {Catechins are a group of flavonoids found primarily in green tea, fruits, and berries; they play a significant role in the modulation of the gut microbiota, thereby having an impact on gut health and cancer prevention. Owing to their low bioavailability, catechins are transformed by the gut microbiota into various bioactive metabolites such as valerolactones and glucuronides, which support the growth of several beneficial bacterial species including Bifidobacterium and Lactobacillus while inhibiting harmful strains like Clostridium difficile and Escherichia coli. These interactions enhance metabolic balance, reduce inflammation, and help maintain gut homeostasis, which is critical for preventing gut dysbiosis. Dysbiosis is characterized by a shift from symbiotic to pathogenic microbial populations and is closely associated with cancer development, especially in the gut. This review explores how catechins, particularly epigallocatechin gallate (EGCG), contribute to cancer prevention by promoting a symbiotic microbial environment, supporting immune modulation, and inhibiting inflammatory pathways. By examining the role of catechins in both health and cancer, this paper aims to emphasize their therapeutic potential as dietary supplements in maintaining gut health and reducing cancer risk.},
}

@article {pmid42689470,
year = {2026},
author = {Qiao, Y and Qiao, J and Berendsen, RL and Cheng, X and Pieterse, CMJ and Song, Y},
title = {Ecological Filtering by Tuber Compartments Shapes Stable Core Microbiomes That Underpin Potato Plant Growth Across Environments.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70843},
pmid = {42689470},
issn = {1365-3040},
support = {101060393//Horizon Europe research and innovation programme./ ; OCENW.XS25.2.311//Dutch Research Council (NWO) Open Competition Domain Science - XS./ ; },
abstract = {Harnessing plant microbiomes for sustainable agriculture requires understanding not only whether they can boost crop performance, but also how ecological processes govern their assembly, stability, and functional contributions across environments. While we previously showed that seed tuber microbiomes can predict potato vigour using machine learning, it remained unclear how ecological processes shape tuber microbiome stability and functionality across host genotypes, tuber compartments, soil types, and years. Here, we analyzed the national-scale dataset of 240 field-collected potato seedlots, spanning six genotypes, two soil types, and two growing years, with a focus on the spatially distinct heel and eye compartments of the potato tuber. By profiling over 1200 bacterial and fungal communities and linking microbiome composition to plant performance, we show that plant genotype and tuber compartment are the strongest determinants of microbial diversity and composition. Compartment-specific enrichment of functional traits revealed spatial partitioning of microbial functions, with organic compound conversion and nitrogen cycling dominant in the heel, and energy metabolism enriched in the eye. Applying a macroecological abundance-occupancy framework, we identified a stable core microbiome of bacterial and fungal taxa that persisted across all environments and years. These core members were more strongly associated with plant growth-related traits than non-core taxa, and core taxa in different tuber compartments showed distinct correlations with taxa of potential pathogenic relevance. Together, our findings demonstrate that tuber compartments act as ecological filters that structure persistent, functionally specialised microbiomes linked to plant growth-related traits across environments. By providing an ecological and functional framework for compartment-resolved, stable core microbiomes, this study advances mechanistic understanding of plant-microbe interactions and identifies stable microbial partners as promising targets for improving potato resilience and productivity.},
}

@article {pmid42689993,
year = {2026},
author = {Kaewkaen, P},
title = {From Neuroinflammation to Precision Stroke Recovery: A Phase-Specific Immune-Metabolic Framework.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {31},
number = {8},
pages = {54110},
doi = {10.31083/FBL54110},
pmid = {42689993},
issn = {2768-6698},
mesh = {Humans ; *Stroke/metabolism/immunology ; *Neuroinflammatory Diseases/metabolism/immunology ; Animals ; *Recovery of Function ; Blood-Brain Barrier/metabolism/immunology ; *Stroke Rehabilitation/methods ; Inflammation/metabolism/immunology ; },
abstract = {Stroke recovery varies markedly among patients and cannot be fully predicted by infarct size, lesion location, or acute treatment success. This variability suggests that recovery is shaped by evolving interactions among neural injury, immune activation, neurovascular integrity, metabolic reserve, and repair-related plasticity. This review proposes a phase-specific immune-metabolic framework for precision stroke recovery. Rather than treating neuroinflammation as a uniformly detrimental process, this review conceptualizes neuroinflammation as a time-dependent biological gate that may either amplify injury or support repair, depending on the phase, cellular context, blood-brain barrier integrity, and systemic metabolic state. In the acute phase, regulated cell death, oxidative stress, inflammasome activation, blood-brain barrier disruption, and proteolytic remodeling contribute to secondary injury and neurovascular instability. During the subacute phase, controlled immune responses may facilitate debris clearance, angiogenesis, synaptic remodeling, and rehabilitation-induced neuroplasticity. In contrast, persistent low-grade inflammation in the chronic phase may impair network reorganization, promote glial reactivity, and contribute to delayed neurodegeneration or poor functional recovery. The available evidence suggests that metabolic and microbiome-related factors are not secondary modifiers but integral components of recovery biology. Nutritional status, sarcopenia, metabolic imbalance, and post-stroke gut dysbiosis may influence immune tone, blood-brain barrier function, microbial metabolite signaling, and neuroplastic potential. These interactions provide a rationale for defining biological recovery endotypes that integrate inflammatory, neurovascular, metabolic, microbiome-related, and plasticity-related signatures. By linking neuroinflammation with immune-metabolic regulation and repair biology, this review reframes stroke recovery as a phase-dependent and biologically stratified process. The framework may support the development of multimodal biomarkers, phase-matched interventions, and patient-stratification strategies for precision stroke recovery trials.},
}

Humans
*Stroke/metabolism/immunology
*Neuroinflammatory Diseases/metabolism/immunology
Animals
*Recovery of Function
Blood-Brain Barrier/metabolism/immunology
*Stroke Rehabilitation/methods
Inflammation/metabolism/immunology

@article {pmid42690051,
year = {2026},
author = {Liu, G and Li, Y and Yang, S and Jiang, H and Ma, L and Jia, Q and Bai, T and Shao, L},
title = {Skin commensal bacterium Staphylococcus epidermidis CCSM0287 cell-free supernatant protects HaCaT cells from UVB irradiation-induced photodamage and improves skin barrier function.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0364925},
doi = {10.1128/spectrum.03649-25},
pmid = {42690051},
issn = {2165-0497},
abstract = {Ultraviolet B (UVB) radiation is a major environmental stressor that induces oxidative stress, inflammation, and skin barrier dysfunction. Although Staphylococcus epidermidis (S. epidermidis) is a beneficial skin commensal, current evidence on its protective effects against UVB-induced skin damage has primarily focused on reference strains or a limited number of individual metabolites. The broader photoprotective potential of postbiotics derived from newly isolated skin commensal strains remains insufficiently characterized. Here, we investigated the anti-photodamage activity and underlying mechanisms of the cell-free supernatant of S. epidermidis CCSM0287 (SE 287-CFS), a multifunctional skin commensal isolated from healthy skin, in UVB-induced HaCaT cells. SE 287-CFS significantly reduced intracellular reactive oxygen species (ROS), malondialdehyde (MDA), and pro-inflammatory cytokines, while enhancing antioxidant enzyme activity and interleukin-10 (IL-10) secretion. Mechanistically, SE 287-CFS inhibited p65 nuclear translocation and suppressed activation of the ROS/MAPK/NF-κB signaling pathway. In addition, SE 287-CFS increased transepithelial electrical resistance (TEER) and promoted keratinocyte proliferation and migration, indicating improved skin barrier function. Non-targeted metabolomics combined with correlation analysis suggested that butyric and adipic acids were primarily associated with antioxidative and anti-inflammatory effects. Other organic acids, including succinic, acetic, and propanoic acids, may contribute to skin barrier repair. Together, this study demonstrates that SE 287-CFS protects against UVB-induced photodamage by modulating oxidative stress, suppressing inflammation, and improving skin barrier function. It also highlights the potential of postbiotics derived from skin commensals as candidates for microbiome-based skin photoprotection.IMPORTANCEStaphylococcus epidermidis is a dominant commensal skin bacterium that plays a crucial role in maintaining skin homeostasis and defending against various external stressors. UV radiation is a primary environmental factor that induces oxidative stress and inflammatory responses, resulting in photodamage and impaired skin barrier function. This study demonstrated the significant protective effect of SE 287-CFS in counteracting ultraviolet B (UVB)-induced skin damage. By modulating the reactive oxygen species (ROS)/MAPK/NF-κB signaling pathways, SE 287-CFS effectively alleviated oxidative stress, reduced inflammatory cytokine production, and enhanced skin barrier function. This research highlighted the potential of using skin commensal bacteria as a novel therapeutic strategy to enhance skin protection against UVB-induced damage, providing a promising approach to improve skin health under environmental stressors like UV radiation.},
}

@article {pmid42690065,
year = {2026},
author = {Langlois, A and Vincent, AT and Lauzon, K and Brouard, J-S and Bueno Dalto, D and Gagnon, N and Talbot, G and Lapointe, J and Poulin-Laprade, D},
title = {Characterization of the gut microbiome and resistome of piglets supplemented with low, moderate, and high concentrations of zinc oxide.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0005926},
doi = {10.1128/spectrum.00059-26},
pmid = {42690065},
issn = {2165-0497},
abstract = {UNLABELLED: The livestock sector is standing out for its substantial use of antimicrobials but is also investing in the development of mitigation strategies. Supranutritional concentrations of zinc (Zn) are served to piglets to prevent post-weaning diarrhea. This practice is detrimental to the piglet's assimilation of nutrients and can impact the environment through the excretion of unassimilated Zn, contributing to the persistence of antibiotic resistance by co-selection. In this study, the ileum and colon microbiome of piglets fed low (175 ppm), moderate (953 ppm), or high (2,991 ppm) concentrations of zinc oxide for 21 days after weaning were investigated using metagenomics and 16S rRNA amplicon sequencing. The pH and volatile fatty acids (VFA) were measured in cecum and colon. The colon resistome was investigated using metagenomics and PCR. The high Zn supplementation led to an increase in pH and a decrease in the VFA in both the cecum and colon. The bacterial diversity in colon was negatively impacted by the high Zn diet, with thriving Clostridiaceae and depletion of beneficial populations (e.g., Lactobacillaceae and Selenomonadaceae). Of concern, higher abundances of blaCTX-M and intI1 were observed in piglets fed with the moderate Zn diet. The findings from this study support the limitation of Zn to low concentrations.

IMPORTANCE: Developing alternatives to antibiotics is imperative to mitigate the global antimicrobial resistance crisis, particularly within the livestock sector, the predominant consumer of these agents. Yet, interventions introduced without due consideration may precipitate unintended consequences. In North American swine production, supranutritional zinc supplementation in pig feed has been adopted to prevent post-weaning diarrhea and sustain profitability. However, excessive zinc disrupts iron and copper metabolism and perturbs mitochondrial homeostasis, impairing energy metabolism, antioxidant defenses, and innate immunity. Moreover, high dietary zinc increases the excretion of this heavy metal, contributing to environmental pollution and fostering antibiotic-resistant bacteria through co-selection. This study provides further evidence supporting the restriction of zinc supplementation to nutritional needs, as supranutritional diets compromised the fermentative capacity of the pig gut microbiome and increased the frequency of clinically relevant antimicrobial resistance markers.},
}

@article {pmid42690073,
year = {2026},
author = {Fraley, AE and Rust, M and Wagner, M and Hipfinger, IR and Böhm, PJN and Dieterich, CL and Field, CM and Page, MJ and Owen, JG and Keyzers, RA and Sunagawa, S and Piel, J},
title = {Noncanonical Peloruside A Biosynthesis by an Uncultivated Verrucomicrobiota Symbiont.},
journal = {Angewandte Chemie (International ed. in English)},
volume = {},
number = {},
pages = {e2011872},
doi = {10.1002/anie.2011872},
pmid = {42690073},
issn = {1521-3773},
support = {//Gordon and Betty Moore Foundation/ ; 205320_185077/SNSF_/Swiss National Science Foundation/Switzerland ; 10.002.732/SNSF_/Swiss National Science Foundation/Switzerland ; //Boehringer Ingelheim Fonds/ ; },
abstract = {Peloruside A, a polyketide macrolide identified in the marine sponge Mycale hentscheli, is a promising anticancer drug candidate due to its ability to stabilize tubulin at a nontaxoid binding site. Substantial efforts were made to improve the supply of this scarce substance through chemical synthesis and mariculture, however, sustainable production has yet to be achieved. Recent microbiome sequencing suggested that bacterial producers are responsible for all M. hentscheli bioactive compounds, but the identity of the peloruside producer remained unknown. Furthermore, a candidate peloruside polyketide synthase (PKS) was identified in silico, but its highly aberrant architecture prevented a confident biosynthetic prediction for the pharmacologically important exocyclic double bond. Here, we reveal an unusually complex modular PKS pathway comprising nonelongating ketosynthases (KSs), two internal thioesterases (TEs), and an acetyl coenzyme A ligase that orchestrate O-acetylation/elimination, acetyl-CoA recycling, and configurational proof-reading to facilitate selective Z-double bond incorporation. The first internal TE falls into a previously characterized O-acylating TE family but contains key amino acid substitutions that facilitate bifunctional acylation/elimination activity. Furthermore, we identified the peloruside producer as 'Candidatus Pelorusia occulta', a member of the biochemically underexplored Lentisphaeria class within the phylum Verrucomicrobiota. This work provides the biochemical and microbiological foundation for heterologous peloruside production.},
}

@article {pmid42690389,
year = {2026},
author = {Yang, GS and Hegde, UP and Guan, Z and Maas, KR and Patel, S and Redeker, NS and Cong, X},
title = {Longitudinal Analysis of Psychoneurological Symptoms and the Gut Microbiome in Patients With Melanoma Receiving Immune Checkpoint Inhibitors.},
journal = {Oncology nursing forum},
volume = {53},
number = {5},
pages = {1-8},
doi = {10.1188/26.ONF.e26535372},
pmid = {42690389},
issn = {1538-0688},
mesh = {Humans ; Female ; Male ; Aged ; *Gastrointestinal Microbiome/drug effects ; *Immune Checkpoint Inhibitors/adverse effects/therapeutic use ; *Melanoma/drug therapy/psychology/microbiology ; Longitudinal Studies ; Middle Aged ; *Fatigue ; Aged, 80 and over ; Symptom Burden ; },
abstract = {OBJECTIVES: To characterize the severity of psychoneurological (PN) symptoms in cancer survivors who initiated immune checkpoint inhibitors (ICIs) at baseline and 12 weeks post-treatment and to examine the associations between PN symptoms and gut microbiome patterns.

SAMPLE AND SETTING: 15 patients (n = 9 males and n = 6 females, mean age = 70.9 years) with solid tumors who initiated ICIs were recruited from a cancer center.

METHODS AND VARIABLES: PN symptoms were assessed using self-report questionnaires, and stool samples were analyzed using 16S rRNA sequencing. Alpha and beta diversity indices were calculated, and a least absolute shrinkage and selection operator regression model was fitted to assess associations between each symptom and the log-ratio of the genus abundance.

