Search Results (1,002)

Ectopic olfactory receptors (ORs) are G protein-coupled chemosensors expressed outside the olfactory epithelium, where they may couple local chemical inputs to cell-specific signaling. The oral cavity is continuously exposed to food-derived compounds, microbial metabolites, volatile organic compounds, and inflammation-associated metabolites, yet the molecular roles of oral ORs remain incompletely defined. This review critically synthesizes current evidence for OR expression and signaling in oral tissues and associated cell populations, with emphasis on ligand–receptor–signaling relationships and disease relevance. Functional OR signaling has been demonstrated in mammalian taste cells, while emerging transcriptomic studies in oral mucosa and transcriptomic/localization studies in the periodontal ligament indicate OR-related programs during tissue-specific or repair-associated states. Candidate metabolic axes, including short-chain fatty acids and lactate linked to OR51E1/OR51E2/Olfr78-related pathways in non-oral models, provide testable mechanistic hypotheses for microbiome–host communication in periodontitis and oral cancer; however, direct causal validation in oral disease models remains limited. We propose an evidence-tiered framework integrating spatial expression mapping, metabolomics-guided deorphanization, receptor perturbation, and longitudinal oral-fluid profiling. Oral ORs should currently be regarded as candidate molecular modulators and components of multimodal biomarker strategies rather than validated standalone diagnostic or therapeutic targets. Full article

The circadian rhythm is an internal timing system formed by the body’s adaptation to the Earth’s rotation, which helps maintain homeostasis by regulating physiological, metabolic, and behavioral activities. The gut microbiota (GM), the largest microbial ecosystem in the human body, exhibits a bidirectional regulatory relationship with the host circadian clock. Emerging evidence indicates that circadian rhythm disruption (CRD) is linked to disturbances in the diurnal oscillations and compositional balance of the GM, accompanied by reduced short-chain fatty acid levels, increased lipopolysaccharide leakage, and altered tryptophan metabolism. These microbial abnormalities may be involved in anxiety-like behaviors through three major pathways: neuroendocrine (hyperactivation of the HPA axis), immune (microglia-mediated neuroinflammation), and neurotransmitter (imbalance of the serotonergic and dopaminergic systems). Conversely, microbial metabolites such as butyrate and secondary bile acids may reciprocally regulate peripheral clock gene expression, forming a complex “circadian rhythm–GM–anxiety” interaction network. This review summarizes the molecular basis of circadian–GM interactions, potential GM-mediated mechanisms linking CRD with anxiety, and emerging intervention strategies including chrononutrition (time-restricted feeding, sequential nutrient intake), microbiota-targeted therapies (probiotics/prebiotics, fecal microbiota transplantation), and light therapy and melatonin supplementation. Future directions should focus on cell-specific mechanisms using single-cell and spatial transcriptomics, developing personalized interventions that integrate chronotype and microbiome profiling, and conducting large-scale randomized controlled trials to facilitate clinical translation. This review provides a framework for understanding the integrative role of circadian biology and gut microbiota in anxiety and may help develop precision intervention paradigms. Full article

The gut microbiome of rainbow trout (Oncorhynchus mykiss) and Atlantic salmon (Salmo salar) is increasingly recognized as a functional interface linking dietary inputs, epithelial barrier integrity, mucosal immunity, environmental stress, disease susceptibility, and antimicrobial-resistance risk in intensive aquaculture. Based on available salmonid studies and relevant evidence from broader fish and aquaculture systems, this review synthesizes current knowledge on salmonid gut microbial composition, nutritional modulation, microbiome–mucosal immune interactions, aquaculture stressors, antibiotic exposure, antibiotic resistance genes (ARGs), mobile genetic elements (MGEs), metagenomics, multi-omics, and emerging microbiome-informed decision-support tools. Current evidence does not support a universally stable single-core microbiota in these species. Instead, community structure is shaped by developmental stage, freshwater–seawater transition, intestinal segment, digesta versus mucosa sampling, diet, temperature, stress, health status, and methodological workflow. Feed substitution and functional additives can remodel the gut microbiota, but these shifts should be interpreted alongside histology, barrier function, metabolic profiles, immune indicators, and disease-resistance phenotypes. Antibiotic exposure may reduce acute bacterial disease pressure while disturbing community structure and potentially enriching ARGs or ARG–MGE associations. Risk assessment should therefore move beyond ARG abundance toward host–ARG–MGE linkage using shotgun metagenomics, metagenome-assembled genomes, long-read sequencing, Hi-C, and externally validated multi-omics models. Machine learning and artificial intelligence approaches may support feature screening, risk stratification, and decision support, but their application in salmonid gut-health management remains at an early stage and requires external validation across sites, production stages, diets, and seasons. Full article

