@article {pmid42861963,
year = {2026},
author = {Xie, P and Luo, M and Fan, J and Xiong, L},
title = {A global atlas of the gut virome reveals subtype-specific and functional alterations in irritable bowel syndrome.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0090126},
doi = {10.1128/msystems.00901-26},
pmid = {42861963},
issn = {2379-5077},
abstract = {The gut virome is a critical component of the microbiome-gut-brain axis; however, its role in irritable bowel syndrome (IBS) remains poorly understood due to limited sample sizes and geographic bias. We aimed to construct a comprehensive global atlas of the IBS gut virome to elucidate its composition, functional potential, and clinical relevance across diverse populations and IBS subtypes. We integrated multi-cohort data comprising 1,104 samples (790 IBS patients and 314 healthy controls) from 11 cohorts across 10 geographic regions. A standardized bioinformatic pipeline was employed to perform viral mining from metagenomic and virus-like particle-enriched metaviromic data. The IBS virome exhibited significant taxonomic alterations, with specific viral signatures distinguishing IBS-D, IBS-C, and IBS-M subtypes. Geographic region was identified as a significant factor influencing the viral community structure. Functionally, the IBS virome was enriched in auxiliary metabolic genes involved in carbon metabolism and neurotransmitter precursor synthesis (histidine and tryptophan metabolism), as well as a distinct profile of virulence factors and antibiotic resistance genes. Furthermore, in a specific cohort, certain viral taxa were significantly correlated with the severity of anxiety and depression. Machine learning models based on viral signatures achieved robust performance for IBS subtyping (area under the curve = 0.92). This study establishes a global baseline for the IBS gut virome, demonstrating that viral communities are dynamically shaped by geography and disease subtypes while encoding gene repertoires with the potential to influence host physiology, thereby providing a foundational resource for precision medicine.IMPORTANCEResearch on the human gut microbiome in IBS has focused primarily on bacteria, leaving the viral component as a vast and poorly understood reservoir. By profiling over 1,000 human samples globally, this study characterizes the taxonomic and functional features of the IBS gut virome. We demonstrate that these viral communities vary across geographic populations and IBS subtypes and are enriched in specific auxiliary metabolic genes, virulence factors, and antibiotic resistance genes. In addition, certain viral profiles show significant correlations with patient psychological symptoms such as anxiety and depression. This study also evaluates the potential of virome-based diagnostic biomarkers. Consequently, our findings provide a valuable reference for future in-depth research into the specific roles and mechanistic contributions of the gut virome in the pathogenesis of IBS.},
}

@article {pmid42861989,
year = {2026},
author = {Wang, G and Zhang, N and Peng, Y and Wen, X and Chen, X and Zou, M and Gao, S and Min, C and Min, X and Huang, J},
title = {Association of quantitative sputum Candida load with respiratory dysbiosis and airway inflammation in suspected invasive pulmonary candidiasis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0083726},
doi = {10.1128/msystems.00837-26},
pmid = {42861989},
issn = {2379-5077},
abstract = {UNLABELLED: The clinical significance of Candida species isolation from sputum remains ambiguous due to the colonization-infection dilemma. Integrating quantitative culture with microbiome profiling may clarify its role, yet systematic evidence is scarce. In this exploratory study (June 2023-June 2026), we enrolled 140 hospitalized patients suspected of invasive pulmonary candidiasis (IPC) and stratified them into possible IPC (n = 36), probable IPC (n = 71), and negative control (n = 33) groups based on clinical criteria. All underwent quantitative fungal culture of sputum and metagenomic next-generation sequencing (mNGS). Patients were stratified by sputum Candida species load into low (<10[5] CFU/mL), high (≥10[5] CFU/mL), and negative control (0 CFU/mL) groups. We investigated associations between Candida species burden, respiratory microbiota, local inflammation (IL-8), and clinical outcomes. Higher Candida species load was significantly associated with prolonged hospitalization, elevated sputum IL-8, an increased microbial dysbiosis index, and depletion of key commensals (e.g., Neisseria, Prevotella, Rothia, Streptococcus, and Veillonella). Counterintuitively, it correlated negatively with several classic bacterial pathogens (such as Acinetobacter baumannii, Escherichia coli, Klebsiella pneumoniae, Mycobacterium tuberculosis, and Pseudomonas aeruginosa). A random forest model identified a nine-species microbiome signature that effectively discriminated probable from possible IPC (AUC, 0.877; 95% CI, 0.662-0.944). In patients with suspected IPC, higher sputum Candida species load is associated with exacerbated respiratory dysbiosis and airway inflammation. Quantitative Candida species assessment combined with microbiome signatures may serve as a complementary tool for stratifying disease severity and ecological disruption, meriting further validation in larger, multicenter cohorts.

IMPORTANCE: Respiratory specimens dominate clinical fungal cultures, yet interpreting the role of Candida spp. in sputum remains a diagnostic dilemma. Here, by integrating quantitative culture with metagenomic sequencing, we show that a high sputum Candida species load is a marker of profound ecological disruption. High Candida species burden was associated with significant depletion of key commensals, an elevated dysbiosis index, and heightened local inflammation. Counterintuitively, it correlated negatively with several classic bacterial pathogens, revealing a distinct dysbiotic signature. Moreover, a microbiome-based model accurately discriminated patients with probable invasive pulmonary candidiasis. Our findings suggest that quantitative sputum Candida species load, interpreted within the context of the microbial community, may be a practical biomarker for identifying patients with significant respiratory dysbiosis and inflammation, offering a path toward more refined, ecology-informed therapeutic strategies.},
}

@article {pmid42861994,
year = {2026},
author = {Melis-Arcos, F and Arita, M and Garrido, D},
title = {Comparative transcriptional network analysis reveals ecological specialization in infant-associated species of Bifidobacterium.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0108226},
doi = {10.1128/msystems.01082-26},
pmid = {42861994},
issn = {2379-5077},
abstract = {UNLABELLED: Bifidobacterium species are important microorganisms in the infant gut microbiota displaying substantial genomic diversity, yet how this variability is reflected in transcriptional regulatory architecture remains an open question. Here, we integrated pangenome analysis with transcription factor binding site inference and network-based approaches to compare regulatory architectures across Bifidobacterium longum subsp. infantis, Bifidobacterium breve, and B. longum subsp. longum using over 300 high-quality genomes. All three species exhibited open pangenomes, with regulatory interactions frequently involving accessory genes. Inferred network metrics were compared with score-randomized controls across motif-score thresholds. Increasing score stringency reduced network size while increasing the number of detected communities, indicating greater fragmentation of the retained networks rather than a measured increase in modularity. NrdR showed an intermediate overlap in the Clusters of Orthologous Groups (COG) category sets represented among its predicted targets and species-dependent target prevalence. HMO-related regulators (FucR, NanR, and NagR) differed descriptively between Bifidobacterium infantis and B. breve, the two species included in the complete three-regulator comparison, in predicted target counts, represented COG category sets, and genomic-prevalence patterns; only FucR showed a significant difference in accessory-target fraction. These findings identify species-dependent differences in predicted regulon composition and genomic prevalence and provide testable hypotheses about how regulatory architecture may relate to ecological specialization in the infant gut.

IMPORTANCE: Bifidobacterium species are among the most abundant microorganisms in the breast-fed infant gut microbiota, where they display distinct patterns of genomic diversification and host association. However, the transcriptional regulatory mechanisms underlying these species-specific differences remain incompletely characterized. Here, we reconstructed and compared genome-scale transcriptional regulatory networks across three infant-associated Bifidobacterium species, integrating pangenome structure with transcription factor binding site inference across more than 300 genomes. Our analyses identified predicted regulatory interactions involving accessory genes and species-specific differences in network structure, regulon composition, and target prevalence. These associations provide hypotheses for experimental studies of how gene content and regulatory architecture may contribute to niche adaptation. This pangenome-scale framework can support the prioritization of regulatory hypotheses for future functional studies of infant-associated Bifidobacterium.},
}

@article {pmid42862002,
year = {2026},
author = {Zhang, M and Ge, L and Liu, K and Liu, Y and Zhao, G and Kwok, LY and Sun, Z and Sun, Z and Zhang, W},
title = {Sex- and Time-Resolved Physiological and Gut Ecosystem Responses to a Food-Grade Microbiome-Targeted Intervention in Collegiate Endurance Athletes.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e77664},
pmid = {42862002},
issn = {2198-3844},
support = {NMGLLY2025-02//Inner Mongolia Autonomous Region Special Project for Scientific and Technological Innovation Research in Key Fields of the "Two Barriers," "Two Bases," and "One Bridgehead" Initiative/ ; 32325040//National Natural Science Foundation of China/ ; 32502149//National Natural Science Foundation of China/ ; U25A20733//National Natural Science Foundation of China/ ; CARS36//Earmarked Fund for China Agriculture Research System/ ; },
abstract = {Endurance athletes experience sustained physiological demands during high-volume training, yet evidence for microbiome-targeted interventions in real-world settings remains limited. We conducted a two-stage, randomized, double-blind, placebo-controlled trial in 150 athletes allocated 2:1 to combined probiotics-yeast extract (CPYE) or placebo for 6 weeks; 44 completers confirmed for the 12th Inner Mongolia Autonomous Region University Games entered an exploratory 6-week extension with intensified training. Integrating wearable-derived phenotyping, field-based cardiorespiratory indices, clinical assessments, fecal metagenomics, and metabolomics, we found that during the randomized short-term phase, CPYE was associated with changes in device-estimated maximal oxygen uptake, exercise heart-rate indices, lactate, and redox biomarkers versus placebo. Exploratory sex-stratified analyses suggested heterogeneous response patterns, while the selected long-term extension indicated time-dependent changes requiring confirmation. Multi-omics identified sex- and phase-associated differences in microbial taxa, functions, metabolites, and network topology. Indirect-effect models nominated candidate features (rmlD, PISD-linked phosphatidylethanolamine pathways, Bacteroides ovatus, and folate-related functions) as potential indirect correlates of host outcomes. These findings support further evaluation of CPYE-associated responses in collegiate endurance athletes; subgroup, long-term, network, and indirect-effect results are hypothesis-generating.},
}

@article {pmid42862088,
year = {2026},
author = {Hoque, MN and Rahman, MS and Hossain, MG and Rahman, MT and Islam, T and Hossain, MA},
title = {Subclinical Mastitis and Antibiotic Exposure Reshape the Milk Bacteriome, Resistome, and Metabolic Functional Profiles in Dairy Cows.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70440},
pmid = {42862088},
issn = {2045-8827},
support = {LS20221764//Bangladesh Bureau of Educational Information & Statistics (BANBEIS), Ministry of Education/ ; },
mesh = {Animals ; *Milk/microbiology ; Female ; *Anti-Bacterial Agents/pharmacology/therapeutic use ; Cattle ; *Bacteria/drug effects/classification/genetics/isolation & purification ; *Mastitis, Bovine/microbiology/drug therapy ; Metagenomics ; *Microbiota/drug effects ; Drug Resistance, Bacterial ; },
abstract = {Subclinical mastitis (SCM) reduces milk yield and promotes antibiotic use, contributing to antimicrobial resistance. However, information on milk microbiome dysbiosis and resistome alterations in dairy cows remains limited. We performed shotgun metagenomic sequencing of 30 milk samples from 20 cows classified as SCM (n = 10), antibiotic-treated (ANT; n = 10), and healthy milk (HM; n = 10). Bacteriome, resistome, and metabolic functions were analyzed using bioinformatic tools. Microbial alpha diversity was significantly higher in HM than SCM and ANT samples (p < 0.05), with the greatest richness observed in Local Zebu and Middle-aged (5-8 years) cows. However, beta diversity did not differ significantly among groups (PERMANOVA, p > 0.05). A total of 665 bacterial species belonging to 15 phyla were identified, with Pseudomonadota, Actinomycetota, and Bacillota comprising 90%-99% of total abundance. SCM milk was dominated by Actinoalloteichus sp. (40.55%) and Vibrio furnissii (37.01%), while Staphylococcus aureus was enriched (1.74%) compared with HM and ANT (< 0.01%). ANT milk showed increased abundance of Acinetobacter johnsonii (10.52%), whereas HM samples contained beneficial commensals, including Pseudomonas lundensis, Bacteroides thetaiotaomicron, and Lactococcus lactis. Similar taxonomic shifts were observed across breeds and age groups. In total, 194 antimicrobial resistance genes (ARGs) were detected, with SCM harboring the largest repertoire (n = 161). Nevertheless, macrolide-, aminoglycoside-, and β-lactam-resistance genes were significantly enriched in ANT samples (p < 0.01). Correlation analyses linked Escherichia coli and A. johnsonii with multiple ARGs, while Acinetobacter and Pseudomonas were associated with lipid metabolism, membrane transport, and xenobiotic biodegradation pathways. These findings reveal bacteriome disruption, ARG enrichment, and functional alterations in SCM and antibiotic-exposed milk.},
}

Animals
*Milk/microbiology
Female
*Anti-Bacterial Agents/pharmacology/therapeutic use
Cattle
*Bacteria/drug effects/classification/genetics/isolation & purification
*Mastitis, Bovine/microbiology/drug therapy
Metagenomics
*Microbiota/drug effects
Drug Resistance, Bacterial

@article {pmid42862338,
year = {2026},
author = {Kubica, A and Maszczyk, W},
title = {Dietary modulation of the gut microbiota in type 2 diabetes and obesity: mechanisms, interventions, and clinical perspectives.},
journal = {Acta diabetologica},
volume = {},
number = {},
pages = {},
pmid = {42862338},
issn = {1432-5233},
abstract = {Obesity and type 2 diabetes mellitus (T2DM) are associated with heterogeneous changes in gut microbial composition and function, while mechanistic studies support plausible links among diet, microbial metabolism, intestinal barrier function, immune signaling, and host metabolism. This narrative review integrates diet-microbiome mechanisms, dietary-assessment and multi-omics methodology, major dietary patterns, quantitative clinical intervention evidence, treatment-related microbiome modulation, and implications for precision nutrition. High-fiber, Mediterranean, plant-based, and Western-style dietary patterns can modify microbial functions and metabolites, but responses vary across populations, substrates, baseline microbiota, medications, and study methods. Randomized trials and meta-analyses show selected metabolic effects of dietary and microbiome-targeted interventions; effects are generally modest and heterogeneous, and prebiotics, probiotics, synbiotics, and postbiotics are not interchangeable across products or populations. Medication and procedural exposures can also alter microbiome and metabolome readouts and confound interpretation. Current evidence does not provide a validated basis for routine microbiome-guided pharmacological or surgical treatment selection. Integration of dietary, microbiome, metabolome, and clinical data may identify metabotypes and candidate response patterns, but individualized microbiome-based nutrition remains an emerging, validation-dependent research domain rather than routine clinical practice.},
}

@article {pmid42862350,
year = {2026},
author = {Han, Q and Zhang, X and Li, S},
title = {Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.},
journal = {Inflammation research : official journal of the European Histamine Research Society ... [et al.]},
volume = {75},
number = {1},
pages = {},
pmid = {42862350},
issn = {1420-908X},
mesh = {Humans ; *Inflammatory Bowel Diseases/epidemiology/therapy/microbiology/genetics/complications/immunology ; *Breast Neoplasms/epidemiology/therapy/genetics/immunology ; Female ; Animals ; Gastrointestinal Microbiome ; },
abstract = {OBJECTIVE AND DESIGN: This narrative review examines epidemiological, genetic, mechanistic, microbial, and therapeutic evidence concerning inflammatory bowel disease (IBD) and breast cancer.

METHODS: Relevant literature was identified through targeted PubMed searches completed through May 2026 and reference-list screening. Evidence was selected for its relevance to epidemiology, candidate mechanisms, microbiome-related pathways, and treatment interactions.

RESULTS: Pooled cohort evidence does not show a significant overall increase in breast cancer risk among patients with IBD. Several inflammatory, stromal, microbial, and endocrine pathways are relevant to both diseases, although most evidence comes from separate study populations and experimental models. Studies of patients with prior malignancy have not shown a clear increase in new or recurrent cancer during commonly used IBD therapies, but few analyses have focused specifically on breast cancer. Microbiome-directed treatments have been studied in IBD and, more recently, in oncology; their value for patients with both diseases is unknown.

CONCLUSIONS: Current evidence does not support classifying IBD as a breast cancer risk state. The main clinical concern is the interaction between treatments for the two diseases, which requires individualized assessment and coordinated gastroenterology and oncology care.},
}

Humans
*Inflammatory Bowel Diseases/epidemiology/therapy/microbiology/genetics/complications/immunology
*Breast Neoplasms/epidemiology/therapy/genetics/immunology
Female
Animals
Gastrointestinal Microbiome

@article {pmid42862369,
year = {2026},
author = {Filippatos, F and Michos, A and Kakleas, K},
title = {Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.},
journal = {European journal of pediatrics},
volume = {185},
number = {11},
pages = {},
pmid = {42862369},
issn = {1432-1076},
mesh = {Humans ; *Asthma/immunology/microbiology ; Child ; *Mycoplasma pneumoniae/immunology ; *Pneumonia, Mycoplasma/immunology/complications ; *Immunity, Innate/immunology ; Phenotype ; *Adaptive Immunity ; },
abstract = {UNLABELLED: Mycoplasma pneumoniae (Mp) is repeatedly detected during pediatric wheeze and asthma exacerbations, but its clinical significance depends on the host-response context. This review evaluates the clinical and mechanistic evidence linking Mp to pediatric asthma phenotypes and examines approaches for distinguishing biologically meaningful infection from incidental detection. We narratively synthesized clinical, experimental, immunological, toxin, and proteomic literature addressing Mp-associated wheeze, asthma exacerbation, epithelial injury, allergic amplification, and inflammatory endotyping. Evidence was distinguished by population and experimental system. Experimental studies show that Mp adheres to airway epithelium; disrupts mucociliary function; activates TLR2/TLR4, NF-κB, autophagy, and inflammasome pathways; and promotes cytokine networks that overlap with allergic asthma. In experimental allergic-airway models, epithelial alarmins, IgE responses, mast cells, and type 2 inflammation may amplify Mp-driven signals, whereas IL-23/IL-17 pathways recruit neutrophils and suggest mixed endotypes; altered corticosteroid responsiveness has not been established in pediatric Mp-associated asthma. CARDS toxin induces eosinophilic inflammation, mucus metaplasia, airway hyperresponsiveness, functional IgE responses, and worsening allergen-driven disease in experimental models. Upper-airway PCR positivity, however, may reflect carriage or prolonged detection rather than active lower-airway infection.

CONCLUSION:  Quantitative pathogen testing, paired serology, viral co-detection, age, atopy, microbiome context, and host-response biomarkers merit integrated evaluation in research. Proteomic and multi-omics signatures may support precision endotyping, improve causal attribution, and strengthen pediatric asthma trial design. Their diagnostic and treatment-predictive value remains unvalidated.

WHAT IS KNOWN: • M. pneumoniae is linked to pediatric wheeze and asthma exacerbations, but upper-airway PCR may reflect carriage rather than active lower-airway infection. • Epithelial injury, type 2/Th17 responses, and CARDS toxin can promote asthma-like inflammation in experimental systems.

WHAT IS NEW: • This review integrates diagnostic attribution, toxin biology, immune crosstalk, and proteomic endotyping in one pediatric framework. • It proposes an unvalidated combined pathogen-load and host-response assessment to investigate clinically meaningful M. pneumoniae-driven endotypes and guide trials.},
}

Humans
*Asthma/immunology/microbiology
Child
*Mycoplasma pneumoniae/immunology
*Pneumonia, Mycoplasma/immunology/complications
*Immunity, Innate/immunology
Phenotype
*Adaptive Immunity

@article {pmid42862416,
year = {2026},
author = {Ani, OG},
title = {Race, Diet, and Cardiometabolic Risk in US Young Adults: A Biosocial Framework Integrating Biological Mechanisms and Structural Inequities Toward Precision Nutrition.},
journal = {Current nutrition reports},
volume = {15},
number = {1},
pages = {},
pmid = {42862416},
issn = {2161-3311},
mesh = {Humans ; *Diet ; United States/epidemiology ; *Cardiovascular Diseases/ethnology/epidemiology ; *Cardiometabolic Risk Factors ; Precision Medicine ; *Health Status Disparities ; Gastrointestinal Microbiome ; *Racial Groups ; Black or African American ; },
abstract = {Cardiometabolic disease disproportionately affects Black populations in the US, yet dietary interventions have not reduced these disparities. This review examines race as a biosocial construct integrating ancestry-related biology and structural exposures to understand cardiometabolic risk and dietary response in precision nutrition RECENT FINDINGS: Evidence suggests racial differences in glucoregulatory physiology, metabolically relevant allele frequencies, stress-related epigenetic regulation, gut microbiome composition, and metabolomic profiles. Functional foods, including fruits, vegetables, and nuts, target pathways linked to these phenotypes. However, most intervention studies involve older, predominantly White populations, limiting understanding of race-specific responses. The review proposes the "cumulative racial biological phenotype" framework, where ancestry-related biology and structural exposures jointly influence cardiometabolic risk. It advances the greater plasticity hypothesis, suggesting greater baseline biological perturbation may predict larger dietary responses. Testing these concepts requires race-stratified, multi-omics dietary intervention trials in young adults using culturally and structurally responsive designs to improve the effectiveness and equity of precision nutrition.},
}

Humans
*Diet
United States/epidemiology
*Cardiovascular Diseases/ethnology/epidemiology
*Cardiometabolic Risk Factors
Precision Medicine
*Health Status Disparities
Gastrointestinal Microbiome
*Racial Groups
Black or African American

@article {pmid42862482,
year = {2026},
author = {Gadelmawla, AF and El-Farargy, SH and Alsubaiei, AA and AlSejari, NY and Sharara, MR and Abdul-Hafez, HA and Mohamed, AE and Hageen, AW and Alharran, AM and Andò, G and Aronow, WS},
title = {Toxic Metals and Metalloids Exposure and the Gut-Cardiometabolic Axis: A Narrative Review of Microbiome Dysbiosis, Gut Barrier Dysfunction, and Metabolic Inflammation.},
journal = {Cardiovascular toxicology},
volume = {26},
number = {11},
pages = {},
pmid = {42862482},
issn = {1559-0259},
mesh = {Humans ; *Intestinal Barrier Function/drug effects ; Animals ; Dysbiosis ; *Gastrointestinal Microbiome/drug effects ; *Inflammation Mediators/metabolism ; *Metalloids/adverse effects ; *Bacteria/metabolism/drug effects ; *Inflammation/metabolism/chemically induced/microbiology ; *Intestines/microbiology/drug effects/physiopathology ; Host-Pathogen Interactions ; *Metals ; *Environmental Exposure/adverse effects ; Risk Assessment ; *Environmental Pollutants/adverse effects ; Cardiotoxicity ; },
abstract = {Toxic elements and metalloids exposure is an important environmental contributor to cardiometabolic disease, yet the gut-mediated mechanisms linking toxic elements to systemic metabolic and vascular injury remain incompletely understood. Lead, cadmium, arsenic, and mercury can enter the gastrointestinal tract through contaminated food, water, dust, smoking, seafood, and occupational sources, allowing direct interaction with the intestinal lumen, epithelial barrier, immune system, and gut microbiome. This narrative review examines the gut-cardiometabolic axis as a mechanistic framework connecting toxic metal exposure to microbiome dysbiosis, barrier dysfunction, endotoxemia, microbial metabolite imbalance, and chronic metabolic inflammation. Available evidence, derived from human, animal, and in-vitro studies of varying quality, suggests that toxic elements may alter microbial diversity and function, affect tight-junction integrity, and increase intestinal permeability; however, a consistent metal-specific signature and a complete causal chain have not been established. These changes may promote lipopolysaccharide passage through the intestinal barrier, activate innate immune pathways, and maintain systemic inflammatory signaling. At the same time, disruption of microbial metabolite profiles, including lower short-chain fatty acid production and altered trimethylamine N-oxide, bile acid and uremic toxin pathways, may promote insulin resistance, dyslipidemia, endothelial dysfunction, hypertension, atherosclerosis and overall cardiometabolic vulnerability. Viewing toxic-metal exposure through the gut-cardiometabolic axis provides a hypothesis-generating framework for integrating exposure reduction with conventional cardiometabolic risk management; the clinical value of microbiome-targeted strategies remains to be established. Longitudinal and multi-omics studies are still needed to define causal relationships and identify populations at greatest susceptibility.},
}

Humans
*Intestinal Barrier Function/drug effects
Animals
Dysbiosis
*Gastrointestinal Microbiome/drug effects
*Inflammation Mediators/metabolism
*Metalloids/adverse effects
*Bacteria/metabolism/drug effects
*Inflammation/metabolism/chemically induced/microbiology
*Intestines/microbiology/drug effects/physiopathology
Host-Pathogen Interactions
*Metals
*Environmental Exposure/adverse effects
Risk Assessment
*Environmental Pollutants/adverse effects
Cardiotoxicity

@article {pmid42862527,
year = {2026},
author = {Mishra, P and PramodKumar, TA and Pradhan, B and Ghosh, U and Mishra, PK and Dash, P and Anjana, RM and Patra, SK and Mohan, V},
title = {The Bidirectional Relationship Between Diabetes and Cancer: Mechanistic Insights, Epigenetic Intermediaries, and Therapeutic Approaches.},
journal = {Diabetes therapy : research, treatment and education of diabetes and related disorders},
volume = {},
number = {},
pages = {},
pmid = {42862527},
issn = {1869-6953},
abstract = {OBJECTIVES: The global rise in diabetes mellitus parallels an increasing cancer burden, highlighting an incompletely understood relationship between these two complex diseases. Accumulating epidemiological evidence indicates that diabetes is associated with an increased incidence and mortality of several site-specific cancers, whereas cancer and its treatment may contribute to dysglycemia and diabetes through diverse mechanisms. In addition, shared metabolic and environmental risk factors further contribute to the observed association between these conditions.

METHODOLOGY: This narrative review comprehensively examined peer-reviewed literature retrieved from PubMed, Scopus, Web of Science, and Google Scholar, focusing on the epidemiological, mechanistic, and epigenetic links between diabetes and cancer.