RESULTS: Average fatigue levels increased during 12 weeks. The microbiome community varied by age, sex, and their interaction. At 12 weeks post-treatment, Oscillibacter (beta = -0.141), Limosilactobacillus (beta = 0.088), and Erysipelotrichaceae (beta = -0.021) were associated with average levels of fatigue, whereas Tannerellaceae (beta = -0.011), Bacteroides (beta = 0.474), and Acidaminococcus (beta = 0.193) were associated with pain severity (all p < 0.05).

IMPLICATIONS FOR NURSING: Given the potential association between the gut microbiome and PN symptoms during ICI treatment, nurses are encouraged to assess dysbiosis risk, screen for treatment-related adverse symptoms, and educate patients about gut health while receiving ICIs.},
}

Humans
Female
Male
Aged
*Gastrointestinal Microbiome/drug effects
*Immune Checkpoint Inhibitors/adverse effects/therapeutic use
*Melanoma/drug therapy/psychology/microbiology
Longitudinal Studies
Middle Aged
*Fatigue
Aged, 80 and over
Symptom Burden

@article {pmid42690486,
year = {2026},
author = {Wen, Y and Luo, Z and Li, Z and Li, K and Li, J and Yin, S and Zou, Y and Zhang, H and Zhang, Y and Chen, K and Zhang, Y and Liu, S and Chen, Z and Yu, L and Ding, Y},
title = {Oral and gut microbiota profiles in patients with locally advanced rectal cancer with varying responses to neoadjuvant chemoradiotherapy.},
journal = {Functional & integrative genomics},
volume = {26},
number = {1},
pages = {},
pmid = {42690486},
issn = {1438-7948},
support = {2023A0060//Science and Technology Plan Project of Jiangxi Provincial Administration of Traditional Chinese Medicine/ ; 2024A1515013292//Guangdong Basic and Applied Basic Research Fundation/ ; 2025A1515010567//Guangdong Basic and Applied Basic Research Fundation/ ; 2026A1515012094//Guangdong Basic and Applied Basic Research Fundation/ ; 32300085//National Natural Science Foundation of China/ ; 82504340//National Natural Science Foundation of China/ ; 82473567//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Rectal Neoplasms/microbiology/therapy/pathology ; *Neoadjuvant Therapy ; *Gastrointestinal Microbiome/genetics ; Male ; Female ; Middle Aged ; *Chemoradiotherapy ; Aged ; Feces/microbiology ; Saliva/microbiology ; },
abstract = {Recent research has focused on gut bacteria in colorectal cancer, but the influence of other microbiota, including oral and nonbacterial gut microbiota, on treatment efficacy remains insufficiently explored. This study aimed to investigate their relationship with the efficacy of neoadjuvant chemoradiotherapy (nCRT) in locally advanced rectal cancer (LARC). Saliva and fecal samples were collected from patients with LARC before treatment. Shotgun metagenomic sequencing was used to profile bacterial, archaeal, eukaryotic, and viral taxonomic groups and to examine oral and gut microbial functions. An artificial intelligence-based prediction model was developed by integrating oral and gut microbiome data with clinical information. Statistical analyses compared diversity and response-associated microbial features between responders and non-responders to nCRT. Response-associated differences were observed in bacterial and nonbacterial taxonomic profiles and in oral and gut microbial functional profiles. In the internal test subset, the integrated analysis yielded an observed AUC of 0.917. Given the small cohort and the exploratory comparison of candidate classifiers, this estimate requires confirmation in larger, independent cohorts. Baseline oral and gut microbiome profiles were associated with response to nCRT. Integrating microbiome and clinical features showed potential for response prediction, but the model remains exploratory and requires validation in larger, independent cohorts before clinical application. Retrospectively registered on 01/08/2026, NCT07346729.},
}

Humans
*Rectal Neoplasms/microbiology/therapy/pathology
*Neoadjuvant Therapy
*Gastrointestinal Microbiome/genetics
Male
Female
Middle Aged
*Chemoradiotherapy
Aged
Feces/microbiology
Saliva/microbiology

@article {pmid42690736,
year = {2026},
author = {Chu, P and Wu, J},
title = {Efficacy and safety evaluation of Weifuchun in preventing recurrence and treating mucosal lesions after endoscopic resection of intestinal polyps: A potential modulation of gut microbiome.},
journal = {Acta microbiologica et immunologica Hungarica},
volume = {},
number = {},
pages = {},
doi = {10.1556/030.2026.03051},
pmid = {42690736},
issn = {1588-2640},
abstract = {We evaluated Weifuchun tablets (composed of red ginseng, chamomile, and roasted shell) for preventing intestinal polyp recurrence and treating mucosal lesions after endoscopic resection, and to analyze its mechanism via gut microbiome regulation. This study prospectively enrolled 218 patients who underwent endoscopic intestinal polyp resection (April 2022-April 2024). The observation group (n = 109) received routine postoperative care plus oral Weifuchun tablets for three months, while the control group (n = 109) received routine care alone. Propensity score matching (PSM) was used to balance baseline characteristics. Primary outcomes included one-year polyp recurrence, mucosal injury scores, and gut microbiome alterations (16S rDNA sequencing). Safety and independent protective factors for recurrence (multivariate logistic regression) were also assessed. After PSM, the observation group had a significantly lower one-year recurrence rate than the control group (31.00% vs. 42.16%, P = 0.025). Weifuchun significantly reduced intestinal mucosal injury scores (P < 0.001). Crucially, microbiome analysis revealed that Weifuchun markedly increased gut microbial diversity (Sorensen index, P < 0.05) and significantly boosted the relative abundance of beneficial bacteria such as Bifidobacterium and Lactobacillus, while decreasing harmful bacteria including Escherichia coli and Bacteroides (all P < 0.001). Furthermore, Weifuchun significantly reduced postoperative complications (2.00% vs. 8.82%, P = 0.032) and was identified as an independent protective factor against recurrence (OR = 0.456, 95% CI: 0.304-0.683, P < 0.001). Weifuchun effectively prevents polyp recurrence and promotes mucosal repair post-endoscopic resection. Its mechanism is closely linked to beneficial modulation of the gut microbiome, restoring microbial balance and enhancing the intestinal microenvironment, and demonstrates a favorable safety profile.},
}

@article {pmid42691205,
year = {2026},
author = {Cui, X and Du, W},
title = {Gut-Intervertebral Disc Axis: Gut Microbiome-Driven Immune-Metabolic Imbalance and Intervertebral Disc Degeneration.},
journal = {Journal of cellular physiology},
volume = {241},
number = {9},
pages = {e70222},
pmid = {42691205},
issn = {1097-4652},
support = {22JR11RA072//Gansu Provincial Department of Education-Gansu Province University Teachers' Innovation Fund Project/ ; },
mesh = {Humans ; *Intervertebral Disc Degeneration/microbiology/immunology/metabolism/pathology ; *Gastrointestinal Microbiome/immunology ; Animals ; *Intervertebral Disc/metabolism/immunology/pathology/microbiology ; Dysbiosis/immunology/microbiology ; },
abstract = {Intervertebral disc degeneration (IDD) serves as a critical structural basis for chronic low back pain, severely impairing patients' quality of life and imposing a significant socioeconomic burden. Current interventions remain largely limited to symptomatic treatments including pharmacological analgesia and surgical intervention. The recently proposed "gut-disc axis" suggests that the gut microbiome can reshape the endplate-disc microenvironment by influencing intestinal barrier integrity, microbial metabolite profiles, and host immune-metabolic status. Existing evidence indicates that dysbiosis-related increases in endotoxin load, dysregulated metabolism of short-chain fatty acids, tryptophan, and bile acids, systemic low-grade inflammation, and shifts in immune cell lineages may collectively promote nucleus pulposus cell senescence and apoptosis, matrix degradation, and endplate pathology. Mendelian randomization studies have also suggested potential causal links between certain gut microbiota and disc diseases. However, the determination of whether "microbial signals" detected within the intervertebral disc represent true colonization is currently hindered by methodological limitations, particularly low-biomass contamination. This review focuses on mechanisms through which gut microbiota influence the endplate-disc microenvironment via immune-metabolic pathways, including the LPS/TLR4/NF-κB axis, SCFAs-AhR axis, and lipid/iron metabolism, while only briefly addressing studies related to mechanical injury and surgery. Building on these insights, we integrate advances from clinical cohorts, animal models, and multiomics studies, summarize key actionable intervention nodes, and propose a preliminary patient stratification framework and validation pathway based on gut-immune-metabolic typing, providing a theoretical foundation for developing microbiome-guided disease-modifying interventions.},
}

Humans
*Intervertebral Disc Degeneration/microbiology/immunology/metabolism/pathology
*Gastrointestinal Microbiome/immunology
Animals
*Intervertebral Disc/metabolism/immunology/pathology/microbiology
Dysbiosis/immunology/microbiology

@article {pmid42691543,
year = {2026},
author = {Lv, B and Zhang, X and Liu, T and Wang, W and Xu, L and Zhong, S and Jin, F and Xu, Y and Cao, J and Chen, G},
title = {Hybrid bacteriophage hydrogels deplete intratumoral bacteria to potentiate oncolytic immunotherapy.},
journal = {Biomaterials},
volume = {338},
number = {Pt A},
pages = {124598},
doi = {10.1016/j.biomaterials.2026.124598},
pmid = {42691543},
issn = {1878-5905},
abstract = {Oncolytic viruses act as in situ cancer vaccines by inducing antigen release to boost antitumor immunity. Specific intratumoral bacteria exacerbate immunosuppression; however, their influence on oncolytic immunotherapy remains unknown. Here, we report a hybrid bacteriophage hydrogel composed of engineered oncolytic M13 phage (eM13) and Escherichia coli (E. coli) phage Tequatrovirus YZ2, which suppresses breast cancer progression and metastasis by boosting antitumor immunity through selective elimination of intratumoral E. coli. Particularly, YZ2 is conjugated with photosensitizer CyI to produce YZ2-CyI (YC), and the hydrogel is prepared by cross-linking YC and eM13 using pH-sensitive coordinating molecules through the formation of dynamic Schiff base bonds. Within the acidic tumor microenvironment, eM13 and YC are gradually released for targeted oncolysis and E. coli eradication, respectively. Intratumoral bacterial clearance enhances dendritic cell and CD8[+] T cell activation, while suppressing immunosuppressive M2 macrophages, regulatory T cells, and myeloid-derived suppressor cells. In poorly immunogenic triple-negative breast cancer models, depleting intratumoral E. coli potentiates oncolytic therapy against tumor progression, recurrence, and metastasis. Notably, the bacteriophage formulation shows favorable safety without disrupting gut microbiota homeostasis. These results support its potential clinical application in microbiome-infiltrated tumors and ability to improve oncolytic immunotherapy outcomes.},
}

@article {pmid42691667,
year = {2026},
author = {Su, W and Fan, H and Zheng, Y and Wang, T and Li, Y and Fan, J and Guo, S and Cheng, Y and Zheng, B and Xiang, X},
title = {Micro-nano bubble-assisted fasting improves the meat quality of Pelodiscus sinensis by modulating gut microbiota and metabolic profiles.},
journal = {Food chemistry},
volume = {528},
number = {},
pages = {150678},
doi = {10.1016/j.foodchem.2026.150678},
pmid = {42691667},
issn = {1873-7072},
abstract = {This study investigated the effects of micro-nano bubble (MNB)-assisted fasting on the meat quality of Chinese soft-shelled turtle (Pelodiscus sinensis). Compared to conventional fasting, MNB treatment significantly improved muscle elasticity and enhanced umami intensity by retaining higher levels of glutamic and aspartic acids. GC-IMS and electronic nose analyses confirmed that MNBs effectively reduced off-flavors (e.g., dimethyl sulfide, hexanal) while preserving polyunsaturated fatty acids (EPA, DHA). Integrated metabolomics and microbiome analyses revealed that MNBs remodeled the gut microbiota-enriching beneficial Romboutsia and suppressing spoilage-associated Aeromonas. This microbial shift, alongside the oxidative modulation of the aquatic environment, curbed the generation of sulfur-containing off-flavors and preserved lipid nutrients. Consequently, MNB-assisted fasting emerges as a valuable ecological strategy to enhance the sensory and nutritional quality of cultured turtles.},
}

@article {pmid42691785,
year = {2026},
author = {Wang, J and Liu, Y and Nie, CZ and Wang, XS and Huang, XH and Qin, L},
title = {Mechanisms of volatile flavor formation in fermented meat products and prospects of artificial intelligence-based prediction.},
journal = {Meat science},
volume = {243},
number = {},
pages = {110209},
doi = {10.1016/j.meatsci.2026.110209},
pmid = {42691785},
issn = {1873-4138},
abstract = {Volatile flavor formation in fermented meat products is governed by complex interactions among raw materials, microbial metabolism, proteolysis, lipid oxidation, amino acid conversion, processing conditions, and ripening. These processes generate diverse volatile compounds, including aldehydes, ketones, alcohols, acids, esters, and sulfur- and nitrogen-containing compounds, which collectively determine product aroma and sensory quality. However, their dynamic, nonlinear, and multi-factorial nature makes accurate prediction and mechanism interpretation challenging using conventional statistical approaches alone. This review summarizes the major volatile compounds, formation pathways, and key factors affecting flavor development in fermented meat products. It further discusses the data foundations required for artificial intelligence-based modeling, including physicochemical indices, process parameters, volatile profiles, electronic nose and GC-IMS fingerprints, sensory evaluation, microbiome, and multi-omics data. The potential applications of machine learning, deep learning, time-series modeling, multi-omics integration, and explainable AI are highlighted for flavor prediction, maturity identification, key factor screening, sensory perception prediction, and mechanism analysis. Future studies should focus on standardized databases, external validation, and interpretable, transferable multimodal models to support precise flavor regulation and intelligent quality control in fermented meat products.},
}

@article {pmid42691837,
year = {2026},
author = {Wohlmann, S and Steniczka, G and Karwautz, C and Griebler, C},
title = {Acute and chronic toxicity of nitrate to the stygobiont amphipods Niphargus inopinatus and N. grandii.},
journal = {Ecotoxicology and environmental safety},
volume = {323},
number = {},
pages = {120736},
doi = {10.1016/j.ecoenv.2026.120736},
pmid = {42691837},
issn = {1090-2414},
abstract = {Nitrate is the predominant groundwater pollutant within the European union (EU), despite comprehensive legislation. In this study, acute (up to 96 h) and time-independent toxicity of nitrate (NO3[-]) were investigated for two groundwater amphipod species, Niphargus inopinatus and N. grandii. Nitrate concentrations applied ranged from 10 to 5000 mg/L NO3[-]. Bulk stable nitrogen isotope analysis was used to assess the potential uptake and exchange of nitrate derived nitrogen into biomass. Furthermore, we challenged the hypothesis that amphipods via their gut microbiome contribute to nitrate removal from contaminated groundwater. Acute sublethal effects occurred after 24 h of exposure only at 5000 mg/L, the highest nitrate concentration tested. Mortality remained at 0% for both species after 96 h. The 96-h EC50 values were 397 mg/L for N. inopinatus and 1298 mg/L for N. grandii, whereas the time-independent ultimate EC50 were calculated with 127 mg/L and 164 mg/L NO3[-], respectively, matching nitrate concentrations frequently found in contaminated groundwaters. These values were reached already after 6 and 10 days, respectively. A time-independent LC50 of 386 mg/L NO3[-] could be estimated for only N. inopinatus. The NOEC of NO3[-] after 4 weeks of exposure was 100 mg/L for both species. Chronic nitrate exposure, did not change the δ[1] [5]N signature of test animals' bulk biomass. No evidence was collected for a nitrate reduction in groundwater mediated by the invertebrates. The present study underlines the need for further studies with stygobiont organisms, but also emphasizes its limitations.},
}