The planthopper pests Geisha distinctissima and Ricanula fujianensis are major threats to tea plantations. Although insect endosymbionts are functionally important, their communities in these pests are poorly understood. This study, conducted in the representative tea-growing region of Guiyang in southwestern China, employed high-throughput sequencing to analyze the bacterial and fungal endosymbionts of both species. We found that bacterial communities were dominated by Proteobacteria and Firmicutes, with core genera such as Enterobacter and Rickettsia showing significant interspecific variation. Fungal communities were primarily composed of Ascomycota and Basidiomycota, and key genera like Fusarium exhibited host-specific patterns. Most notably, we discovered an intriguing pattern: bacterial communities differed in structure but showed conserved predicted functions, whereas fungal communities were structurally similar yet functionally divergent. This suggests that bacterial symbionts may underpin core physiological stability, while fungal symbionts could act as key drivers of host-specific adaptation. These results provide critical insights into planthopper–microbe interactions and establish a theoretical basis for developing targeted, microbiome-based pest management strategies. Full article

Background/Objectives. The intestinal microbiota is a key contributor to postoperative complications, yet direct interventions targeting dysbiosis—antibiotics, probiotics, and synbiotics—have produced inconsistent results. This paradox indicates a fundamental gap in understanding host–microbiota interactions under surgical stress. We aimed to re-examine the causal role of dysbiosis in postoperative pathogenesis and propose a revised therapeutic paradigm centered on host barrier protection. Methods. A narrative literature review was conducted, searching PubMed/MEDLINE, Scopus, and Web of Science for articles published between 2009 and 2025. Reference lists of included publications were additionally screened. Studies in English and Russian were eligible; 107 references were included. Results. We hypothesize that dysbiosis in surgical patients may, at least in part, represent a predictable ecological response to systemic hypoperfusion, pharmacological burden, and ischemia–reperfusion injury, rather than acting solely as an independent pathogenic agent. Microbial shifts, characterized by the depletion of short-chain fatty acid-producing commensals and the expansion of pathobionts, frequently accompany epithelial injury; however, available human data are predominantly observational and do not permit definitive determination of the temporal sequence. This hypothesis provides the conceptual foundation for the proposed therapeutic reorientation. Conclusions. The present findings support the rationale for transitioning from microbiome manipulation to a “host-first” strategy, which prioritizes the restoration of intestinal barrier integrity through the administration of cytoprotective agents and targeted metabolic substrates (glutamine and butyrate). We propose the Gut Resilience Index (GRI) as a theoretical construct to identify patients approaching a critical threshold necessitating rescue therapy. It must be emphasized that both the “host-first” strategy and the GRI remain hypothetical frameworks requiring prospective validation. The most critical next steps include the development and validation of the GRI in prospective cohort studies, as well as randomized controlled trials directly comparing barrier-oriented strategies with standard care. Full article