RESULTS: Beyond shared lifestyle risk factors, converging molecular mechanisms-including chronic hyperglycemia, insulin resistance, low-grade inflammation, oxidative stress, and metabolic reprogramming-provide a biological framework linking diabetes and cancer. Emerging evidence suggests that epigenetic dysregulation acts as a central intermediary in this relationship by integrating metabolic stress with sustained alterations in gene expression through DNA methylation, histone modifications, non-coding RNAs, chromatin remodeling, and epigenetic aging. Diabetes-related epigenetic memory, microbiome-driven epigenetic modulation, and sex-specific epigenetic signatures may further contribute to cancer susceptibility and disease heterogeneity, although the strength of evidence varies across experimental and clinical studies.

CONCLUSIONS: This review synthesizes current epidemiological, mechanistic, and epigenetic evidence linking diabetes and cancer, with particular emphasis on metabolic-epigenetic crosstalk and clinically relevant signaling pathways. It also critically evaluates the dual metabolic and oncologic effects of antidiabetic and anticancer therapies while highlighting current evidence gaps and the need for precision medicine approaches in the prevention and management of both diseases.},
}

@article {pmid42863060,
year = {2026},
author = {Dalvano, BE and Covington, BC and Seyedsayamdost, MR},
title = {Discovery and characterization of miranthins, "Trojan horse" antibiotic modulators of bacterial composition in the oral microbiome.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {42},
pages = {e2621138123},
doi = {10.1073/pnas.2621138123},
pmid = {42863060},
issn = {1091-6490},
support = {R35 GM152049//HHS | NIH | National Institute of General Medical Sciences (NIGMS)/ ; 2023A004123//Leona M. and Harry B. Helmsley Charitable Trust (Helmsley)/ ; Fellowship//John D. and Catherine T. MacArthur Foundation (JDCTMF)/ ; },
mesh = {*Microbiota/drug effects ; Humans ; *Anti-Bacterial Agents/pharmacology/chemistry ; *Mouth/microbiology ; *Streptococcus mitis/drug effects/metabolism ; *Peptides/pharmacology/chemistry ; Biological Products/pharmacology/chemistry ; },
abstract = {Bacteria of the human microbiota encode an abundance of natural products that likely mediate bacterial competition, local colonization patterns, and human health and disease. However, very few of these compounds have been identified and characterized to date. During our investigation of Streptococcus mitis, an important early colonizer of the oral cavity, we identified and structurally characterized a family of peptide natural products, termed miranthins herein, that contain an unusual macrocycle formed by an Asp-Cys β-carbon thioether crosslink. We determined that the most abundantly secreted miranthin is a "Trojan horse" antibiotic that enters sensitive cells via the Ami oligopeptide transporter, is hydrolyzed and activated by aminopeptidase N, and subsequently inhibits ribosomal translation to curb the growth of streptococcal competitors. The miranthins are narrow-spectrum antibiotics that could enable S. mitis to modulate community dynamics in the oral cavity, highlighting the importance of peptide natural products in interspecies competition in the microbiome.},
}

*Microbiota/drug effects
Humans
*Anti-Bacterial Agents/pharmacology/chemistry
*Mouth/microbiology
*Streptococcus mitis/drug effects/metabolism
*Peptides/pharmacology/chemistry
Biological Products/pharmacology/chemistry

@article {pmid42863159,
year = {2026},
author = {Siddiqui, R and Maciver, SK and Lloyd, D and Khan, NA},
title = {Integrating free-living amoebae into climate-microbiome and One Health frameworks.},
journal = {Protist},
volume = {183},
number = {},
pages = {126188},
doi = {10.1016/j.protis.2026.126188},
pmid = {42863159},
issn = {1618-0941},
abstract = {Climate change is altering microbial ecosystems at a global scale, yet the role of free-living amoebae within these shifting microbiomes remains incompletely understood. Free-living amoebae occupy soil, water, air, and built environments, where they contribute to microbial diversity, regulate nutrient cycling, and host diverse bacterial, fungal, and viral microorganisms. As temperature, moisture, and land-use patterns change, amoebal behaviour and their associated microbiomes may shift in ways that may affect soil fertility, water quality, microbial network stability, and the persistence of opportunistic pathogens. Through grazing, amoebae regulate bacterial turnover and mineral nutrient release from microbial biomass, providing a mechanistic link between nutrient cycling and plant accessible nutrient pools that underpin soil fertility. Understanding these dynamics is essential for planetary microbiome research and for strengthening One Health approaches that link environmental, animal, and human health. Herein, we discuss free-living amoebae in the context of climate change, the planetary microbiome, and One Health, and consider how their ecological roles may relate to broader shifts in microbial systems. We synthesise current evidence linking free-living amoebae to climate-responsive microbiome dynamics and propose their inclusion within planetary microbiome and One Health frameworks as responsive ecological indicators. Integrating amoebae into surveillance, ecological modelling, and climate-adaptation strategies may improve predictive capacity for tracking climate-driven microbial change.},
}

@article {pmid42863256,
year = {2026},
author = {Lima, PPABM and Paulino, PG and Reis, TL and Valentim, JK and Santos, LM and Cavalheiro, MF and Dilelis, F and Maitre, A and Kratou, M and Cabezas-Cruz, A and Santos, HA},
title = {Temporal dynamics of cecal microbiota composition and diversity in broiler chickens challenged with different doses of Eimeria spp.},
journal = {Veterinary parasitology},
volume = {348},
number = {},
pages = {110932},
doi = {10.1016/j.vetpar.2026.110932},
pmid = {42863256},
issn = {1873-2550},
abstract = {Coccidiosis, caused by Eimeria spp., is one of the major enteric diseases affecting broiler chickens, compromising gut integrity and altering gut microbiota composition. This study aimed to evaluate the effects of different Fortegra® Eimeria spp. challenge doses on the composition and diversity of the cecal microbiota over time postinfection. Broiler chickens were allocated into three groups: a control group receiving PBS, G1 challenged with a 10 × vaccine dose, and G2 challenged with a 20 × vaccine dose. Cecal content samples were collected at 7, 14, and 21 days post-inoculation and analyzed using 16S rRNA next-generation sequencing (NGS). Across all groups, the dominant bacterial phyla were Firmicutes and Bacteroidota. A transient increase in Proteobacteria was observed at 7 days postinfection, suggesting an early phase of microbial instability. Taxonomic shifts indicated an initial disruption of the cecal microbiota, followed by progressive microbial reorganization over time. Alpha diversity analysis revealed marked temporal changes in both G1 and G2, with increased richness and diversity at later time points, consistent with a process of microbial succession. In terms of beta diversity, Jaccard distance analysis demonstrated temporal shifts in taxa presence and absence. G1 exhibited a pronounced temporal pattern characterized by continuous species turnover, whereas G2 showed a constrained temporal shift with indications of progressive stabilization. Overall, the findings suggest that temporal dynamics exert a greater influence than challenge intensity in shaping the gut microbiota, reflecting a succession process associated with the partial restoration of gut homeostasis.},
}

@article {pmid42863282,
year = {2026},
author = {Cappelli, E and Cappelli, MA and Cappelli, F and Addis, E and Nazeri, A and Pesce, M and De Vita, D},
title = {Digital health technologies for the prevention and management of urinary tract infections in menopausal women: A systematic review.},
journal = {Maturitas},
volume = {214},
number = {},
pages = {109151},
doi = {10.1016/j.maturitas.2026.109151},
pmid = {42863282},
issn = {1873-4111},
abstract = {BACKGROUND: Urinary tract infections are among the most common infectious diseases in women, with incidence increasing after menopause. The genitourinary syndrome of menopause increases susceptibility to recurrent urinary tract infections through urogenital atrophy and microbiome disruption, compounding the risk of antimicrobial resistance.

OBJECTIVE: To synthesise evidence on digital health technologies for the prevention and management of urinary tract infections in menopausal women.

METHODS: Four databases (PubMed/MEDLINE, Scopus, Web of Science, Cochrane) were systematically searched from January 2000 to March 2026 following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Study quality was assessed using risk-of-bias and critical appraisal tools. Menopausal status was classified as explicitly, proxy or not reported.

RESULTS: Of 9935 records identified, 14 studies met the inclusion criteria. Certainty of evidence ranged from very low to moderate. Four technology clusters emerged: patient-facing digital interventions (n = 4), predictive machine-learning models (n = 7), clinician-facing electronic health record-integrated decision support systems (n = 2), and point-of-care biosensors (n = 1). Digital tools reduced inappropriate antibiotic prescribing by up to 60% and ciprofloxacin use by 80.5%. Predictive models achieved discrimination values of 0.57-0.96 but lacked prospective validation. No study applied formal staging criteria for reproductive aging or integrated hormonal variables. Time to diagnosis and treatment were not assessed.

CONCLUSIONS: Digital health technologies show potential for antimicrobial stewardship in menopausal women with urinary tract infections but remain largely insensitive to menopause-specific biological factors. One randomised controlled trial demonstrated increased uptake of vaginal oestrogen therapy with the use of these technologies, providing evidence of digitally supported non-antibiotic prevention. Future research should integrate menopausal staging, hormonal variables, and user-centred design.

PROSPERO REGISTRATION: CRD420251052764.},
}

@article {pmid42863410,
year = {2026},
author = {Villa-Rodríguez, E and Ferguson, S and Stougaard, J and Radutoiu, S},
title = {Understanding genetic determinants of bacterial adaptation to plant niches: Toward more robust bioinoculant design.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128760},
doi = {10.1016/j.micres.2026.128760},
pmid = {42863410},
issn = {1618-0623},
abstract = {Plant-associated bacteria offer a sustainable alternative to chemical inputs in agriculture, yet the field performance of microbial inoculants remains inconsistent. A central but frequently overlooked cause is that bioprospecting pipelines still select strains on the basis of plant-growth-promoting activities, while the bacterial genetic traits that determine whether a strain can reach, colonise and persist in a given root compartment are rarely assessed. Previous reviews have largely catalogued growth-promoting functions or described root microbiome assembly from the plant's perspective, here we take the bacterium's. We trace the journey of a bacterium from bulk soil to its final niche and, at each stage, identify the genes and pathways (genetic determinants) that encode key bacterial traits involved, such as chemotaxis and motility, nutrient acquisition and metabolic independence, competitive and defensive arsenals, attachment and biofilm formation, evasion of plant immunity, and endophytic entry and persistence. Throughout, we use evidence from comparative genomics and metagenomics, (meta)transcriptomics, targeted mutagenesis and genome-wide screens such as Tn-seq, obtained in systems ranging from binary interactions to synthetic communities and natural soils. For each stage we examine the current state of knowledge, identify critical gaps, and propose avenues to deepen our mechanistic understanding of the bacterial traits involved in plant colonisation. We argue that this mechanistic understanding is the missing foundation for developing inoculants with more consistent and robust performance across diverse agroecosystems.},
}

@article {pmid42863670,
year = {2026},
author = {Gurung, M and Chandrashekar, R and Thomson, JL and Landry, AS and Read, QD and Martinez, AE and Andres, A and Yeruva, L},
title = {Associations between fermented dairy food intake during pregnancy and gestational weight gain, macrosomia, and gut microbiota.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105194},
doi = {10.1016/j.clnesp.2026.105194},
pmid = {42863670},
issn = {2405-4577},
abstract = {BACKGROUND AND AIMS: Fermented dairy food (FDF) operationalized in this study as cheese and yogurt, contains beneficial microbes and bioactive metabolites that may support maternal and offspring health, yet FDF intake and its association with maternal-offspring health outcomes is understudied in the US population. We evaluated the associations between FDF intake during pregnancy from the participants of The Growing Life, Optimizing Wellness Study (GLOWING, ClinicalTrials.gov ID: NCT01131117) and gestational weight gain (GWG), macrosomia (body weight ≥4000g at birth), and mother and infant microbiota composition.

METHODS: Dietary data were collected using 3-day food records at six pregnancy visits and FDF intake (cheese, yogurt) were extracted based on food descriptions and codes. Maternal microbiota composition was evaluated at each trimester of pregnancy, while the infant microbiota composition was assessed at one month, 6 months and 12 months of age using 16S rRNA gene sequencing.

RESULTS: In this cohort, the mean FDF intake during pregnancy was 63 g/day. Higher FDF intake was positively associated with healthier body weight at enrollment and overall Healthy Eating Index score during pregnancy. No significant associations between FDF intake and GWG or macrosomia were observed. FDF intake during pregnancy was negatively associated with only one taxon, Bacteroidetes (now Bacteroidota) in infants aged 6 months.

CONCLUSION: While FDF intake during pregnancy was positively associated with healthier pre- or early pregnancy weight and diet quality during pregnancy, it was not associated with GWG, macrosomia, or maternal microbiome. These results need to be interpreted in the context of the limited variety and amount of fermented food consumed during pregnancy in this cohort. Future studies that include participants from larger geographical locations with broader FDF intakes could provide more insight into the associations between FDF and maternal and infant health outcomes.},
}

@article {pmid42863687,
year = {2026},
author = {Czarnowski, P and Czajkowska, A and Rubik, J and Kocur, A},
title = {LC-MS/MS quantification of trimethylamine N-oxide in plasma and volumetric absorptive microsamples: analytical validation and feasibility in pediatric kidney transplant recipients.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {},
number = {},
pages = {122894},
doi = {10.1016/j.cca.2026.122894},
pmid = {42863687},
issn = {1873-3492},
abstract = {Trimethylamine N-oxide (TMAO) is a gut microbiome-related metabolite that may be associated with kidney injury and cardiovascular risk. Measuring TMAO in children after kidney transplantation may support investigation of the gut-kidney-cardiovascular axis; however, repeated venous sampling is often impractical in pediatric longitudinal studies. This study aimed to validate a rapid LC-MS/MS method for measuring TMAO in plasma and 10 μL dried capillary blood samples collected using volumetric absorptive microsampling (VAMS). TMAO was quantified using its stable-isotope-labelled internal standard, TMAO-d9, by hydrophilic interaction chromatography (HILIC) with positive electrospray ionization. For TMAO, an endogenous analyte, the calibration curves were determined using a surrogate matrix of 5% bovine serum albumin in phosphate-buffered saline (PBS) for plasma and a surrogate whole-blood matrix for VAMS. Quality control samples were prepared in authentic matrices. The validation process involved examining the calibration curve, LLOQ, accuracy, precision, recovery, matrix effect, stability, incurred sample reanalysis, matrix parallelism, and comparability of plasma-VAMS results. The assay calibration curve was linear from 0.1 to 20 μmol/L. The LLOQ was 0.1 μmol/L for both matrices. The mean calibration R[2] values were 0.9989 ± 0.0007 for plasma and 0.9981 ± 0.0011 for VAMS. The surrogate and true matrices exhibited similar parallelism (slopes of 0.97 and 0.93 for plasma and VAMS, respectively). In the pediatric kidney transplant population, plasma TMAO was highly correlated with serum creatinine (r = 0.964) and inversely correlated with eGFR (r = -0.788). Similar associations were observed between VAMS plasma-estimated TMAO and creatinine (r = 0.951) and eGFR (r = -0.784). The validated method enables reliable quantification of TMAO in both plasma and VAMS microsamples and demonstrates analytical feasibility for future longitudinal biomarker studies in pediatric kidney transplantation. However, these clinical findings should be considered exploratory rather than evidence of clinical utility.},
}

@article {pmid42864232,
year = {2026},
author = {Delvigne, F and Roeloffs, F and Josselin, L and Pressé, S and Olsson, L and Grünberger, A},
title = {Subpopulation networks: a scaling principle for engineering living systems.},
journal = {Trends in biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tibtech.2026.09.018},
pmid = {42864232},
issn = {1879-3096},
abstract = {Cell populations underpin applications ranging from bioproduction and biotherapeutics to microbiome engineering and biocomputing. However, treating them as bulk quantities rather than as structured systems limits our understanding of population-level stability, productivity, and robustness. Cellular populations self-organize into coexisting subpopulations (SPs) representing phenotypically distinct states that emerge from the interplay of biological noise and selective pressures. We propose that networks of interacting SPs constitute a fundamental organizational layer for engineering stable cell population dynamics. Surveying published single-cell studies across bacterial, yeast, and mammalian systems, we show that populations consistently self-organize into a limited number of SPs. This dimensional reduction can be captured experimentally by clustering single-cell data and gives rise to scaling laws that link population structure to collective performance.},
}

@article {pmid42864263,
year = {2027},
author = {Wysokińska, M and Mysza, M and Uryga, AE and Kołodziejczyk, AA},
title = {Gut microbiota shaping fatty liver disease progression.},
journal = {Life science alliance},
volume = {10},
number = {1},
pages = {},
doi = {10.26508/lsa.202603756},
pmid = {42864263},
issn = {2575-1077},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Fatty Liver/microbiology/metabolism ; Animals ; Disease Progression ; Liver/metabolism ; Intestinal Barrier Function ; Methylamines/metabolism ; Lipid Metabolism ; Bacteria/metabolism ; Bile Acids and Salts/metabolism ; Fatty Acids, Volatile/metabolism ; },
abstract = {The gut-liver axis is an important regulator of homeostasis, and its dysregulation has been implicated in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). In this review, we summarize current knowledge on both compositional alterations of the gut microbiome in MASLD and the functional consequences of these changes. We first discuss changes across major microbial domains, including bacteria, archaea, eukaryota, and bacteriophages, and then focus on microbiota-derived metabolites, such as short-chain fatty acids, trimethylamine and its derivative trimethylamine N-oxide, tryptophan-derived indoles, secondary bile acids, and other bioactive compounds. Their complex impacts on intestinal barrier integrity, inflammation, lipid and glucose metabolism, and immune and hormonal signaling in the liver are highlighted. We further examine mechanisms involving the translocation of microbial products and the modulation of nuclear and membrane receptors. Finally, we outline current challenges and knowledge gaps that need to be addressed to better understand the role of the gut microbiota in MASLD.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Fatty Liver/microbiology/metabolism
Animals
Disease Progression
Liver/metabolism
Intestinal Barrier Function
Methylamines/metabolism
Lipid Metabolism
Bacteria/metabolism
Bile Acids and Salts/metabolism
Fatty Acids, Volatile/metabolism

@article {pmid42864402,
year = {2026},
author = {Chadwick, BP and Dicker, AJ and Hansen, R},
title = {Infant microbiome development: a renewed focus on the second six months and complementary feeding.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42864402},
issn = {1530-0447},
}

@article {pmid42864764,
year = {2026},
author = {Yang, Y and Tang, X and Chen, R and Wang, Z},
title = {The Microbiome-Gut-Lung axis in Respiratory Diseases: From Biological Mechanisms to Clinical Translation.},
journal = {Respirology (Carlton, Vic.)},
volume = {},
number = {},
pages = {},
doi = {10.1002/resp.70329},
pmid = {42864764},
issn = {1440-1843},
support = {2022YFA1304300//National Key Research and Development Program of China/ ; 82495200//National Natural Science Foundation of China/ ; 82495201//National Natural Science Foundation of China/ ; 82404633//National Natural Science Foundation of China/ ; GZNL2023A02001//Major Project of Guangzhou National Laboratory/ ; 2024ZD0528400//Noncommunicable Chronic Diseases-National Science and Technology Major Project/ ; 2026ZD0555400//Noncommunicable Chronic Diseases-National Science and Technology Major Project/ ; SKLRD-Z-202507//Open Project of State Key Laboratory of Respiratory Disease/ ; 2026A1515011144//Basic and Applied Basic Research Foundation of Guangdong Province/ ; },
abstract = {Respiratory diseases exhibit substantial heterogeneity in clinical phenotypes and underlying pathobiology that cannot be fully captured by conventional lung-centred frameworks. Accumulating evidence implicates a role for the microbiome-gut-lung axis in respiratory disease pathogenesis. Within this bidirectional axis, gut-derived microbial metabolites and structural components can modulate pulmonary immunity, whereas respiratory infection and exposures can reciprocally influence the gut microbiota. Dysregulation of the microbiome-gut-lung axis may influence respiratory disease susceptibility, progression, and clinical presentation. In this Review, we outline core mechanisms of gut-lung crosstalk, including metabolite-driven immunomodulation, pattern recognition receptor signalling and reciprocal immune-ecological remodelling. We synthesize phenotype-specific evidence linking the axis to major chronic inflammatory airway diseases (asthma, chronic obstructive pulmonary disease, cystic fibrosis and bronchiectasis) and acute respiratory disorders (pneumonia and sepsis-associated acute respiratory distress syndrome), emphasizing mechanistic and clinical evidence. We discuss the translational promise of gut-lung signatures as biomarkers and treatable traits and review current therapies with microbiome effects and emerging microbiome-targeted interventions. Finally, we address key challenges and propose future research priorities to advance clinical management leveraging the gut-lung axis.},
}

@article {pmid42864827,
year = {2026},
author = {Yu, H and Feng, J and Li, M and Zhao, Y and Wang, Y},
title = {Wheat straw biochar enhances rhizosphere colonization of Bacillus amyloliquefaciens B1408 for biocontrol of cucumber Fusarium wilt.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.71400},
pmid = {42864827},
issn = {1526-4998},
support = {32072474//the Natural Science Foundation of China/ ; 2017YFD0201203//National Key Research and Development Program of China/ ; 2020zdzx03-03-01//major Science and Technology Projects of Shaanxi Province/ ; },
abstract = {BACKGROUND: Plant growth-promoting rhizobacteria (PGPR) offer a sustainable alternative for managing soilborne diseases, yet their field efficacy is often compromised by poor rhizosphere persistence. Here, we tracked the spatiotemporal colonization dynamics of a GFP-labeled Bacillus amyloliquefaciens B1408 strain and developed a wheat straw biochar-based formulation to overcome this bottleneck.

RESULTS: At 120 days post-inoculation, the biochar formulation increased B1408 populations from 7.49 × 10[3] to 4.96 × 10[4] CFU g[-1] in the rhizosphere soil and from 1.41 × 10[4] to 7.58 × 10[4] CFU g[-1] on the rhizoplane, corresponding to 6.62- and 5.36-fold increases, respectively. In pot trials, the formulation reduced the cucumber Fusarium wilt disease index from 73.33% to 20%. The WSBA treatment was associated with enhanced soil nutrient-cycling enzyme and plant antioxidant enzyme activities, altered rhizosphere microbial community structure, reduced the connectivity of FOC-associated microbial co-occurrence networks, and enriched several indigenous bacterial genera, including Allorhizobium and Sphingomonas. In validation assays, Allorhizobium sp. 813 and Ensifer sp. 4724 isolated from the WSBA-treated rhizosphere significantly increased cucumber plant height and fresh weight.

CONCLUSION: These findings demonstrate that wheat straw biochar enhances the rhizosphere persistence and biocontrol efficacy of B1408 and is associated with changes in rhizosphere microbial composition and network connectivity. This formulation provides a promising strategy for improving the stability and performance of B. amyloliquefaciens-based biocontrol agents. © 2026 Society of Chemical Industry.},
}

@article {pmid42864833,
year = {2026},
author = {Wang, Z and Luo, Z and Wang, L and Tang, J and Zhang, Z and Fan, X},
title = {Targeting the Tumor Microenvironment Network to Overcome Immunotherapy Resistance in Non-Small Cell Lung Cancer: Mechanisms to Clinical Translation.},
journal = {Cancer medicine},
volume = {15},
number = {10},
pages = {e72335},
doi = {10.1002/cam4.72335},
pmid = {42864833},
issn = {2045-7634},
support = {202301AY070001-090//The Science and Technology Department of Yunnan Province-Kunming Medical University Joint Special Project/ ; 202501AS070099//The Basic Research Key Project of Science and Technology Department of Yunnan Province/ ; RLMY20220004//The Yunnan Xingdian Talent Support Program-Famous Doctor Training Object/ ; RLMY20220011//The Yunnan Xingdian Talent Support Program-Famous Doctor Training Object/ ; //The National Collaborative "Flagship" Department of Chinese and Western Medicine/ ; 2025-TD-03//The Kunming Medical University First Affiliated Hospital Undergraduate Education Teaching High-Quality Development Research Project-Respiratory Medicine Teaching Master Team/ ; },
mesh = {Humans ; *Tumor Microenvironment/immunology/drug effects ; *Carcinoma, Non-Small-Cell Lung/immunology/drug therapy/therapy/pathology ; *Lung Neoplasms/immunology/drug therapy/therapy/pathology ; *Immunotherapy/methods ; *Drug Resistance, Neoplasm/drug effects ; Animals ; Translational Research, Biomedical ; Metabolic Reprogramming ; },
abstract = {BACKGROUND: Immunotherapy has transformed the treatment landscape for advanced non-small cell lung cancer (NSCLC), yet resistance mediated by the tumor microenvironment (TME) limits its efficacy in most patients. This review aims to synthesize the current understanding of the TME as an integrated network driving immunotherapy resistance and to evaluate emerging therapeutic strategies aimed at overcoming it.

METHODS: We conducted a comprehensive narrative review of key literature in the field, sourced from PubMed and major conference proceedings. The focus was on mechanistic studies elucidating immunosuppressive cell circuits, metabolic reprogramming, epigenetic regulation, spatial heterogeneity, and microbiome interactions within the lung cancer TME. Preclinical and clinical evidence for TME-targeted combination therapies and biomarker development was also critically analyzed.

RESULTS: The TME orchestrates resistance through highly interconnected axes: (1) cellular circuits including myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and M2-polarized tumor-associated macrophages (M2-TAMs), (2) metabolic barriers (lactate acidosis, nutrient depletion), (3) epigenetic reprogramming, and (4) systemic communication via exosomes and the microbiome. Spatial transcriptomics reveals that driver mutations (e.g., EGFR, KRAS) shape distinct immune-excluded architectures. To disrupt this network, rational combination strategies-such as immune checkpoint inhibitors with metabolic modulators (LDHAi), epigenetic drugs, targeted agents (METi), or microbiome interventions-show synergistic potential in early-phase trials. Furthermore, a tiered biomarker system integrating spatial, metabolic, and microbial features is proposed to guide patient stratification.