@article {pmid42691895,
year = {2026},
author = {Majhi, B and Semwal, P and Pandey, DD and Mishra, SK and Yadav, N and Chauhan, PS},
title = {Synthetic microbial community-assisted regulation of arsenic transport and metabolism reduces grain arsenic accumulation in rice across developmental stages.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128704},
doi = {10.1016/j.micres.2026.128704},
pmid = {42691895},
issn = {1618-0623},
abstract = {Arsenic contamination in paddy soils threatens crop productivity and results in the accumulation of toxic arsenic in rice grains. Here, we demonstrate that a defined synthetic microbial community (SynCom) of Priestia flexa and Pseudomonas putida mitigates arsenic toxicity and restricts arsenic accumulation in rice (Oryza sativa var. Sarju-52). Under arsenic stress [As(III), 18 mg/kg; As(V), 50 mg/kg], plants exhibited impaired growth, reduced photosynthetic performance, and increased oxidative stress. Inoculation with SynCom restored physiological function and metabolic balance, as evidenced by improved photosynthesis, increased soluble sugars, and reduced proline accumulation. Accompanied by attenuation of antioxidant enzyme overactivation, which indicates effective control of reactive oxygen species. Mechanistically, SynCom substantially reduced arsenic accumulation in roots, shoots and grains by coordinate downregulation of arsenic transporter genes (Lsi1, Lsi2, Lsi3, OsNIP1;1, and OsNIP3;3), which limits arsenic uptake and translocation. Metabolomic profiling also indicated stress-associated metabolite suppression and enrichment of growth-related pathways. These results demonstrate that microbiome engineering can reprogram plant responses to arsenic stress and provide a scalable strategy to reduce dietary arsenic exposure from staple crops. Additionally, this study lays a strong foundation for developing SynCom as an effective and sustainable biotechnological intervention to improve food safety and agricultural resilience in arsenic-contaminated areas.},
}

@article {pmid42691903,
year = {2026},
author = {Li, Y and Tang, C and Mo, Y and Shan, Y and He, Z and Huang, Y and Wan, C and Wu, R and Zhang, C and Liang, J and Zhu, T and Yu, F},
title = {Enhanced phytoextraction of manganese and cadmium by Polygonum lapathifolium L. via Enterobacter sp. inoculation: Roles of rhizosphere regulation and endophytic microbiome assembly.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143481},
doi = {10.1016/j.jhazmat.2026.143481},
pmid = {42691903},
issn = {1873-3336},
abstract = {Plant growth-promoting bacteria (PGPB) can enhance phytoremediation, but whether inoculation alters rhizosphere microbial abundance and elicits tissue-specific endophytic responses remains unclear. Here, Enterobacter sp. was applied to improve Mn/Cd phytoextraction by Polygonum lapathifolium L. Inoculation decreased rhizosphere pH and increased acid-extractable Mn and Cd by 11.8% and 45.5%, respectively, accompanied by enhanced nutrient availability and C, N and P cycling enzyme activities. It also altered rhizosphere bacterial and fungal community structure, increased their absolute abundances and functional potential, and markedly increased rhizosphere Enterobacter abundance. In parallel, inoculation induced adaptive shifts in plant endophytic microbial communities, as reflected by higher root bacterial community-level rrn copy numbers but lower values in leaves, together with enhanced modularity of the endophytic interaction network under the C1.0 (9.50 ×10[10] CFU/pot) treatment, predominated by Pseudomonadota and Actinomycetota. Path analysis revealed that rhizosphere bacteria indirectly promoted Mn/Cd phytoextraction by regulating soil properties, while alleviation of oxidative stress sustained metal uptake. Inoculation reduced H2O2 and ·O2[-] levels, enhanced antioxidant capacity, and increased plant growth and metal accumulation. Overall, Enterobacter sp. inoculation enhanced phytoextraction through quantitative and compositional changes in rhizosphere microbiota, tissue-specific endophytic responses, and improved plant stress tolerance, supporting its application in Mn-Cd contaminated soils.},
}

@article {pmid42692023,
year = {2026},
author = {Santoro, EP and Raimundo, I and Beenham, L and Garcias-Bonet, N and García, FC and Schultz, J and Curdia, J and Antony, CP and Delgadillo-Ordoñez, N and Singh, U and Rosado, AS and Jaremko, M and Jaremko, L and Peixoto, RS},
title = {Probiotic and postbiotic treatment improves coral health and promotes specific metabolic and microbiome changes in situ during a heatwave.},
journal = {Cell reports},
volume = {},
number = {},
pages = {117839},
doi = {10.1016/j.celrep.2026.117839},
pmid = {42692023},
issn = {2211-1247},
abstract = {Microbial therapies are emerging as promising tools for coral protection against heat stress, yet such application was not tested in situ. We tested two coral-derived probiotic consortia and their heat-killed counterparts (postbiotics) on bleaching Acropora cf. valida in the Red Sea during a marine heatwave. Over 15 days, both live and one of the heat-killed treatments maintained photosynthetic efficiency (Fv/Fm), whereas placebo-treated corals exhibited significant thermal stress-induced decline. 16S rRNA gene sequencing profiling showed enrichment of putatively beneficial genera (e.g., Terasakiispira spp., Pseudoalteromonas spp.), and untargeted metabolomics resolved treatment-specific metabolic signatures that differed among consortia and between live and inactivated formulations. These molecular fingerprints suggest potential underlying protective mechanisms and host-microbiome interactions under heat stress. Together, our results position microbial therapies (probiotics and specific postbiotics) as field-validated interventions capable of minimizing impacts on corals during real-world thermal extremes and provide design cues for further development and deployment.},
}

@article {pmid42692152,
year = {2026},
author = {Ntuli, Y and Nehme Ibrahimi, M and Kronsten, VT and Shawcross, DL},
title = {Hepatic encephalopathy in chronic liver disease: Emerging insights from the gut microbiome.},
journal = {JHEP reports : innovation in hepatology},
volume = {},
number = {},
pages = {102022},
doi = {10.1016/j.jhepr.2026.102022},
pmid = {42692152},
issn = {2589-5559},
abstract = {Hepatic encephalopathy remains an underserved complication of chronic liver disease. Reliable diagnostic and prognostic biomarkers linked to disease pathophysiology are currently lacking, as are options for treatment that reduce mortality beyond lactulose and rifaximin. However, with the advent of high-throughput sequencing and multi-omics techniques to interrogate microbial taxonomy and metabolic pathways, our understanding of the gut-liver-brain-axis has moved beyond the ammonia-inflammation hypothesis. This review summarises recent studies that have aimed to characterise the role of the gut-liver-brain axis in hepatic encephalopathy and how this can be leveraged to create novel diagnostic, prognostic and therapeutic agents.},
}

@article {pmid42630008,
year = {2026},
author = {Encarnacion, J and Wolfgang, MJ},
title = {Impact of intestinal propionate metabolism on systemic metabolic homeostasis.},
journal = {American journal of physiology. Endocrinology and metabolism},
volume = {331},
number = {3},
pages = {E414-E424},
doi = {10.1152/ajpendo.00168.2026},
pmid = {42630008},
issn = {1522-1555},
support = {1//Propionic Acidemia Foundation (PAF)/ ; },
mesh = {Animals ; *Propionates/metabolism ; *Homeostasis ; Male ; Mice ; Female ; Liver/metabolism ; *Intestinal Mucosa/metabolism ; *Propionyl-Coenzyme A Carboxylase/genetics/metabolism ; Mice, Knockout ; Gastrointestinal Microbiome/physiology ; Colon/metabolism ; },
abstract = {Propionate is an abundant short-chain fatty acid largely derived from gut microbiota in mammals. Propionate metabolism is essential to maintain systemic homeostasis, and inborn errors of essential metabolic enzymes in this pathway cause severe illness. The juxtaposition of high concentrations of propionate with the intestinal epithelium suggests a need for propionate catabolism. To understand the requirement of propionate metabolism in intestinal epithelium, we generated mice with a conditional knockout of propionyl-CoA carboxylase A (Pcca) specifically in the intestine (Pcca[Vil-Cre]). Male and female Pcca[Vil-Cre] mice were born and weaned at the expected Mendelian ratio and gained weight normally on chow and high-fat diets. Liver metabolomics of Pcca[Vil-Cre] mice suggest that propionate metabolism affects the gut-liver axis. However, the loss of Pcca in the intestine did not affect the colonic transcriptome. These data suggest that intestinal propionate metabolism is largely dispensable, and that hepatic capture and metabolism of propionate dominate systemic physiology.NEW & NOTEWORTHY Propionate generated by the microbiome is extremely high in the lumen of the gut. To determine the requirement of propionate metabolism in the gut, we generated and characterized mice with an intestine-specific knockout of propionyl-CoA carboxcylase alpha (PCCA), the first step in propionyl-CoA metabolism. Overall, mice that are unable to use propionate in the intestine are relatively normal with alterations in the gut-liver axis.},
}

Animals
*Propionates/metabolism
*Homeostasis
Male
Mice
Female
Liver/metabolism
*Intestinal Mucosa/metabolism
*Propionyl-Coenzyme A Carboxylase/genetics/metabolism
Mice, Knockout
Gastrointestinal Microbiome/physiology
Colon/metabolism

@article {pmid42679417,
year = {2026},
author = {Li, H and Gao, H and Fu, J and Yang, S and Chen, L and Zhou, J},
title = {Comparative analysis of microbial communities, assembly processes, and life-history strategies in a mariculture-impacted eutrophic bay and adjacent coastal sediments.},
journal = {Ecotoxicology and environmental safety},
volume = {323},
number = {},
pages = {120750},
doi = {10.1016/j.ecoenv.2026.120750},
pmid = {42679417},
issn = {1090-2414},
abstract = {Coastal embayments are increasingly subjected to intensive mariculture, which delivers sustained nutrient, organic matter, and antibiotics to sediments, yet microbiome responses remain poorly understood. Here we compared sediment microbiomes of the eutrophic Xiangshan Bay (XSB) and oligotrophic East China Sea (ECS), integrating cell counts, 16S rRNA amplicon, metagenomics, and cultivation-based resistance assays. Cell counts and amplicon data showed that XSB harbored higher microbial abundance (1.28 ×10[8]-1.34 ×10[9] vs. 2.07 ×10[7]-4.43 ×10[8] cells g[-1]), Chao1 richness (10,374-16,674 vs. 8311-12,281), and Shannon diversity (6.31-7.43 vs. 5.95-6.68). Amplicon-based null and neutral models indicated that community assembly in XSB was less stochastic and more deterministically selected than in the ECS. Life-history traits inferred directly from metagenomic data were consistently elevated in XSB relative to ECS, including 16S rRNA gene copy number (3.35 vs. 2.37), codon usage bias (0.0219 vs. 0.0188), maximum growth potential (0.1208 vs. 0.0844 h[-1]), genome size (5.63 vs. 5.38 Mb), GC content (56.26% vs. 54.48%), and transposase abundance (3.91% vs. 2.55%), collectively indicating a transition from K- to r-selected life-history strategies. Moreover, metagenomic annotation revealed a similarly expanded resistome in XSB, with 4.5-fold higher antibiotic resistance gene abundance (17.40-45.37 vs. 7.96-25.96 RPM) dominated by efflux-pump mechanisms, while plate assays showed roughly two-fold higher phenotypic resistance to macrolides, tetracyclines, and sulfonamides. These findings demonstrate that microbial community, life-history strategies, and antibiotic resistance respond as a coupled system to mariculture-driven eutrophication, providing a trait-based framework for predicting microbiome trajectories under anthropogenic nutrient enrichment.},
}

@article {pmid42679497,
year = {2026},
author = {Bagchi, R and Pant, B and Wang, HL and Kabir, AH},
title = {Localized root colonization by Trichoderma afroharzianum T22 is associated with host transcriptional reprogramming and beneficial bacterial enrichment under salinity stress in sorghum.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128703},
doi = {10.1016/j.micres.2026.128703},
pmid = {42679497},
issn = {1618-0623},
abstract = {Salinity is a major abiotic stress that severely restricts crop productivity. Despite considerable potential, the role of Trichoderma afroharzianum T22 in the molecular responses and root microbiome dynamics associated with salinity tolerance remains poorly understood in sorghum. In this study, T. afroharzianum inoculation alleviated salinity-induced stress by improving chlorophyll content, growth parameters, and nutrient balance, while restricting root-to-shoot Na[+] translocation. Split-root experiments showed that T. afroharzianum application to a single root compartment was insufficient to improve whole-plant performance under salinity, whereas inoculation of both compartments restored growth and chlorophyll-related traits. RNA-seq analysis showed the upregulation of genes involved in symbiosis, hormone signaling, antioxidant defense, and ion homeostasis, accompanied by repression of genes involved in ethylene biosynthesis and senescence in the roots. KEGG enrichment analysis further revealed activation of secondary metabolic pathways involved in stress adaptation. Furthermore, 16S rRNA sequencing showed that T. afroharzianum inoculation was associated with shifts in the root bacterial community without significantly altering alpha diversity, while selectively enriching putatively beneficial taxa, including Dyella mobilis, Luteibacter rhizovicinus, and Luteibacter yeojuensis under salinity. In addition, a conserved core microbiome was retained across treatments and was dominated by Streptomyces, Rhizobium, Dyella, and Labrys. Further, Janibacter was identified as a characteristic indicator taxon of T. afroharzianum inoculation, while Streptomyces showed the highest overall indicator value. Multi-omics integration analysis revealed that T. afroharzianum-associated microbial taxa were strongly associated with hormone signaling, redox homeostasis, mineral transport, and secondary metabolism under salinity stress. Particularly, Streptomyces and Luteibacter were the two genera most strongly associated with plant growth traits, whereas Rhizobium and Mucilaginibacter showed stronger positive correlations with tissue Na[+] accumulation. Collectively, these findings provide new insights into T. afroharzianum-mediated salinity tolerance in sorghum and highlight its potential as a microbial biostimulant, warranting further validation across diverse sorghum genotypes in field conditions.},
}

@article {pmid42679498,
year = {2026},
author = {Chen, X and Zhang, J and Gao, F and Du, H},
title = {Bacteriophages as emerging modulators of antitumor immunity in the tumor microenvironment.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128700},
doi = {10.1016/j.micres.2026.128700},
pmid = {42679498},
issn = {1618-0623},
abstract = {The tumor microenvironment (TME) is increasingly recognized as a complex ecosystem shaped by dynamic interactions among tumor cells, immune cells, and microbial components. While growing evidence has established the microbiota as a key regulator of antitumor immunity and immunotherapy response, the contribution of bacteriophages, the most abundant biological entities within microbial communities, has remained largely overlooked. Recent studies suggest that bacteriophages are not merely passive regulators of bacterial populations but can actively modulate host immune responses and influence tumor-associated immune landscapes. In this review, we summarize emerging evidence suggesting that bacteriophages may influence antitumor immunity through both direct and indirect mechanisms. Evidence from immune-cell and non-cancer experimental systems indicates that phage nucleic acids can engage TLR9-dependent sensing and, for selected phages, STING-associated inflammatory signaling; however, the relevance of these pathways within human tumors remains to be established. Indirectly, phages may alter microbial community structure and metabolic outputs, which could influence systemic immune tone and the composition of immune infiltrates within the TME. We further discuss accumulating data linking phageome features with tumor progression and responses to immune checkpoint blockade and other cancer therapies. However, much of the available evidence remains preclinical, indirect, or correlative, and causal roles for endogenous phages in human tumor immunity still require further validation. Distinct from the putative ecological and immunological roles of naturally occurring phages, engineered bacteriophages are being developed as therapeutic platforms for cancer immunotherapy, including tumor-antigen display, targeted delivery of immune agonists, cytokines or nucleic acids, and combination strategies with existing treatments. Finally, we address key methodological, mechanistic, and safety challenges that must be overcome to translate phage-based immunomodulation into clinical applications. Collectively, this review highlights the phageome as an emerging regulatory layer of tumor immunity and a promising, yet underexplored, target for therapeutic intervention.},
}