Carbohydrate-active enzymes (CAZymes) encoded by the human gut microbiome are central mediators of dietary glycan metabolism and host–microbe biochemical homeostasis. Among these, β-glucuronidases represent functionally pivotal hydrolases implicated in metabolism, intestinal physiology, and therapeutic modulation. The present study performs an integrative in silico structural and functional interrogation of β-glucuronidases derived from Acidobacterium capsulatum (3VNY), Bacteroides ovatus (6D8K), and Faecalibacterium prausnitzii (6ED2). An integrated computational framework encompassing physicochemical parameters profiling, hierarchical structural prediction, tertiary-structure validation, salt-bridge energetics, functional domain and motif annotation, protein–protein interaction reconstruction, ligand-binding thermodynamics via molecular docking, and residue-resolved non-covalent interaction network mapping using the Protein Contacts Atlas (PCA) was employed. Physicochemical analyses indicated that all enzymes are thermostable, intracellular, and hydrophilic, while secondary-structure organization revealed a functional balance between helix-mediated rigidity and coil-driven flexibility. Structural validation metrics identified 6ED2 as the most conformationally stable architecture, whereas 6D8K displayed enhanced functional complexity, including enriched motif composition, membrane-associated features, and superior ligand-binding affinity. Docking simulations highlighted castanospermine and calcium saccharate as the most favorable interacting ligands across enzyme variants. Importantly, PCA-based interaction analysis revealed distinct ligand-centered atomic contact networks, with immediate contact counts of 57 (3VNY), 32 (6D8K), and 41 (6ED2), providing residue-level insight into stabilization mechanisms and interaction topology beyond conventional docking metrics. Collectively, these findings establish a multidimensional computational framework linking structural stability, functional diversification, ligand recognition, and atomic interaction networks in gut microbial β-glucuronidases, thereby supporting future biochemical validation, microbiome-targeted therapeutics, and biotechnological or cosmeceutical applications. Full article

The TM7x strain is a genetic variant of the bacterium Nanosynbacter lyticus, which belongs to the Saccharibacteria phylum within the Candidate Phyla Radiation (CPR) or Patescibacteria group. Its biology differs significantly from that of other bacterial phyla, and its ecological role in the oral cavity remains largely undefined. Through a organyzed and comprehensive literature review, we aim to define the role this bacterium plays within the oral ecosystem. We identified relevant studies from primary sources, including scientific articles from preclinical and clinical studies obtained from three digital databases. The bacterial strain TM7x is an obligate epibiont that exhibits autonomous energy metabolism and utilizes a type IV pili system to adhere to its direct host, Schaalia odontolytica. It interacts with its host in two stages: initially as an epipatobiont and subsequently as an episymbiont. TM7x plays a complex ecological role by modulating the host’s metabolism and structure toward a less virulent phenotype resistant to phage attack, while also influencing the human host through immunomodulation and tissue protection. This organism has transitioned from being considered ‘biological dark matter’ to a key model for understanding coevolution within the human microbiome. Its ability to protect the host from phages, induce protective biofilms, and suppress destructive inflammatory responses suggests its potential role as a speculative modulator of human oral microbiome homeostasis, although direct clinical confirmation in human subjects is still lacking. Full article