CONCLUSION: Overcoming immunotherapy resistance requires a paradigm shift from single-target to network-targeted therapy. This review provides an integrated framework for understanding TME-mediated resistance and translates these insights into a roadmap for clinical translation. Future efforts must prioritize biomarker-validated, rationally designed combination therapies to improve outcomes for patients with resistant NSCLC.},
}

Humans
*Tumor Microenvironment/immunology/drug effects
*Carcinoma, Non-Small-Cell Lung/immunology/drug therapy/therapy/pathology
*Lung Neoplasms/immunology/drug therapy/therapy/pathology
*Immunotherapy/methods
*Drug Resistance, Neoplasm/drug effects
Animals
Translational Research, Biomedical
Metabolic Reprogramming

@article {pmid42864924,
year = {2026},
author = {Suresh, N and Singh, V and Rathore, A and Dwivedi, S and Bansal, A},
title = {The Gut Microbiota-inflammation-immune Axis in Cancer: Anti-inflammatory Mechanisms and Therapeutic Implications.},
journal = {Anti-inflammatory & anti-allergy agents in medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715230502786261001104534},
pmid = {42864924},
issn = {1875-614X},
abstract = {Through its mediation between inflammatory and immune pathways, the gut microbiota has proved to be a key regulator of cancer development, progression, and treatment response. Changes in microbial composition known as dysbiosis might facilitate chronic inflammation, immune dysregulation, and genomic instability, thereby facilitating carcinogenesis. Conversely, positive commensal microbes can generate short-chain fatty acids, bile acids, and tryptophan derivatives, which help maintain the epithelial barrier, cytokine signaling, and innate and adaptive immune responses. These microbial metabolites regulate immune cell differentiation, including regulatory T cells, dendritic cells, macrophages, and cytotoxic CD8+ T cells, thereby impacting the tumor microenvironment and tumor progression. Recent research highlights the microbiota as an outcome of response to cancer therapies, particularly immune checkpoint inhibitors, chemotherapy, and targeted therapies. Certain microbial genera, e.g., Akkermansia muciniphila, Bifidobacterium species, and Faecalibacterium prausnitzii, have been linked to augmented antitumor immunity and treatment efficacy. To enhance treatment outcomes and minimize toxicity during therapy, therapeutic interventions that target the regulation of the gut microbiome, such as dietary interventions, probiotics, prebiotics, fecal microbiota transplantation, and engineered microbial platforms, are under investigation. Moreover, improvements in metagenomics, metabolomics, and immunomics are now enabling the discovery of microbiome-based biomarkers to inform precision oncology. Knowledge of the gut microbiota-inflammation-immune axis thus presents promising possibilities in creating new treatment modalities and in designing individualized treatments in cancer management.},
}

@article {pmid42865133,
year = {2026},
author = {Lv, Y and Shi, M and Zhao, Y and Yu, Y and Lv, J and Zhao, H},
title = {Context-dependent TREM2 signalling in myeloid cells: Molecular mechanisms and immunotherapeutic divergence in neurodegeneration and cancer.},
journal = {Clinical and translational medicine},
volume = {16},
number = {10},
pages = {e70863},
doi = {10.1002/ctm2.70863},
pmid = {42865133},
issn = {2001-1326},
support = {ZR2022QH372//Shandong Province Natural Science Foundation/ ; },
mesh = {Humans ; *Receptors, Immunologic/metabolism ; *Membrane Glycoproteins/metabolism ; *Signal Transduction ; *Myeloid Cells/metabolism/immunology ; *Neoplasms/therapy/immunology ; Animals ; *Immunotherapy/methods ; *Neurodegenerative Diseases/therapy/immunology ; },
abstract = {BACKGROUND: Triggering receptor expressed on myeloid cells 2 (TREM2) is a pivotal lipid-sensing receptor that governs the functional plasticity and metabolic fitness of mononuclear phagocytes, including microglia, osteoclasts, dendritic cells and tissue-resident macrophages. While originally identified as a genetic risk factor for Alzheimer's disease (AD), TREM2 functions as a context-dependent immunometabolic checkpoint rather than a uniform phenotypic driver, exerting divergent biological outputs dictated by distinct tissue microenvironments and ligand repertoires.

SUMMARY OF KEY CONTENTS: This review provides a comprehensive synthesis of TREM2 immunobiology, detailing how ligand engagement-including cell-surface phospholipids and apolipoprotein E (ApoE)-activates the DAP12/DAP10-SYK-PI3K-mTOR signalling axis. This coordinated intracellular cascade instructively drives myeloid adaptation towards metabolically competent disease-associated microglia (DAM) and lipid-associated macrophage (LAM) states, sustaining bioenergetics and debris clearance under pathological stress. Across neurodegenerative proteinopathies and acute cerebral ischemia, TREM2 signalling is predominantly neuroprotective by promoting aggregate compaction and mitigating secondary excitotoxicity, although chronic dysregulated activation may drive stage-dependent neuroinflammation. In peripheral inflammatory pathologies such as rheumatoid arthritis and sepsis, TREM2 fine-tunes macrophage efferocytosis and systemic metabolic thresholds. In oncology, TREM2 displays a complex, microenvironment-dependent divergence: in central nervous system malignancies such as glioblastoma (GBM), TREM2 exerts controversial, stage-dependent effects, spanning microglial tumour containment in early stages versus pro-tumoural myelin recycling and immunosuppression by monocyte-derived macrophages in post-treatment recurrence; conversely, in peripheral solid tumours, monocyte-derived TREM2+ tumour-associated macrophages (TAMs) predominantly orchestrate an immunosuppressive, nutrient-deprived niche that impairs cytotoxic T-cell function. Furthermore, we synthesise emerging paradigms along the bidirectional microbiome-gut-brain-tumour axis, elucidating how commensal and intra-tumoural microbial cues dynamically calibrate myeloid signalling tone and therapeutic susceptibility.

CONCLUSION: We address translation bottlenecks-including blood-brain barrier (BBB) shuttles, human trial scarcity and soluble TREM2 (sTREM2) biomarker harmonisation-outlining a biomarker-guided, context-tailored precision therapeutic framework for targeting the TREM2 axis.},
}

Humans
*Receptors, Immunologic/metabolism
*Membrane Glycoproteins/metabolism
*Signal Transduction
*Myeloid Cells/metabolism/immunology
*Neoplasms/therapy/immunology
Animals
*Immunotherapy/methods
*Neurodegenerative Diseases/therapy/immunology

@article {pmid42865179,
year = {2026},
author = {Parveen, N and Kumar, M and Das, M and Singh, N and Patel, AK and Kumar, D and Singh, LP and Goswami, PK},
title = {Pathophysiology and Pharmacological Management of Chronic Liver Injury: Current Challenges and Future Directions.},
journal = {Current drug research reviews},
volume = {},
number = {},
pages = {},
doi = {10.2174/0125899775508122261001092450},
pmid = {42865179},
issn = {2589-9783},
abstract = {INTRODUCTION: Chronic liver injury results from persistent hepatic injuries such as metabolic disorders, alcohol consumption, viral infections, drug toxicity, autoimmune conditions, and genetic factors. It is a major global health concern due to its progression to fibrosis, cirrhosis, and hepatocellular carcinoma. This review aims to summarize key pathophysiological mechanisms and evaluate current and emerging pharmacological strategies.

METHODS: A narrative review of preclinical and clinical studies was conducted, focusing on inflammation, oxidative stress, immune dysfunction, fibrogenesis, and therapeutic approaches, including conventional drugs, antifibrotics, metabolic modulators, and advanced drug delivery systems. A total of 352 records were identified, of which 158 studies were included in the review.

RESULTS: Chronic liver injury is characterized by persistent inflammation, oxidative stress, hepatocyte death, impaired regeneration, and activation of hepatic stellate cells, leading to extracellular matrix accumulation and fibrosis. Current therapies are largely etiology-based and slow disease progression but rarely reverse fibrosis. Emerging therapies targeting nuclear receptors, metabolic pathways, gene-based interventions, microbiome modulation, and nanocarrier-based systems show promising potential.

DISCUSSION: These findings indicate that chronic liver injury is a complex, multifactorial process involving interconnected molecular pathways, limiting the effectiveness of single-target therapies. The gap between mechanistic insights and clinical translation remains a key challenge. Multi-targeted, combination, and precision-based therapeutic approaches, along with targeted drug delivery systems, may enhance treatment efficacy and overcome current limitations.

CONCLUSION: Despite advances in understanding disease mechanisms, effective diseasemodifying therapies remain limited. The development of combination and personalized treatment strategies is essential for improving outcomes and preventing disease progression.},
}

@article {pmid42865215,
year = {2026},
author = {Ullah, A},
title = {Dietary and Microbial Determinants of Intestinal Sulfur Gas and Malodor: Mechanisms, Phenotypes, and Nutritional Mitigation.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70806},
pmid = {42865215},
issn = {1440-1746},
abstract = {Intestinal gas and malodor are common nutrition-related concerns that may influence dietary adherence, gastrointestinal symptoms, and quality of life. Although gas volume and odor are often treated as a single outcome, they arise from partly distinct processes. Bulk intestinal gas is generated principally through swallowed air, acid-bicarbonate reactions, and microbial fermentation, whereas malodor is determined mainly by trace volatile sulfur compounds, including hydrogen sulfide, methanethiol, and dimethyl sulfide. Their production depends on dietary sulfur amino acids, sulfate, taurine, host-derived substrates, microbial cross-feeding, intestinal transit, luminal chemistry, and gas-liquid partitioning. This review integrates evidence concerning dietary determinants of intestinal gas, gut microbial sulfur metabolism, nutritional and microbiome-directed interventions, and downstream odor-control strategies. The concept of conditional sound-odor discordance is retained as a secondary framework illustrating that gas volume, acoustic intensity, and odor burden should not be considered interchangeable endpoints. Human dietary trials indicate that low-FODMAP diets and substrate-specific enzymes may reduce fermentation-related symptoms or total gas production, but they do not necessarily suppress sulfur-derived odorants. Probiotic evidence remains strain-specific and largely indirect, whereas sulfide-binding compounds and external adsorptive devices target odor-active molecules more directly. Future nutritional studies should combine controlled dietary exposure with measurements of gas volume, volatile sulfur compounds, microbial functional pathways, intestinal transit, and perceived odor.},
}

@article {pmid42865226,
year = {2026},
author = {Hu, S and Chen, Z and Li, Y and Liao, Q and Luo, M and Song, D and Yu, H and Gao, Y and Yang, S and Wan, S and Zhang, S and Luo, C and Zhao, LY},
title = {Oral and Fecal Microbial Dysbiosis as Non-Invasive Diagnostic Biomarkers for Gastrointestinal Cancers: A Systematic Review and Meta-Analysis of Diagnostic Accuracy.},
journal = {International journal of cancer},
volume = {},
number = {},
pages = {},
doi = {10.1002/ijc.70779},
pmid = {42865226},
issn = {1097-0215},
abstract = {Gastrointestinal (GI) cancers, including esophageal (EC), gastric (GC), and colorectal cancer (CRC), impose a substantial global burden, with early detection remaining crucial for improving patient outcomes. The oral and gut microbiota are increasingly implicated in cancer development and hold promise as sources of non-invasive biomarkers. However, current evidence on microbiome-based diagnostics remains fragmented, and a systematic comparison of the diagnostic accuracy between oral and fecal sampling across multiple GI cancer types is lacking. To address this gap, a systematic search of PubMed, Embase, and Scopus up to December 31, 2025, identified 43 case-control studies (59 cohorts) comprising 4452 cancer patients and 5809 controls. The pooled area under the curve (AUC) was 0.846 (95% CI: 0.824-0.867), though with substantial heterogeneity (I[2] = 86.5%). By cancer type, pooled AUCs were 0.746 for EC (5 cohorts), 0.886 for GC (8 cohorts), and 0.850 for CRC (46 cohorts). A bivariate analysis of 20 cohorts comparing sample types found no statistically significant difference in diagnostic performance between oral (sAUC = 0.863) and fecal sampling (sAUC = 0.820; p = 0.369). While these exploratory findings suggest that oral and fecal microbial biomarkers may offer comparable diagnostic accuracy for GI cancers, with oral sampling presenting a more practical option for screening, the results are preliminary. Significant heterogeneity, a limited number of oral cohorts, and the absence of clinical control groups highlight the need for large-scale prospective studies with direct comparisons and real-world validation to validate these biomarkers for clinical translation.},
}

@article {pmid42865259,
year = {2026},
author = {Doane, MP and Martin, B and Kerr, E and Dinsdale, EA and Rangers, MM and Guida, L and Kyne, PM},
title = {Patterns of Functional Redundancy and Anaerobic Metabolic Potential Characterise the Skin Microbiome of a Critically Endangered Sawfish.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {e70442},
doi = {10.1111/1462-2920.70442},
pmid = {42865259},
issn = {1462-2920},
support = {//Charles Darwin University 2021 Institute of Advanced Studies (IAS) Rainmaker Start Up/ ; //Australian Marine Conservation Society (AMCS)/ ; //Flinders Accelerator for Microbiome Exploration/ ; },
mesh = {Animals ; *Skin Microbiome ; Anaerobiosis ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Endangered Species ; *Microbiota ; Metagenomics ; *Skin/microbiology ; Phylogeny ; },
abstract = {Using shotgun metagenomics of largetooth sawfish (Pristis pristis) skin and paired pool water samples, we provide the first taxonomic and functional characterisation of a sawfish skin microbiome and assess its ecological distinctiveness, assembly, and resilience relative to the surrounding water column. The skin microbiome was strongly host-associated and compositionally distinct, with lower taxonomic richness than the water column but dominated by Bacillota, particularly spore-forming Bacilli. Functional profiling revealed genes associated with sporulation, dormancy, anaerobic metabolism, and peptide transport, consistent with low-oxygen, low-flow conditions. In contrast, water-column microbiomes were more taxonomically diverse and enriched in phototrophic and polysaccharide-utilisation pathways. Sawfish skin communities exhibited patterns consistent with greater functional redundancy, with gene functions accumulating more rapidly per taxon. Together with greater among-individual taxonomic dispersion, this pattern is consistent with a host-filtered, lottery-like assembly process in which taxonomically variable communities maintain similar functional potential. The enrichment of dormancy and anaerobic pathways suggests the skin microbiome persists through periods of host quiescence and environmental stress while maintaining metabolic potential. Together, these results demonstrate that the sawfish skin supports a resilient, functionally robust microbiome distinct from ambient aquatic communities, highlighting the potential for integrating microbial functional data into conservation strategies for Critically Endangered vertebrates.},
}

Animals
*Skin Microbiome
Anaerobiosis
*Bacteria/classification/genetics/isolation & purification/metabolism
Endangered Species
*Microbiota
Metagenomics
*Skin/microbiology
Phylogeny

@article {pmid42865466,
year = {2026},
author = {Sandak, A and Pajerski, W and Gubenšek, A and Butina Ogorelec, K and Černoša, A},
title = {The archibiome: extending engineered living materials to multiscale built environments.},
journal = {Frontiers in systems biology},
volume = {6},
number = {},
pages = {1943876},
pmid = {42865466},
issn = {2674-0702},
abstract = {The integration of living systems into architecture is advancing rapidly through developments in biotechnology, materials science, and design approaches grounded in regenerative principles. Engineered Living Materials (ELMs) and living artefacts demonstrate how microbial systems can be embedded within materials to enable responsiveness, metabolic activity, and adaptive functionality. However, current applications remain largely confined to discrete material components, overlooking the complex and dynamic microbial ecosystems already present within buildings. This opinion paper introduces the concept of the archibiome as a framework for extending ELMs from isolated systems to interconnected architectural environments. The archibiome conceptualizes buildings as dynamic microbial ecosystems in which engineered systems, material interfaces, and native microbial communities interact across spatial and temporal scales. While this shift offers opportunities for adaptive and regenerative design, it also introduces challenges related to system stability, environmental variability, biosafety, and regulatory constraints. Addressing these challenges requires interdisciplinary approaches that integrate microbial ecology, materials engineering, architectural design, and regulatory science. Ultimately, the archibiome positions microbial life as a design variable, enabling a transition toward predictive, systems-level strategies for living architecture.},
}

@article {pmid42865524,
year = {2026},
author = {Yan, JY and Zhou, Y and Ni, L and Ding, ZJ and Lin, C},
title = {Effects of trait stacking on the maize phyllosphere microbiome: a shotgun metagenomic comparison.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1904641},
pmid = {42865524},
issn = {1664-302X},
abstract = {Current safety assessments for stacked-trait transgenic crops underrepresent the phyllosphere, a critical interface directly exposed to transgenic products, warranting strengthened risk evaluation. Here, we employed metagenomics to characterize the phyllosphere of three maize lines under herbicide-free conditions: wild-type (Corn.CK), herbicide-resistant single-trait (transgene of cp4-epsps, Corn.S), and insect- and herbicide-resistant stacked-trait (transgene of cry1Ab and cp4-epsps, Corn.D). Shannon diversity showed a consistent trend toward higher values in the cp4-epsps single-trait line than in the wild type (not significant after correction for multiple comparisons), whereas the stacked-trait line showed an intermediate increase. Transgenic events were associated with bidirectional taxonomic remodeling, characterized by the depletion of Enterobacterales and enrichment of environmentally adapted taxa. Functionally, transgenic lines displayed pervasive metabolic depletion across KEGG pathways and CAZyme categories, alongside reduced abundance of virulence-associated gene homologs (e.g., T6SS and Enterobactin) and lower antibiotic resistance gene diversity (wild-type > stacked-trait > single-trait), driven by the concomitant loss of Enterobacterales hosts. Notably, in most of the taxonomic, functional, virulence, and resistome dimensions examined, the stacked-trait line exhibited an intermediate microbiome profile between the wild-type and single-trait lines. These findings suggest that, for this genotype combination under these controlled conditions, trait stacking was not associated with microbiome perturbation greater than that observed for the single trait, and provide a preliminary, genotype- and stage-specific reference for phyllosphere biosafety assessment, pending field validation.},
}

@article {pmid42865525,
year = {2026},
author = {Caccamo, A},
title = {Trust your gut: the neuro-gastroenteric mechanics of prediction and expectation.},
journal = {Frontiers in human neuroscience},
volume = {20},
number = {},
pages = {1956182},
pmid = {42865525},
issn = {1662-5161},
abstract = {Living organisms constantly make probabilistic predictions about what they expect to see in their external environment, and actively solicit information from the environment to inform their predictions. This process is foundational for many frameworks including Active Inference and Predictive Processing. It relies on organisms having prior expectations, entailed by an internal generative model of the environment. Posterior expectations are updated based on the selected data, driven by prediction error minimization. However, failures to contextualize the precision or confidence placed in predictions, can give rise to perceptual abnormalities that are at the basis of various psychiatric conditions. Different factors can influence this process. Notably, disruptions in the gut microbiome have been implicated in some psychotic disorders. Gut microbial dysregulation has also been associated with alterations in neurotransmitter synthesis, metabolism, and turnover, which may affect processes involved in the encoding of precision of prediction errors. On the basis of this gut-brain connection, this Hypothesis and Theory article hypothesizes that the gut microbiome plays a role as a modulator of predictive processing, influencing how predictions are formed and expectations updated. Specifically, this article explores the importance of "mental model" embodiment, and considers the role of hippocampal activity in predictive coding and its modulation by the gut microbiome. Finally, it offers a novel perspective on the use of cortico-hippocampal-gastroenteric frameworks for inferring personalized dietary interventions in nutritional psychiatry.},
}

@article {pmid42865545,
year = {2026},
author = {Chen, Z and Gan, W and Cao, F and Yu, F and Lin, W and Wang, X and Hong, Y and Yang, M and Hong, L and Chen, C and Wu, J and Liu, X and Zhang, W and Lian, Y},
title = {Intratumoral microbiota-host gene associations characterize stage-associated microecological patterns in colorectal cancer.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1934580},
pmid = {42865545},
issn = {1664-302X},
abstract = {INTRODUCTION: Intratumoral microbiota are emerging as important ecological components of the colorectal cancer (CRC) microenvironment. However, their stage-associated patterns and coordination with host gene expression remain poorly understood. This study aimed to characterize stage-associated associations between intratumoral microbiota and the host transcriptome in CRC.

METHODS: We profiled 73 regional tumor specimens from 30 independent, treatment-naïve CRC patients using full-length 16S rRNA gene sequencing and mRNA sequencing. Microbial diversity, predicted functional profiles, co-occurrence networks, differential abundance, and microbiota-host transcriptome associations were analyzed. Regularized canonical correlation analysis and machine-learning modeling with SHAP-based feature interpretation were performed to identify stage-discriminative features. Candidate associations were evaluated in two independent public microbiome datasets. Mendelian randomization and immune-infiltration analyses were further conducted to explore the potential biological relevance of representative microbiota-gene associations.

RESULTS: Disease stage was a major factor shaping intratumoral microbial composition. Advanced-stage CRC exhibited increased microbial α-diversity, distinct predicted functional profiles, and altered microbial co-occurrence patterns. Integrated microbiota-transcriptome analysis identified ten genus-level and six species-level candidate microbiota-gene association pairs. Core genera showed reproducible stage-discriminative signals in two independent public microbiome datasets. SHAP analysis identified the principal microbial and host transcriptomic features contributing to stage classification. Integrating microbial and host gene signatures improved classification performance, with the combined model achieving an AUROC greater than 0.90. The Alloprevotella-MDH1 pair was selected as a representative association axis. Alloprevotella abundance was negatively correlated with MDH1 expression, while low MDH1 expression was associated with poorer survival and distinct metabolic-immune states in CRC. Exploratory Mendelian randomization analysis provided preliminary genetic epidemiological support for an association between Alloprevotella abundance and CRC risk.

DISCUSSION: Intratumoral microbiota and host transcriptional profiles exhibit coordinated, stage-associated alterations in CRC. The identified microbiota-gene associations, particularly the Alloprevotella-MDH1 axis, provide potential biological links between tumor microbial ecology, host metabolism, immune states, and CRC progression. These findings support the value of integrated microbiome-transcriptome analysis for characterizing the intratumoral microenvironment and identifying candidate microbial-host regulatory relationships.},
}

@article {pmid42865837,
year = {2026},
author = {Ge, QY and Wang, CY and Zheng, C and Zheng, HT and Wen, YX and Luo, J and Qiang, Y and Wang, YQ and Cong, ZZ and Shen, Y},
title = {Short-term clinical outcomes of nasoduodenal tube versus feeding jejunostomy after minimally invasive esophagectomy: a retrospective cohort study with exploratory microbiome analysis.},
journal = {Journal of thoracic disease},
volume = {18},
number = {9},
pages = {1024},
pmid = {42865837},
issn = {2072-1439},
abstract = {BACKGROUND: Esophagectomy remains an effective treatment for esophageal cancer but is associated with severe postoperative complications, in which nutritional status plays a critical role. The optimal route for enteral feeding remains uncertain. To address this uncertainty, we compared the short-term clinical outcomes of the two approaches and exploratorily analyzed the differences in gut microbiota.

METHODS: This retrospective cohort study enrolled patients who underwent minimally invasive esophagectomy (MIE) for esophageal squamous cell carcinoma (ESCC) between July 2018 and June 2021. Primary outcomes were surgery-related complications (including anastomotic leakage, anastomotic stenosis, pneumonia, respiratory failure, cardiac events, chylothorax, intestinal fistula and bowel obstruction) and catheter-related outcomes (including occlusion, accidental removal, displacement and retention time). Baseline data were extracted from medical records. Propensity score matching (PSM) was applied to control for potential confounders. Intestinal fluid and fecal samples were collected after enteral nutrition for 16S ribosomal DNA (16S rDNA) sequencing.

RESULTS: After PSM, a total of 381 patients (nasoduodenal tube: 282; feeding jejunostomy: 153) was finally included. The feeding jejunostomy group exhibited a higher incidence of pneumonia (21.49% vs. 33.99%, P=0.007), respiratory failure (3.07% vs. 13.07%, P<0.001), anastomotic stenosis (1.32% vs. 5.23%, P=0.03) and bowel obstruction (0% vs. 2.16%, P=0.03). Nasoduodenal tube placement was associated with more accidental removal (13.16% vs. 0.65%, P<0.001) and catheter displacement (13.60% vs. 6.54%, P=0.03). The catheter retention time {37 [interquartile range (IQR): 15-40] days vs. 39 (IQR: 37-42) days, P<0.001}
was also shorter in nasoduodenal tube group.