@article {pmid42679573,
year = {2026},
author = {Liu, B and Shen, Z and Shen, Y and Ren, J and Zhang, Z and Li, T and Li, W and Zhou, Q and Wu, T and Sun, J},
title = {Microplastic aging drives convergence of the plastisphere microbiome and resistome toward agricultural soils.},
journal = {Journal of hazardous materials},
volume = {516},
number = {},
pages = {143426},
doi = {10.1016/j.jhazmat.2026.143426},
pmid = {42679573},
issn = {1873-3336},
abstract = {The degree of microplastic (MP) aging varies substantially in agricultural soils; however, how this common aging gradient influences the plastisphere microbiome and resistome remains largely unknown. We therefore collected polyethylene MPs from long‑term mulched farmlands and classified them into low‑aged plastispheres (LAPs) and high‑aged plastispheres (HAPs). Bacterial community dissimilarity to soil decreased progressively from LAPs to HAPs, accompanied by broadening niche breadth, increasing bacterial diversity, and a shift toward more stochastic community assembly. The diversity and abundance of antibiotic resistance genes (ARGs) declined significantly along the aging gradient, with clinically relevant high-risk ARGs (e.g., vanR, ugd, and aac(6')-I) decreasing by 53.34-84.01%. Furthermore, the ARG hosts shifted from Actinomycetota in LAPs to Pseudomonadota in soils. Variance partitioning showed that the carbonyl index uniquely explained 57.03% of the variation in plastisphere ARG profile distance toward soil, identifying MP aging as the primary driver of resistome convergence. Collectively, these findings demonstrate that natural MP aging drives a progressive convergence of the plastisphere resistome toward that of the surrounding soil, indicating that aged MPs may pose a reduced risk of antibiotic resistance compared to newly formed MPs. This convergence underscores the need to incorporate plastic aging into future risk assessment frameworks for plastisphere-associated ARGs.},
}

@article {pmid42679639,
year = {2026},
author = {Ahmad, I and Zia, MA and Tavares, RG and Spanevello, RM and Stefanello, FM},
title = {AMPK and macrophage crosstalk in diabetes: Mechanisms, inflammation, and therapeutic perspectives.},
journal = {Cytokine & growth factor reviews},
volume = {91},
number = {},
pages = {161-172},
doi = {10.1016/j.cytogfr.2026.08.002},
pmid = {42679639},
issn = {1879-0305},
abstract = {Diabetes mellitus, especially type 2 diabetes (T2DM), is a complex metabolic disease marked by persistent low-grade inflammation and insulin resistance. In diabetes, adipose tissue macrophages adopt a pro-inflammatory M1 phenotype, secreting cytokines including TNF-α, IL-6, and IL-1β that disrupt insulin signaling and cause metabolic dysfunction. AMP-activated protein kinase (AMPK), a cellular energy sensor, is a key regulator of macrophage polarization. It suppresses M1 responses by inhibiting NF-κB and JNK signaling, activating CREB/SIRT1 pathways, and promoting oxidative metabolism. Therefore, this review investigates the bidirectional interaction between AMPK signaling and macrophage function in diabetes, focusing on how metabolic stress affects AMPK activity, increasing inflammation and insulin resistance, whereas AMPK activation restores immune-metabolic balance. The gut microbiome further influences this axis, with short-chain fatty acids activating AMPK via GPR41/43, promoting M2 polarization and improving metabolic outcomes. Metformin, SGLT2 inhibitors, new direct AMPK activators such as PXL770, and lifestyle changes are also potential therapeutic treatments. However, considerable hurdles remain, including the prevalence of preclinical findings, a lack of macrophage-specific AMPK activators, simplicity of the M1/M2 paradigm, and uncertainty about long-term safety. Future research must focus on macrophage-targeted drug delivery, tissue-specific regulatory networks, biomarker discovery, and rigorous clinical trials with immunological outcomes. In conclusion, the AMPK-macrophage axis is a critical immune-metabolic gatekeeper in diabetes, and targeting this pathway offers a potential technique for restoring immune-metabolic balance, while significant difficulties must be overcome before practical use.},
}

@article {pmid42679805,
year = {2026},
author = {Samarra, A and Alcañiz, AJ and Quijada, NM and Renwick, S and George, S and Sinha, T and Martínez-Costa, C and Segata, N and Zhernakova, A and Bode, L and Collado, MC},
title = {Maternal secretor status and human milk oligosaccharides influence the infant gut resistome.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103007},
doi = {10.1016/j.xcrm.2026.103007},
pmid = {42679805},
issn = {2666-3791},
abstract = {The infant gut resistome is established early in life and is shaped by perinatal exposures, yet the mechanisms underlying its modulation remain unclear. We combined shotgun metagenomics of fecal samples from 57 one-month-old infants and paired milk samples from 50 mothers in the MAMI cohort to investigate the influence of maternal secretor status on early-life resistome development. Longitudinal follow-up at 6 and 12 months, and also further validation in the independent Lifelines NEXT (LLNEXT) cohort, support our findings. Cesarean section (C-section) was associated with increased antibiotic resistance gene (ARG) diversity, whereas exclusive breastfeeding reduced ARG abundance and diversity. Maternal secretor status further modified resistome composition among exclusively breastfed infants. Human milk oligosaccharide profiling identified specific glycans underlying these associations, with 2'-fucosyllactose and 6'-sialyllactose showing negative correlations with distinct ARG classes. These findings identify human milk composition as a key determinant of early-life resistome assembly and a potential target for modulating antimicrobial resistance.},
}

@article {pmid42680070,
year = {2026},
author = {Wang, J and Luo, L and Zhang, J and Yu, L and Cui, L},
title = {The Gut Microbiota and Gut-Brain Axis in Alzheimer's Disease: From Pathogenesis to Treatment.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103345},
doi = {10.1016/j.arr.2026.103345},
pmid = {42680070},
issn = {1872-9649},
abstract = {Alzheimer's disease (AD) is a progressive neurodegenerative disorder whose pathological course involves amyloid-β (Aβ) deposition, tau abnormalities, neuroinflammation, and neurovascular dysfunction. Interest in the microbiota-gut-brain axis does not arise because gut dysbiosis has been established as an independent initiating cause of sporadic AD, but because this axis connects modifiable peripheral factors-including diet, medication, ageing, and intestinal physiology-with barrier homeostasis, immunometabolic state, neural afferent signaling, and the brain's response to pathology. Human studies have detected microbiota differences in biomarker-positive preclinical AD and suggest that barrier abnormalities may be associated with subsequent cognitive change; patient-derived microbiota transfer, APOE-dependent tau models, and immune-vagal circuit studies further support phenotype modifiability under defined experimental conditions. This review therefore integrates barrier, immune, metabolic, and neural pathways and emphasizes that diverse microbial alterations may converge on a limited set of measurable functional nodes that could be more informative than individual genera for mechanistic validation, risk stratification, and treatment monitoring. Although clinical intervention evidence remains at an early stage, the peripheral accessibility and modifiability of the microbiota provide a rationale for investigating it as an adjunctive target alongside standard AD therapy. Future work should concurrently evaluate the microbiome, metabolites, both barriers, and immune and neural readouts in longitudinal cohorts and stratified randomized trials to determine which patients, disease stages, and intervention modalities are most likely to benefit.},
}

@article {pmid42680280,
year = {2026},
author = {Yu, K and Wang, S and Shi, H and Luo, R and Chen, Z and Xia, Y and Zeng, Q and Ma, Y and Han, D},
title = {Climate and soil shape Daqu wheat quality and seed microbiome via rhizosphere taxa and microbial assembly.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {119958},
doi = {10.1016/j.foodres.2026.119958},
pmid = {42680280},
issn = {1873-7145},
mesh = {*Triticum/microbiology ; *Rhizosphere ; *Soil Microbiology ; *Seeds/microbiology ; *Microbiota ; *Climate ; *Soil/chemistry ; Bacteria/classification ; Fungi/classification ; },
abstract = {The grain quality and seed microbiome of Daqu wheat are fundamental determinants of Daqu fermentation performance; however, the mechanisms by which cultivation environments influence these traits via rhizosphere microbial communities remain unclear. Bacterial and fungal communities across the bulk soil-rhizosphere-seed continuum of three wheat cultivars grown in four ecoregions were characterized using absolute quantitative amplicon sequencing. The rhizosphere microbiome was treated as a central intermediary, while the response variables were seed microbial diversity and grain-quality traits, including starch content, protein content, and grain hardness. Twelve physicochemical properties of soil and 11 climatic factors were integrated into a multidimensional association framework. Environmental conditions exerted stronger influences on both seed quality traits and microbial diversity than cultivar identity. Distinct regional signatures were also evident in rhizosphere microbiomes, with environmental gradients explaining community variation more effectively than geographic distance. Bacterial communities exhibited greater sensitivity to environmental fluctuations than fungi. Mantel analyses identified available nitrogen, precipitation, and atmospheric pressure as significant drivers of core rhizosphere taxa (P < 0.05). iCAMP revealed that stochastic processes predominantly governed rhizosphere bacterial assembly, whereas stochastic and deterministic mechanisms jointly shaped fungal assembly. Partial least squares path modeling further uncovered a rhizosphere-mediated environment-seed cascade, wherein sunlight intensity and duration, atmospheric pressure, and soil nitrogen directly or indirectly affected seed wet gluten content, grain hardness, and seed microbial diversity through their influences on rhizosphere microbiota. Rhizosphere bacterial diversity was negatively associated with seed bacterial diversity (path coefficient = -0.118, P < 0.05), indicating that rhizosphere communities may shape seed endophytic bacterial assemblages via environmental filtering and competitive interactions. Collectively, these findings elucidate how environments shape the quality and seed microbiomes of Daqu wheat, providing scientific guidance for optimal site selection and the standardized production of high-quality brewing wheat for industrial Baijiu.},
}

*Triticum/microbiology
*Rhizosphere
*Soil Microbiology
*Seeds/microbiology
*Microbiota
*Climate
*Soil/chemistry
Bacteria/classification
Fungi/classification

@article {pmid42680295,
year = {2026},
author = {Shafi, Z and Waheed, A and Shahid, M and Rasool, A and Ali, S},
title = {Beyond protein source: The structure-gut microbiome axis in alternative protein digestion, fermentation, and health.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {119983},
doi = {10.1016/j.foodres.2026.119983},
pmid = {42680295},
issn = {1873-7145},
mesh = {*Fermentation ; *Digestion/physiology ; Humans ; *Gastrointestinal Microbiome/physiology ; *Dietary Proteins/metabolism ; Animals ; },
abstract = {Alternative proteins from plant, algal, fungal, and microbial sources are increasingly recognized for their potential to influence gut microbiota. However, the role of protein structure in shaping these interactions remains poorly understood. This review examines how key structural attributes of alternative proteins-including amino acid composition, folding characteristics, aggregation behavior, and enzymatic accessibility, govern gastrointestinal digestion. It also explores how these structural features affect microbial fermentation and the subsequent nutritional and functional outcomes. Structural variations influence peptide generation, microbial substrate utilization, and the production of metabolites such as short-chain fatty acids and proteolytic compounds. Current evidence indicates that protein conformation and digestibility, rather than source alone, are major determinants of microbiome responses. However, progress is hindered by limited multi-omics integration and a lack of standardized models and in-vivo validation. Collectively, current evidence supports a structure-driven framework for predicting microbiome interactions with alternative proteins. It also highlights key research priorities for developing functional protein ingredients that support gut and metabolic health.},
}

*Fermentation
*Digestion/physiology
Humans
*Gastrointestinal Microbiome/physiology
*Dietary Proteins/metabolism
Animals

@article {pmid42680304,
year = {2026},
author = {Li, Y and Wang, Y and Prabhakaran, P and Ouyang, F and Zhou, W and Guan, H and Chen, Y and Li, D and Sun-Waterhouse, D and Li, F},
title = {Food-derived phenolic compounds in precision nutrition: computational and AI-assisted approaches for target identification and health intervention.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {120000},
doi = {10.1016/j.foodres.2026.120000},
pmid = {42680304},
issn = {1873-7145},
mesh = {Humans ; *Phenols ; *Precision Medicine/methods ; *Artificial Intelligence ; },
abstract = {Precision nutrition refers to nutritional interventions tailored to individual biological variability (e.g., genetics, gut microbiome, and metabolic status). Within this framework, identifying bioactive food components that modulate disease-relevant targets and pathways in an individualized manner is a central goal. Targeted interventions are increasingly used for cancer, autoimmune disorders, and metabolic diseases, but are often limited by high prices and adverse effects. Dietary phenolic compounds have therefore attracted attention as safer and more sustainable candidates for health intervention strategies, owing to their ability to interact with disease-relevant protein targets. Examples include EGCG targeting the p53-MDM2 interaction, quercetin modulating HSP90-related ferroptosis, and sesamin inhibiting Syk activation in food allergy. Their structural diversity and bioactivity make them valuable for candidate screening and personalized intervention design. However, these features also create challenges for target identification and functional evaluation. More systematic and predictive strategies are therefore needed to accelerate the identification, evaluation, and optimization of phenolic bioactives. In this context, computational and AI-assisted approaches (e.g., molecular docking, machine learning, and network pharmacology) offer new opportunities to improve target discovery, candidate prioritization, and response prediction. These approaches can integrate individual-level genetic, microbiome, metabolic, dietary, and clinical data. This integration may help predict personalized molecular targets, phenolic metabolism, bioavailability, and intervention responses, thereby supporting tailored phenolic-based nutrition strategies. This review summarizes the therapeutic potential, computational discovery strategies, molecular targets, and translational gaps in applying phenolic compounds to precision nutrition.},
}