Mulberry species (Morus spp.) provide phytochemically distinct plant materials in which leaves are typically characterized by high levels of iminosugars (notably 1-deoxynojirimycin), flavonols/flavones, and polysaccharides, whereas fruits—especially Morus nigra—contain substantial amounts of anthocyanins alongside other phenolic compounds and polysaccharides. Importantly, the composition and biological properties of mulberry-derived products depend not only on species and plant part (leaf vs. fruit), but also on preparation and processing variables, including drying, maceration, fermentation, and extraction, or fractionation strategy (e.g., aqueous vs. hydroalcoholic extracts or enriched fractions). Such technological factors may substantially influence the chemical composition, bioavailability, and functionality of mulberry-derived preparations and thereby modify their interactions with gut microbiota and host metabolic processes. Available preclinical studies indicate that mulberry leaf- and fruit-derived preparations can affect gut microbial composition or activity in experimental models of metabolic dysfunction. Reported findings frequently include enrichment of microbial taxa commonly regarded as beneficial, such as Bifidobacterium, Lactobacillus, and Akkermansia, normalization of dysbiosis-associated microbial patterns, and increased production of short-chain fatty acids, particularly acetate, propionate, and butyrate. These microbial changes are sometimes observed alongside improvements in metabolic parameters such as glucose regulation, lipid profile, adiposity, or inflammatory markers. However, reported responses differ across plant parts, species, and preparation approaches, indicating that phytochemical composition and processing strategy are likely to influence biological outcomes. Interpretation of the current evidence is limited by the predominance of non-human studies and by incomplete or inconsistent reporting of extract composition, processing conditions, and standardization procedures. These factors reduce comparability between studies and complicate mechanistic interpretation of microbiome-related effects. Overall, existing preclinical data support the possibility that mulberry-derived preparations may influence metabolic health through microbiota-associated pathways shaped by both botanical origin and preparative technology. Well-designed human intervention studies using chemically characterized and standardized preparations, together with comprehensive gut microbiome analyses, are needed to determine the translational relevance of these observations and to identify which mulberry-derived preparations offer the greatest potential for supporting gut and metabolic health. Full article

Lipids (sphingolipids, fatty acids, phospholipids, and lipoproteins) are vital to intestinal barrier integrity, as precursors for pro-inflammatory and pro-resolving mediators and undergo remodelling through host microbiome interactions. Accumulating evidence implicates the Western diet—high in long-chain saturated and omega-6 polyunsaturated fatty acids and low in omega-3—in both the onset and progression of IBD. In contrast, microbiota derived lipid metabolites, including short-chain fatty acids and secondary bile acids, contribute to mucosal homeostasis and immune regulation. This review is structured around three interconnected pillars. First, we classified lipidomic alterations in IBD across major lipid classes: sphingolipids, fatty acids, phospholipids, and lipoproteins by integrating host, dietary, and microbiome contributions. Second, we examined the potential of lipidomics in IBD as a source of prognostic, diagnostic and therapy response biomarkers. Third, we critically assessed the challenges that currently limit clinical implementation including analytical variability, pre-analytical confounding, small cohort sizes, and the lack of prospective validation. Addressing these barriers will be essential to fully realise the potential of lipidomics in advancing personalised care for patients with IBD. Full article

Background/Objectives: Mushroom-derived phenolic compounds are gaining attention as bioactive molecules with potential roles in gut microbiota modulation, intestinal health, and metabolic regulation. Although mushroom polysaccharides are well established as fermentable substrates, the contribution of fungal phenolics to microbiota–host interactions remains less defined. This review aimed to critically analyse the evidence supporting mushroom-derived phenolic compounds as emerging prebiotic-like modulators of gut microbiota, intestinal function, and host metabolism. Methods: A narrative critical review was conducted using scientific literature retrieved from PubMed, Scopus, Web of Science, and Google Scholar. Studies addressing phenolic profiling in edible and medicinal mushrooms, gastrointestinal digestion, colonic fermentation, microbial biotransformation, gut microbiota modulation, intestinal barrier function, inflammation, and metabolic outcomes were considered. Particular attention was given to chromatographic and mass spectrometry-based studies, in vitro digestion/fermentation models, mechanistic studies, animal experiments, clinical trials, systematic reviews, and meta-analyses. Results: Current evidence shows that mushrooms contain diverse phenolic compounds, mainly phenolic acids such as gallic, protocatechuic, caffeic, p-coumaric, ferulic, vanillic, syringic, and cinnamic acids. Due to limited small intestine absorption, a substantial fraction of these compounds may reach the colon, where they undergo microbial biotransformation into smaller phenolic metabolites. These metabolites may influence microbial ecology, support beneficial taxa, modulate short-chain fatty acid production indirectly, attenuate oxidative stress and inflammatory signaling, and contribute to intestinal barrier integrity. However, most evidence derives from in vitro and preclinical studies, while human data remain limited and are mainly based on whole-mushroom interventions. Conclusions: Mushroom-derived phenolic compounds are promising prebiotic-like modulators within the microbiota–metabolite–host axis. Nevertheless, their specific contribution cannot yet be quantitatively distinguished from that of other mushroom constituents, particularly β-glucans, chitin, and other fungal polysaccharides, because most available evidence derives from whole-mushroom matrices, crude extracts, or polysaccharide-rich preparations rather than isolated phenolic fractions. Future studies should compare whole mushroom preparations, polysaccharide-rich fractions, and standardized phenolic-rich extracts, integrating metabolomics, microbiome profiling, and well-designed clinical trials to clarify the relative mechanistic and therapeutic relevance of mushroom phenolics. Future studies should use standardized phenolic-rich extracts, metabolomics, microbiome analysis, and well-designed clinical trials to clarify their mechanistic relevance, clinical significance, and translational potential. Full article