CONCLUSIONS: In this study, nasoduodenal tube placement was associated with a higher incidence of catheter-related complications, whereas feeding jejunostomy was linked to more surgery-related complications. Nasoduodenal tube placement also showed potential functional advantages for the gut microbiome. However, future multi-center randomized controlled trials are still needed to minimize potential confounders and validate the differences between the two enteral nutrition routes.},
}

@article {pmid42865919,
year = {2026},
author = {Krishna S, G and Reeja, N and Sadanandan, S and Mappurath, B and Chatterjee, A and Antony, G and Grace, T},
title = {Decoding host-microbiome interactions through integrative multi-omics and artificial intelligence: from biological mechanisms to predictive modelling.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1906484},
pmid = {42865919},
issn = {2813-4338},
abstract = {The mutual communication between the human host and its microbiome plays a fundamental role in maintaining metabolic and immunological homeostasis. Disruptions in this delicate ecosystem are heavily linked to severe pathologies like inflammatory bowel disease (IBD), metabolic syndromes, and cancer. Whilst traditional single-omics approaches offer limited taxonomic snapshots, multi-omics strategies are bridging the gap by mapping the complex, multi-layered networks driving host-microbe interactions. However, integrating these highly dimensional, heterogeneous datasets creates significant computational bottlenecks. Artificial Intelligence (AI), spanning machine learning and deep learning architectures, has emerged as a critical catalyst to resolve this crisis. AI transforms complex data into predictive models for early diagnosis, clinical biomarker discovery, and personalised therapeutics. Despite persistent hurdles in model generalisation and data standardisation, the convergence of multi-omics and AI is actively driving the future of precision medicine.},
}

@article {pmid42865978,
year = {2026},
author = {Gao, Y and Lv, X and Sun, Z},
title = {Seminal dysbiosis in idiopathic male infertility: toward a seminal dysbiosis-inflammatory/oxidative endophenotype-SDF axis.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1943471},
pmid = {42865978},
issn = {1664-2392},
mesh = {Humans ; Male ; *Infertility, Male/metabolism/pathology/etiology ; *Semen/microbiology/metabolism ; *Dysbiosis/metabolism ; *Oxidative Stress ; *Inflammation/pathology/metabolism ; *Endophenotypes ; *DNA Fragmentation ; *Spermatozoa/pathology/metabolism ; },
abstract = {Idiopathic male infertility (IMI) usually refers to abnormal semen parameters after known causes have been excluded. However, its clinical stratification and intervention evidence remain difficult to reconcile. Based on low biomass in semen, this review proposes an SD-IO-SDF axis linking seminal dysbiosis (SD), inflammatory/oxidative endophenotype (IO), and sperm DNA fragmentation (SDF) in subsets of IMI. It integrates three mechanisms of evidence strength: (i) inflammation-oxidative injury pathway (leukocyte-dependent); (ii) leukocyte-independent redox imbalance; and (iii) a metabolic-epigenetic route (SAM cycle, butyrate) as a testable hypothesis. Existing evidence suggests that the association between SD and SDF concentrates in specific IO activation states and IMI subtypes. IO stratification may reduce effect dilution across mixed populations and make the hypothesis more directly testable. For research implementation, we propose IO indicators grouped by measurement type (inflammatory: leukocytospermia and/or PMN-elastase; oxidative: sORP), with validation against SDF platforms as a subsequent step. This approach provides a falsifiable structure for IMI and provides a template for future trial designs based on SD×IO stratification.},
}

Humans
Male
*Infertility, Male/metabolism/pathology/etiology
*Semen/microbiology/metabolism
*Dysbiosis/metabolism
*Oxidative Stress
*Inflammation/pathology/metabolism
*Endophenotypes
*DNA Fragmentation
*Spermatozoa/pathology/metabolism

@article {pmid42865986,
year = {2026},
author = {Chen, Y and Li, Y and Lu, H and Jia, S and Jiang, Y},
title = {New insights into the gut-heart axis: microbial metabolite biomarkers, multi-omics, and engineered bacterial delivery systems.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1987882},
pmid = {42865986},
issn = {1664-302X},
abstract = {Despite rapid growth in gut-heart axis research, clinical translation remains limited. This review addresses that gap by critically synthesizing recent evidence on microbiota-derived metabolites, biomarkers, multi-omics workflows, and engineered bacterial interventions in cardiovascular disease (CVD). We examine how TMAO, short-chain fatty acids, bile acids, indole derivatives, and phenylacetylglutamine exert context-dependent cardiovascular effects, and why functional microbial gene markers and integrated biomarker panels may outperform single-taxon signatures. We then evaluate multi-omics strategies, metagenomics, metabolomics, proteomics, single-cell and spatial omics, and bioinformatics integration, for causal inference and biomarker validation. Finally, we assess engineered bacterial delivery systems, including gene circuit design, colonization control, biocontainment, and safety, and outline short-, medium-, and long-term milestones for clinical translation, cost-effectiveness, and intellectual property. The key takeaway is that precision microbiome medicine in CVD will require standardized assays, prospective validation, robust regulatory pathways, and equitable commercialization. By linking mechanistic insights with translational requirements, this review provides a framework for developing microbiome-targeted diagnostics and therapeutics in CVD.},
}

@article {pmid42865996,
year = {2026},
author = {Zhang, Y and Feng, M and Xue, Q and Ma, R and Liu, F},
title = {Applications of artificial intelligence in personalized nutrition interventions.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1974199},
pmid = {42865996},
issn = {2296-861X},
abstract = {Unhealthy dietary patterns remain a major modifiable contributor to the global burden of obesity, type 2 diabetes mellitus (T2DM), cardiovascular disease, and cancer. However, individuals can respond markedly differently to identical foods, limiting the effectiveness of one-size-fits-all dietary guidance. This review examines the application of artificial intelligence (AI) to personalized nutrition interventions across three interconnected layers. At the biological level, inter-individual variability can be characterized by three mechanistic dimensions: nutrigenomic variation, which influences nutrient metabolism and disease susceptibility; metabolomic biomarkers, which objectively capture dietary exposure and early metabolic alterations; and the gut microbiome, which bidirectionally mediates diet-host interactions. At the technological level, AI integrates these dimensions into multimodal digital profiles. Machine learning models predict individual postprandial glycemic and lipemic responses, with reported correlations of up to r = 0.77 in large cohorts; deep learning and computer vision automate dietary assessment; natural language processing and large language models (LLMs) support nutrition counseling; knowledge graphs enable constraint-aware food recommendations; and digital-twin and adaptive closed-loop systems incorporating continuous glucose monitoring and wearable-device data support real-time nutritional interventions. However, the strength of clinical evidence varies across disease domains. Glycemic management in T2DM and prediabetes currently has the most mature randomized controlled trial evidence: an AI-enabled personalized intervention combining algorithmic dietary personalization with CGM-linked feedback improved glycemic endpoints compared with a Mediterranean diet, while a fully automated AI-delivered diabetes prevention program achieved outcomes non-inferior to those of human coaching. In obesity, cardiovascular disease, oncology, and gastrointestinal disorders, the evidence remains mixed or preliminary. Clinical translation also faces substantial challenges, including biased and inconsistently standardized dietary and multi-omics data; the underrepresentation of non-European populations, which limits model generalizability and raises concerns about health equity; limited model explainability; privacy and data-governance challenges; immature regulatory pathways for adaptive software as a medical device; and specific risks associated with LLMs, such as hallucinated or guideline-discordant dietary advice. AI-enabled personalized nutrition is therefore progressing from proof of concept toward clinical translation. Realizing its potential equitably will require multi-ethnic nutrition-omics cohorts, privacy-preserving multicenter collaboration, dietitian-led human-AI collaboration, and lifecycle safety governance for generative models.},
}

@article {pmid42866007,
year = {2026},
author = {Ni, FX and Pan, CF and Chen, HH and Huang, DH and Jiang, ZB},
title = {From gut to lung: the microbiome-directed causal mechanisms and therapeutic horizons in asthma.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1935791},
pmid = {42866007},
issn = {1664-3224},
mesh = {Humans ; *Asthma/therapy/microbiology/immunology/metabolism/etiology ; Animals ; *Lung/immunology/microbiology/metabolism ; *Gastrointestinal Microbiome/immunology ; Dysbiosis/immunology ; Probiotics/therapeutic use ; },
abstract = {The gut-lung axis represents a predominantly gut-to-lung communication network through which gut microbiota and their metabolites influence pulmonary immunity. In asthma, gut dysbiosis-characterized by reduced microbial diversity, depletion of short-chain fatty acid (SCFA)-producing taxa, and expansion of pro-inflammatory pathobionts-has been consistently associated with disease severity and type 2 inflammation. While the axis is conceptually bidirectional, the vast majority of mechanistic evidence to date describes unidirectional gut to lung regulation. This review critically synthesizes evidence on the gut-lung axis in asthma. We evaluate multi-kingdom microbial ecology, evaluating contributions from bacterial, fungal, protozoan, and phage. We examine metabolite-specific immune reprogramming via SCFAs, bile acids, and tryptophan derivatives, explicitly acknowledging unresolved controversies including the SCFA concentration paradox. We integrate causal inference frameworks that combine Mendelian randomization, gnotobiotic models, and experimental triangulation. We also present precision therapeutic pipelines with evidence-based grading of interventions ranging from probiotics to engineered live biotherapeutics. We propose that targeting the gut-lung axis represents a foundational strategy for asthma modification and outline a roadmap from multi-omics discovery to biomarker-guided clinical trials. Distinguishing this review from prior work, we explicitly separate established mechanisms from speculative pathways and provide actionable criteria for clinical translation. We also critically identify the reverse (lung to gut) pathway as a major knowledge gap requiring urgent investigation.},
}

Humans
*Asthma/therapy/microbiology/immunology/metabolism/etiology
Animals
*Lung/immunology/microbiology/metabolism
*Gastrointestinal Microbiome/immunology
Dysbiosis/immunology
Probiotics/therapeutic use

@article {pmid42866012,
year = {2026},
author = {Dumbuya, JS and Li, Y and He, B and Li, G and Liu, Y and Zhong, Y and Huang, S and Chen, X},
title = {Gut microbiota and health-related quality of life in paediatric inherited metabolic disorders: a narrative review and conceptual framework.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1928657},
pmid = {42866012},
issn = {1664-302X},
abstract = {Inherited metabolic disorders (IMDs) comprise more than 1,400 rare genetic conditions affecting paediatric patients worldwide. Despite advances in newborn screening and dietary management, many children experience chronic complications, gastrointestinal symptoms, and reduced health-related quality of life (HRQoL). Emerging evidence-predominantly from phenylketonuria (PKU)-suggests that gut microbiota may influence metabolic homeostasis and patient-centred outcomes in affected children. Because of substantial methodological heterogeneity and the rarity of individual disorders, we elected a narrative review format to synthesise current evidence rather than a formal quantitative synthesis. Electronic searches were performed in PubMed, Embase, and Web of Science from inception to February 2026. We synthesise current evidence regarding gut microbiota composition in major paediatric IMDs, including PKU, organic acidemias, glycogen storage diseases, lysosomal storage disorders, and mitochondrial diseases. For PKU, controlled studies report reduced microbial diversity and depletion of butyrate-producing taxa associated with long-term dietary treatment. For the remaining disorders, direct paediatric microbiome data are sparse or absent, and proposed links rely on mechanistic extrapolation from non-IMD populations. We present the gut microbiota-metabolism-quality of life axis as a conceptual framework that integrates microbial metabolites, intestinal barrier function, immune signalling, and patient-reported outcomes, while emphasising that direct causal evidence linking microbiota alterations to HRQoL in paediatric IMDs is currently lacking. Microbiota-directed interventions remain preliminary. Future multicentre longitudinal studies integrating microbiome profiling, multi-omics technologies, and validated patient-reported outcomes are needed to clarify causal mechanisms and therapeutic potential. Importantly, the available evidence is heterogeneous: direct paediatric microbiome evidence is strongest for PKU, whereas evidence for other IMDs is sparse and often observational, preclinical, or extrapolated from non-IMD populations. The proposed microbiota-metabolism-HRQoL axis is therefore presented as a hypothesis-generating framework rather than an established causal pathway.},
}

@article {pmid42866017,
year = {2026},
author = {Herrera, G and Hua, X and Wu, Z and Liao, LM and Wan, Y and Dagnall, CL and Jones, K and Hicks, BD and Hutchinson, A and Gail, MH and Shi, J and Gierach, GL and Sinha, R and Vogtmann, E},
title = {Oral microbiome and postmenopausal breast cancer risk: findings from the NIH-AARP diet and health study.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2728745},
pmid = {42866017},
issn = {2000-2297},
abstract = {INTRODUCTION: Breast cancer is the most frequently diagnosed cancer among women worldwide. Some case-control studies have reported associations between the oral microbiome and breast cancer, but the temporality of the association remains unclear. Therefore, we examined this association prospectively in the NIH-AARP Diet and Health Study.

METHODS: In 2005, oral wash samples were collected from a subset of the NIH-AARP cohort. We identified 318 women who developed breast cancer after collection and 318 controls, incidence-density matched on age at collection, race/ethnicity and smoking. DNA was extracted using the DNeasy PowerSoil Pro Kit, followed by shotgun metagenomic sequencing. Conditional logistic regression was used to calculate the odds ratios (OR) for associations between alpha- and beta-diversity and species- and gene-level metrics with breast cancer risk, adjusting for potential confounders.

RESULTS: Cases developed breast cancer on average 3.4 years after sample collection. Overall, the majority of the microbial metrics, including species and genes, showed largely null associations with the exception of Pielou's evenness (OR = 0.82; 95% CI = 0.70-0.95). When stratified by time to diagnosis, the inverse association with Pielou's evenness was only detected among women diagnosed within 2 years (29% of cases). In this subgroup, some previously reported associations, like the inverse association with the presence of Treponema (OR = 0.37; 95% CI = 0.17-0.78), were replicated. Null associations were predominantly observed for cases diagnosed more than 2 years after sample collection.

CONCLUSIONS: The oral microbiome was generally not prospectively associated with postmenopausal breast cancer in a US population and results suggested previous findings may reflect reverse causation.},
}

@article {pmid42866036,
year = {2026},
author = {Schmidt, MA and Schmidt, CM and Schmidt, JC and Meydan, C and Afshin, EE and Overbey, EG and Kim, J and Singh, RS and Beheshti, A and Mason, CE},
title = {Systemic elevation of gut derived p-cresol during one year in space: implications for brain, heart, bone, liver and microbiome in astronauts.},
journal = {Frontiers in physiology},
volume = {17},
number = {},
pages = {1878680},
pmid = {42866036},
issn = {1664-042X},
abstract = {INTRODUCTION: We observed the elevation of p-cresol in the untargeted metabolome of the multiomics portion of the NASA Twins Study of One Year in Space. p-Cresol is a uremic and neurotoxin that is produced via the metabolism of dietary tyrosine by gut bacteria. Intestinally produced p-cresol is absorbed into systemic circulation where it exerts its adverse metabolic effects and drives phenotypic changes relevant to astronauts, including the brain, heart, bone, liver, kidney, and colon.

METHODS: A pair of monozygotic twins were studied for 25 months, during which one subject spent 340 days aboard the International Space Station (ISS), while his identical twin remained on Earth. Molecular analyses included genome, epigenome, transcriptome, proteome, metabolome, immunome, and microbiome. Our metabolite feature extraction was focused on plasma p-cresol (p-cresyl sulfate [pCS] and p-cresol glucuronide [pCG]), along with associated biological dynamics that govern p-cresol production and metabolism.

RESULTS: Significance was observed for pCG when comparing Post-flight vs. Inflight (adj p = 0.016). pCS values were significantly altered Post-flight vs. Inflight (adj p = 0.002) and Post-flight vs. Late-flight (adj p = 0.037). pCS values for Early-flight vs. Pre-flight approached significance (adj p = 0.08). In alignment with elevated plasma p-cresol values at certain stages of spaceflight, we found an increase in count-normalized abundance (raw reads) for the major p-cresol producer Clostridioides difficile in TW (Flight) vs. HR (Ground) for Post-flight, Inflight, and Overall (adj p = 0.014, adj p = 0.0006, and adj p = 2.02x10¯[5], respectively). Concomitantly, we observed a significant increase in count-normalized abundance for another of the major p-cresol producers Olsenella uli in TW vs. HR for Post-flight, Inflight, and Overall (adj p = 0.0045, adj p = 0.00043, adj p = 0.0016, respectively), including Interaction for Inflight vs. Pre-flight (adj p = 0.028).

DISCUSSION: We observed an elevation of p-cresol during one year in space, which may have significant implications for astronaut health and performance. Molecular findings and p-cresol countermeasure candidates are discussed. We also explore the process from untargeted molecular feature extraction to description of biological meaning, to new hypothesis generation, to plausible countermeasure development for human spaceflight.},
}

@article {pmid42866058,
year = {2026},
author = {Zhai, J and Lu, Y and Fan, JG},
title = {Omics-based Decoding of Metabolic Dysfunction-associated Fatty Liver Disease: From Pathogenesis to Clinical Translation.},
journal = {Journal of clinical and translational hepatology},
volume = {14},
number = {9},
pages = {949-959},
pmid = {42866058},
issn = {2310-8819},
abstract = {Metabolic dysfunction-associated fatty liver disease (MAFLD) is a multifactorial disorder driven by complex interactions among genetic, epigenetic, transcriptional, proteomic, metabolic, and microbiome factors. Single-omics technologies have provided valuable insights into disease mechanisms, yet each layer captures only a partial view of MAFLD pathogenesis. Recent advances in multi-omics integration allow systematic dissection of molecular networks, cell differentiation trajectories, intercellular communication, and spatial organization, revealing causal links between molecular alterations and tissue phenotypes. Horizontal integration connects different omic layers within the same biological state, while longitudinal integration captures dynamic changes across disease stages. Emerging spatial transcriptomics, proteomics, and metabolomics techniques further enable in situ mapping of cellular and molecular heterogeneity, uncovering spatially defined pathogenic niches and regulatory hubs. Collectively, these integrated approaches offer a multidimensional framework for understanding MAFLD progression, identifying potential biomarkers, and guiding precision therapeutic strategies. Future efforts should focus on standardized multi-omics pipelines, interdisciplinary collaboration, and functional validation to translate these insights into clinical applications.},
}

@article {pmid42866068,
year = {2026},
author = {Pedrino, IC and Lacava, PT},
title = {Nano-enabled microbial bioinputs for sustainable agriculture: advances, mechanisms, applications, and future challenges.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1925672},
pmid = {42866068},
issn = {1664-462X},
abstract = {Microbial bioinputs have emerged as key components of sustainable agriculture owing to their ability to promote plant growth, improve nutrient acquisition, enhance tolerance to biotic and abiotic stresses, and suppress phytopathogens. Despite their considerable potential, the widespread adoption of these technologies remains constrained by limited environmental persistence, reduced formulation stability, and inconsistent performance under field conditions. In this context, nanotechnology has emerged as a promising approach to improve the stability, delivery efficiency, and agronomic reliability of microbial bioinputs. This review provides a critical and comprehensive assessment of recent advances in nano-enabled microbial bioinputs, discussing the mechanisms through which nanomaterials enhance microbial protection, stabilization, controlled release, delivery efficiency, and functional persistence. Particular emphasis is placed on bionanofertilizers and bionanopesticides as emerging technologies for improving nutrient use efficiency, biological crop protection, and soil-plant-microbiome interactions while reducing dependence on conventional agrochemicals. The review also critically examines current knowledge on biosafety, ecological impacts, regulatory frameworks, and the practical challenges associated with large-scale agricultural implementation. Current evidence indicates that nano-enabled formulations can address several limitations associated with conventional microbial bioinputs and contribute to more consistent agronomic performance under environmentally variable conditions. However, most available studies remain limited to laboratory and greenhouse experiments, while robust long-term validation under diverse field conditions is still lacking. In addition, uncertainties regarding environmental fate, nanoparticle-microbiome interactions, standardized biosafety assessment, scalable manufacturing, regulatory harmonization, and economic feasibility continue to constrain broader commercial adoption. Overall, nano-enabled microbial bioinputs represent a promising technological platform for bridging the gap between laboratory innovation and consistent field performance. Their successful implementation will depend on integrating advances in microbiology, nanotechnology, formulation engineering, and environmental risk assessment with rigorous field validation, scalable production strategies, and harmonized regulatory frameworks. Addressing these challenges will be essential to support the development of resilient, resource-efficient, and environmentally sustainable agricultural systems.},
}

@article {pmid42866189,
year = {2026},
author = {Clavero-Jimeno, A and Martin-Olmedo, JJ and Gatti, A and Cortés-Martín, A and Camacho-Cardenosa, A and Jurado-Fasoli, L and Dote-Montero, M and Molina-Fernandez, M and López-Vázquez, A and Lopez-Pascual, A and Ávila, MA and Petrina, E and Zugasti, A and Urdiain, I and Concepción, M and Cabeza, R and Martín-Rodríguez, JL and Labayen, I and R Ruiz, J},
title = {Divergent ectopic fat distribution and adipokine/hepatokine levels characterize the metabolically healthy overweight/obesity phenotype.},
journal = {iScience},
volume = {29},
number = {10},
pages = {117672},
pmid = {42866189},
issn = {2589-0042},
abstract = {The metabolically healthy overweight/obesity (MHOO) phenotype combines excess adiposity with preserved cardiometabolic health. We compared specific fat depots, circulating adipokine and hepatokine levels, and fecal microbiota composition between 384 adults classified as MHOO (n = 99) or metabolically unhealthy overweight/obesity (MUOO; n = 285). Magnetic resonance imaging was used to quantify visceral adipose tissue (VAT) volume, hepatic and pancreatic fat fractions, abdominal and mid-thigh intermuscular adipose tissue (IMAT), and subcutaneous adipose tissue (SAT). Despite similar whole-body fat mass, MHOO showed lower VAT volume, hepatic and pancreatic fat fractions, abdominal IMAT volume, abdominal VAT-to-SAT ratio, and mid-thigh IMAT area, together with higher mid-thigh SAT area. MHOO also had higher adiponectin and sex hormone-binding globulin (SHBG) and lower retinol-binding protein 4 (RBP4) levels. Fecal microbiota composition was similar between groups. VAT volume and hepatic fat fraction were the strongest discriminative features, supporting fat distribution rather than total adiposity as a key feature of preserved metabolic health.},
}

@article {pmid42866308,
year = {2026},
author = {Xu, H and Jiang, T and Li, M and Jiang, D},
title = {The hormone-microbiota-NET framework in gynecologic diseases: evidence, controversies, and translational opportunities.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1929292},
pmid = {42866308},
issn = {1664-3224},
mesh = {Humans ; Female ; *Genital Diseases, Female/microbiology/immunology/metabolism/etiology ; *Microbiota/immunology ; *Extracellular Traps/immunology/metabolism ; Animals ; Pregnancy ; *Gonadal Steroid Hormones/metabolism ; Translational Research, Biomedical ; },
abstract = {Gynecologic diseases, including infectious disorders, endocrine-related conditions, gynecologic malignancies, and pregnancy complications, are clinically diverse yet frequently share features of hormonal imbalance, microbial dysbiosis, and dysregulated inflammation. Current research has largely examined these processes separately, limiting integrated understanding of their potential interactions. This review synthesizes current evidence and proposes a hormone-microbiota-neutrophil extracellular trap (NET) framework as a conceptual tool for understanding common and disease-specific mechanisms across gynecologic disorders. We first summarize the core molecular basis of NET formation, with emphasis on peptidylarginine deiminase 4 as a candidate regulatory node. We then examine the effects of sex hormones on NET regulation, the role of the microbiota in shaping mucosal immune responses, and potential mechanistic links between microbial products, extracellular matrix components, and NET dysregulation. Evidence is further integrated across representative infectious, endocrine-related, malignant, and pregnancy-associated conditions, including pelvic inflammatory disease, bacterial vaginosis, endometriosis, polycystic ovary syndrome, ovarian, cervical, and endometrial cancers, and preeclampsia. The available literature indicates that hormone-dependent immune modulation, pathogen- or microbiota-associated inflammatory signaling, and NET-related tissue injury may converge in multiple gynecologic settings, although the strength of evidence differs substantially across specific pathways and diseases. Direct support is strongest for selected hormone-NET effects in defined experimental or pregnancy-associated settings and for pathogen/microbial product-NET interactions in infectious contexts, whereas the complete hormone-microbiota-NET framework and the proposed glycosaminoglycan-peptidylarginine deiminase 4 (GAG-PAD4) bridge remain insufficiently validated. Overall, this review provides an evidence-based integrative framework for organizing current knowledge, identifying mechanistic gaps, and informing future biomarker development, patient stratification, and translational research in gynecologic disease.},
}

Humans
Female
*Genital Diseases, Female/microbiology/immunology/metabolism/etiology
*Microbiota/immunology
*Extracellular Traps/immunology/metabolism
Animals
Pregnancy
*Gonadal Steroid Hormones/metabolism
Translational Research, Biomedical

@article {pmid42866455,
year = {2026},
author = {de Aguiar, LS and Echeverria, LS and Genaro, LM and Rodrigues, BAG and de Paula Pessoa Bezerra, M and Costa, FO and Pascoal, LB and de Sene Portel Oliveira, P and de Lourdes Setsuko Ayrizono, M and Leal, RF},
title = {Gut microbiota profile and response to neoadjuvant chemoradiotherapy in patients with rectal cancer: a systematic review.},
journal = {Translational gastroenterology and hepatology},
volume = {11},
number = {},
pages = {111},
pmid = {42866455},
issn = {2415-1289},
abstract = {BACKGROUND: Rectal cancer (RC) accounts for approximately 30% of all colorectal cancers, with pathological complete response (pCR) rates following neoadjuvant chemoradiotherapy (nCRT) ranging from 10-15% and reaching up to 38% with total neoadjuvant therapy. The intestinal microbiota has emerged as a potential modulator of treatment efficacy, offering opportunities for patient stratification and personalized therapy. This review aimed to the best of our knowledge, no robust systematic review has focused on the microbiota profile as a biomarker of response to nCRT in RC. Most studies focus on the effect of the microbiota on the adjuvant response to chemotherapy. To synthesize the available evidence and fill the gap in knowledge on the role of the intestinal microbiota in modulating treatment response and prognosis in patients with RC undergoing nCRT.

METHODS: This systematic review was registered in PROSPERO (CRD420251174787). A comprehensive search was conducted across PubMed, PubMed Central (PMC), Virtual Health Library (BVS), Scopus, Web of Science, Embase, and Cochrane Library. Studies evaluating the association between the intestinal microbiota and treatment response or prognosis in adult patients with RC were included. Two independent reviewers selected studies, and data were extracted from eligible studies.

RESULTS: Seventeen studies were included, all published after 2020, with 11 published between 2023 and 2025. Most studies originated from China (11/17). Sequencing methodologies included 16S rRNA sequencing (9 studies), shotgun metagenomics (6 studies), RNA-sequencing (2 studies), and whole-exome sequencing with Path-seq (1 study). A total of 868 patients were evaluated. Alpha-diversity did not differ significantly between responders and non-responders in most studies. Beta-diversity results were heterogeneous. Responders were associated with genera such as Bacteroides, Campylobacter, Faecalibacterium, and Lactobacillus, while non-responders showed enrichment of Akkermansia, Streptococcus, and Prevotella. Functional pathway analyses revealed that responders showed enrichment in pathways related to anaerobic energy metabolism, amino acid synthesis, and innate immune activation [cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway], whereas non-responders showed enrichment of fatty acid metabolism and anti-apoptotic pathways. Nine studies developed predictive models with AUC values ranging from 0.707 to 0.980.