Humans
*Phenols
*Precision Medicine/methods
*Artificial Intelligence

@article {pmid42680335,
year = {2026},
author = {Christman, L and Mai, C and Gu, L},
title = {Dealcoholized muscadine wine improved skin elasticity and oxidative stress biomarkers without affecting gut microbiome in women over 40 in a randomized controlled trial.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 3},
pages = {120042},
doi = {10.1016/j.foodres.2026.120042},
pmid = {42680335},
issn = {1873-7145},
mesh = {Humans ; *Oxidative Stress/drug effects ; Female ; Biomarkers/blood ; *Wine/analysis ; Adult ; *Gastrointestinal Microbiome/drug effects ; Single-Blind Method ; Cross-Over Studies ; *Elasticity/drug effects ; Middle Aged ; Polyphenols/pharmacology ; *Skin/drug effects ; Glycation End Products, Advanced/blood ; *Skin Physiological Phenomena/drug effects ; Vitis/chemistry ; Matrix Metalloproteinase 9/blood ; },
abstract = {Muscadine wine has a unique polyphenol profile distinct from that of common wine, and limited research exists on its health benefits. This study aimed to investigate the effects of intake of dealcoholized muscadine wine (DMW) on skin health, oxidative stress, inflammatory biomarkers, and the gut microbiome. Seventeen healthy women were randomly assigned to consume 300 mL of DMW or a placebo daily for 6 weeks, separated by a 3-week washout period, in a randomized, single-blinded, crossover design. Skin health parameters were measured on the face and forearm. Oxidative stress and inflammatory biomarkers were assessed in plasma. Fecal bacterial DNA was sequenced using shotgun sequencing. DMW did not affect UVB-induced erythema compared to placebo. However, it significantly decreased transepidermal water loss and increased facial gross elasticity. Skin elasticity significantly improved on the forearm, whereas other skin parameters were not affected. DMW significantly decreased plasma levels of matrix metalloproteinase-9 and advanced glycation end products compared with placebo. However, the abundance, diversity, and functions of the gut microbiome were not affected. Polyphenol-rich DMW administered for six weeks improved certain skin health parameters and reduced oxidative and inflammatory stress, without affecting the gut microbiome in healthy women.},
}

Humans
*Oxidative Stress/drug effects
Female
Biomarkers/blood
*Wine/analysis
Adult
*Gastrointestinal Microbiome/drug effects
Single-Blind Method
Cross-Over Studies
*Elasticity/drug effects
Middle Aged
Polyphenols/pharmacology
*Skin/drug effects
Glycation End Products, Advanced/blood
*Skin Physiological Phenomena/drug effects
Vitis/chemistry
Matrix Metalloproteinase 9/blood

@article {pmid42680466,
year = {2026},
author = {Javan, GT and Di Nunzio, M and Grassi, S and Iancu, L and Procopio, N},
title = {Drug-induced dysbiosis as a forensic biomarker: Implications for post-mortem interval estimation and forensic diagnostics.},
journal = {Science & justice : journal of the Forensic Science Society},
volume = {66},
number = {5},
pages = {101493},
doi = {10.1016/j.scijus.2026.101493},
pmid = {42680466},
issn = {1876-4452},
mesh = {Humans ; *Dysbiosis/chemically induced ; *Postmortem Changes ; *Substance-Related Disorders ; Biomarkers ; *Gastrointestinal Microbiome/drug effects ; Animals ; },
abstract = {Substance use disorders (SUDs) and drug-related deaths represent a growing global burden. Increasing evidence highlights substances ability to reshape the gut microbiome, a highly dynamic and metabolically active ecosystem that contributes to host homeostasis through interactions with neural, endocrine, and immune systems. Alterations in microbial diversity, depletion of short-chain fatty acid-producing taxa, disruption of epithelial barrier integrity, and systemic inflammation have been consistently associated with substance exposure. While these changes are increasingly characterized in living individuals, their persistence and impact after death remain less explored. In forensic contexts, drug-related fatalities are difficult to interpret due to non-specific autopsy findings, analytical limitations of toxicological methods, post-mortem redistribution, and the absence of clear lethal thresholds. The emerging study of thanatomicrobiome offers a novel avenue to address these challenges, as antemortem dysbiosis may influence post-mortem microbial succession and, consequently, post-mortem interval (PMI) estimation. This narrative review synthesises current knowledge on substance-induced microbiome alterations across antemortem and postmortem contexts, and extends this perspective to entomotoxicology, highlighting how drug-related microbial changes may influence both insect colonisation and insect-associated microbiomes. It also emphasises current methodological heterogeneity and the need for standardised approaches, outlining opportunities for future forensic applications.},
}

Humans
*Dysbiosis/chemically induced
*Postmortem Changes
*Substance-Related Disorders
Biomarkers
*Gastrointestinal Microbiome/drug effects
Animals

@article {pmid42680481,
year = {2026},
author = {Kim, S and Lee, HY and Kim, SY and Lee, JY},
title = {Sperm as a multilayered epigenetic information system: encoding and transmission of paternal environmental signals.},
journal = {BMB reports},
volume = {},
number = {},
pages = {},
pmid = {42680481},
issn = {1976-670X},
abstract = {Spermatozoa are increasingly recognized as carriers of non-genetic paternal information, rather than passive vehicles for the haploid genome. During spermatogenesis and post-testicular epididymal maturation, the paternal germline establishes a compact but functionally organized epigenome composed of DNA methylation, retained histones and histone modifications, chromatin-associated factors, and diverse small RNAs. These layers are environmentally responsive. In animal models, paternal diet, stress, toxicant exposure, and inflammatory or microbiome-related challenges can alter sperm DNA methylation, chromatin states, and small RNA cargo, with many changes mapping to loci involved in development, metabolism, and stress-response pathways. After fertilization, the paternal genome undergoes extensive epigenetic reprogramming; nevertheless, a subset of DNA methylation and chromatin features can resist erasure or be functionally relayed, while sperm-derived RNAs can influence early embryonic gene expression. Recent work, including studies of diet-induced sperm mitochondrial tRNAs, further supports the concept that defined paternal exposures may be transmitted to the embryo through discrete RNA-mediated mechanisms. In humans, lifestyle and environmental exposures are associated with measurable sperm epigenomic variation and with offspring health outcomes, but most evidence remains observational and is vulnerable to confounding by genetics, maternal factors, and shared environments. A central challenge is therefore to connect specific sperm epigenetic alterations to molecular effects in the early embryo and to subsequent offspring phenotypes. Here, we review how paternal environmental information is encoded during spermatogenesis and epididymal maturation, reshaped by environmental exposures, and interpreted by the early embryo, emphasizing multilayer integration and the evidence required to move from association to mechanism.},
}

@article {pmid42680679,
year = {2026},
author = {Yang, X and Peng, AD and Cheng, JH and Huang, YH and Zhong, HT and Zhou, HT and Liu, PQ and Ji, XH and Li, C and Zhang, SR and Lai, JL and Luo, XG and Wen, G},
title = {A legacy pollutant deciphered by multiomics toxicology and targeted remediation by a synthetic microbial consortium: a case study of 2-chloroacetophenone from abandoned chemical weapons.},
journal = {Water research},
volume = {},
number = {},
pages = {126776},
doi = {10.1016/j.watres.2026.126776},
pmid = {42680679},
issn = {1879-2448},
abstract = {2-Chloroacetophenone (2-CA) is a typical organic poison found in abandoned Japanese chemical weapons, yet systematic research on its ecological risks and bioremediation strategies in aquatic environments remains scarce. Through a 120-day exposure experiment across three concentration gradients (10, 50, and 100 mg·L[-1]) coupled with multiomics analysis (physicochemical profiling, ionomics, 16S rRNA sequencing, metagenomics, and metabolomics), we systematically characterized the toxic effects of 2-CA on aquatic microbial communities and their molecular response mechanisms. The glutathione (GSH) metabolic pathway was identified as the core defense hub against 2-CA-induced oxidative stress, with multiomics data revealing its transition from compensatory activation to irreversible collapse. Guided by these mechanistic insights, we directionally isolated three cascade-degrading bacteria (Pseudomonas abietaniphila, Bacillus sp., and Arthrobacter agilis) harboring the key genes hapA, yjfP, and catA, which encode the three consecutive steps of Baeyer-Villiger oxidation, ester bond hydrolysis, and aromatic ring cleavage. The synthetic microbiome assembled from these three wild-type strains achieved 100% removal of 100 mg·L[-1] 2-CA within 24 h in vitro and within 10 days in simulated contaminated water, with the sequential detection of predicted intermediates (phenyl 2-chloroacetate, phenol, and pyruvic acid) confirming the operation of the cascade pathway. This study establishes a "toxicology diagnosis-functional deconstruction-synthetic reconstruction" paradigm, providing mechanistic understanding and a potential bioremediation strategy for organic toxicants at sites contaminated by relic Japanese chemical weapons, although direct ecotoxicological validation of detoxification remains to be confirmed.},
}

@article {pmid42680742,
year = {2026},
author = {Low, A and Yang, Z and Anantaya, KT and Zhao, S and Tan, WC and Perez, RL and Chung The, H and Lim, SZY and Liu, L and Gounot, JS and Kwah, JS and Ong, RT and Nagarajan, N and Lee, JWJ and Mo, Y},
title = {Microbiome features associated with persistent intestinal carriages of Escherichia coli ST131 in a Southeast Asian cohort study.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42680742},
issn = {2041-1723},
mesh = {Humans ; *Escherichia coli/genetics/isolation & purification/classification ; *Escherichia coli Infections/microbiology/epidemiology ; Feces/microbiology ; *Gastrointestinal Microbiome/genetics ; Cohort Studies ; Metagenomics ; *Carrier State/microbiology ; Asia, Southeastern/epidemiology ; Intestines/microbiology ; },
abstract = {Escherichia coli sequence-type 131 (ST131) is the dominant global extraintestinal pathogen capable of asymptomatic intestinal carriage and sustained household transmission, challenging infection control. Despite its clinical significance, the ecological determinants of gut persistence remain poorly understood. We performed shotgun metagenomics on fecal samples to investigate gut microbiome features associated with ST131-positive samples, distinct host carrier statuses (persistent, intermittent and non-carriers) and household risks in a study of a Southeast Asian cohort. Here, we show that ST131 carriage was associated with compositional shifts without reducing species alpha-diversity. Regression analyses identified depletion of commensal taxa and the 1,5-anhydrofructose degradation pathway in ST131-positive samples. Persistent carriers exhibited highly perturbed microbiome enriched with pathobionts, aerobactin- and lipopolysaccharide (LPS)-biosynthesis pathways. Comparing household risk groups to control, revealed that biotin biosynthesis and 1,5-anhydrofructose degradation may influence ST131 co-colonization through both direct and indirect mechanisms. Machine learning analyses identified metabolic pathways as stronger discriminators of persistent carriage than taxonomic features. Genomic-resolved analysis of clinical ST131 isolates revealed conserved genes for iron-acquisition, LPS and antibiotic resistance determinants. Overall, while commensals and metabolism may influence initial ST131 colonization, persistent carriage is associated with specific microbial and metabolic adaptations, providing potential targets to limit intestinal ST131 persistence.},
}

Humans
*Escherichia coli/genetics/isolation & purification/classification
*Escherichia coli Infections/microbiology/epidemiology
Feces/microbiology
*Gastrointestinal Microbiome/genetics
Cohort Studies
Metagenomics
*Carrier State/microbiology
Asia, Southeastern/epidemiology
Intestines/microbiology

@article {pmid42680796,
year = {2026},
author = {Mu, C and Yusuf, K and Hasan, SU},
title = {Early-life fentanyl exposure, microbiome-brain axis and neurodevelopment.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42680796},
issn = {1530-0447},
}

@article {pmid42680951,
year = {2026},
author = {Pan, X and Conroy, A and Ngima, TS and Mesko, M and Morzhanaeva, O and Li, A and Marino, J and Westblade, LF and Grier, A and Bacher, P and Longman, RS and Scherl, EJ and Iliev, ID},
title = {Antifungal therapy improves microbiome dynamics in inflammatory bowel disease.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {42680951},
issn = {1546-170X},
abstract = {Gut fungal dysbiosis has been implicated in inflammatory bowel disease (IBD), yet strategies for targeting the gut mycobiota in IBD remain unexplored. Here we leveraged the observation that Candida albicans strains are shared between the oral cavity and gut in patients with IBD with mild oral thrush, a condition caused by Candida overgrowth, to design a prospective observational study comparing oral antifungal therapy (swish-and-spit nystatin; oral nystatin fungal targeting (ORNT); n = 18) with orogastrointestinal antifungal therapy (fluconazole; gastrointestinal and oral fluconazole fungal targeting (GIFT); n = 35). Among 53 patients with mild-to-moderate ulcerative colitis or Crohn's disease, fluconazole, but not nystatin, effectively reduced intestinal Candida burden and reshaped gut fungal-community composition. Fluconazole treatment was accompanied by increased bacterial diversity, expansion of short-chain fatty-acid-producing taxa, restoration of anti-inflammatory microbial metabolites and durable shifts in cross-kingdom microbial networks. These microbiome and metabolomic changes coincided with improved disease activity indices and a decreased risk of disease progression over the 8-week follow-up period. These findings demonstrate the feasibility of mycobiome-based patient stratification, provide evidence that targeted antifungal therapy can reshape the intestinal microbiota in IBD and establish a framework for implementing antifungal cotherapy in patients with fungal-associated disease manifestations.},
}

@article {pmid42681027,
year = {2026},
author = {John, E and Kuan, JE and Djamei, A},
title = {Induction of Ustilago maydis Appressorium and Filamentation.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3050},
number = {},
pages = {17-27},
pmid = {42681027},
issn = {1940-6029},
mesh = {*Zea mays/microbiology ; *Ustilago/growth & development ; *Plant Diseases/microbiology ; *Hyphae/growth & development ; Culture Media/chemistry ; Basidiomycota ; },
abstract = {Ustilago maydis is a model smut-causing fungus infecting maize. Two compatible mating-type isolates of the fungus must form the infectious dikaryotic filaments that form infection. However, several laboratory techniques and strains have been developed that can induce this phenotype under controlled conditions, in order to study the pathogen outside the complexities of the host and microbiome. Three such methods are described here, which cover the use of charcoal-supplemented agar to induce filamentation, appressorium formation on hydrophic surfaces with 16-hydroxyhexadecanoic acid, as well as inducing b-dependent filamentation in liquid culture with engineered strains.},
}

*Zea mays/microbiology
*Ustilago/growth & development
*Plant Diseases/microbiology
*Hyphae/growth & development
Culture Media/chemistry
Basidiomycota

@article {pmid42681450,
year = {2026},
author = {Choa, R and Sun, L and Kambayashi, T},
title = {Extraction and Quantification of Skin Immune Cells and Skin Lipids.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3053},
number = {},
pages = {785-797},
pmid = {42681450},
issn = {1940-6029},
mesh = {Animals ; *Skin/immunology/cytology/metabolism/chemistry ; Mice ; *Lipids/isolation & purification/analysis ; Chromatography, Thin Layer/methods ; Sebum/metabolism/immunology/chemistry ; T-Lymphocytes/immunology/metabolism ; Flow Cytometry/methods ; Lipid Metabolism ; },
abstract = {We have recently shown that the immune system, specifically T cells stimulated by the skin-derived cytokine thymic stromal lymphopoietin, can promote total body adipose loss. This effect is caused by the regulation of lipid metabolism in the skin, whereby T cells induce the release of a lipid-rich substance called sebum. The adoptive transfer of thymic stromal lymphopoietin-stimulated T cells can also induce adipose loss and sebum secretion, making this approach applicable to cellular therapies for metabolic and dermatologic diseases. The skin is the body's largest organ system and provides a critical barrier surface that senses and protects the host from the outside environment. Sebocytes within the skin secrete sebum, a lipid-rich substance that coats the skin and protects it against water, pathogens, and sun damage while also regulating the skin immune landscape and microbiome. Methods to quantify and characterize sebum production are needed to better investigate the role of sebum in skin immunobiology. Here, we describe a protocol that we developed to extract lipids from mouse fur followed by thin layer chromatography analysis of the various lipid classes. We also describe a protocol to maximally extract immune cells from the skin for flow cytometric analysis, which has previously been limited by low cell numbers. These methods will be useful to study skin immunobiology including, but not limited to, its impact on sebum secretion.},
}