The gut microbiome plays a central role in regulating nutrient utilization, immune function, and disease resistance, thereby directly influencing growth performance and feed efficiency. Existing microbiome modulation strategies, including probiotics, prebiotics, dietary interventions, and antibiotic alternatives, are critically evaluated. Despite their reported benefits, the effectiveness of these approaches often remains inconsistent across production systems. Evidence suggests that this variability is largely driven by complex interactions among microbial communities, host factors, and environmental and management conditions, which are frequently overlooked in conventional intervention-based approaches. To address this gap, this review proposes an integrated microbiome–host–environment framework that links microbial ecology with host physiology and production conditions. The framework provides a systems-level perspective for understanding the factors governing microbiome stability and production responses, offering a basis for more targeted and reliable microbiome management strategies. Finally, current challenges and future research priorities are discussed, including the integration of multi-omics technologies, precision nutrition, and data-driven approaches to support next-generation poultry production systems. By emphasizing the interconnected nature of microbiome regulation, this review contributes a conceptual foundation for improving broiler productivity and sustainability through more consistent and effective microbiome optimization. Full article

The tumor microbiome has been implicated in pancreatic ductal adenocarcinoma (PDAC)’s poor response to treatment, demanding new methods for understanding host-microbe interactions in therapy. Traditional 2D systems, while widely used, fail to adequately recapitulate human PDAC due to insufficient representation of structural, immunological and stromal components. Differences in cancer-specific microbiomes, microbe-immune interactions, and the unique physiological and immunosuppressive features unique to PDAC have hindered the clinical translation of immune therapies. Reproducible 3D culture systems that integrate the human microbe-tumor-immune (MTI) axis represent a promising avenue for treatment research, yet they remain underexplored in PDAC. In this narrative review, we discuss the key microbial determinants of therapy resistance, explore the current 3D multicellular modeling approaches in other cancer types, and provide a path forward for similar integrative translational models in PDAC. Full article

Gestational diabetes mellitus (GDM) is an increasingly prevalent metabolic disorder of pregnancy, driven by rising maternal age, obesity, and complex metabolic–inflammatory interactions. Emerging evidence implicates the maternal microbiome as a key modulator of metabolic adaptation during gestation; however, its precise role in GDM pathogenesis remains incompletely defined. This narrative review synthesizes current knowledge on microbiome alterations across gut, vaginal, and oral niches, focusing on their contribution to insulin resistance, metabolic endotoxemia, and immune dysregulation. GDM is consistently associated with reduced microbial diversity, depletion of beneficial taxa (e.g., Akkermansia, Bifidobacterium, Faecalibacterium), and expansion of pro-inflammatory pathobionts, which collectively may impair intestinal barrier integrity and promote low-grade systemic inflammation. These mechanisms are linked to altered insulin signaling and adverse maternal–fetal outcomes. In parallel, microbiome-derived metabolites and early taxonomic signatures have been proposed as potential biomarkers for first-trimester risk stratification, offering an opportunity to overcome the limitations of late diagnostic approaches such as the oral glucose tolerance test. Despite these advances, most available evidence remains associative, with substantial heterogeneity across studies and limited mechanistic validation. The clinical utility of microbiome-based interventions—including dietary modulation, prebiotics, and probiotics—remains promising but inconclusive, with outcomes highly dependent on individual, microbial, and methodological factors. Overall, the maternal microbiome represents a compelling but still evolving target in GDM research. Future progress will depend on standardized methodologies, longitudinal multi-omics studies, and the development of precision medicine approaches capable of integrating microbial, metabolic, and host data. Such advances may enable earlier diagnosis, targeted prevention, and ultimately the disruption of intergenerational metabolic risk. Full article