CONCLUSIONS: The intestinal microbiota may play a relevant role in modulating response to nCRT in RC, particularly through functional metabolic pathways rather than taxonomic composition alone. Predictive models based on microbial signatures show promising accuracy, although standardization of methodologies and validation in diverse populations are needed before clinical implementation.},
}

@article {pmid42866476,
year = {2026},
author = {Zhuo, W and Yu, Z and Liu, K and Zhang, W and Ma, Z and Xu, Z and Wang, J and Li, T and Zhu, G and Wang, B and Xiong, R and Li, C and Zhang, H and Wang, W},
title = {Remodeling the gut microbiota: mechanistic insights into probiotic-mediated alleviation of weaning stress in piglets.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1964247},
pmid = {42866476},
issn = {1664-3224},
mesh = {Animals ; *Probiotics ; *Weaning ; *Gastrointestinal Microbiome ; Swine ; *Stress, Physiological ; Intestinal Barrier Function ; },
abstract = {Early weaning, characterized by the replacement of maternal milk with solid diets, is widely recognized as one of the most stressful developmental events affecting piglets in intensive production systems. During this stage, the digestive, immune, and metabolic systems remain immature, rendering piglets highly susceptible to environmental and nutritional stressors as well as opportunistic pathogens. These challenges frequently disrupt intestinal microbial homeostasis, impair gut barrier integrity, and trigger immune and metabolic disturbances, ultimately leading to post-weaning diarrhea, intestinal inflammation, growth retardation, and reduced production performance. For decades, dietary antibiotics have been extensively used to mitigate weaning-associated diseases. However, the emergence and dissemination of antimicrobial resistance, together with concerns regarding antibiotic residues and microbiota disruption, accelerated the search for safe, effective, and sustainable alternatives to maintain intestinal health in antibiotic-free swine production. As one of the most promising microbiota-targeted strategies, probiotics have demonstrated considerable potential for alleviating weaning stress by restoring the structure and function of the gut microbial ecosystem. This review systematically summarizes weaning-induced alterations in gut microbial composition, ecological succession, and microbial metabolic dysfunction, and discusses how these changes contribute to intestinal dysfunction in piglets. Emphasis is placed on the mechanisms by which probiotics remodel the intestinal microbiota, promote the establishment of health-associated microbial communities, and restore key microbial metabolic pathways, including short-chain fatty acid (SCFA), secondary bile acid, and tryptophan metabolism. Although probiotics may interact directly with host tissues, their effects are primarily mediated through restoration of the gut microbial ecosystem and re-establishing microbiota-derived metabolic signaling, thereby coordinating intestinal barrier repair, immune homeostasis, and redox balance while alleviating post-weaning diarrhea and growth impairment. Probiotic-mediated restoration of gut microbial structure and metabolic function represents the central mechanism underlying protection against weaning stress and can be conceptualized as a sequential process involving microbial ecosystem reconstruction, metabolic recovery, and host functional restoration. These insights provide a mechanistic framework for developing precision microbiome-based interventions and sustainable antibiotic-free strategies to improve intestinal health and production efficiency in modern swine production systems.},
}

Animals
*Probiotics
*Weaning
*Gastrointestinal Microbiome
Swine
*Stress, Physiological
Intestinal Barrier Function

@article {pmid42866484,
year = {2026},
author = {Durão, G and Boyer, E and Bonnaure-Mallet, M and Verin, M and Auffret, M and Meuric, V},
title = {Gut oralisation signatures in Parkinson's disease: an integrative multi-study analysis.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2737700},
pmid = {42866484},
issn = {2000-2297},
abstract = {BACKGROUND: Parkinson's disease (PD) compromises oral hygiene and oral health, potentially increasing oral bacterial input to the gut. Whether PD is associated with reproducible faecal enrichment of oral disease-linked taxa remains unclear.

OBJECTIVE: To determine whether oral disease-linked taxa are enriched in the faecal microbiota of individuals with PD.

METHODS: We conducted a pooled re-analysis of 23 faecal 16S rRNA datasets, comprising 3,594 PD and control samples. eHOMD was used to resolve oral-associated taxa, including caries/endodontic- and periodontitis-linked taxa. SILVA-based profiles were used to assess community diversity and ordination patterns. Differential-abundance analyses accounted for variation between studies.

RESULTS: PD samples showed heterogeneous but reproducible enrichment of oral disease-linked taxa, with a prominent caries/endodontic-associated component. The cariogenic-enriched subgroup showed reduced evenness and increased representation of oral taxa including Streptococcus mutans. Beta-diversity analyses showed substantial PD-control overlap and an oralization-related compositional gradient rather than a discrete PD-specific cluster.

CONCLUSIONS: This pooled re-analysis identifies a gut oralization-associated signal in a subset of individuals with PD. Faecal enrichment of oral-associated taxa may represent one component of gut microbiome heterogeneity and may indirectly reflect variation in oral ecosystem status, supporting oral health assessment in future PD microbiome studies.},
}

@article {pmid42866531,
year = {2026},
author = {Day, AS and Armet, AM and Kamath, S and Joyce, PM and Bryant, RV and Armstrong, HK},
title = {Microbiome-targeted dietary therapy in health and disease: Challenges, opportunities, and pathways forward.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2744027},
pmid = {42866531},
issn = {2993-3935},
abstract = {The gut microbiome has an established role in health and disease, and can be manipulated by diet, positioning microbiome-targeted dietary therapies as potential therapeutics. Mounting evidence supports dietary patterns rich in fermentable fibers and lower in nutrient-poor processed foods; however, there are individual, local, and system-wide complexities to adopting and sustaining dietary change as part of therapeutic dietary strategies. Wider adoption of diet therapy is also limited by critical factors that interfere and influence treatment outcomes, the most significant being inter-individual variability in response to dietary therapy, which remains poorly characterized and understood, hindering advancements in precision nutrition. This review examines the role of the gut microbiome in health and disease and describes barriers and solutions for developing and implementing microbiome-targeted dietary interventions as therapeutic strategies. We organize these barriers into three domains: biological, behavioral, and policy and systems, moving from molecular and individual-level mechanisms to population-level systems, and identify evidence gaps and candidate measurable outcomes to guide future research and dietary guideline development.},
}

@article {pmid42866582,
year = {2026},
author = {Walder, F and Hartman, K and Edlinger, A and Herzog, C and Valzano-Held, AY and Romdhane, S and Philippot, L and Banerjee, S and van der Heijden, MGA},
title = {Compost application more strongly shapes soil fungal than bacterial communities across arable fields.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag259},
pmid = {42866582},
issn = {2730-6151},
abstract = {Organic amendments such as compost are widely promoted for enriching soil microbial communities and supporting key soil functions, yet their effects across diverse farming systems and pedoclimatic conditions remain poorly understood. Most evidence originates from controlled experiments that cannot account for the variability inherent in real agronomic settings. Here, using data from 56 commercially managed wheat fields under different fertilizer regimes (compost, solid digestate, or manure) across Switzerland, we show that compost application reshapes soil microbial communities under real farming conditions. Compost increased fungal diversity, shifted fungal community composition, and markedly enhanced fungal network complexity (+50%), exceeding effects of the overall management system (organic versus conventional). While compost effects were strongest for fungal communities, 13 bacterial and nine fungal taxa also increased in abundance following frequent compost application. We further identified a distinct microbial cluster enriched with compost-responsive taxa, including thermophilic taxa from both bacterial (Thermoactinomycetaceae) and fungal (Thermomyces) lineages characteristic of composting processes, suggesting establishment of compost-derived microbes in agricultural soils. In contrast, solid digestate from biogas plants had weaker and more variable effects on soil microbial communities. Structural equation modelling suggested that compost was associated with higher soil respiration mediated primarily through soil physicochemical properties and to a lesser extent microbial community traits. Together, the results provide evidence that compost application structures soil microbial communities across a wide range of pedoclimatic conditions and management backgrounds within Swiss agroecosystems, supporting its role as an effective practice for strengthening microbially mediated soil processes and promoting sustainable soil management.},
}

@article {pmid42866813,
year = {2026},
author = {Amedorme, D and Addy, H and Osei-Poku, P and Kwarteng, A},
title = {Inferred functional potential of microbial communities in traditional African fermented dairy products using 16S rRNA.},
journal = {Access microbiology},
volume = {8},
number = {10},
pages = {},
pmid = {42866813},
issn = {2516-8290},
abstract = {Background. Africa is home to several indigenous dairy products that span the continent. These dairy products are widely consumed and cherished for their rich nutritional profile and distinctive taste, shaped by microbial fermentation. However, their microbiome remains largely unexplored, thus limiting knowledge of microbial composition, diversity and functional inference. These limitations have implications for product quality and safety and scientific documentation. Methods. The 16S rRNA dataset on five popularly consumed dairy products, Nono, Wara, Kwerionik, Ghee and Nunu, with the SRA accession number PRJNA532858, was collected for taxonomic classification and diversity analysis using the Quantitative Insights into Microbial Ecology 2 pipeline. Functional inference was conducted using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States 2 version 2. Results. In this dataset, an average of 12 phyla were observed, including Firmicutes, Proteobacteria, Actinobacteria and Bacteroidetes. At the genus level, lactic acid bacteria, particularly Lactobacillus and Streptococcus, were predominant in Nono, Wara and Nunu, with relative abundances: 57.7, 33.5 and 39.3% for Lactobacillus and 16.6, 36.7 and 39.5% for Streptococcus. Functional predictions revealed both shared and product-specific metabolic capabilities, with varying taxonomic contributions to key pathways across samples. Conclusion. Across the analysed samples, the products exhibit both conserved and distinct predicted functional signatures inferred from the 16S rRNA gene data. Particularly, those related to ATP-binding cassette transporters, amino acid metabolism, sugar utilization and biosynthetic pathways. Streptococcus dominated in the purine-rich environments of Nono and Nunu; Wara displayed lactic acid bacteria co-dominance, with a focus on peptidoglycan metabolism; Kwerionik exhibited broader microbial diversity, with a three-way taxonomic distribution; and Ghee stood out with Acetobacter-driven lipid and oxidative metabolism, showcasing the community's adaptive plasticity to distinct environmental and processing conditions. These findings suggest that traditional dairy fermentations function as complex microbial ecosystems and highlight their potential importance in food systems and microbial ecology.},
}

@article {pmid42866839,
year = {2026},
author = {Dohoczky, D and Šantić, R and Mustapić, S and Knežević, B and Kumrić, M and Banić, M and Božić, J},
title = {A narrative review of sex-related differences in inflammatory bowel disease-associated cardiovascular and thrombotic risk: epidemiology, mechanisms, and prevention strategies.},
journal = {Translational gastroenterology and hepatology},
volume = {11},
number = {},
pages = {112},
pmid = {42866839},
issn = {2415-1289},
abstract = {BACKGROUND AND OBJECTIVE: Inflammatory bowel disease (IBD) is increasingly recognized as a systemic inflammatory disorder associated not only with gastrointestinal morbidity but also with arterial atherosclerotic cardiovascular disease (ASCVD) and venous thromboembolism (VTE). Although men generally retain a higher absolute cardiovascular event burden in the general population, women with IBD, particularly younger and premenopausal women, may experience a disproportionate relative increase in selected arterial events. This narrative review aimed to summarize sex-related differences in IBD-associated cardiovascular and thrombotic risk, with emphasis on epidemiology, biological mechanisms, and prevention strategies.

METHODS: Targeted searches of PubMed/MEDLINE and major society statements were performed, prioritizing meta-analyses, population-based cohorts, sex-stratified studies, consensus documents, mechanistic studies, and selected clinical trials. Evidence was synthesized narratively across four domains: epidemiology of ASCVD and VTE in IBD, sex-specific risk patterns, mechanistic pathways linking intestinal inflammation to vascular dysfunction and thrombosis, and practical prevention approaches.

KEY CONTENT AND FINDINGS: Available evidence supports a modest but significant increase in arterial cardiovascular risk in IBD and a more pronounced increase in VTE risk, particularly during active disease, hospitalization, corticosteroid exposure, and sustained systemic inflammation. Sex-related differences appear most relevant for relative arterial risk estimates, while interpretation must distinguish relative from absolute risk. Proposed mechanisms include endothelial and microvascular dysfunction, platelet activation, increased thrombin generation, altered estrogen signaling, estrogen receptor beta dysregulation, menopause, exogenous hormone exposure, and the potential contribution of the estrobolome as a gut microbiome-estrogen interface. Additional modifiers include obesity, smoking, pregnancy/postpartum status, and advanced therapies such as JAK inhibitors, whose cardiovascular safety profile remains heterogeneous.

CONCLUSIONS: Cardiovascular prevention in IBD should integrate conventional risk-factor assessment with IBD-specific risk enhancers, careful interpretation of sex-stratified data, aggressive inflammatory control, steroid-sparing treatment, individualized hormone assessment, and appropriate thromboprophylaxis. Future studies should report both relative and absolute cardiovascular risk and better define sex-specific mechanisms and prevention pathways in IBD.},
}

@article {pmid42866850,
year = {2026},
author = {Gu, L and Chen, Y and Jin, L and Liu, Y},
title = {A narrative review of the gut microbiota-testis axis: mechanisms and implications for male reproductive health.},
journal = {Translational andrology and urology},
volume = {15},
number = {9},
pages = {350},
pmid = {42866850},
issn = {2223-4691},
abstract = {BACKGROUND AND OBJECTIVE: Infertility affects approximately 8-12% of couples worldwide, with male factors accounting for nearly half of all cases. The gut microbiota is widely recognized as a key regulator of host physiology, yet its specific role in male reproductive health remains to be elucidated. This narrative review synthesizes current evidence on the "gut microbiota-testis axis" and provides a critical evaluation of the strength of evidence derived from different study designs.

METHODS: We conducted a comprehensive literature search in PubMed/MEDLINE up to May 2026 using Boolean search strategies combining terms related to the gut microbiota (e.g., "Gastrointestinal Microbiome", "gut microbiota", "gut microbiome") with terms related to male reproduction (e.g., "Semen Analysis", "Spermatozoa", "Infertility, Male", "semen quality", "sperm quality"). Separate search strategies were developed for human and animal studies. Literature screening and data extraction were performed independently by two reviewers according to predefined inclusion and exclusion criteria.

KEY CONTENT AND FINDINGS: Although human studies remain preliminary, several genera, including Anaerotruncus, Bacteroides, and Faecalibacterium prausnitzii, have been reproducibly associated with semen quality, with microbial metabolites such as butyrate, trimethylamine-N-oxide (TMAO), and succinate potentially serving as important mediators. At the mechanistic level, microbiota-derived metabolic and inflammatory signals act on Leydig cells, Sertoli cells, and germ cells, thereby influencing testosterone synthesis and spermatogenesis. Fecal microbiota transplantation (FMT) experiments in animal models have provided direct evidence for these causal links.

CONCLUSIONS: The gut microbiota-testis axis has emerged as a critical physiological pathway linking the microbiome to male reproductive function. This review provides an evidence-based framework for understanding this axis and highlights key knowledge gaps that must be addressed. Future research should integrate large-scale longitudinal cohorts, mechanistic exploration, and randomized controlled trials with fertility outcomes as primary endpoints to advance the field from descriptive correlations toward mechanism-driven clinical translation.},
}

@article {pmid42867140,
year = {2026},
author = {Izquierdo, VS and Brauner, CC and Sousa, LM and Rocha, CC and Laporta, J and Peñagaricano, F and Binelli, M and Bittar, JHJ and Burdick Sanchez, NC and Cooke, RF and Vendramini, JMB and Moriel, P},
title = {Gestational heat stress alters maternal vaginal microbiome, plasma metabolic markers, and preweaning offspring performance in Bos indicus-influenced cow-calf pairs.},
journal = {Journal of animal science},
volume = {},
number = {},
pages = {},
doi = {10.1093/jas/skag335},
pmid = {42867140},
issn = {1525-3163},
abstract = {This 3-year study evaluated the effects of gestational access to shade on maternal performance, vaginal microbiome composition, and offspring preweaning performance in beef cows. On day 0 of each year (92 ± 20 days prepartum), 176 multiparous, pregnant Brangus crossbred beef cows (25 to 37.5% Bos indicus) were stratified by bull, body weight (BW; 548 ± 51 kg) and body condition score (BCS; 5.52 ± 0.70; scale of 1 to 9), and randomly assigned to 1 of 16 bahiagrass (Paspalum notatum) pastures (11 cows and 8.1 ha per pasture). Treatments were randomly assigned to pastures on day 0 of each year (8 pastures per treatment) and consisted of cows provided (SH) or not (NSH) access to artificial shade (3.27 m2 per cow) from day 0 to 90. Cows were provided free-choice access to artificial shade from day 91 until calf weaning on day 330 (240 ± 20 days of age). Non-binary and binary data were analyzed as a complete randomized study using the MIXED and GLIMMIX procedure of SAS, respectively. Effects of treatment × day × year and treatment × year were not detected (P ≥ 0.11) for any variable, except for calf preweaning BW (P = 0.01). Shade access improved (P ≤ 0.05) cow BCS on days 30, 60, and 150 and modified plasma metabolites, including lower cortisol on day 30 and greater glucose and IGF-1 but lower urea nitrogen on day 60. Shade also reduced (P ≤ 0.05) body surface and rectal temperatures on day 60, respiration rates, and intravaginal temperatures from 1000 to 1400 h. Plasma non-esterified fatty acids, whole blood mRNA expression of heat shock proteins, and reproductive success did not differ (P ≥ 0.12) between treatments. Relative abundance of Blautia and Methanobrevibacter on day 30 were greater (P ≤ 0.05) in SH vs. NSH cows. At birth, gestational access to shade did not impact (P ≥ 0.41) calf plasma cortisol and serum immunoglobulin G but increased (P ≤ 0.05) calf plasma haptoglobin and BW. At weaning, calf BW was greater (P ≤ 0.04) in year 1 but was less (P = 0.05) in years 2 and 3 for NSH vs. SH calves. In conclusion, gestational shade access improved maternal thermoregulation, body condition, and metabolic profile, while modestly shifting the prepartum vaginal microbiome. These maternal responses were accompanied by greater calf birth weight, although weaning performance varied by year, underscoring the dynamic nature of gestational heat stress impacts in subtropical grazing systems.},
}

@article {pmid42867154,
year = {2026},
author = {Zhang, Y and Wang, J and Shen, J and Galloway-Peña, J and Shelburne, S and Wang, L and Hu, J},
title = {Inverse probability weighting-based mediation analysis for microbiome data.},
journal = {Bioinformatics (Oxford, England)},
volume = {},
number = {},
pages = {},
doi = {10.1093/bioinformatics/btag750},
pmid = {42867154},
issn = {1367-4811},
abstract = {MOTIVATION: Mediation analysis is an important tool for elucidating causal mechanisms in biomedical research and has recently gained increasing attention in microbiome studies. Motivated by a microbiome study of acute myeloid leukemia (AML) patients, we investigate whether the effect of induction chemotherapy intensity on infection status is mediated through gut microbial taxa. This problem poses substantial methodological challenges due to the high dimensionality, zero inflation, and dependence of microbial mediators, as well as the presence of an exposure-induced mediator-outcome confounder, antibiotic use.

RESULTS: To address these challenges, we propose a novel nonparametric identification formula for the interventional indirect effect, a causal mediation estimand that remains identifiable in the presence of exposure-induced mediator-outcome confounding. Building on this identification result, we develop an inverse probability weighting estimator and construct standard normal bootstrap confidence intervals for inference. Simulation studies demonstrate that the proposed method achieves accurate effect estimation and maintains appropriate type I error rates and power in finite samples. Application to the AML microbiome study provides evidence of a statistically significant interventional indirect effect of induction chemotherapy intensity on infection risk through alterations in the gut microbiome.

The R code for the simulation studies is available at https://github.com/YX-ZHANG-1/CausalMediationMicrobiome and archived on Zenodo at https://doi.org/10.5281/zenodo.21960802.},
}

@article {pmid42867185,
year = {2026},
author = {Jang, S and Yang, H and Lee, S and Kim, P and Yun, BS and Kim, D and Ryu, CM},
title = {Silicate fertilizer mitigates methane emissions from rice paddies by enriching Burkholderia to modulate microbial interactions.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag255},
pmid = {42867185},
issn = {1751-7370},
abstract = {Methane emissions from rice paddies are a major source of greenhouse gases, and silicate fertilizer (SF) derived from blast furnace slag has emerged as an environmentally friendly amendment that reduces methane release. SF modifies the soil redox environment by supplying electron acceptors such as iron, but the microbial mechanisms underlying methane mitigation remain unclear. Here, we combined metagenomic profiling, microbial isolation, and greenhouse experiments to show that SF consistently enriched Burkholderia vietnamiensis together with the methanotrophs in the rice rhizosphere. Inoculation of B. vietnamiensis strain HU01 alone reproduced the methane-suppressing effect of SF and increased methanotroph abundance. Cell-free culture supernatants of HU01 stimulated the growth of Methylococcus geothermalis and Methylocystis parvus through secreted, low-molecular-weight, heat-stable metabolites. Although metabolic modeling predicted primary metabolites such as L-glutamate and cobalamin as candidate cross-feeding factors, LC-MS/MS analysis of the highly active fractions indicated that the robust bioactivity was primarily driven by a chemically complex metabolite mixture rather than these ubiquitous single compounds. These results provide direct evidence that enrichment of a single heterotrophic species can enhance methane oxidation by stimulating methanotroph activity through metabolite exchange. B. vietnamiensis HU01 represents a promising microbial resource for methane mitigation and illustrates how targeted heterotroph-methanotroph interactions can be leveraged for climate-smart rice cultivation.},
}

@article {pmid42867188,
year = {2026},
author = {Chen, W and Yang, F and Wu, B and Xiang, G and Lu, X and Ma, J and Xu, Y and Mo, L and Sun, X and He, J},
title = {Harnessing the Bacterial Membrane-Derived Oral Vaccine to Potentiate Antitumor Immunity and Metabolic Control of T Cells.},
journal = {Advanced materials (Deerfield Beach, Fla.)},
volume = {},
number = {},
pages = {e75342},
doi = {10.1002/adma.75342},
pmid = {42867188},
issn = {1521-4095},
support = {82674954//National Natural Science Foundation of China/ ; 32601842//National Natural Science Foundation of China/ ; W2611112//National Natural Science Foundation of China/ ; U24A20676//National Natural Science Foundation of China/ ; 82270923//National Natural Science Foundation of China/ ; //Innovation Group Project/ ; 2023NSFSC1993//Science and Technology Department of Sichuan Province/ ; DSQZ-ZD-20250104//State Key Laboratory of Advanced Drug Delivery and Release Systems/ ; //National Clinical Research Center for Geriatrics/ ; Z2024YY003//West China Hospital, Sichuan University/ ; HXQMX0118//"Qimingxing" Research Fund for Young Talents/ ; ZYGD24006//1.3.5 Project for Disciplines of Excellence/ ; 2026NSFSC0565//Sichuan Provincial Science and Technology Support Program/ ; },
abstract = {The fluctuating gastrointestinal milieu and its restrictive epithelial barrier represent critical challenges for the design of oral cancer vaccines. Nevertheless, leveraging the gut microbiome as an interventional strategy has recently gained traction, especially in patients on immune checkpoint inhibitor (ICI) therapy. Here, microbial-derived double-layered membrane vesicles are developed as adjuvants and cell-free carriers, fused with cell-penetrating peptide-modified antigens, and encapsulated in an alginate/chitosan-microsystem to engineer oral vaccines. This design strategically harnesses the crosstalk between the gut microbiome and gut-associated lymphoid tissues, driving dendritic cell maturation, plasma cell activation, and production of immune-stimulatory cytokines within the mesenteric lymph nodes and lamina propria. In mouse prophylactic and therapeutic tumor models, the select Bifidobacterium bifidum-derived oral vaccine combined with anti-PD1 treatment enhances cytotoxic antitumor responses, along with Th1-, Th17-immunity, leading to potent tumor suppression, prolonged survival, and long-term protection against tumor rechallenge. Mechanistically, the vaccine promotes interferon-γ-producing T cells and antitumor efficacy with ICI therapy via the improved microbiota diversity and signaling metabolites, with an indole-3-acetic-acid (3IAA) enriched diet profoundly shaping T-cell recruitment and differentiation. Our findings uncover a tryptophan metabolite-driven immune axis that amplifies the specific antitumor immune response, redefining oral vaccines as a powerful tool for cancer immunotherapy.},
}

@article {pmid42867216,
year = {2026},
author = {Palmer, MA and Garland, MJ and Hanna, H and Richmond, A and O'Connell, NE},
title = {Changes in the broiler litter bacterial microbiome during production on UK farms.},
journal = {Journal of applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jambio/lxag253},
pmid = {42867216},
issn = {1365-2672},
abstract = {AIM: The management and characteristics of broiler chicken litter are important for bird health and production. The bacterial community within the litter is an area of increasing interest. This work aimed to develop a profile of the bacterial microbiota in broiler litter throughout production on UK commercial farms.

METHODS AND RESULTS: Litter samples were taken from broiler houses on six UK farms during two consecutive production cycles. Sampling points were in the Early (day 5-10), Mid (day 25-30) and Late (post-thin, day 32-42) parts of the cycle. Three of the farms used wood shavings litter, two used straw crumb and one used cut straw. Bacterial community composition was determined using 16 s rRNA amplicon sequencing (v3-v4). Functional potential was predicted from this using PICRUSt2. The bacterial community composition (and predicted functional potential) was most variable at the Early sampling point and changed between the Early and Mid points. The relative abundance of seven of the ten most abundant bacterial genera also changed between the Early and Mid points, but not between the Mid and Late points.

CONCLUSIONS: Results of this applied study demonstrate changes in the community composition and predicted metabolic potential of the bacterial microbiome in broiler litter during the production cycle on UK commercial farms.},
}

@article {pmid42867232,
year = {2026},
author = {Zavos, C},
title = {Dental Status and the Reflux Microbiome.},
journal = {Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery},
volume = {},
number = {},
pages = {},
doi = {10.1002/ohn.70487},
pmid = {42867232},
issn = {1097-6817},
}

@article {pmid42858690,
year = {2026},
author = {Guler Cekic, S and Vatansever, C and Akpinar, A and Belge, S and Shahrokhi, G and Unal, C and Altintas, A and Aydin, S and Can, F},
title = {Interactions between vaginal, periurethral and urinary microbiota in genitourinary syndrome of menopause and the effects of local estrogen therapy.},
journal = {Maturitas},
volume = {214},
number = {},
pages = {109146},
doi = {10.1016/j.maturitas.2026.109146},
pmid = {42858690},
issn = {1873-4111},
abstract = {OBJECTIVES: Alterations to the vaginal microbiota have been investigated in genitourinary syndrome of menopause but data regarding periurethral and urinary microbiota remain limited. We aimed to characterize vaginal, periurethral, and urinary microbiota in clinically stratified postmenopausal women and to evaluate the effects of estrogen therapy.

STUDY DESIGN: In this prospective study, postmenopausal women were categorized as controls without atrophy or symptoms, women with clinical atrophy without symptoms, symptomatic women, and symptomatic women receiving 12 weeks of vaginal estriol. Vaginal, periurethral, and bladder samples were collected.

MAIN OUTCOME MEASURES: Microbiota composition and diversity (alpha diversity - Shannon index; and beta diversity - Bray-Curtis dissimilarity) across urogenital niches and changes in these following estrogen therapy.

RESULTS: Vaginal and periurethral alpha diversity was higher in women with asymptomatic atrophy and symptomatic women at baseline than in controls and estrogen-treated women. Beta diversity analyses demonstrated separation of controls and estrogen-treated women from the atrophy groups at baseline. Controls exhibited Lactobacillus-enriched periurethral communities and Klebsiella-dominant urinary profiles. Women with asymptomatic atrophy and symptomatic women showed reduced Lactobacillus and increased anaerobic taxa in vaginal and periurethral niches, while urinary samples were characterized by Escherichia predominance. Notably, in women with asymptomatic atrophy, Lactobacillus abundance was higher in periurethral than vaginal samples. Estrogen therapy increased Lactobacillus abundance in vaginal and periurethral compartments and shifted urinary microbiota toward a control-like composition. Periurethral Streptococcus abundance correlated with sexual symptom scores.