Animals
*Skin/immunology/cytology/metabolism/chemistry
Mice
*Lipids/isolation & purification/analysis
Chromatography, Thin Layer/methods
Sebum/metabolism/immunology/chemistry
T-Lymphocytes/immunology/metabolism
Flow Cytometry/methods
Lipid Metabolism

@article {pmid42681656,
year = {2026},
author = {Alnuaimi, F and Yassin, LK and Alketbi, S and Skrabulyte-Barbulescu, J and Almazrouei, S and Alremeithi, D and Alahbabi, N and Almarzooqi, S and Shamma, H and Hamad, MIK},
title = {Human milk microbiome as a modulator of the early-life gut-brain axis: mechanisms and translational opportunities for neurodevelopment.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {42681656},
issn = {1479-5876},
mesh = {Humans ; *Milk, Human/microbiology ; *Neurodevelopment ; *Brain/growth & development ; *Gastrointestinal Microbiome ; *Translational Research, Biomedical ; *Microbiota ; Infant, Newborn ; *Translational Science, Biomedical ; },
abstract = {The first 1000 days of life represent a critical developmental window during which early microbial colonization contributes to immune, metabolic, and neurodevelopmental programming. Human milk is increasingly recognized as a biologically active fluid that shapes infant gut microbiome assembly through microorganisms, human milk oligosaccharides (HMOs), immune factors, and microbial metabolites. Within this framework, the human milk microbiome has emerged as a potential contributor to the milk-gut-brain axis (MGBA), a bidirectional communication network linking the gut microbiota with neural, immune, endocrine, and metabolic pathways involved in brain development. This review summarizes current evidence regarding the origins, determinants, and functional relevance of the human milk microbiome and its potential role in early-life neurodevelopment. Proposed microbial sources include maternal skin, the infant oral cavity, environmental exposure, and the entero-mammary pathway, while key determinants include lactational stage, delivery mode, antibiotic exposure, maternal diet, obesity, and prematurity. Mechanistic pathways linking milk-associated microbes with neurodevelopment are discussed, including microbial colonization, immune and barrier maturation, vagal and neuroendocrine signalling, and production of short-chain fatty acids (SCFAs) and tryptophan-derived metabolites. We further evaluate evidence relating breastfeeding and milk-associated microbial exposures to cognitive, behavioural, and neurodevelopmental outcomes, particularly in preterm and medically vulnerable infants. Although experimental and observational evidence supports biologically plausible links between the human milk microbiome and the developing microbiota-gut-brain axis, major uncertainties remain regarding microbial viability, sustained colonization, causality, and long-term functional significance. Methodological limitations, including low microbial biomass, contamination susceptibility, and heterogeneity in analytical approaches, continue to complicate interpretation across studies. Future progress will require longitudinal, mechanistically informed studies integrating microbiome profiling with metabolomics, immune phenotyping, neuroimaging, and validated neurodevelopmental outcomes.},
}

Humans
*Milk, Human/microbiology
*Neurodevelopment
*Brain/growth & development
*Gastrointestinal Microbiome
*Translational Research, Biomedical
*Microbiota
Infant, Newborn
*Translational Science, Biomedical

@article {pmid42681689,
year = {2026},
author = {Feng, F and Wu, Z and Xu, H and Li, Z and Wu, H and Zhang, J and Xu, Z and Zhang, S and Li, Y},
title = {Pathogens in rheumatoid arthritis: epidemiological, mechanistic, and clinical insights.},
journal = {Biomarker research},
volume = {14},
number = {1},
pages = {},
pmid = {42681689},
issn = {2050-7771},
abstract = {Rheumatoid arthritis is a chronic systemic autoimmune disease characterized by synovial inflammation, joint destruction, and systemic comorbidities. Emerging evidence highlights the critical involvement of the microbiome in disease pathogenesis, encompassing bacteria, viruses, fungi, and mycoplasmas. This review synthesizes recent findings on microbiome alterations, summarizing epidemiological, molecular, and mechanistic data. Among the evaluated pathogens, Porphyromonas gingivalis and Prevotella copri currently demonstrate the strongest causal evidence for initiating autoimmunity. Porphyromonas gingivalis directly catalyzes host protein citrullination via its unique peptidylarginine deiminase, driving anti-citrullinated protein antibody production, while Prevotella copri expands during the preclinical phase to drive T helper 17 cell polarization. Furthermore, chronic Hepatitis C virus infection presents compelling causal links, as continuous viral stimulation triggers robust autoantibody production in atypical memory B cells. Other infectious agents, including Epstein-Barr virus and Proteus mirabilis, act as environmental triggers through molecular mimicry, whereas opportunistic pathogens like Pneumocystis jirovecii emerge as severe secondary complications resulting from profound pharmacological immunosuppression. In terms of immediate clinical translation, several microbiome-targeted strategies are poised for routine practice. These include non-surgical periodontal therapy and oral hygiene optimization to reduce systemic disease activity, the utilization of direct-acting antivirals for Hepatitis C virus to concurrently resolve joint inflammation, and targeted prophylaxis using sulfasalazine to prevent Pneumocystis jirovecii pneumonia in highly immunosuppressed populations. Additionally, the immunomodulatory application of Ganoderma lucidum polysaccharides for symptomatic pain relief and the preclinical development of bacterial virulence factor inhibitors represent promising therapeutic avenues. Together, these findings confirm that the microbiome acts as a critical modifier of the inflammatory milieu. Future studies integrating longitudinal cohorts and precision interventional trials will further solidify causality and refine these microbiome-targeted therapies.},
}

@article {pmid42681694,
year = {2026},
author = {Shi, C and Deng, J and Zhang, H and Li, Y and Zhang, S and Wang, H and Min, S and Luo, Y and Zhang, Z and Hao, J and Wang, Y and Cao, B and He, Y and Su, H},
title = {Dietary green tea residue improves growth and antioxidant capacity via rumen microbiota and glutathione modulation in finishing beef cattle.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42681694},
issn = {1674-9782},
support = {CARS-37//China Agriculture Research Systems of MOF and MARA/ ; 2023YFD1300904//the National Key R&D Program of China/ ; },
abstract = {BACKGROUND: Green tea residue (GTR) is an abundant by-product rich in polyphenols. This study aimed to investigate the effects of GTR on growth performance, rumen microbiota, and systemic metabolism in finishing beef cattle.

RESULTS: Forty-five 18‑month‑old finishing Angus steers with an average initial body weight of 474.44 ± 14.03 kg (mean ± SD) were individually housed and randomly assigned to three dietary treatments (n = 15 per group) using stratified randomization by initial body weight: control group (CG group, 150 g rice straw), low-dose GTR group (LG group, 75 g rice straw +75 g GTR), and high-dose GTR group (HG group, 150 g GTR). The feeding trial lasted 70 d with a 10-day adaptation period. To elucidate the regulatory mechanisms of GTR on beef cattle growth, we thoroughly assessed growth performance, nutrient digestibility, ruminal fermentation parameters, conducted bacterial 16S rRNA sequencing, analysed plasma biochemical and antioxidant markers, and executed an untargeted plasma metabolomic analysis. The LG group tended to increase average daily gain (ADG). Meanwhile, the LG group exhibited elevated plasma concentrations of β-hydroxybutyrate and glucose, increased activities of superoxide dismutase and glutathione S-transferase, an increased glutathione (GSH)/glutathione disulfide (GSSG) ratio, and reduced GSSG content. GTR treatment decreased reactive oxygen species and oxidative stress index. Furthermore, dietary GTR significantly modified the rumen microbial community structure, enriching Xylanibacter and Prevotellaceae_UCG-003, while reducing the abundance of Rikenellaceae_RC9_gut_group. Plasma metabolomics revealed that GTR treatment enriched GSH Metabolism and the Pentose Phosphate Pathway. Notably, gamma-glutamylcysteine was identified as a key mediator of the association between Xylanibacter and ADG in fattening beef cattle supplemented with GTR.

CONCLUSIONS: Dietary supplementation with 75 g/steer/d GTR improved growth performance and systemic antioxidant capacity in finishing beef cattle by modulating the rumen microbiota and activating the glutathione system. GTR represents a promising functional feed additive that simultaneously valorizes tea by‑products and enhances livestock productivity.},
}

@article {pmid42681814,
year = {2026},
author = {Lu, X and Zou, J and Han, G and Zhao, M and Luo, T and Feng, X and Zhu, L and Chen, Y and Ji, X and Jin, J and Zhao, L},
title = {Oligosaccharides With Defined Glycosidic Bonds Shape Gut Microbial Succession and Metabolism Via Bond-Specific Microbial Responders.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e77488},
doi = {10.1002/advs.77488},
pmid = {42681814},
issn = {2198-3844},
support = {32302102//National Natural Science Foundation of China/ ; 23ZR1415400//Natural Science Foundation of Shanghai/ ; 23YF1409800//Shanghai Sailing Program/ ; //Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism (Shanghai Municipal Education Commission)/ ; },
abstract = {Functional oligosaccharides are important prebiotic ingredients, but the structure-function relationships and mechanisms by which defined glycosidic bonds shape microbial responses remain unclear. Five glucose disaccharides, trehalose (α-1,1), maltose (α-1,4), isomaltose (α-1,6), cellobiose (β-1,4), and gentiobiose (β-1,6), were used as minimal oligosaccharide models to isolate glycosidic bond effects. Absolute time-series profiling combined with Bayesian generalized Lotka-Volterra modeling identified bond-specific microbial responders, operationally defined as taxa with statistically supported substrate-associated growth advantages beyond endpoint dominance. α-Linked disaccharides mainly recruited Bifidobacterium pseudocatenulatum and Megamonas funiformis, cellobiose enriched Faecalibacterium prausnitzii, and gentiobiose enriched B. pseudocatenulatum. Monoculture assays confirmed direct cognate disaccharide utilization. Metaproteomics revealed linkage-matched modules: isomaltose responders upregulated GanO/ChvE and oligo-1,6-glucosidase; cellobiose responders expressed CebE/ChvE, ABC.MS.S, CelB, cellobiose phosphorylase, and β-glucosidases; whereas the molecular evidence for gentiobiose was based mainly on ABC.MS.S and general β-glucosidases. Metabolically, gentiobiose favored acetic acid accumulation, cellobiose yielded the highest butyric acid concentration, and isomaltose elevated trans-4-hydroxy-L-proline and 7,8-dihydroneopterin associated with redox and immune-related cofactor pathways. Guided by these ecological and molecular observations, microbial responder-centered synthetic microbial communities utilized cognate disaccharides, recapitulated glycosidic bond-specific ecological succession, showed greater net short-chain fatty acid (SCFA) accumulation than matched complex communities under equal initial substrate input in vitro, and elevated fecal SCFAs in mice, with cellobiose increasing butyric acid by 2.1-fold. These results support a mechanistically informed pathway linking glycosidic bond structure, microbial succession, and metabolic outputs, providing a basis for structure‑guided microbiome modulation.},
}

@article {pmid42681862,
year = {2026},
author = {Gretgrix, LJ and Scanlan, JL and Martoni, F and Blacket, MJ and Rodoni, BC and Piper, AM},
title = {Quantitative metabarcoding for invertebrate pest monitoring and management.},
journal = {Journal of economic entomology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jee/toag264},
pmid = {42681862},
issn = {1938-291X},
support = {//Agriculture Victoria/ ; DEE2305-004RTX//National Grains Diagnostic and Surveillance Initiative/ ; //Grains Research and Development Corporation (GRDC)/ ; ULA2601-003RSX//Australian Government Research Training Program Scholarship and GRDC/ ; },
abstract = {Invertebrate pests pose one of the most significant threats to global agriculture. Trap-based surveillance is widely used to monitor the presence and abundance of pests, beneficial taxa and broader agroecosystem communities; however nonselective traps often collect hundreds or even thousands of individuals per sample, making conventional sorting and morphological identification labor-intensive and delaying the delivery of actionable information. Metabarcoding offers a scalable alternative for rapidly identifying agriculturally significant taxa in mixed trap samples, while providing more precise identifications (i.e. to species level). However, metabarcoding currently only provides semiquantitative estimates of relative abundance, rather than the accurate absolute abundance information required for many pest-monitoring and management decisions. Improving the quantitative capacity of metabarcoding is therefore an important and rapidly developing area of research across ecological, medical, microbiome, and environmental DNA research. This review summarizes progress toward quantitative metabarcoding of bulk invertebrate samples, highlighting key sources of bias, emerging correction methods, and the opportunities and challenges associated with their translation into agricultural monitoring systems. By consolidating insights from diverse ecological applications, we present a practical roadmap for improving the quantitative outputs and interpretation of metabarcoding data and integrating these novel approaches into agricultural pest monitoring and management.},
}

@article {pmid42681875,
year = {2026},
author = {Mahdiabadi, MA and Moghaddam, A and Erfanian, N},
title = {Microbiome-Derived Tryptophan Metabolites Regulate AhR Signaling to Restore Epithelial Barrier Integrity in Inflammatory Bowel Disease.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70386},
doi = {10.1002/mbo3.70386},
pmid = {42681875},
issn = {2045-8827},
mesh = {*Receptors, Aryl Hydrocarbon/metabolism ; Humans ; *Inflammatory Bowel Diseases/metabolism/microbiology ; *Tryptophan/metabolism ; *Signal Transduction ; Intestinal Barrier Function ; Animals ; *Intestinal Mucosa/metabolism ; *Gastrointestinal Microbiome ; Indoles/metabolism ; Basic Helix-Loop-Helix Proteins ; },
abstract = {Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation and compromised epithelial barrier integrity. Emerging evidence demonstrates that gut microbiota-derived tryptophan metabolites serve as endogenous ligands for the aryl hydrocarbon receptor (AhR), initiating protective signaling cascades that restore mucosal homeostasis. This review synthesizes current mechanistic insights into how microbial tryptophan catabolites including indole-3-aldehyde, indole-3-propionic acid, indole-3-lactic acid, and indole-3-acetic acid activate AhR to enhance epithelial barrier function. However, this protective capacity is specific to activation by physiological, low-affinity microbial ligands and should not be generalized to AhR signaling irrespective of ligand identity, dose, or duration of exposure. Key bacterial producers include Lactobacillus species (L. reuteri and L. plantarum), Clostridium sporogenes, and Allobaculum species. AhR activation by these metabolites triggers multiple downstream pathways, including AMP-activated protein kinase (AMPK) activation, which promotes autophagy and mitochondrial homeostasis; nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant responses; nuclear factor-κB (NF-κB) inhibition, which reduces pro-inflammatory cytokine production; and interleukin-22 (IL-22) induction, which supports epithelial regeneration. These signaling events converge to upregulate tight junction proteins, preserve mucus layer integrity, and reduce actomyosin-mediated permeability through decreased myosin light chain phosphorylation. Preclinical studies demonstrate AhR-dependent barrier restoration, with protective effects abolished by AhR antagonists. Despite these preclinical findings, their therapeutic utility in IBD remains to be established in human interventional studies. Importantly, the protective effects of AhR are highly context-dependent, as kynurenine pathway ligands and sustained receptor activation may exert immunosuppressive or pro-tumorigenic effects, highlighting the importance of ligand selectivity in therapeutic development.},
}