Chronic wounds represent a substantial and growing clinical burden, yet durable healing remains difficult to achieve in a large proportion of patients. The skin microbiome plays a central role in this challenge: in healthy tissue, resident microorganisms support barrier integrity and calibrate immune responses, whereas in chronic wounds, community disruption—often combined with persistent biofilm formation—drives non-resolving inflammation, impairs re-epithelialisation, and increases antimicrobial tolerance. As antibiotic resistance escalates, these features strengthen the rationale for microbiome-directed strategies that target wound ecology while reducing reliance on conventional antimicrobials. Current evidence is still dominated by mechanistic and preclinical studies, with only early clinical signals for selected approaches; therefore, next-generation probiotics, including Lactiplantibacillus/Lactobacillus spp., as well as defined prebiotic and postbiotic formulations, should be interpreted as promising adjuncts rather than clinically established therapies. Causal mechanisms, optimal formulations, reproducibility, and patient-level determinants of response remain insufficiently defined, representing a critical knowledge gap that limits translation. Here, we synthesise current evidence linking microbial ecology to key wound-healing pathways and propose a precision framework that integrates metagenomics, transcriptomics, metabolomics, and spatial profiling to map host–microbe interactions, identify predictive biomarkers, and guide stratified therapy. We further highlight combinatorial approaches pairing ecological engineering with biofilm-disruptive materials and immune-modulatory molecules. Realising the potential of these interventions will require mechanism-resolved clinical trials, standardised outcome frameworks, and patient stratification tools—advances that could improve chronic wound management while reducing selective pressure for antimicrobial resistance. Full article

Autoimmune and immune-mediated inflammatory diseases (IMIDs) develop when genetically and environmentally susceptible hosts lose stable immune tolerance. The gut ecosystem is increasingly recognized as a biologically active interface in this process. Its bacterial, fungal, and viral components may shape mucosal and systemic immunity through antigenic stimulation, barrier regulation, and metabolite-dependent signaling, although the strength of evidence is uneven: bacteriome data are currently the most mature, whereas mycobiome, virome, and phageome findings remain more disease-specific and emerging. Dysbiosis may influence autoimmunity through overlapping routes, including epithelial barrier failure, altered short-chain fatty acid, bile acid, and tryptophan metabolism, molecular mimicry, and cross-kingdom microbial interactions. Nutrition is central to this network because dietary substrates determine microbial growth, metabolic output, epithelial integrity, and immune-cell differentiation. In this narrative review, we integrate evidence on disease-associated bacteriome, mycobiome, and virome patterns in systemic autoimmune diseases, with emphasis on rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome, systemic sclerosis, spondyloarthritis, vasculitides, and idiopathic inflammatory myopathies. COVID-19 is considered not as a proven causal driver of autoimmunity, but as an example of an environmental and infectious insult capable of perturbing microbiome–barrier–immune communication. Finally, we discuss diet-based and microbiome-targeted approaches, including probiotics, prebiotics, synbiotics, and postbiotics, as adjunctive strategies that may help restore microbial resilience and immune balance. A better understanding of the diet–microbiome–host immunity axis may support more personalized preventive and therapeutic concepts in autoimmune disease. Full article