CONCLUSIONS: Microbial alterations in genitourinary syndrome of menopause are compartment-specific and extend beyond the vagina. Periurethral microbiota may contribute to symptom expression, while local estrogen therapy promotes restoration of Lactobacillus-dominant urogenital microbiota.

CLINICALTRIALS: gov registration: NCT06633705.},
}

@article {pmid42858922,
year = {2026},
author = {Eftekharian, S and Rastkar, S},
title = {The Oral Microbiome in the Biological and Clinical Response to Photobiomodulation During Cancer Supportive Care: A Critical Mechanistic and Translational Review.},
journal = {Photodiagnosis and photodynamic therapy},
volume = {},
number = {},
pages = {105682},
doi = {10.1016/j.pdpdt.2026.105682},
pmid = {42858922},
issn = {1873-1597},
abstract = {Cancer therapy can disrupt the oral microbial ecosystem through mucosal injury, salivary dysfunction, immune suppression, antimicrobial exposure, dietary change, and altered oral hygiene. Photobiomodulation therapy (PBMT) is guideline-supported for prevention of oral mucositis in selected oncologic settings, but whether the oral microbiome contributes to PBMT response remains uncertain. This critical narrative review reframes the question from whether PBMT changes the oral microbiome to what role, if any, microbial ecology plays in the biological and clinical response to PBMT during cancer supportive care. Evidence is organized as direct clinical evidence, indirect clinical evidence, experimental microbial evidence, and mechanistic hypothesis. Direct clinical evidence is sparse and internally mixed: a four-patient uncontrolled pilot reported concurrent cytokine and microbiome shifts after PBMT, whereas a 2023 head-and-neck cancer case series reported clinical improvement in mucositis without significant pre-post changes in salivary bacterial community structure. The strongest current rationale therefore supports a host-first model in which PBMT modifies epithelial integrity, inflammatory and redox signaling, tissue repair, and possibly salivary physiology, thereby changing the ecological conditions experienced by oral microorganisms. Direct microbial photobiological effects remain plausible but are highly dependent on wavelength, irradiance, radiant exposure, oxygen availability, organism, and biofilm state, and should not be conflated with antimicrobial photodynamic therapy. We propose four non-equivalent roles for microbiome change: mediator, modifier, biomarker, or consequence of treatment response. Oral mucositis is the most informative clinical model, but causal interpretation requires longitudinal sampling, functional microbial assays, complete PBMT dosimetry, validated clinical and patient-reported outcomes, and rigorous control of antimicrobials, periodontal status, oral hygiene, diet, feeding support, and anticancer treatment. Microbiome modulation should currently be regarded as an emerging mechanistic hypothesis and research endpoint rather than an established mechanism of PBMT efficacy.},
}

@article {pmid42859003,
year = {2026},
author = {Dong, L and Luo, S and Misbahullah, SM and Xu, J and Wan, S and Gao, H and Qin, Z},
title = {Polymerization-dependent gut microbiome responses to curdlan β-1,3-glucan and its oligosaccharides.},
journal = {Food research international (Ottawa, Ont.)},
volume = {244},
number = {},
pages = {120524},
doi = {10.1016/j.foodres.2026.120524},
pmid = {42859003},
issn = {1873-7145},
mesh = {*beta-Glucans/metabolism/chemistry ; Humans ; *Gastrointestinal Microbiome/drug effects/physiology ; Feces/microbiology ; *Oligosaccharides/metabolism/chemistry ; Polymerization ; Fermentation ; Dietary Fiber/metabolism ; Fatty Acids, Volatile/metabolism ; Glucose/metabolism ; RNA, Ribosomal, 16S/genetics ; },
abstract = {β-1,3-Glucan is a dietary fiber with microbiome-modulating potential, yet the role of polymerization degree on microbial composition and metabolism remains unclear. Curdlan is an insoluble linear β-1,3-glucan widely used as a food hydrocolloid that provides a model to examine structure-dependent microbiome responses. We compared glucose, curdlan (CBG), and curdlan-derived β-1,3-glucan oligosaccharides (OBG) using anaerobic in vitro fermentation of pooled human feces. A multi-omics approach integrating 16S rRNA sequencing, shotgun metagenomics, short-chain fatty acid (SCFA) quantification, and untargeted metabolomics was applied to resolve taxonomic, functional, and metabolic shifts. Both CBG and OBG enriched Bacteroidota and enhanced carbohydrate metabolism relative to glucose, but through distinct pathways. CBG promoted polymer-associated carbohydrate processing, with enrichment of β-1,3-glucan-degrading enzymes such as GH16, Sus-like transport systems, and polysaccharide-specialized taxa (e.g., Prevotella and Bifidobacterium), and butyrate production. In contrast, OBG favored transporter-mediated substrate uptake, broader microbial participation (e.g. Parabacteroides and Enterobacteriaceae), and a metabolite profile enriched in amino acid-derived compounds and branched-chain SCFAs. These findings demonstrate that β-1,3-glucan polymerization degree governs microbiome functional routing and highlight polymerization degree as a tunable parameter for designing microbiome-directed carbohydrate ingredients with predictable metabolic outcomes.},
}

*beta-Glucans/metabolism/chemistry
Humans
*Gastrointestinal Microbiome/drug effects/physiology
Feces/microbiology
*Oligosaccharides/metabolism/chemistry
Polymerization
Fermentation
Dietary Fiber/metabolism
Fatty Acids, Volatile/metabolism
Glucose/metabolism
RNA, Ribosomal, 16S/genetics

@article {pmid42859016,
year = {2026},
author = {Ji, Q and Qu, H and Chen, D and Li, Q and Zong, L and Liu, Y and Huang, Y and Gu, R},
title = {Matrix-associated spatial structure contributes to compositional stability of a complex multispecies starter culture under microbial perturbation: Insights from kefir grains.},
journal = {Food research international (Ottawa, Ont.)},
volume = {244},
number = {},
pages = {120540},
doi = {10.1016/j.foodres.2026.120540},
pmid = {42859016},
issn = {1873-7145},
mesh = {*Kefir/microbiology ; Fermentation ; *Food Microbiology/methods ; *Microbiota ; Cultured Milk Products/microbiology ; },
abstract = {Complex multispecies starter cultures can enrich the metabolic and sensory diversity of fermented foods, but industrial use is limited by compositional drift, overgrowth of dominant taxa, and vulnerability to exogenous microbial contamination. Kefir grains (KG), a matrix-encapsulated complex starter culture with stable serial propagation, provide a model for how spatial structure contributes to starter stability. We compared matrix-associated KG with free kefir-fermented milk (FKFM), representing a grain-free liquid-phase kefir microbial community, under a large-scale microbial challenge. During the acute 24 h challenge, target-taxon drift estimated from PMA-qPCR data was lower in KG than in the liquid compartments. Ten-generation serial transfer caused stronger community restructuring and Shannon diversity loss in FKFM, whereas KG showed constrained compositional adjustment and remained relatively clustered in Bray-Curtis ordination space. Species-level metagenomic tracking showed broader expansion, retention, and cumulative drift of species-level signals corresponding to exogenous challenge strains in FKFM, while more of these signals in KG followed restricted/stable trajectories. Kefir cell-free supernatant inhibited multiple challenge strains beyond the effect of low pH, indicating a contribution of diffusible inhibitory factors. SEM and live/dead staining revealed rough matrix-associated surfaces and heterogeneous cell states in KG. Together, the results support a model in which spatial structure, prior niche occupancy, and diffusible inhibition jointly contribute to the compositional stability and anti-perturbation capacity of this complex starter culture, informing the design of spatially structured synthetic starter consortia for industrial fermentation.},
}

*Kefir/microbiology
Fermentation
*Food Microbiology/methods
*Microbiota
Cultured Milk Products/microbiology

@article {pmid42859175,
year = {2026},
author = {Khan, I and Khan, I and Noor, U and Irfan, M and Zhiqiang, L},
title = {Artificial intelligence in human microbiome research: from data integration to explainable translation.},
journal = {Archives of microbiology},
volume = {209},
number = {1},
pages = {},
pmid = {42859175},
issn = {1432-072X},
mesh = {Humans ; *Artificial Intelligence ; *Microbiota ; Multiomics ; Precision Medicine ; Translational Research, Biomedical ; Machine Learning ; Genomics ; },
abstract = {The human microbiome is integral to health, metabolism, immunity, and physical protection, with dysbiosis linked to metabolic disorders, autoimmune conditions, and cancer. High-throughput sequencing has generated massive datasets, but analyzing these complex, multidimensional data poses significant challenges. Artificial intelligence (AI), including machine learning, deep learning, and related approaches, offers powerful solutions for data integration, pattern recognition, functional annotation, and predictive modeling. AI applications in microbiome research include identifying microbial biomarkers, predicting disease susceptibility, elucidating microbial interactions, and optimizing personalized interventions. AI also enables integration of microbiome data with host genomics, transcriptomics, and clinical metadata, providing a holistic view of host-microbiome dynamics. Despite advances, challenges such as data heterogeneity, model interpretability, and limited sample sizes remain. This narrative review synthesizes literature from 2015 to 2025 without a formal systematic methodology. We conclude with three priority areas for AI-microbiome translation: improved interpretability, longitudinal modeling, and clinical integration. Leveraging AI in this field holds significant promise for accelerating precision medicine, improving diagnostics, and developing microbiome-targeted therapies, if interpretability and validation challenges are addressed.},
}

Humans
*Artificial Intelligence
*Microbiota
Multiomics
Precision Medicine
Translational Research, Biomedical
Machine Learning
Genomics

@article {pmid42859354,
year = {2026},
author = {Yu, S and Zheng, W and Pan, Y and Chen, L and Ma, J and Gao, M and Zou, W and Lu, Y and Zhao, Y},
title = {Cerebral cavernous malformations: epidemiology, molecular pathogenesis, diagnosis and therapy.},
journal = {Molecular biomedicine},
volume = {7},
number = {1},
pages = {},
pmid = {42859354},
issn = {2662-8651},
support = {82274233//National Natural Science Foundation of China/ ; BK20240146//Natural Science Foundation of Jiangsu Province/ ; 22KJA360007//Natural Science Research of Jiangsu Higher Education Institutions of China/ ; ZD202403//Jiangsu Province Traditional Chinese Medicine Science and Technology Development Plan Key Project/ ; },
mesh = {Humans ; *Hemangioma, Cavernous, Central Nervous System/therapy/epidemiology/diagnosis/genetics ; Animals ; Mutation ; },
abstract = {Cerebral cavernous malformations (CCMs) are cerebrovascular diseases characterized by vascular lesions of the central nervous system (CNS) that can result in epileptic seizures, headaches, focal neurologic deficits (FNDs), and hemorrhagic stroke. Germline and somatic loss-of-function (LOF) mutations in one of the three established CCM-associated genes, namely CCM1 (or krev interaction trapped protein 1, KRIT1), CCM2, and CCM3 (or programmed cell death 10, PDCD10), which have been validated as core drivers of CCM pathogenesis and progression. Over the past few decades, a substantially improved understanding of the hallmarks and molecular basis of CCMs has been achieved. Key pathological hallmarks include but are not limited to excessive angiogenesis, vascular leakage, endothelial-mesenchymal transition (EndMT), defective autophagy, inflammation and immune response, oxidative stress, influenced gut microbiome and altered brain vascular microenvironment. These hallmarks are orchestrated by dysregulated signaling cascades, notably MEKK3-KLF2/4, PI3K-mTOR, and RhoA-ROCK, which integrate genetic, inflammatory, and hemodynamic cues. Concurrently, sophisticated neuroimaging (MRI with SWI/QSM) and genetic testing now enable precise diagnosis and risk stratification. Although surgical resection remains the mainstay for accessible symptomatic lesions, a wave of mechanism‑based pharmacological candidates has shown promising efficacy in preclinical models, and several have advanced to early‑phase clinical trials. This review summarizes the current understanding of CCM epidemiology, molecular pathogenesis, diagnosis and therapy, highlighting how the evolving multi‑hit concept and the dissection of downstream signaling are paving the way towards personalized management of this complicated vascular disease.},
}

Humans
*Hemangioma, Cavernous, Central Nervous System/therapy/epidemiology/diagnosis/genetics
Animals
Mutation

@article {pmid42859437,
year = {2026},
author = {Saimee, Y and Okada, R and Inoue, D and Ike, M},
title = {Characterization of duckweed-associated bacteria from the Wolffia globosa microbiome: Strain-level effects on host growth and key determinants.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {508-525},
pmid = {42859437},
issn = {2471-1888},
abstract = {Wolffia, a rootless duckweed in the family Lemnaceae, is increasingly recognized as a sustainable bioresource for food, animal feed, bioenergy, and biomaterials. Its productivity depends strongly on the associated microbiome, yet the functional roles of individual duckweed-associated bacteria (DAB) remain poorly understood. In this study, we evaluated the effects of DAB isolated from Wolffia globosa microbiomes on host plant growth and characterized their physiological traits. A total of 98 DAB strains were isolated from seven W. globosa microbiomes and individually co-cultivated with W. globosa, exhibiting diverse effects on host growth ranging from promotion to inhibition, with -14.6 to +12.9% of final effects on plant growth. Ten strains consistently promoted host growth and nine strains inhibited growth, which were identified as plant growth-promoting and growth-inhibiting bacteria, respectively. Of these, seven and four strains were identified within the core taxa of W. globosa microbiomes. At the community level, growth-promoting strains tended to be enriched in the growth-promoting microbiomes, whereas neutral or negative strains appeared to be enriched in the growth-inhibiting microbiomes. Taxonomic evaluation demonstrated that prominent promotive and inhibitory phenotypes occurred across six and five genera, respectively, with strain-level characteristics likely determining plant growth effects. Indole-related compound production by DAB emerged as a key physiological determinant associated with Wolffia growth. These findings provide a traceable strain set to advance our understanding of Wolffia-microbiome interactions and offer practical clues on microbiome engineering strategies to enhance Wolffia biomass productivity.},
}

@article {pmid42859514,
year = {2026},
author = {Khanday, S and Darmaki, AA and Malahifci, R and Alvavi, R and Ahmed, S and Nasr, DS},
title = {Gut microbiota and the gut-brain axis in autism spectrum disorder and attention-deficit/hyperactivity disorder: A scoping review of shared and disorder-specific mechanistic pathways.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {548-563},
pmid = {42859514},
issn = {2471-1888},
abstract = {BACKGROUND: Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are among the most prevalent neurodevelopmental conditions worldwide, yet the biological mechanisms driving their onset and phenotypic variability remain incompletely understood. The gut-brain axis (GBA), a bidirectional network linking intestinal microbial communities to central nervous system function through endocrine, immune, neural, and metabolic pathways, has emerged as a candidate mechanism through which environmental factors interact with genetic susceptibility to shape neurodevelopmental outcomes.

OBJECTIVE: To systematically map the peer-reviewed evidence on gut microbiome-related mechanistic pathways in ASD and ADHD, we delineated features common to both disorders and identified areas of divergence and knowledge gaps requiring further investigation.

METHODS: A scoping review was performed following the PRISMA Extension for the Scoping Reviews (PRISMA-ScR) framework. PubMed, Scopus, and Google Scholar were searched for peer-reviewed studies published January 2018 through March 2025. Studies addressing gut microbiome composition, GBA signaling, or microbiome-directed interventions in ASD or ADHD were eligible for inclusion. Extracted data were synthesized using inductive thematic analysis via Covidence software.

RESULTS: Forty-five studies satisfied the eligibility criteria. Inductive analysis produced five mechanistic themes: Endocrine dysregulation and microbial metabolite signaling; neuronal signaling and neurotransmitter modulation; immune activation and neuroinflammation; gene-microbiota-environment interactions; and microbiota-targeted interventions. Studies on both disorders demonstrated modifications involving taxa with short-chain-fatty-acid-producing capacity; however, findings were varied and did not prove a common reduction in butyrate production. ASD was marked by pronounced dysregulation of the serotonergic system and tryptophan-kynurenine pathway and increased hypothalamic-pituitary-adrenal (HPA) axis responsiveness. On the other hand, the results in ADHD were majorly cross-sectional or preliminary, and the widely-m recognized dopaminergic dysfunction in ADHD has not been associated to specific microbiota alterations to date.

CONCLUSIONS: Evidence demonstrates the GBA as a useful research conceptual for investigating ASD and ADHD, although the strength of mechanistic evidence differs substantially between the two disorders. Translating these insights into therapeutic strategies will require longitudinal, multi-omic research designs capable of establishing causality and enabling patient stratification for precision microbiome-based interventions.},
}

@article {pmid42859518,
year = {2026},
author = {Wang, F and Zhang, S and Xu, L and Qian, J and Zou, B and Huo, S and Ma, A and Zhuang, G},
title = {Biocontrol of phytopathogenic fungi by Bacillus spp.: Strain screening, regulatory mechanisms, and field application.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {564-594},
pmid = {42859518},
issn = {2471-1888},
abstract = {Bacillus species, which are among the most extensively studied and widely used rhizobacteria, have demonstrated potent antagonistic activity against a broad spectrum of phytopathogenic fungi, making them ideal microorganisms for biological control. Phytopathogenic fungi cause severe preharvest and postharvest losses in global crop production, significantly reducing yield and quality. The prolonged and heavy reliance on traditional chemical fungicides has resulted in environmental pollution and poses risks to human health. In this context, Bacillus-based biological control has emerged as an environmentally friendly, cost-effective, and sustainable alternative strategy. In this review, we provide a comprehensive overview of the screening of Bacillus strains for the biocontrol of phytopathogenic fungi. The possible mechanisms, including the production of a wide array of antifungal metabolites, the induction of systemic resistance in host plants, and indirect suppression through competition for nutrients and space, were also evaluated. Furthermore, the effects of multistrain synergistic consortia and the development of multifunctional Bacillus strains on biocontrol efficacy are discussed, and research advances in the application of Bacillus spp. in the control of soilborne diseases and phytopathogenic fungi are summarized. Finally, this review provides suggestions for the development of efficient Bacillus-based biocontrol agents, thereby promoting sustainable agricultural development.},
}

@article {pmid42859529,
year = {2026},
author = {Celeski, M and Marchetta, M and Sammartini, E and Sorropago, A and Basile, M and Morello, M and Salzillo, C and Bernardi, M and Mollo, P and Romeo, FJ and Cesaro, A and Golino, M},
title = {Inflammation After Transcatheter Aortic Valve Implantation: Mechanisms, Risk Stratification, and Therapeutic Implications.},
journal = {Reviews in cardiovascular medicine},
volume = {27},
number = {9},
pages = {52850},
pmid = {42859529},
issn = {2153-8174},
abstract = {Transcatheter aortic valve implantation (TAVI) elicits a sterile inflammatory response that is almost universal, yet highly heterogeneous in both magnitude and clinical impact. Initiated by endothelial injury, ischemia-reperfusion, and residual bioprosthetic immunogenicity, peri-procedural inflammation converges on activation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and downstream interleukin-1β (IL-1β) and IL-6 signaling, leading to increased C-reactive protein levels. This response is further modulated by patient susceptibility, procedural complexity, and device-specific characteristics. While a controlled response promotes tissue repair and healing, exaggerated activation, which manifests as systemic inflammatory response syndrome in up to two-thirds of patients, has been consistently associated with higher mortality, conduction disturbances, new-onset atrial fibrillation, acute kidney injury (AKI), and subclinical leaflet thrombosis. Emerging evidence also implicates gut microbiome-derived metabolites and xenoantigen-driven adaptive immunity as additional contributors to the overall inflammatory burden. Serial biomarker assessment, including C-reactive protein trajectories, neutrophil-to-lymphocyte ratio, cancer antigen 125 (CA-125), and novel composite indices such as the neutrophil percentage-to-albumin ratio, combined with multimodality imaging, allows increasingly refined risk stratification. However, no anti-inflammatory therapy is currently established for routine use after TAVI. Colchicine has shown proof-of-concept signals, sodium-glucose cotransporter 2 inhibitors have demonstrated clinical benefit with pleiotropic anti-inflammatory properties, and lessons from IL-1 and IL-6 inhibition trials in ischemic heart disease provide a translational roadmap. This narrative review synthesizes the epidemiology, mechanisms, clinical consequences, and assessment of peri-TAVI inflammation. Moreover, this review proposes a pragmatic inflammatory subphenotyping framework that integrates baseline risk, procedural exposure, and biomarker kinetics. Such a framework may help bridge the gap between observational associations and precision-based therapeutic strategies, shifting peri-TAVI inflammation from a prognostic marker to a modifiable determinant of outcome.},
}

@article {pmid42859540,
year = {2026},
author = {Li, Y and Mo, C and Xie, Y and Huang, Z and Chen, L and Xie, X and Luo, J and Huang, S and Jiang, S and Zhang, T and Zhang, J and Wu, R and Wu, Q},
title = {The stone-degrading metabolic potential of the urinary microbiome: Sexual dimorphism and dysbiosis in urolithiasis.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {595-609},
pmid = {42859540},
issn = {2471-1888},
abstract = {Urolithiasis is a prevalent global health burden characterized by high recurrence rates and marked sexual dimorphism. While the gut microbiome's role in oxalate degradation is established, the functional capacity of the local urinary microbiome remains largely unexplored. This study investigated the composition and function of the urinary microbiome in 40 healthy volunteers and 61 urolithiasis patients using 16S rRNA amplicon sequencing, alongside a retrospective analysis of stone composition in 2027 patients. We identified a diverse, ecologically structured microbiome in healthy urine dominated by genera such as Lactobacillus, Streptococcus, and Gardnerella. Significant sex-dependent differences were observed: While males exhibited higher microbial α-diversity, females demonstrated a distinct compositional structure with superior predicted functional capacity for stone degradation. Specifically, the female microbiome was enriched with enzymes including oxalyl-CoA decarboxylase, formyl-CoA transferase, urate oxidase, and purine nucleosidase. Correlation analysis identified Lactobacillus, Enterococcus, and Gardnerella as key contributors to this litholytic potential. Conversely, urolithiasis patients displayed significant dysbiosis, characterized by disrupted microbial networks and a marked reduction in these stone-degrading enzymes. Clinical data supported these findings, revealing a significantly higher prevalence of uric acid stones in males, consistent with their lower microbial degradation capacity. These findings suggest that the healthy urinary microbiome functions as a metabolically active defense system against stone formation. The observed sex-specific variations in microbial composition and enzymatic function provide a novel mechanistic explanation for the epidemiological sex disparities in urolithiasis, highlighting the urinary-kidney axis as a potential therapeutic target.},
}

@article {pmid42859560,
year = {2026},
author = {Dewan, A and Goulart, DB and Mascellino, MT},
title = {Gut microbiota dysbiosis: Pathogenic drivers and emerging phage-based therapeutics.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {632-665},
pmid = {42859560},
issn = {2471-1888},
abstract = {Gut microbiota dysbiosis driven by pathogenic and opportunistic bacteria, including Clostridioides difficile, adherent-invasive Escherichia coli (AIEC), Salmonella enterica serovar Typhimurium, Fusobacterium nucleatum, Klebsiella pneumoniae, Enterococcus faecalis, and Campylobacter spp., disrupts colonization resistance, epithelial barrier integrity, and immune homeostasis, thereby contributing to the development of inflammatory and metabolic diseases. In this review, we summarize the mechanisms through which these microorganisms promote gut dysbiosis and critically evaluate current microbiome-targeted therapeutic strategies, including fecal microbiota transplantation (FMT), live biotherapeutic products (LBPs), probiotics, and bacteriophage (phage) therapy. We review the preclinical and emerging clinical evidence supporting phage-based targeting of major dysbiosis-associated pathogens and examine the principal challenges limiting clinical translation, including phage resistance, immune-mediated clearance, safety considerations related to temperate phages, manufacturing and delivery constraints, and regulatory barriers. Although evidence remains predominantly preclinical, advances in phage engineering, artificial intelligence-guided phage selection, and systems-level microbiome modeling are expanding the potential of personalized phage therapeutics. Collectively, these developments position bacteriophage therapy as a promising addition to future microbiome-directed strategies for restoring gut microbial homeostasis and managing dysbiosis-associated disease.},
}

@article {pmid42859703,
year = {2026},
author = {Bateman, A},
title = {Peer Bork (1963-2026): pioneer of computational biology, architect of bioinformatics resources, and visionary microbiome researcher.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag227},
pmid = {42859703},
issn = {2635-0041},
}

@article {pmid42859978,
year = {2026},
author = {Gulyás-Oldal, V and Patay, G and Dézsi, C and Bezzegh, A and Szili, K},
title = {[The gut-muscle axis and the role of Roseburia inulinivorans in age-related muscle loss: a narrative review].},
journal = {Orvosi hetilap},
volume = {167},
number = {41},
pages = {1646-1654},
doi = {10.1556/650.2026.33641},
pmid = {42859978},
issn = {1788-6120},
mesh = {Humans ; *Sarcopenia/microbiology/physiopathology ; *Gastrointestinal Microbiome/physiology ; *Muscle, Skeletal ; Animals ; *Aging/physiology ; Muscle Strength/physiology ; Aged ; },
abstract = {Age-related muscle loss (sarcopenia) represents one of the most significant health burdens in a globally ageing population. The relationship between the gut microbiome and skeletal muscle, referred to as the gut-muscle axis, is the subject of increasing research, yet the identification of specific responsible microbial species and mechanisms has remained limited. This review aims to summarize the current evidence on the gut-muscle axis, with particular focus on the association between the intestinal bacterium Roseburia inulinivorans and muscle performance reported in a 2026 Gut publication, and to evaluate its clinical and therapeutic relevance. Narrative review based primarily on the study by Martinez-Tellez et al. (2026), supplemented by relevant literature on the gut-muscle axis, sarcopenia, and the ageing microbiome. The relative abundance of R. inulinivorans positively correlated with handgrip strength, leg press and bench press performance. Older adults with detectable R. inulinivorans showed 29% higher handgrip strength without a concomitant increase in cardiorespiratory capacity. In a murine model, oral supplementation produced approximately 30% increase in forelimb grip strength. The mechanism may operate not via butyrate but through activation of the purine and pentose phosphate pathways in muscle tissue. R. inulinivorans shows a species-specific association with muscle strength and represents a candidate target for nutraceutical interventions against sarcopenia and cachexia. Human randomized clinical trials and longitudinal studies accounting for sex differences are required to confirm these findings. Orv Hetil. 2026; 167(41): 1646-1654.},
}