*Receptors, Aryl Hydrocarbon/metabolism
Humans
*Inflammatory Bowel Diseases/metabolism/microbiology
*Tryptophan/metabolism
*Signal Transduction
Intestinal Barrier Function
Animals
*Intestinal Mucosa/metabolism
*Gastrointestinal Microbiome
Indoles/metabolism
Basic Helix-Loop-Helix Proteins

@article {pmid42681893,
year = {2026},
author = {Khan, KU and Zahid, MT and Mustafa, G and Tanpure, RS and Tahir, HM and Kumar, R and Kim, DW and Park, HK and Jeon, BH},
title = {Gut Microbiome Diversity, Functional Potential, and Ecological Relevance of Hottentotta tamulus.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70373},
doi = {10.1002/mbo3.70373},
pmid = {42681893},
issn = {2045-8827},
support = {2026-RISE-01-027-01//Regional Innovation System & Education (RISE)"/ ; RS-2025-00520940//National Research Foundation of Korea (NRF)/ ; },
mesh = {Animals ; RNA, Ribosomal, 16S/genetics ; *Bacteria/classification/genetics/isolation & purification ; *Gastrointestinal Microbiome ; Phylogeny ; DNA, Bacterial/genetics ; Biodiversity ; Sequence Analysis, DNA ; Animals, Poisonous ; Scorpions ; },
abstract = {Scorpions are ancient arachnids of medical and ecological importance; they prey on insects and other arthropods while serving as prey to birds and reptiles. In this study, we reported for the first time on the characterization of the gut intestinal microbiome of Hottentotta tamulus native to northeastern Pakistan. The scorpions were identified on a morphological basis and the Cytochrome c oxidase subunit 1 gene sequence, while the gut microbiome was characterized through full-length 16S rRNA (V1-V9) Nanopore sequencing. The gut microbiota exhibited low to moderate alpha diversity with Chao1 and Shannon indices of 126 ± 90.54 and 0.85 ± 0.21, respectively. The intestinal microbial community was dominated by the phyla Firmicutes (79.48%-90.43%), followed by Proteobacteria (9.46%-20.48%), whereas Actinobacteriota (0.03%-0.11%) and Bacteroidota (0.00%-0.01%) were present at very low relative abundance. The functional profiling identified 23 notable pathways involved in energy metabolism, biomolecule synthesis, the biodegradation of various xenobiotics, and nucleotide metabolism, highlighting the role of the gut microbiome in metabolic homeostasis. The dominance of Bacillus and Mycoplasma in gut microbial communities may enhance host adaptation to low-resource environments.},
}

Animals
RNA, Ribosomal, 16S/genetics
*Bacteria/classification/genetics/isolation & purification
*Gastrointestinal Microbiome
Phylogeny
DNA, Bacterial/genetics
Biodiversity
Sequence Analysis, DNA
Animals, Poisonous
Scorpions

@article {pmid42681944,
year = {2026},
author = {Funnicelli, MIG and do Amaral, RB and de Mello, VVC and Bassini-Silva, R and Micolta, LFB and Buysse, M and de Assis, WO and da Silva, AR and Herrera, HM and Machado, RZ and Barros-Battesti, DM and Pinheiro, DG and Duron, O and André, MR},
title = {Bacterial composition of Polygenis (Polygenis) bohlsi bohlsi (Wagner, 1901) (Siphonaptera: Rhopalopsyllidae) associated with Thrichomys fosteri (Rodentia: Echimyidae) in the Brazilian Pantanal wetland.},
journal = {Medical and veterinary entomology},
volume = {},
number = {},
pages = {},
doi = {10.1111/mve.70111},
pmid = {42681944},
issn = {1365-2915},
support = {2022/05615-2//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2023/16710-9//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2024/20336-8//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 303701/2021-8//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; },
abstract = {Fleas (Insecta: Siphonaptera) are important vectors of zoonotic bacterial pathogens. However, the bacterial communities hosted by fleas remain poorly understood, especially regarding the interactions between nonpathogenic bacteria and pathogens, as well as the factors shaping these bacterial communities. This study aimed to explore the bacterial composition and diversity between female and male Polygenis (Polygenis) bohlsi bohlsi fleas collected from free-living Thrichomys fosteri (Rodentia: Echimyidae) in the Nhecolândia region of central-western Brazil. Here, bacterial profiling of fleas was performed using a Next-Generation Sequencing approach targeting the V3-V4 hypervariable region of the 16S rRNA gene to assess community structure. Bacterial diversity in P. (P.) bohlsi bohlsi fleas varied by sex, as indicated by significant differences in alpha diversity, while beta diversity showed a trend toward separation between sexes. Pseudomonadota was the predominant phylum in the flea microbiome. Ten bacterial genera showed differentially abundance between male and female fleas, including Bartonella spp., which was detected exclusively in males, and Wolbachia spp., which was more abundant in females than in males. Phylogenetic analysis positioned Bartonella gltA sequences detected in two fleas within the same clade as Bartonella harrusi. While the Wolbachia wsp and 16S rRNA sequences detected in P. (P.) bohlsi bohlsi grouped within the supergroups S (associated with pseudoscorpions), gatB sequences grouped with V (cat flea-related). These findings suggest sex-associated differences in the microbiome of P. (P.) bohlsi bohlsi fleas and highlight the need for further investigation into the potential role of Wolbachia spp. in shaping flea-associated microbial communities and their interactions with Bartonella spp.},
}

@article {pmid42681956,
year = {2026},
author = {Ren, K and Zhao, T and Li, L and Lin, L and Ren, S and Ni, X and Gao, Z and Zhang, W and Duan, X and Hai, X},
title = {Gut microbiota-derived indole-3-propionic acid attenuates Arsenic trioxide-induced cognitive impairment by inhibiting ubiquitination and degradation of BRD4.},
journal = {British journal of pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bph.70632},
pmid = {42681956},
issn = {1476-5381},
support = {82274028//National Natural Science Foundation of China/ ; 320.6750.2024-18-37//Scientific Research Project of Wu Jieping Medical Foundation/ ; LH2023H032//Natural Science Foundation of Heilongjiang Province/ ; PL2025H098//Natural Science Foundation of Heilongjiang Province/ ; ZL2024H005//Key Project of Natural Science Foundation of Heilongjiang Province/ ; 2025M781968//China Postdoctoral Science Foundation/ ; 2025//provincial universities in heilongjiang province/ ; },
abstract = {BACKGROUND AND PURPOSE: Arsenic trioxide (ATO) therapy for acute promyelocytic leukaemia (APL) can induce neurological disorders, including cognitive impairment (CI) and depression, severely impacting patient quality of life, yet effective interventions are lacking. Clinical observations indicate ATO treatment is associated with gut microbiota dysbiosis. Given the crucial role of gut microbes and their metabolites in neurological health, this study investigated indole-3-propionic acid (IPA), a neuroprotective microbiota-derived metabolite capable of crossing the blood-brain barrier.

RESULTS: In ATO-treated mice, behavioural tests confirmed significant cognitive decline. 16S rRNA genotyping revealed a reduction in Bifidobacterium abundance, and metabolomics identified a concomitant decrease in its metabolite, IPA, alongside disruptions in the tricarboxylic acid cycle and glycolysis. IPA supplementation alleviated ATO-induced intestinal inflammation and behavioural deficits. Mechanistically, IPA inhibited ATO-induced BRD4 degradation and the associated reduction in H4 acetylation, thereby restoring the expression of the metabolic enzyme PFKM and the synaptic protein PSD95.

CONCLUSION: IPA mitigates ATO-induced intestinal injury and glycolytic dysfunction via the 'BRD4-H4ac-PFKM' axis, providing novel insights for preventing and treating ATO-induced neurotoxicity.},
}

@article {pmid42681978,
year = {2026},
author = {Deringer, R and Silva, CS and Klein, D},
title = {Nutrition support in gastroenterology: opinion on current literature.},
journal = {Current opinion in gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1097/MOG.0000000000001194},
pmid = {42681978},
issn = {1531-7056},
abstract = {PURPOSE OF REVIEW: Historically, enteral nutrition has been the preferred therapy due to its physiologic benefits, with parenteral nutrition selected if enteral nutrition was contraindicated or insufficient; however, recent advances in nutrition support have prompted reevaluation of this process. This review summarizes the current evidence regarding enteral nutrition and parenteral nutrition in gastrointestinal oncology, inflammatory bowel disease (IBD), critical care, and gastrointestinal surgery.

RECENT FINDINGS: In gastric cancer, parenteral nutrition may improve the nutritional status and clinical outcomes of treatment-related gastrointestinal dysfunction. In IBD, exclusive enteral nutrition may be effective for inducing remission and promoting mucosal healing, whereas parenteral nutrition is preferred in intestinal failure and severe complications. Studies have shown the value of early parenteral nutrition when enteral nutrition is contraindicated or insufficient, specifically for improving nutrient delivery and reducing complications in critically ill and surgical patients. Additional areas of interest include caloric and protein dosing, indirect calorimetry, and the effect of nutrition support on the gut microbiome.

SUMMARY: Current evidence supports a patient-centered approach to nutrition support with enteral nutrition remaining as the preference when the gastrointestinal tract can be utilized and parenteral nutrition as an important alternative or adjunct in select populations. Future research should focus on the refinement of supplemental parenteral nutrition practices and the development of evidence-based approaches for specific disease states.},
}

@article {pmid42682004,
year = {2026},
author = {Sufiyan, R and Nadeem, M and Bokhari, SMS and Khan, BS and Fatima, M},
title = {Vaginal microbiome metabolite shifts as early predictors of premature ovarian insufficiency in adolescents with novel gene variants.},
journal = {Turkish journal of obstetrics and gynecology},
volume = {},
number = {},
pages = {},
doi = {10.4274/tjod.galenos.2026.72418},
pmid = {42682004},
issn = {2149-9322},
}

@article {pmid42682077,
year = {2026},
author = {Sadr, Z and Fallahpour, B and Dastgheib, AA and Bahrami, R and Tafti, MG and Shiri, A and Masoudi, A and Nematzadeh, F and Neamatzadeh, H},
title = {A Critical Synthesis of Machine Learning in Autism Spectrum Disorder Genomic Research: From Transcriptomics to Microbiome.},
journal = {Medeniyet medical journal},
volume = {},
number = {},
pages = {},
doi = {10.4274/MMJ.galenos.2026.69259},
pmid = {42682077},
issn = {2149-2042},
abstract = {Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by persistent impairments in social communication, restricted interests, and repetitive behaviors. This narrative review synthesizes advances in machine learning applications to ASD genomic research through May 2026, spanning gene expression analysis, whole-exome sequencing (WES), non-coding variant interpretation, multi-omics integration, single-cell transcriptomics, epigenetic profiling, and gut microbiome analysis. A purposive, thematic literature synthesis approach was employed, allowing broad coverage of emerging methodological innovations and biological insights. We critically evaluate state-of-the-art deep learning architectures-including the Separate Translated Autism Research Neural Network and SHapley Additive exPlanations-based explainable artificial intelligence frameworks. Reported discrimination across the field varies widely, from receiver operating characteristic-area under the curve (ROC-AUC) values near 0.66 to implausibly perfect values of 1.00; the best-validated specialized genomic architecture achieves only modest discrimination (ROC-AUC≈0.73). We emphasize that interpretability and predictive performance are orthogonal properties: specialized architectures yield biologically interpretable feature attributions despite modest discriminative power; and several extreme AUC values in the literature are, in our assessment, more consistent with overfitting or data leakage than with genuine signal, although the primary reports did not always provide the information needed to definitively attribute them. Key themes include: (1) identification of differentially expressed genes through meta-analysis of transcriptomic data; (2) validation of predictive gene features from large-scale WES; (3) detection of non-coding regulatory mutations affecting synaptic transmission pathways; (4) discovery of gut microbiome signatures associated with ASD classification; and (5) discovery of data-driven subtypes enabling precision medicine stratification. Critical challenges include population bias toward European ancestry, socioeconomic ascertainment bias, modest predictive effect sizes, conflation of association with causation, and gaps between computational prediction and clinical utility. Future directions emphasize multi-modal data integration, diverse cohort expansion, engagement with neurodiversity perspectives, and regulatory science development.},
}

@article {pmid42682281,
year = {2026},
author = {You, G and Ren, Y and Du, Y},
title = {Comment on "Global clinical trial landscape of microbiome modulator therapy in sepsis: gut microbiota interventions and challenges".},
journal = {International journal of surgery (London, England)},
volume = {112},
number = {6},
pages = {12987-12988},
pmid = {42682281},
issn = {1743-9159},
}

@article {pmid42682404,
year = {2026},
author = {Liu, Y and Tian, Y and Pu, C and Yang, Y and Peng, X and Zhu, H and Fan, J and Zhang, R and Yuan, H and Zhang, J and Liu, J and Zhao, G},
title = {Metronidazole-mediated gut anaerobe remodeling is associated with transplant rejection.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1874387},
pmid = {42682404},
issn = {2235-2988},
mesh = {*Metronidazole/pharmacology/administration & dosage ; Animals ; *Graft Rejection/prevention & control/microbiology/immunology ; Mice ; *Gastrointestinal Microbiome/drug effects ; RNA, Ribosomal, 16S/genetics ; Humans ; *Bacteria, Anaerobic/drug effects/classification/genetics ; *Islets of Langerhans Transplantation/adverse effects ; Graft Survival/drug effects ; Mice, Inbred C57BL ; Disease Models, Animal ; Male ; },
abstract = {BACKGROUND: The gut microbiome has emerged as a potential modulator of transplant rejection. However, the relevance of anaerobe-associated gut microbial communities to transplant rejection responses remains unclear.

METHODS: In a murine islet transplantation model, we assessed the effects of metronidazole pretreatment on allograft survival and function. 16S rRNA sequencing was performed to characterize treatment-associated changes in gut microbial composition. Separately, an exploratory two-sample MR analysis using human GWAS data was performed to prioritize gut microbial taxa associated with a composite outcome of transplant failure or rejection. Biological annotation was subsequently used to prioritize candidate host pathways. Immunohistochemistry and flow cytometry were used to evaluate post-transplant immune responses after metronidazole pretreatment.

RESULTS: Metronidazole treatment remodeled gut microbiota composition and significantly delayed islet allograft rejection. MR analyses identified several anaerobe-associated gut microbial taxa potentially relevant to transplant rejection risk, including the family Defluviitaleaceae and the genera Intestinibacter, Bilophila, Ruminococcus and Eubacterium fissicatena. Integrative biological annotation highlighted glycosylation-related pathways and prioritized ST3GAL4 for subsequent expression assessment in the murine transplant model. Furthermore, metronidazole treatment reduced CD4[+] T-cell infiltration around the allograft and Th17-related inflammatory responses.