Humans
*Sarcopenia/microbiology/physiopathology
*Gastrointestinal Microbiome/physiology
*Muscle, Skeletal
Animals
*Aging/physiology
Muscle Strength/physiology
Aged

@article {pmid42860030,
year = {2026},
author = {Mousa, AA and Zhang, H and Shen, J and Mao, S and Sun, X},
title = {Excessive Feed Sorting Is Associated With Altered Plasma Metabolism and Distinct Fermentation Responses of Pooled Rumen Microbiota in Dairy Cows.},
journal = {Journal of animal physiology and animal nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1111/jpn.70119},
pmid = {42860030},
issn = {1439-0396},
support = {32530100//Key Program of the National Natural Science Foundation of China/ ; ZJ26195012//Fundamental Research Funds for the Central Universities/ ; },
abstract = {Feed sorting behaviour in dairy cows alters dietary structure and has been associated with rumen dysfunction, but its systemic metabolic consequences and microbial acidogenic potential remain unclear. This study combined in vivo and in vitro approaches to investigate associations between feed sorting behaviour, host metabolism, and rumen microbial fermentation. Twenty-four mid-lactation Holstein cows were monitored for 28 days, from which 12 cows representing extreme feed-sorting phenotypes were selected: severe sorters for fine particles (SES; n = 6) and slight sorters (SLS; n = 6). Blood samples were collected for biochemical and metabolomic analyses, and pooled rumen fluid from selected cows within each sorting category was incubated in vitro with high-concentrate or high-forage substrates. Excessive sorting cows exhibited higher alanine aminotransferase, total cholesterol, and low-density lipoprotein cholesterol concentrations. Metabolomic analysis revealed alterations in carbohydrate, lipid, and amino acid metabolism, including changes in D-mannose, fumaric acid, mevalonic acid, oleic acid, glutamic acid, tryptophan, and gamma-aminobutyric acid concentrations. These changes were accompanied by increased concentrations of PGE2, histamine, and arachidonoyl ethanolamide, consistent with altered inflammatory and endocannabinoid signalling. In vitro incubation of pooled SES- and SLS-derived inocula with high-concentrate and high-forage substrates generated distinct fermentation profiles. Treatments containing SES-derived inocula were characterised by lower pH and greater total volatile fatty acid concentrations, particularly under high-concentrate conditions. These fermentation patterns were associated with higher relative abundances of Succinivibrionaceae UCG-002, Lachnobacterium, and Pseudobutyrivibrio. Overall, these findings suggest that feed sorting behaviour is associated with alterations in systemic metabolism and rumen microbial fermentation characteristics, providing new insight into the relationship between feeding behaviour and metabolic health in dairy cows.},
}

@article {pmid42860089,
year = {2026},
author = {Yan, Y and Zhang, W and Yu, F and Tang, Z and Ding, Y and Wang, D and Li, Y},
title = {Bistability of rhizosphere microbiomes shapes phosphorus partitioning in river networks under water diversion.},
journal = {Water research},
volume = {309},
number = {Pt A},
pages = {127113},
doi = {10.1016/j.watres.2026.127113},
pmid = {42860089},
issn = {1879-2448},
abstract = {Inter-basin water transfer projects are critical for mitigating water scarcity yet impose complex environmental disturbances, altering phosphorus (P) partitioning in recipient river networks. In these ecosystems, rhizosphere microbial communities (RMCs) act as biogeochemical engines regulating P partitioning among water, sediment, and biological phases. This regulatory capacity relies on structural and functional traits of RMC states. However, given their environmental sensitivity, RMCs are susceptible to water diversion disturbances. It remains unclear whether these disturbances drive state transitions and how these shifts reshape P partitioning. Here, we developed a stability landscape framework to characterize RMC states, identify their key environmental drivers, and examine effects on P partitioning in receiving river networks. Results revealed RMC bistability driven by the combination of the coefficient of variation of flow rate (CV_rate), turbidity, and temperature. One stable state maintained low water total P (WTP) and microbial biomass P (MBP), and high plant total P. This low-WTP state featured enrichment of Actinomycetota and Acidobacteriota, enhanced positive network cohesion, and abundant inorganic phosphorus solubilization genes (ppa, ppx). Conversely, the alternative state exhibited elevated WTP and MBP, enriching Cyanobacteriota and Bacteroidota, with simplified networks and enhanced organic phosphorus mineralization and transport genes (phoA, phnW, ugpAC, pstS). Furthermore, this stability landscape framework identified reference values for individual environmental drivers (temperature = 11.93°C, CV_rate = 5.93, turbidity = 21.92 NTU) to inform regulation favoring the low-WTP state. These findings provide a transferable quantitative framework, enabling water diversion operations to shift from reactive P pollution control toward proactive ecological regulation.},
}

@article {pmid42860111,
year = {2026},
author = {Tal, S},
title = {From dam to neonate: microbial, metabolic, and functional pathways shaping early-life development in dogs.},
journal = {Theriogenology},
volume = {268},
number = {},
pages = {118245},
doi = {10.1016/j.theriogenology.2026.118245},
pmid = {42860111},
issn = {1879-3231},
abstract = {Within minutes, the canine neonate transitions from placental support to respiration, thermoregulation, glucose homeostasis, feeding, and microbial colonization. These events are often considered separately, yet they form a connected developmental process that begins in the dam and continues through birth and lactation. This narrative review integrates evidence on maternal, microbial, metabolic, and functional determinants of early-life development in dogs. During gestation, maternal nutrition, metabolism, endocrine adaptation, and the maternal microbiota can influence fetal growth and maturation without requiring a viable fetal microbiota. At birth, loss of placental support coincides with physiological transition and rapid exposure to maternal and environmental microorganisms. Delivery mode, intrapartum care, antimicrobial exposure, and the interval to effective suckling can therefore affect several components of neonatal adaptation simultaneously. Colostrum and milk continue maternal support by supplying immunoglobulins, energy, growth-promoting factors, microorganisms, and a changing metabolite profile. The neonatal intestinal microbiota changes during the first weeks of life, in parallel with maturation of intestinal, immune, and metabolic functions. Low birth weight, inadequate early growth, hypothermia, hypoglycemia, impaired passive immune transfer, and altered intestinal microbial composition are associated with poor outcome, but their causal relationships remain incompletely resolved. Evidence supports careful management of the dam, prompt neonatal assessment, early colostrum intake, thermal and nutritional support, and longitudinal monitoring of weight and clinical activity. Microbiome-based risk prediction and targeted microbial interventions are plausible, but require prospective, multicenter validation before routine clinical use. An integrated dam-to-neonate framework may improve mechanistic research and early recognition of puppies at risk.},
}

@article {pmid42860129,
year = {2026},
author = {Dextro, RB and Rossmann, M and Freitas, AS and Domini, JA and Martins, GL and Shoichiro, U and Coutinho, LL and Cruz, AF and Ono, N and Tsai, SM},
title = {Management-Driven Effects in Soil Physicochemical Properties and Microbial Communities in Eastern Amazonian Agroforests.},
journal = {Environmental microbiology reports},
volume = {18},
number = {5},
pages = {e70432},
pmid = {42860129},
issn = {1758-2229},
support = {2022/13186-4//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2023/08974-6//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2024/03870-0//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2021/10626-0//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2024/06334-2//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; JK20231012//Japan Science and Technology Agency/ ; Finance Code 001//Coordenação de Aperfeiçoamento de Pessoal de Nível Superior/ ; 384253/2023-7//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 130852/2023-6//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 314806/2021-0//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 300104/2025-1//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 423437/2021-6//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; },
mesh = {*Soil Microbiology ; Brazil ; *Soil/chemistry ; Fungi/classification/genetics/isolation & purification ; *Microbiota ; Forests ; Bacteria/classification/genetics/isolation & purification ; Agriculture ; RNA, Ribosomal, 16S/genetics ; Agroecology ; Biodiversity ; Forestry ; },
abstract = {Agroforestry systems (AFS) are a promising bioeconomic strategy for sustainable land use and soil recovery in tropical regions. However, the potential effects of different management practices on soil microbial communities remain poorly understood. This study compared two neighbouring AFS in Tomé-Açu (PA, Brazil) with similar land-use, size, and productivity but contrasting management: organic inputs (AGF19) vs. chemical fertilization (AGF27), alongside a native forest reference area. Soil samples were evaluated through physicochemical properties, litter composition, and amplicon sequencing (16S rRNA and ITS) across three soil depths. Despite similar soil and litter characteristics, AGF19 showed a lower abundance of phytopathogenic fungi and associations with beneficial fungal taxa as biomarkers. In contrast, AGF27 exhibited signs of a microbiota shift towards a stress-related community. These findings could be partially associated with modest management changes like favouring organic inputs, influencing microbial diversity, functional guilds, and soil chemistry. Differences in management could be potentially linked with the identification of a phytopathogenic fungal taxon (e.g., Fusarium) as a biological marker of the community sampled in the AGF27 soil. Although different from the native forest, the results strengthen the role of AFS as a sustainable agroecological strategy. Regular soil monitoring and microbiome-informed practices are essential for sustainable management.},
}

*Soil Microbiology
Brazil
*Soil/chemistry
Fungi/classification/genetics/isolation & purification
*Microbiota
Forests
Bacteria/classification/genetics/isolation & purification
Agriculture
RNA, Ribosomal, 16S/genetics
Agroecology
Biodiversity
Forestry

@article {pmid42860166,
year = {2026},
author = {Omaima, HAAA and Saihood, SS and Burhan, AH and Aboomaima, WAA and Rostami, M and Raoufinia, R and Mahmoudi, A},
title = {Precision medicine in MASLD: Integrating genetics, multi-omics, and artificial intelligence for risk stratification and targeted therapy.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {},
number = {},
pages = {122892},
doi = {10.1016/j.cca.2026.122892},
pmid = {42860166},
issn = {1873-3492},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly termed nonalcoholic fatty liver disease (NAFLD), encompasses a heterogeneous clinical spectrum ranging from isolated hepatic steatosis to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis, and hepatocellular carcinoma. Differences in susceptibility to disease, progression and extrahepatic complications between individuals are due to many different variables, such as genetic, metabolic and environmental factors, sex, reproductive status and gut microbiota. Precision medicine offers a framework to navigate this complexity by combining clinical phenotyping with inherited genetic variation and large-scale multi-omics data including transcriptomics, epigenomics, proteomics, metabolomics, lipidomics, glycomics and microbiome analysis. Here we review the current evidence on important susceptibility genes, novel multi-omics biomarkers and polygenic risk scores, and discuss how these tools can improve risk prediction and sub-phenotyping. We also discuss artificial intelligence and machine learning algorithms that integrate clinical, imaging and molecular information to allow for non-invasive diagnosis and staging. Finally, we highlight precision-based therapeutic approaches such as oligonucleotide-based agents, genotype-stratified lifestyle and pharmacological interventions, and digitally supported personalized lifestyle programs. We outline the remaining challenges and research priorities needed to integrate precision hepatology into routine care, highlighting the identification of clinically actionable MASLD subtypes and the equitable translation of findings into improved long-term outcomes.},
}

@article {pmid42860290,
year = {2026},
author = {Liang, C and Chen, D and Sun, S and Yang, A and Qiao, J and Wu, S},
title = {Relay Architectures and Ecological Strategies of Quorum Sensing Effects on Microbial Interactions.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {e70440},
doi = {10.1111/1462-2920.70440},
pmid = {42860290},
issn = {1462-2920},
support = {2024YFA0920200//National Key Research and Development Program of China/ ; 32300022//National Natural Science Foundation of China/ ; },
mesh = {*Quorum Sensing ; *Microbial Interactions ; Ecosystem ; Bacteria/metabolism ; *Bacterial Physiological Phenomena ; },
abstract = {Microbial communities assemble in heterogeneous habitats, where quorum sensing (QS) influences interactions beyond signalling populations. Yet QS studies are commonly organized by signal type, circuit, or phenotype, obscuring the routes by which a QS event reaches neighbouring populations and why they prevail in particular settings. This Review synthesizes evidence from host-associated, terrestrial, marine, and aquatic systems to develop a two-dimensional framework for QS-mediated ecological effects. The framework distinguishes three relay architectures by which QS activity in one population affects another: direct perception of the source signal, exposure to a QS-regulated chemical effector, or response to a QS-associated change in a shared host or environment. It then identifies the ecological strategies that these architectures can support, including shared signal accessibility, reciprocal coordination, asymmetric cue responsiveness, resource monopolization, and competitive or community restructuring. Across habitats, spatial structure, resource accessibility, host-associated conditions, and temporal variability shape which relay architectures are feasible and the ecological consequences they generate. The framework positions QS as a context-dependent process through which population-state sensing is translated into neighbour responses, changes in habitat conditions, and community assembly. It establishes testable expectations for predicting which QS-mediated interactions arise in a habitat and for designing interventions that steer microbiome function.},
}

*Quorum Sensing
*Microbial Interactions
Ecosystem
Bacteria/metabolism
*Bacterial Physiological Phenomena

@article {pmid42860401,
year = {2026},
author = {Xu, Z and Jiang, H and Huang, W and Chan, A and Lin, Y and Chan, T and Lui, RN and Wong, MTL and Mak, JWY and Chan, FKL and Chevarin, C and Colombel, JF and Buisson, A and Ng, SC},
title = {Fecal microbiota transplantation for the decolonization of mucosal adherent-invasive Escherichia coli in Crohn's disease: an open-label pilot study.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42860401},
issn = {2041-1723},
mesh = {Humans ; *Crohn Disease/therapy/microbiology ; Pilot Projects ; *Fecal Microbiota Transplantation/methods/adverse effects ; Female ; *Escherichia coli/genetics/physiology ; Male ; Feces/microbiology ; Adult ; *Intestinal Mucosa/microbiology ; Middle Aged ; RNA, Ribosomal, 16S/genetics ; *Escherichia coli Infections/therapy/microbiology ; Young Adult ; Gastrointestinal Microbiome ; Treatment Outcome ; },
abstract = {Adherent-invasive Escherichia coli (AIEC) is implicated in Crohn's disease (CD) pathogenesis, but whether fecal microbiota transplantation (FMT) clears mucosal AIEC and alters fecal and mucosal microbiomes has not been studied. In this open-label pilot study, thirty adults with CD and seropositivity for serum anti-E.coli antibody (AEcAb) received a single colonoscopic FMT from one of two donors (ClinicalTrials.gov identifier NCT05611866). The primary outcome was adverse events (AEs) within 12 weeks after FMT; secondary outcomes included changes in mucosal AIEC, clinical measures, and fecal and mucosal microbiome profiles. Shotgun metagenomic sequencing for fecal samples and 16S rRNA sequencing for ileal mucosal samples were performed at baseline and after FMT. Baseline AEcAb levels were higher in patients with mucosal AIEC colonization (p = 0.019) and remained elevated after FMT. No FMT-related serious adverse events were reported. FMT was associated with mucosal AIEC decolonization in all 8 evaluable baseline-positive patients. Mucosal alpha diversity increased after FMT (p = 0.023), which correlated with reduced fecal calprotectin (p = 0.034). Microbial pathway profiles in CD patients resembled those of their respective donors with reduced donor-recipient dissimilarity post-FMT (p = 0.030), particularly among recipients with mucosal AIEC decolonization (p = 0.039). In conclusion, this open-label pilot study demonstrates the feasibility of FMT for modulating mucosal AIEC colonization in CD and highlights the importance of capturing microbial changes at the disease site that may be undetectable in fecal samples.},
}

Humans
*Crohn Disease/therapy/microbiology
Pilot Projects
*Fecal Microbiota Transplantation/methods/adverse effects
Female
*Escherichia coli/genetics/physiology
Male
Feces/microbiology
Adult
*Intestinal Mucosa/microbiology
Middle Aged
RNA, Ribosomal, 16S/genetics
*Escherichia coli Infections/therapy/microbiology
Young Adult
Gastrointestinal Microbiome
Treatment Outcome

@article {pmid42860412,
year = {2026},
author = {Barno, AR and Villela, HDM and Cardoso, PM and García, FC and Cui, G and Delgadillo-Ordoñez, N and Rosado, AS and Thomas, T and Aranda, M and Voolstra, CR and Peixoto, RS},
title = {Bacterial inoculation elicits changes to the coral epigenome.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42860412},
issn = {2041-1723},
mesh = {Animals ; *Anthozoa/microbiology/genetics ; DNA Methylation ; *Vibrio/physiology ; *Epigenome ; *Epigenesis, Genetic ; Probiotics ; Heat-Shock Response/genetics ; },
abstract = {Environmental shifts can cause epigenetic modifications in corals associated with changes in gene expression and physiology, although it remains unclear if associated bacteria can also induce such changes. Here, we inoculate nubbins of the coral Pocillopora verrucosa with an opportunistic pathogen, Vibrio coralliilyticus, and/or a coral probiotic, Cobetia sp., and subject the nubbins to heat stress. We show that pathogen exposure leads to distinct DNA methylation changes compared to the control, probiotic, and co-inoculation groups. We also confirm that DNA methylation broadly correlates with coral gene expression; however, individual correlations are restricted to a subset of genes. We then highlight genes altered by pathogen inoculation that show similar responses in their expression and methylation. Notably, coral probiotic exposure mitigates specific epigenetic changes caused by pathogen inoculation, which correlates with increased stress resilience and higher coral survival rates. Although many aspects remain to be resolved, evidence that bacteria alter coral epigenomes may help clarify the role of microbiome interactions in coral resilience.},
}

Animals
*Anthozoa/microbiology/genetics
DNA Methylation
*Vibrio/physiology
*Epigenome
*Epigenesis, Genetic
Probiotics
Heat-Shock Response/genetics

@article {pmid42860477,
year = {2026},
author = {Li, K and Xie, L and Li, Y and Xiong, Y and Ai, Y},
title = {Gastric Intestinal Metaplasia After Helicobacter pylori Eradication: Reframing the Reversibility Controversy.},
journal = {Digestive diseases and sciences},
volume = {},
number = {},
pages = {},
pmid = {42860477},
issn = {1573-2568},
abstract = {PURPOSE: To critically examine the evidence for and against reversibility of gastric intestinal metaplasia (GIM) after Helicobacter pylori eradication, reframe the two-decade controversy, and propose a hypothesis-generating framework for risk-stratified management.

METHODS: Narrative synthesis of meta-analyses, cohort studies, randomized controlled trials, and mechanistic studies (2007-2026) identified through PubMed and Web of Science.

RESULTS: The evidence has swung from early meta-analyses (2007-2011) concluding against IM reversibility to recent syntheses (2023-2025) demonstrating regression with prolonged follow-up. In early 2026, two reviews reached opposing conclusions: Song and Yu proposed an oncogenic memory model of persistent mucosal injury, epigenetic and immune alterations, and microbiome dysbiosis, while Chen et al. maintained that part of GIM exhibits meaningful reversibility. Extending this framework, we propose a fourth, largely irreversible dimension-histological memory-encompassing spasmolytic polypeptide-expressing metaplasia (SPEM) progression and stem cell niche alteration, which deepens the mucosal injury component of oncogenic memory. Known predictive factors (OLGA/OLGIM stage, subtype, age, eradication timing, and oncogenic memory burden) are organized into a unified reversibility gradient that reframes the binary question in risk-stratified terms, from which a hypothesis-generating three-tier surveillance framework is derived.

CONCLUSION: GIM reversibility is a continuous function of lesion characteristics, host factors, time since eradication, intervention intensity, and oncogenic memory burden rather than a binary property. The clinically relevant question is whose GIM, under what conditions, over what time frame, and with what residual risk reduction. The frameworks are hypothesis-generating, not validated clinical recommendations; prospective validation of risk-stratified surveillance represents the most urgent research priority.},
}

@article {pmid42860521,
year = {2026},
author = {Zhou, Q and Wang, K and Chen, J and Wang, H and Tan, X and Huang, X and Lin, Z and Xu, X and Jin, X and Zhang, S and Xiao, L and Zou, Y and Zhang, T and Liu, X},
title = {Structural Variants in the Human Genome Associated With Gut Microbiome and Blood Metabolic Traits With Potential Causal Links.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e78201},
doi = {10.1002/advs.78201},
pmid = {42860521},
issn = {2198-3844},
support = {32670077//National Natural Science Foundation of China/ ; 32200548//National Natural Science Foundation of China/ ; 2023YFC2509400//National Key R&D Program of China/ ; //Youth S&T Talent Support Programme of Guangdong Provincial Association for Science and Technology/ ; },
abstract = {Research on genetic variants affecting the gut microbiome and blood metabolites has mainly focused on single nucleotide variants (SNPs), leaving structural variants (SVs) largely unexplored. Here, we analyzed high-coverage (∼42×) whole-genome sequencing data from 2002 individuals and constructed a catalog of 138 859 high-confidence SVs, including 44.3% variants not represented in public SV resources. Genome-wide association analyses of 22 519 common SVs identified 30 microbiome-associated and 48 metabolite-associated SV loci, including 19 study-wide significant associations. Notable signals included an Asian-specific 6.5k deletion at TENT2 associated with Coprobacillus sp. 29_1 abundance (β = 0.158, p = 2.5 × 10[-9]) and a deletion covering HBA1/HBA2/HBM/HBQ1 linked to nine blood metabolic traits (strongest for MCV; β = -0.570, p = 1.22 × 10[-91]). Conditional and variance-partitioning analyses indicated that SVs capture complementary genetic information beyond tested SNP signals. SV-based Mendelian randomization delineated putative directional relationships, including Clostridium ramosum with serum uric acid and hyperuricemia. In vitro experiments further supported three predicted metabolite-microbe interactions, showing that vitamin K1 inhibited Coprococcus comes, hydroxyproline inhibited Veillonella parvula, and cysteine promoted Fusobacterium mortiferum growth. Together, our study provides a comprehensive SVs resource and highlights SVs as overlooked genetic determinants of host-microbiome-metabolome interactions relevant to human physiology and disease.},
}

@article {pmid42860590,
year = {2026},
author = {Lee, MJ and Kim, IS and Ahn, SH and Chung, W and Kang, YE and Jeon, SM and An, JH and Pyo, CH and Jeong, J and Kim, YE and Yoon, J and Choi, KY and Lee, SE and Kim, HS and Lee, S and O'Keeffe, S and Park, JO and Lee, JY and Bae, JW and Kim, DE and Lee, H and Kim, SH and Yeo, WH and Yeo, MK and Oh, E and Jo, EK and Heo, JY},
title = {Vagal sensing of altered gut microbiota links to externalizing behaviors.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2743919},
doi = {10.1080/19490976.2026.2743919},
pmid = {42860590},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Vagus Nerve/physiology/metabolism ; Mice ; Mice, Knockout ; Male ; Solitary Nucleus/metabolism ; Amygdala/metabolism ; Mice, Inbred C57BL ; *Behavior, Animal ; },
abstract = {Interoceptive brain responses triggered by intestinal microbiota influence mood-related behaviors such as anxiety and depression. Although genetic mutations can alter the gut microbiome, how alterations in the gut microbiome associated with host genetic variations relate to behavioral outcomes is not fully understood. We investigated how Sirtuin 3 (Sirt3) deficiency is linked to altered gut-brain interactions and mood-related behaviors. Gut microbiota composition and behavior were compared between Sirt3-knockout (KO) and wild-type (WT) mice. Cohousing and heterozygous littermate controls were used to assess microbiome-related contributions to behavioral differences. Transcriptomic profiling assessed region-specific gene expression in the limbic system. Metabolites in the nucleus of the solitary tract (NTS), potentially related to gut-brain vagal signaling, were analyzed. The role of the vagus nerve was further tested using subdiaphragmatic vagotomy in the Sirt3-KO mouse model, along with measurements of plasma choline levels in mice. Sirt3-KO mice displayed mood-related neurobehavioral changes and alterations in synaptic plasticity-related genes in the amygdala and the bed nucleus of the stria terminalis (BNST), accompanied by alterations in gut microbiome composition. Elevated plasma choline levels in Sirt3-KO mice, together with reduced neurotransmitter-related metabolites (e.g., γ-aminobutyric acid [GABA] in the NTS), suggest that externalizing behaviors in Sirt3-KO mice involve vagus nerve-dependent gut-brain axis signaling. Consistent with the involvement of vagal signaling, vagotomized Sirt3-KO mice were similar to WT mice in these measures, including GABA levels in the NTS and synaptic plasticity-related changes in the amygdala and BNST. Our findings support a model in which host genetic variation-associated microbiome alterations are sensed through sustained gut-vagal signaling under non-stressed conditions, correlating with NTS neurotransmitter alterations and externalizing behavioral phenotypes.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Vagus Nerve/physiology/metabolism
Mice
Mice, Knockout
Male
Solitary Nucleus/metabolism
Amygdala/metabolism
Mice, Inbred C57BL
*Behavior, Animal

@article {pmid42860688,
year = {2026},
author = {Liu, Y and Hu, Y and Xu, M and Ma, Z and Li, J and Liu, H and Wei, X},
title = {Integrated Quantitative and Relative Microbiome Profiling Reveals a Bacterial Group Associated With Primary Apical Periodontitis Severity and Sharing a Predicted Virulence-Associated Functional Signature.},
journal = {International endodontic journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/iej.70289},
pmid = {42860688},
issn = {1365-2591},
support = {SHH-2022-YJ-B03//Shanghai Stomatological Hospital Institutional Project/ ; 23Y11910100//Shanghai Science and Technology Innovation Action Medical Innovation Research Project/ ; },
abstract = {AIM: To overcome the confounding effects of taxonomic heterogeneity in primary apical periodontitis (AP), this study aimed to characterize the quantitative and compositional profiles of the root canal microbiota associated with severe clinical features (percussion tenderness, large periapical lesions, and sinus tracts) using integrated relative (RMP) and quantitative microbiome profiling (QMP).

METHODOLOGY: Root canal samples from 52 patients (out of 62 initially enrolled) with primary AP were analysed using spike-in-based 16S rRNA sequencing. Microbial load, diversity, and taxonomic composition were evaluated across these three predefined clinical features (with large lesions defined as ≥ 5 mm). Spearman correlation analysis was applied to assess the associations between differentially abundant genera and clinical severity. Furthermore, PICRUSt2 was used to infer functional profiles and calculate taxonomic contributions to enriched pathways under both RMP and QMP frameworks.