CONCLUSION: Altogether, our findings document gut microbial remodeling and delayed allograft rejection following metronidazole pretreatment. These findings are hypothesis-generating and warrant further mechanistic investigation.},
}

*Metronidazole/pharmacology/administration & dosage
Animals
*Graft Rejection/prevention & control/microbiology/immunology
Mice
*Gastrointestinal Microbiome/drug effects
RNA, Ribosomal, 16S/genetics
Humans
*Bacteria, Anaerobic/drug effects/classification/genetics
*Islets of Langerhans Transplantation/adverse effects
Graft Survival/drug effects
Mice, Inbred C57BL
Disease Models, Animal
Male

@article {pmid42682435,
year = {2026},
author = {Zheng, Y and Wang, Z and Wang, L and Flynn, CR and Shu, XO and English, WJ and Samuels, JM and Chen, Y and Lipworth, L and Gupta, D and Cai, Q and Zheng, W and Yu, D},
title = {Temporal changes in circulating metabolites after metabolic and bariatric surgery and risk of incident coronary heart disease: evidence from prospective cohort and nested case-control studies.},
journal = {International journal of surgery (London, England)},
volume = {112},
number = {7},
pages = {13105-13115},
pmid = {42682435},
issn = {1743-9159},
abstract = {BACKGROUND: Metabolic and bariatric surgery (MBS) has notable cardiovascular benefits beyond weight loss.

METHODS: The Gut Microbiome in Metabolic Surgery Study (GUMMY) enrolled patients who underwent first-time Roux-en-Y gastric bypass or sleeve gastrectomy, with blood samples collected at pre- and 3- and 12-month post-surgery. Significant metabolite changes were identified using paired Wilcoxon signed-rank tests with a false discovery rate (FDR) < 0.05 and |log2 fold change| > log21.5, comparing 3-month post- vs. pre-surgery (early phase) and 12- vs. 3-month post-surgery (late phase). Significantly changed metabolites were classified into three patterns: early changed, late sustained; early changed, late reversed; and early unchanged, late changed. Subsequently, a nested case-control study within the Southern Community Cohort Study (SCCS) assessed the associations between surgery-altered metabolites and incident coronary heart disease (CHD) risk using conditional logistic regression. The same untargeted metabolomic assay was conducted in GUMMY and SCCS plasma samples.

RESULTS: Among 115 surgical patients, the mean (SD) age was 44.9 (9.5) years, and 90 (78%) were women. Significant changes were observed in 224 metabolites, mainly encompassing sustained increases in bile acids and decreases in branched-chain amino acids, lactoyl, and lysine amino acids; reversed changes in some ketone bodies, phospholipids, lysophospholipids, and glycogen metabolites; late increases in taurine, caffeine, benzoate, and some tryptophan metabolites; and late decreases in ceramide metabolites and certain fatty acids. In the SCCS (n = 1194; 597 case-control pairs), 37 surgery-altered metabolites were significantly associated with incident CHD (FDR < 0.1), 28 with concordant effects, i.e., post-surgical increases were associated with reduced CHD risk and vice versa.

CONCLUSIONS: MBS elicits substantial metabolomic alterations, with many altered metabolites associated with incident CHD. These findings provide mechanistic insights into the cardiovascular benefits of MBS and suggest potential therapeutic targets for CHD prevention.},
}

@article {pmid42682509,
year = {2026},
author = {Ren, C and Xiu, Y and Zhang, Y and Wang, X and Zhao, H and Tang, J and Li, Q and Zhang, S and Zhao, F},
title = {Gut microbiome-immune-metabolic mechanisms in cerebrovascular disease: evidence-graded insights from cerebral small vessel disease, ischemic stroke, and intracerebral hemorrhage.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1927904},
pmid = {42682509},
issn = {1664-302X},
abstract = {Cerebrovascular disease is increasingly being examined in relation to the gut microbiome, but the field has not advanced evenly across disease phenotypes. A central challenge is to distinguish broad dysbiosis-based associations from microbial functions, host-facing metabolites, epithelial barrier injury, and immune pathways that may plausibly influence neurovascular vulnerability or recovery. This distinction is particularly important because cerebral small vessel disease, acute ischemic stroke, and intracerebral hemorrhage differ in time scale, vascular pathology, clinical exposure, and available microbiome evidence. This review evaluates gut microbiome-immune-metabolic mechanisms across these cerebrovascular contexts with a focus on microbial ecology, intestinal barrier dysfunction, microbial translocation, short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), bile acid derivatives, tryptophan-linked metabolites, lipopolysaccharide (LPS)-related inflammatory signaling, and emerging multi-kingdom signals, including the gut virome and mycobiome. Current evidence is most convincing in acute ischemic stroke, where human cohort studies and experimental perturbation models link microbiome disruption, microbial metabolites, immune programming, and functional outcome. Evidence for imaging-defined cerebral small vessel disease remains more limited and is largely cross-sectional, whereas intracerebral hemorrhage is an emerging but mechanistically distinct domain. Virome- and mycobiome-related mechanisms remain exploratory and require longitudinal, multi-omics, and perturbation-based validation. This review argues that cerebrovascular microbiome research should move beyond taxonomic association toward time-resolved microbial function, host-facing metabolites, disease-specific host-microbe interfaces, and experimentally testable mechanisms. Candidate microbiome-directed interventions-including dietary, prebiotic, probiotic, postbiotic, fecal microbiota transplantation, defined microbial consortia, metabolite-targeted, and phage-based approaches-remain investigational. Their translation will require disease- and time-window-specific evaluation of biological target engagement, safety, and clinically meaningful outcomes. Longitudinal multi-omics cohorts, disease-specific models, and careful control of diet, antibiotics, vascular medications, hospitalization, and frailty will be essential for determining which gut microbiome-related pathways are causal, context-specific, modifiable, and therapeutically actionable.},
}

@article {pmid42682513,
year = {2026},
author = {Zhang, W and Chen, M and Guo, T and Kuang, G and Ma, N},
title = {Gut microbiota dysbiosis and aromatic amino acid metabolism alterations: a multi-omics analysis of cognitive impairment following aneurysmal subarachnoid hemorrhage.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1870309},
pmid = {42682513},
issn = {1664-302X},
abstract = {BACKGROUND: Aneurysmal subarachnoid hemorrhage (aSAH) is frequently followed by persistent cognitive impairment, characterized by a complex and multifactorial pathological mechanism. While the role of the "microbiota-gut-brain axis" in neurocognition has garnered increasing attention, the specific ways in which gut microbiota and their derived metabolites might be associated with the development and progression of post-aSAH cognitive impairment remain largely undefined. Consequently, there remains a lack of systematic multi-omics evidence to elucidate these potential underlying associations.

METHODS: In this prospective observational study, we enrolled 48 patients with intracranial aneurysms. Among them, patients with aSAH (n = 33) were divided into a cognitive impairment group (aSAH-CI, n = 18) and a group without cognitive impairment (aSAH-WCI, n = 15) based on a 6-month longitudinal neurocognitive assessment. Patients with unruptured intracranial aneurysms (UIA, n = 15) served as the control group. We integrated a multi-omics approach encompassing fecal metagenomics, untargeted metabolomics, and serological profiles of inflammation, oxidative stress, and apoptosis to explore the potential correlations between the host and the microbiome, as well as to identify early diagnostic biomarkers.

RESULTS: Fecal metagenomics revealed distinct gut dysbiosis in aSAH-CI patients, characterized by reduced alpha diversity, depletion of beneficial commensals (e.g., Agathobacter), and expansion of opportunistic pathogens (e.g., Enterococcus). Functional and metabolomic analyses identified a significant alteration in aromatic amino acid biosynthesis. Specifically, tyrosine metabolism was altered, marked by reduced levels of neurotransmitter precursors and elevated neurotoxic trace amines (tyramine and phenylethylamine). Serologically, aSAH-CI patients exhibited heightened systemic inflammation, oxidative stress, and apoptosis. Integrated multi-omics network analysis underscored a strong correlation between elevated trace amines, depleted Agathobacter, and systemic pathological indices. Notably, Agathobacter rectalis and tyramine demonstrated robust potential as early diagnostic biomarkers for cognitive impairment following aSAH.

CONCLUSION: Our findings suggest a potential dual-hit correlative signature via the microbiota-gut-brain axis in cognitive impairment following aSAH. We hypothesize that the depletion of aromatic amino acid-producing microbiota correlates with reduced neurotransmitter precursors, theoretically impairing synaptic repair. Concurrently, observed associations among opportunistic pathogens, trace amines, and systemic inflammatory and oxidative stress markers suggest a synergistic effect potentially linked to further neuronal damage.},
}

@article {pmid42682564,
year = {2026},
author = {Molasy, B and Rachuna, J and Wawszczak-Kasza, M and Dulębska, J and Kuszewska, K and Adamus-Białek, W},
title = {16S rRNA sequencing and conventional culture provide complementary information in hospitalized patients with chronic lower-limb wounds.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1865385},
pmid = {42682564},
issn = {2235-2988},
mesh = {Humans ; *RNA, Ribosomal, 16S/genetics ; Sequence Analysis, DNA ; Female ; Male ; Aged ; Middle Aged ; *Bacteria/classification/genetics/isolation & purification ; Microbiota ; Length of Stay ; DNA, Bacterial/genetics/chemistry ; Aged, 80 and over ; *Wound Infection/microbiology ; DNA, Ribosomal/genetics/chemistry ; Adult ; Hospitalization ; *Wounds and Injuries/microbiology ; },
abstract = {Chronic lower-limb wounds are polymicrobial and difficult to characterize using conventional culture alone. We compared baseline wound microbiota assessed by 16S rRNA sequencing and conventional culture in 62 hospitalized adults with chronic lower-limb wounds and examined associations with subsequent length of stay. Sequencing detected a mean of 11.62 taxa per sample versus 2.24 by culture, with an overall concordance of 51.35%. In sequencing-based analyses, alpha diversity was not associated with length of stay, whereas beta diversity differed significantly according to hospitalization duration (PERMANOVA, R[2] = 0.030, p = 0.005), and six genera were associated with length of stay. Conventional culture showed no significant association with length of stay. No significant associations were found between sequencing-derived baseline microbiota and wound thermal parameters or 12-week healing. These findings indicate that 16S rRNA sequencing and conventional culture provide distinct yet complementary views of chronic wound microbiology.},
}

Humans
*RNA, Ribosomal, 16S/genetics
Sequence Analysis, DNA
Female
Male
Aged
Middle Aged
*Bacteria/classification/genetics/isolation & purification
Microbiota
Length of Stay
DNA, Bacterial/genetics/chemistry
Aged, 80 and over
*Wound Infection/microbiology
DNA, Ribosomal/genetics/chemistry
Adult
Hospitalization
*Wounds and Injuries/microbiology

@article {pmid42682580,
year = {2026},
author = {Yaliniz, G and Tas, Z and Tasdemir, I and Unal, M},
title = {Predictive, Preventive and Personalized Medicine Approaches in Periodontitis: Emerging Technologies from Biomarkers to Artificial Intelligence-Driven Integrated Strategies.},
journal = {The EPMA journal},
volume = {17},
number = {3},
pages = {585-609},
pmid = {42682580},
issn = {1878-5077},
abstract = {RATIONALE AND PURPOSE: Periodontitis is a chronic multifactorial inflammatory disease linked to systemic conditions including cardiovascular disease and diabetes, underscoring the need for a holistic diagnostic approach. Current diagnostics rely on clinical probing and radiography, which detect accumulated damage rather than early biological activity or individual progression risk. This reactive paradigm delays intervention and limits personalization. Within predictive, preventive and personalized medicine (PPPM), this review examines emerging diagnostic technologies and evaluates their potential to enable a paradigm shift toward early prediction, targeted prevention, and individualized periodontal management.

WORKING HYPOTHESIS: The convergence of molecular biomarkers, advanced imaging, microbiome profiling, artificial intelligence, and smart oral technologies into a multimodal framework can support the transition from reactive care to PPPM by enabling detection of suboptimal health states before irreversible damage, continuous digital health monitoring beyond episodic visits, and AI-driven patient stratification for individualized protection against health-to-disease transition and disease progression.

Salivary and gingival crevicular fluid biomarkers detect inflammatory activity prior to clinical attachment loss, supporting early risk identification. Optical coherence tomography and Raman spectroscopy capture structural and biochemical tissue changes non-invasively. Next-generation sequencing reveals early dysbiotic shifts preceding clinical deterioration. Artificial intelligence integrates these heterogeneous datasets into patient-specific risk signatures, with recent PPPM-oriented studies confirming feasibility of automated oral health assessment. Smart oral devices extend monitoring into daily life, enabling continuous surveillance of behavioral and biochemical risk parameters.

For predictive diagnostics, biomarker panels and AI-driven analysis enable identification of preclinical disease activity and individual risk stratification. For targeted prevention, digital monitoring and wearable technologies support continuous risk surveillance and timely individualized interventions. For personalization of medical services, multimodal data integration through AI facilitates patient-specific treatment planning and adaptive care pathways. This integrative framework goes beyond technology-focused reviews by positioning emerging periodontal diagnostics within a unified PPPM paradigm, contributing to the shift from reactive care toward predictive, preventive and personalized disease management.},
}

@article {pmid42682645,
year = {2026},
author = {Bajinka, O and Jallow, L and Li, N and Kuhn, C and Kuhn, W and Stetkarova, I and Golubnitschaja, O and Zhan, X},
title = {Evidence-based recommendations for advancing the chronic pelvic pain syndrome management by the paradigm change from reactive symptom suppression to proactive 3PM-guided patient-centered care.},
journal = {The EPMA journal},
volume = {17},
number = {3},
pages = {715-734},
pmid = {42682645},
issn = {1878-5077},
abstract = {Chronic pelvic pain syndrome (CPPS) encompasses a heterogeneous group of debilitating conditions including interstitial cystitis/bladder pain syndrome (IC/BPS), chronic abacterial prostatitis, endometriosis, and pelvic congestion syndrome, among others. Despite advances in symptomatic management, CPPS remains challenging due to its multifactorial etiology, complex phenotypes, and poor response to conventional reactive treatments. On the other hand, sympathetic overdrive phenotype (SOP) carriers frequently suffer from increased stress sensitivity, chronic sterile inflammation, pain chronification, and mitochondrial stress - all considered the key CPPS/SOP shared pathomechanisms. Further, the dominant vasoconstriction, altered sense regulation (e.g. the reduced feeling of thirst potentially resulting in systemic dehydration) as well as altered multi-drug resistance protein profiles characteristic for SOP (e.g. exemplified by the Flammer syndrome) may predispose affected individuals to the therapy resistance such as CPPS patients with vulvar-vaginal dryness and abacterial prostatitis. This review article highlights the central role of SOP, systemic mitochondrial stress as well as gut and urinary microbiome alterations - all, per evidence, are considered systemic modifiable risk factors of the CPPS manifestation, disease progression, and therapy resistance. The article introduces 3PM-guided patient-centered solutions aiming to improve life quality and individual outcomes in the CPPS patient cohort. Non-invasive mitochondria-based biosensorics, e.g. applied via the tear fluid analysis, and digital health monitoring, per evidence, enable early health risk assessment and patient stratification at the level of reversible damage to health. Recommended targeted preventive strategies encompass individually adapted lifestyle modifications, modulation of the stress-associated mitochondrial homeostasis, and application of supportive nutraceuticals. Personalized 3PM-guided treatment algorithms transform CPPS management into the patient-centered, cause-oriented and cost-effective proactive care, protecting vulnerable individuals against health-to-disease transition and preventing disease progression in stratified patients.},
}