RESULTS: Samples with percussion tenderness exhibited significantly elevated microbial loads, with similar trends observed for large periapical lesions and sinus tracts. Percussion-positive samples also showed significantly higher Inverse Simpson index and Pielou's evenness index, whereas no significant differences in alpha diversity were observed for large periapical lesions or sinus tracts. Beta diversity did not differ significantly across any of the three clinical features under either QMP or RMP. Spearman correlation analysis identified a core bacterial group-Porphyromonas, Treponema, Tannerella, Peptostreptococcus, Selenomonas, Fusobacterium, and Fretibacterium-whose members showed broadly positive associations with all three clinical features in both relative and absolute abundance. Functional inference revealed these taxa collectively accounted for a shared set of virulence-associated pathways (e.g., lipopolysaccharide/peptidoglycan biosynthesis and protein export) consistently enriched in severe cases.

CONCLUSIONS: Despite taxonomic heterogeneity in the root canal microbiota, severe clinical features of primary AP were associated with elevated microbial load and with increased relative and absolute abundances of a candidate bacterial group, whose members converged on a shared set of virulence-associated pathways, suggesting that compositionally diverse communities may nevertheless converge on common virulence-related functions.},
}

@article {pmid42860924,
year = {2026},
author = {},
title = {Correction to "Deciphering Gut Microbiome Dynamics in Irritable Bowel Syndrome Using Deep Learning".},
journal = {Neurogastroenterology and motility},
volume = {38},
number = {10},
pages = {e70445},
doi = {10.1111/nmo.70445},
pmid = {42860924},
issn = {1365-2982},
}

@article {pmid42860978,
year = {2026},
author = {Eleutério Junior, J and Eleutério, RMN and Gonçalves, AK and Giraldo, PC},
title = {Bacterial vaginosis: a narrative review of concepts and best practices.},
journal = {Gynecology and pelvic medicine},
volume = {9},
number = {},
pages = {37},
pmid = {42860978},
issn = {2617-4499},
abstract = {BACKGROUND AND OBJECTIVE: Bacterial vaginosis (BV) is a multifaceted condition characterized by an imbalance of the vaginal microbiota. This disruption includes not only Gardnerella vaginalis but also a range of anaerobic bacteria, with clinical outcomes varying according to the specific bacterial composition. This review aims to provide an updated overview of the concepts, diagnosis, and management of BV.

METHODS: We conducted a search on MEDLINE (Medical Literature Analysis and Retrieval System Online), Google Scholar, and Scopus for publications in English, prior to September 2025, using the keywords [vaginal microbiota] OR [vaginal microbiome] OR [vaginosis] OR [bacterial vaginosis] OR [dysbiosis] AND [vagina] AND [diagnosis] AND [treatment]. We also reviewed the references of the articles obtained through our literature searches.

KEY CONTENT AND FINDINGS: BV is characterized by a shift from aerobic to anaerobic microbiota. Anaerobic bacteria and their metabolites can significantly impact the local immune response, resulting in various complications in women's reproductive health. Although most affected individuals remain asymptomatic, dysbiosis may negatively influence pregnancy outcomes and elevate the risk of sexually transmitted infections. Diagnosis is traditionally based on the Amsel criteria and Nugent Score. More recently, nucleic acid amplification tests, particularly those utilizing multiplex platforms, have been implemented to identify bacterial species such as Gardnerella, Fannyhessea, and Sneathia. Bacterial composition and the presence of biofilm are critical factors influencing treatment outcomes. Alternatives to conventional antibiotic therapy, including biofilm-disrupting agents and probiotics, are essential for addressing persistent and recurrent BV.

CONCLUSIONS: BV has long been recognized, and diagnosis has traditionally been based on Amsel's criteria and Nugent's score. While new diagnostic tools have offered valuable insights, they have also introduced new questions about this complex condition. Metronidazole remains the primary treatment, although adjuvant therapies, such as biofilm disruption and probiotics, are often required. Further large-scale, in-depth studies are needed to address ongoing uncertainties.},
}

@article {pmid42861078,
year = {2026},
author = {Aguilera-Garrido, A and Lemée, A and Claudel, J and Alem, H},
title = {Strategies for modelling the intestinal mucus interface: Focus on drug transport and host-microbiota interactions.},
journal = {International journal of pharmaceutics: X},
volume = {12},
number = {},
pages = {100672},
pmid = {42861078},
issn = {2590-1567},
abstract = {The intestinal mucus barrier is a complex, dynamic hydrogel that plays a central role in host-microbiota interactions, nutrient transport, and protection against pathogens. Understanding its physicochemical properties has become essential for developing predictive in vitro and in silico models for drug delivery, microbiome research, and disease modelling. Over the past decade, advances in polymer chemistry, glycoscience, and microfluidics have enabled the development of increasingly sophisticated mucus models that mimic structural, rheological, and biochemical features of native intestinal mucus. This review provides a comprehensive overview of recent progress in gut-mucus chemical model development, focusing on mucin biochemistry, hydrogel-based synthetic systems, microphysiological platforms, and an introduction on computational modelling approaches. Special emphasis is placed on emerging strategies to reproduce mucus heterogeneity, viscoelasticity, and microbial interactions. We critically assess the strengths and limitations of current models and highlight future directions for improving physiological relevance, including multi-scale integration and personalized mucus modelling. This review aims to provide a framework for researchers developing next-generation mucus models for biomedical and pharmaceutical applications.},
}

@article {pmid42861307,
year = {2026},
author = {Cheung, SM and Cheng, CY and Ponnusamy, VK and Tsai, KF and Kung, CT and Huang, WT and You, HL and Li, SH and Lee, WC and Cheng, FJ and Chaithanya, V},
title = {Endocrine Disruptors, Gut Microbiota, and Type 2 Diabetes: Bridging Mechanisms to Probiotic-Based Therapeutic Approaches.},
journal = {Diabetes, metabolic syndrome and obesity : targets and therapy},
volume = {19},
number = {},
pages = {636877},
pmid = {42861307},
issn = {1178-7007},
abstract = {Genetic and lifestyle factors alone cannot explain the rising global burden of type 2 diabetes mellitus (T2DM). Growing evidence implicates endocrine-disrupting chemicals (EDCs) found in plastics, pesticides, food packaging, industrial products, and contaminated water as significant environmental contributors to metabolic dysfunction. EDCs, including bisphenol A (BPA), phthalates, per- and polyfluoroalkyl substances (PFAS), persistent organic pollutants (POPs), and heavy metals, have been associated with insulin resistance, pancreatic β-cell dysfunction, oxidative stress, mitochondrial impairment, chronic inflammation, and epigenetic modifications that collectively promote T2DM pathogenesis. The gut microbiota has emerged as a potential mediator of EDC-associated metabolic disruption, whereby chemical exposures may alter microbial diversity, disturb the Firmicutes/Bacteroidetes ratio, impair short-chain fatty acid production, decrease intestinal barrier integrity, driving metabolic endotoxemia and systemic inflammation. This narrative review examines the major EDCs associated with diabetes, their molecular and metabolic mechanisms of action, and their interactions with the gut microbiota, drawing on current experimental and epidemiological evidence. Special emphasis is placed on probiotic supplementation as an emerging therapeutic strategy targeting the EDC-gut microbiota-metabolic axis. Current evidence for probiotics in EDC-associated metabolic dysfunction is predominantly preclinical, with studies suggesting improvements in microbial homeostasis, pancreatic oxidative damage, and glucose metabolism. However, available evidence remains heterogeneous and human clinical trials specifically examining probiotic intervention in EDC-exposed populations at risk of T2DM remain absent, representing a fundamental translational gap that future research must urgently address. Advancing precision medicine approaches, integrating microbiome profiling, metabolomics, epigenetic analysis, and coordinated efforts across toxicology, clinical medicine, and public health, will be essential to reducing the growing global burden of environmentally driven type 2 diabetes.},
}

@article {pmid42861577,
year = {2026},
author = {Samra, NA and Suliman, SGI and Al-Hadad, M and Boomsma, DI and Alhantoobi, F and Alsamahi, M and Abufarajallah, H and Al Tikriti, A and Aung, Z and Richards, S and Sajini, A and Mousa, M and Sulaiman, F and Osman, W},
title = {Toward "Obesityomics": Domain-Specific Omics in Precision Obesity Medicine with a Brief AI Perspective.},
journal = {Obesity reviews : an official journal of the International Association for the Study of Obesity},
volume = {},
number = {},
pages = {e70226},
doi = {10.1111/obr.70226},
pmid = {42861577},
issn = {1467-789X},
support = {RIG-2024-017//Khalifa University of Science, Technology and Research/ ; },
abstract = {BACKGROUND: Obesity's global rise has outpaced the effectiveness of "one-size-fits-all" prevention and treatment strategies. The promise of precision medicine lies in addressing the etiological and biological diversity of obesity and transforming it into actionable endotypes.

OBJECTIVES: In a narrative review, we analyze "obesityomics," looking at the contributions each omics layer makes to understanding and managing obesity. The areas we evaluate are genomics (heritability, polygenic risk, and monogenic forms), epigenomics (development and environment imprinting), transcriptomics (tissue-specific programs of adipose, liver, muscle, and hypothalamus), proteomics (signaling networks and adipokines), metabolomics and lipidomics (fuel partitioning, lipotoxicity, and metabolic inflection points), and microbiome science (metabolites, host-microbe interactions, and microbial ecology). Our domain-by-domain (single-omics) approach demonstrates how disease taxonomy, causal pathways, and biomarkers can be refined and targeted therapeutically.

DISCUSSION: We argue that "obesityomics" is a pragmatic approach to aligning omics modalities to the right questions at the right time, not a wholesale merger of datasets. Artificial intelligence (AI)-including machine learning and deep learning-should be used in conjunction with quality control, feature selection, modest data integration, and obesity intervention prediction. Among the key challenges in managing sensitive multilayer data are harmonization, standardization, reproducibility, equitable representation, and governance. The translation priorities include prospective studies related to patient-centered outcomes, biomarker panels that are clinic-ready, interoperability standards, and cost-effectiveness evaluations.

CONCLUSION: The review maps concrete steps to assist people with obesity in making better choices by identifying what each omics domain excels at and introducing a brief AI perspective.},
}

@article {pmid42861589,
year = {2026},
author = {Xie, YZ and Sun, CX and Fu, TT and Jin, Z and Nalinratana, N and Rojsitthisak, P and Zhao, K and Hua, JS and Pei, FY and Wang, XH},
title = {Nanoformulated Curcumin Ameliorates Ulcerative Colitis via Gut Microbiota Modulation and Barrier Function Restoration.},
journal = {The American journal of Chinese medicine},
volume = {},
number = {},
pages = {1-26},
doi = {10.1142/S0192415X26500837},
pmid = {42861589},
issn = {1793-6853},
abstract = {The gut microbiota is increasingly recognized as a key mediator of the anticolitis effects of curcumin (CUR). However, the clinical translation of this promising activity is severely hampered by CUR's low solubility and poor bioavailability. Although nanoencapsulation represents a promising strategy to address these limitations, the preventive effect of nanocurcumin (nano-CUR) against colitis remains largely unexplored. The present study aimed to elucidate the preventive effects of nano-CUR on intestinal barrier function, gut microbiota composition, and metabolic profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis. The results demonstrated that pre-supplementation of nano-CUR significantly ameliorated disease severity, attenuated intestinal barrier disruption, and suppressed colonic inflammation in mice with DSS-induced colitis. Mechanistically, integrated 16S rRNA sequencing and untargeted metabolomics demonstrated that nano-CUR-restored microbial homeostasis and enhanced the production of short-chain fatty acids, linking microbial shifts to anti-inflammatory outcomes. Fecal microbiota transplantation (FMT) further validated the causal role of the nano-CUR-remodeled microbiota in conferring protection. Collectively, these findings decipher the mechanism by which nano-CUR interacts with the gut microbiota, confirming that dietary nano-CUR consumption protects against ulcerative colitis by modulating the gut microbiome and its metabolic output.},
}

@article {pmid42861590,
year = {2026},
author = {Deng, LR and Zhong, YM and Zhu, SF and Wu, ZY and Chen, FJ and Huang, CY and Wu, QY and Tomlinson, B and Tan, HE and Li, YH},
title = {Anemoside B4 from Pulsatilla chinensis Ameliorates Ulcerative Colitis by Inhibiting Inflammatory Responses via the Modulation of the Gut Microbiota-Immune Interplay.},
journal = {The American journal of Chinese medicine},
volume = {},
number = {},
pages = {1-29},
doi = {10.1142/S0192415X26500849},
pmid = {42861590},
issn = {1793-6853},
abstract = {We previously demonstrated that anemoside B4 (AB4) exerts a beneficial effect in a dextran sulfate sodium (DSS)-induced murine model of ulcerative colitis (UC). In this study, we further explored the mechanism of AB4 against UC from the perspective of gut microbiota-immune interplay. The gut microbiota was depleted in two DSS-induced colitis models to investigate the modulatory effects of the gut microbiome on immune responses and the activity of AB4. In parallel, adoptive transfer of CD4[Formula: see text]CD62L[Formula: see text] T cells into Rag1-deficient (Rag1[-/-]) mice was used to elucidate the alterations in the gut microbiota associated with immune-mediated colitis as well as the modulation by AB4. qPCR, ELISA and western blotting were used to determine the inflammatory responses of mice with colitis, while immunohistochemistry and flow cytometry were employed to determine the CD4[Formula: see text] T cell function and the underlying mechanism. Metagenomic sequencing analysis was used to detect changes in the intestinal microbiota. The depletion of the gut microbiota attenuated disease severity and immune responses in mice with DSS-induced acute and chronic colitis. Notably, the inhibitory effects of orally administered AB4 on colitis progression and immune responses were abrogated. In addition, colitis induced by adoptive transfer of CD4[Formula: see text]CD62L[Formula: see text] T cells into Rag1[-/-] mice was accompanied by CD4[Formula: see text] T cell engraftment and alterations in gut microbiota. Remarkably, all these pathological changes were significantly attenuated by AB4. Crucially, we found that AB4 suppresses the proliferation, migration, and differentiation of CD4[Formula: see text] T cells, which provides a mechanistic basis for its immunosuppressive effects. Collectively, these findings indicate that the gut microbiota and the immune system, particularly CD4[Formula: see text] T cells, interact with each other in the initiation of colitis. We show that, by targeting this gut microbiota-immune interplay, AB4 is a promising therapeutic strategy for UC.},
}

@article {pmid42861600,
year = {2026},
author = {Liu, Y and Ning, X and Liu, Y and Yu, Z and Liu, J and Xu, X and Zhao, J and Sun, S},
title = {Potential Roles of Escherichia coli in IgA Nephropathy: Evidence, Mechanistic Hypotheses and Microbiota-Targeted Strategies.},
journal = {Microbial biotechnology},
volume = {19},
number = {10},
pages = {e70455},
doi = {10.1111/1751-7915.70455},
pmid = {42861600},
issn = {1751-7915},
support = {82470735//National Natural Science Foundation of China/ ; 2023TD-02//Shaanxi Provincial Health Commission/ ; 2023-ZDLSF-15//Key Research and Development Program of Shaanxi Province/ ; 2022ZDLSF03-12//Key Research and Development Projects of Shaanxi Province/ ; },
mesh = {Humans ; *Glomerulonephritis, IGA/microbiology/therapy/pathology ; *Escherichia coli/pathogenicity ; Animals ; *Gastrointestinal Microbiome ; Immunoglobulin A/metabolism ; },
abstract = {IgA nephropathy (IgAN), the most common primary glomerular disease, involves mucosa-kidney axis dysregulation, with gut dysbiosis increasingly implicated in its pathogenesis. Certain Escherichia coli (E. coli) strains harbour virulence-associated features that promote intestinal colonization, barrier disruption and immune activation. Recent microbiome and metagenomic studies have reported an enrichment of E. coli in patients with IgAN, suggesting a potential link to the mucosa-kidney axis. Nevertheless, E. coli may contribute to IgAN through two major pathways. First, sustained LPS exposure may induce aberrant production of galactose-deficient IgA1 (Gd-IgA1) by stimulating B cells and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome in macrophages, thereby amplifying systemic and renal inflammation. Second, metabolic reprogramming is associated with increased circulating sphingosine-1-phosphate (S1P) and altered production of indole and trimethylamine (TMA); S1P may promote mesangial proliferation and fibrosis, whereas indole- and TMA-related pathways may contribute to tubulointerstitial injury and chronic kidney disease (CKD) progression. Beyond conventional gut microbiota-targeted interventions, emerging precision therapeutic strategies offer promising new directions for the etiological treatment of IgAN. This review summarizes E. coli virulence factors, pathogenesis, and host, environmental, and ecological factors driving its gut expansion in IgAN patients and outlines corresponding therapeutic strategies.},
}

Humans
*Glomerulonephritis, IGA/microbiology/therapy/pathology
*Escherichia coli/pathogenicity
Animals
*Gastrointestinal Microbiome
Immunoglobulin A/metabolism

@article {pmid42861948,
year = {2026},
author = {Wojtkowiak, A and Shinfuku, MS and Lewin, GR},
title = {No strain, no gain: within-host bacterial microdiversity and human health.},
journal = {Infection and immunity},
volume = {},
number = {},
pages = {e0006226},
doi = {10.1128/iai.00062-26},
pmid = {42861948},
issn = {1098-5522},
abstract = {It is well established that within a bacterial species, genotypic and phenotypic variation leads to differences in virulence, antibiotic susceptibility, and metabolism. However, there is also increasing evidence that often multiple variants of the same species co-inhabit the same site in the human body, both during health and disease. This within-host microdiversity can develop over time for pathogens in chronic infections and has been observed for many members of the microbiota, for instance in the gut and on the skin. Research is just beginning to uncover how this within-host intra-species diversity develops and why it matters. Intra-species diversity is largely stable over time, with occasional selective sweeps of new genotypes, and the overall level of diversity is modulated by both microbe-microbe and microbe-host interactions. Furthermore, data indicate that within-host microdiversity can impact the stability of bacterial communities, their antimicrobial resistance, and the efficacy of probiotics and microbiota transplants. Here, we describe the evolutionary and ecological processes that promote high or low within-host microdiversity and the extent of this diversity in the human microbiota and in infections. In addition, we consider how microdiversity within individuals shapes the functional role of the human microbiota and the progression of disease. Together, within-host microdiversity is a newly developing way to think about the diversity of human-associated microbes, with implications in how we treat chronic infections and manipulate our microbiota to promote health.},
}

@article {pmid42861952,
year = {2026},
author = {Alvarez-Aponte, ZI and Anagu, HI and Mok, KC and Nguyen, ST and Trotter, VV and Taga, ME},
title = {Cobamide-based interactions between soil bacteria can be predicted based on monoculture growth.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0130026},
doi = {10.1128/aem.01300-26},
pmid = {42861952},
issn = {1098-5336},
abstract = {Interactions between microbes shape the structure and function of microbial communities. While studying interactions is key to understanding microbial communities as a whole, gaining a detailed mechanistic view is challenging due to the number of co-occurring interactions. Here, we focus on a single class of shared nutrients, the cobalamin (vitamin B12) family of enzyme cofactors known as cobamides, to study nutrient interactions in laboratory consortia of increasing complexity. Measuring cobamide-dependent growth of two soil Caulobacter isolates in monoculture revealed that each grows faster within a distinct range of cobamide concentrations. Co-culturing the two isolates demonstrated that the cobamide concentration predictably determines which isolate predominates. These results suggest that, although the two organisms appear functionally redundant, with identical metabolic capabilities predicted in their genomes, they may occupy distinct niches in their environment based on cobamide concentration. We further examined the ability of cobamide-producing Mesorhizobium and Priestia isolates to share cobamides and found that both support the cobamide-dependent growth of the two Caulobacter isolates. The Caulobacter isolates could coexist in tri-cultures with each producer following serial passaging, indicating the producers can support the growth of multiple cobamide-dependent organisms. We analyzed the metabolic capacity encoded in the genomes of the four isolates and found that cobamides are likely the main shared nutrient in our co- and tri-cultures. These results highlight the utility of cobamides as a model nutrient to characterize and predict interactions in bacterial consortia of increasing complexity.IMPORTANCEInteractions between microbes shape their communities and the world around them. Because microbial communities are physically and chemically complex, predicting microbial interactions is often difficult. Using a set of four bacteria isolated from the same soil environment, we generated and tested predictions about the interactions involving a family of model nutrients related to cobalamin (vitamin B12). Understanding and predicting interactions can lead to greater insights into microbiome function.},
}

@article {pmid42818378,
year = {2026},
author = {Ghezzi, H and Wolff, R and Jain, A and Burckhardt, JC and Hunter, M and Ng, KM and Carasso, S and Geva-Zatorsky, N and Garud, N and Tropini, C},
title = {Growth capacity and mortality burden shape microbial persistence under osmotic stress in Bacteroides thetaiotaomicron.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42818378},
issn = {2692-8205},
support = {R35 GM151023/GM/NIGMS NIH HHS/United States ; },
abstract = {Microbial persistence in the gut is central to sustaining beneficial host-microbiota interactions; however, characterizing determinants of persistence in vivo can be challenging due to the complexity of native microbial communities interacting with the host. Here, we used a defined microbial consortium to demonstrate that intrinsic in vitro growth capacity becomes increasingly predictive of in vivo relative abundance as intestinal osmolality increases. In Bacteroides thetaiotaomicron, in vivo abundance was higher than predicted from growth capacity alone, indicating that additional physiological factors contribute to persistence. We identify mortality as one such determinant: adaptation to prolonged osmotic stress markedly reduced cell loss without enhancing growth capacity. This adaptive phenotype was associated with rapid and reversible phase variation in cell surface-associated PUL78/80 rather than fixed de novo mutations, with the PUL78/80-OFF state becoming progressively enriched among surviving cells as mortality increased. Our findings demonstrate that in addition to growth capacity, reduced cell loss can provide a distinct route to microbial persistence during environmental perturbation.},
}

@article {pmid42853402,
year = {2026},
author = {Sonji, G and Sonji, N and El Katerji, A},
title = {Beyond gastric acid: pharmacologic modulation of the tumor microenvironment by vonoprazan and its drug-interaction implications for chemotherapy and immunotherapy.},
journal = {Cancer chemotherapy and pharmacology},
volume = {96},
number = {1},
pages = {},
pmid = {42853402},
issn = {1432-0843},
mesh = {*Pyrroles/pharmacology/administration & dosage ; Humans ; *Sulfonamides/pharmacology/administration & dosage ; *Tumor Microenvironment/drug effects ; Animals ; *Antineoplastic Agents/pharmacology ; Drug Interactions ; Gastric Acid/metabolism ; Immunotherapy/methods ; *Neoplasms/drug therapy/pathology ; Proton Pump Inhibitors/pharmacology ; },
abstract = {PURPOSE: Vonoprazan, a potassium-competitive acid blocker, possesses distinct pharmacokinetic and pharmacodynamic properties, including a high pKa , prolonged systemic exposure, and sustained hypochlorhydria, that may have implications beyond gastric acid suppression for anticancer drug interactions and the tumor microenvironment.

METHODS: We critically reviewed preclinical and clinical literature to evaluate vonoprazan's potential effects across two proposed biological axes: the intracellular/organelle axis, involving potential lysosomal drug sequestration, pH regulation, autophagy, and apoptotic signaling, and the systemic microbiome axis, involving acid-suppression-associated microbial alterations and potential consequences for antitumor immunity.

RESULTS: Vonoprazan enhanced cisplatin cytotoxicity in MCF-7 breast cancer cells and attenuated cisplatin-associated nephrotoxicity in rats, while altering autophagy-related markers. Separate cancer-cell studies found no increase in VEGF expression under the tested conditions, in contrast to several proton pump inhibitors. Conversely, a retrospective NSCLC cohort associated vonoprazan exposure with higher hazards of progression and death during immune checkpoint inhibitor therapy, although causality was not established. A 2026 pharmacovigilance analysis also identified increased cholangitis reporting among immune checkpoint inhibitor-exposed reports with co-reported vonoprazan, although causality was not established. Clinical evidence for microbiome alterations is emerging, but their relevance to anticancer treatment outcomes remains uncertain.

CONCLUSION: Available evidence supports a context-dependent pharmacologic framework rather than a uniform oncologic effect. Direct evidence for tumor-cell accumulation and vonoprazan-specific effects on V-ATPase activity in tumors remains limited. Prospective clinical and translational studies are needed to determine the clinical relevance of these potential interactions and to define appropriate use alongside anticancer therapies.},
}

*Pyrroles/pharmacology/administration & dosage
Humans
*Sulfonamides/pharmacology/administration & dosage
*Tumor Microenvironment/drug effects
Animals
*Antineoplastic Agents/pharmacology
Drug Interactions
Gastric Acid/metabolism
Immunotherapy/methods
*Neoplasms/drug therapy/pathology
Proton Pump Inhibitors/pharmacology

@article {pmid42853772,
year = {2026},
author = {Khan, MD and Ali, MA and Chaudhry, AS and Ahsan, A and Ahmad, I},
title = {Fusobacterium nucleatum mediated crosstalk drives cisplatin resistance in head and neck cancer.},
journal = {Oncology},
volume = {},
number = {},
pages = {1},
doi = {10.1159/ocl/aebag021},
pmid = {42853772},
issn = {1423-0232},
abstract = {Cisplatin remains a cornerstone of head and neck cancer (HNC) treatment, yet resistance frequently undermines therapeutic efficacy. Emerging evidence implicates Fusobacterium nucleatum, enriched in the tumour microbiome, in promoting chemoresistance via molecular and microenvironmental mechanisms. This review synthesises evidence from PubMed, Scopus, and Web of Science (January 2015-September 2025) examining F. nucleatum's contribution to cisplatin resistance in HNC. Cisplatin resistance involves tumour-intrinsic pathways, such as nucleotide excision repair, homologous recombination, and ATP7B-mediated drug efflux. F. nucleatum indirectly enhances resistance via Wnt5a/Ca[2+]-NFATc3 signalling, downregulation of p53 and E-cadherin, and activation of the NLRP3 inflammasome, which recruits myeloid-derived suppressor cells. It also amplifies inflammation and chemoresistance by escalating the senescence-associated secretory phenotype, promoting a tumour-supportive microenvironment. These findings highlight microbiome host crosstalk as a therapeutic target, suggesting that microbiota-directed strategies alongside cisplatin may improve outcomes in resistant HNC.},
}