Search Results (3,620)

Direct-acting antivirals (DAAs) cure most chronic hepatitis C virus (HCV) infections, yet whether the gut microbiota returns toward a healthy state after viral clearance remains uncertain. We systematically reviewed DAA-era adult HCV studies using sequencing-based fecal microbiota assessment (PROSPERO CRD420261374682). Longitudinal alpha-diversity change was pooled by REML random-effects meta-analysis with Hartung–Knapp adjustment, and compositional/functional findings were synthesized narratively. Seven studies met qualitative criteria and five longitudinal reports were extractable. Because participant overlap between two Thai reports could not be excluded, the primary conservative non-overlap analysis of four reports (180 paired observations) gave Hedges’ g = 0.13 (95% CI −0.53 to 0.80; I² ≈ 89%); the five-report sensitivity estimate was directionally positive but imprecise (g = 0.35, 95% CI −0.38 to 1.07). Recovery concentrated in richness (Chao1), whereas evenness-weighted diversity (Shannon, Hill) barely moved; beneficial taxa such as Faecalibacterium and Blautia increased after SVR. These findings are consistent with uneven, richness-led microbial recovery, but the overall certainty of the pooled evidence is very low (GRADE); functional and clinical recovery remain insufficiently characterized and undemonstrated. Full article

Prenatal alcohol exposure (PAE) leads to fetal alcohol spectrum disorder (FASD), the most common preventable cause of neurodevelopmental impairment. The classical narrative attributes the clinical picture of FASD exclusively to direct ethanol-induced brain injury. In the present review, we argue that this perspective is incomplete and leads to diagnostic errors, most often to the misdiagnosis of ADHD in children who in fact have FASD. We propose that, alongside the direct neurotoxicity of ethanol, an important and clinically under-recognized complementary mechanism is gut–brain axis dysfunction: alcohol damages the enteric nervous system and enteric glial cells, induces dysbiosis with deep deficits of butyrate and other short-chain fatty acids (SCFAs), damages the enterochromaffin cells responsible for 90% of peripheral serotonin production, and—through translocation of lipopolysaccharide (LPS) and activation of the Toll-like receptor 4 (TLR4)—sustains a neuroinflammatory brain signature. This cascade—superimposed on direct ethanol neurotoxicity—may account for the high rates of depression, anxiety, self-injurious behavior, and suicide attempts observed in individuals with FASD and for the limited efficacy of traditional interventions focused solely on the central nervous system. The 2024 Polish Institute of Mother and Child (Okulicz-Kozaryn et al.) study showed that 50.3% of pregnant women consumed alcohol, and 11% did so regularly, against only 7% who admitted so in questionnaires. The real clinical picture of children with FASD is further complicated by three factors to which we devote separate sections in this paper: prenatal co-exposure to nicotine, cannabinoids, and opioids; the loss of vertical microbiota transmission and breastfeeding in children transferred to foster care (where the prevalence of FASD is 18.8% and in children’s homes in some regions reaches up to 80%); and the substantial over-representation of preterm and small-for-gestational-age (SGA) infants (in the Hasken et al. cohort, 18.4% of children with FASD were born preterm and 51.4% were born SGA). In the final section, we present a structured, staged protocol for nutritional and microbiological intervention grounded in a hierarchy of evidence: from interventions supported by randomized controlled trials (RCT-level; choline) through interventions supported by strong mechanistic rationale and RCTs in related populations (sodium butyrate, Lactobacillus rhamnosus GG, GOS/FOS prebiotics—galacto-oligosaccharides and fructo-oligosaccharides, and omega-3 fatty acids) to experimental interventions. The protocol also covers the window before 2 years of age: we argue that, given the over-representation of preterm and SGA infants among children with FASD, the analogy to preterm infants on parenteral nutrition and to post-institutional infants applies in substantial part to the same patients, which justifies extending the indications for choline and other nutritional interventions. The paper includes a compact table of dosing proposals for each age window (from pregnancy to school-age child) and provides clinicians with concrete answers: where to start, what to avoid, and what to monitor, with explicit signposting of regulatory limitations for individual substances in Poland and the European Union. Full article

Chronic enteropathy (CE) is a common cause of persistent gastrointestinal signs in dogs, and dietary management represents the cornerstone of treatment. Probiotics have been proposed as adjunctive strategies to support intestinal health, although evidence of their efficacy remains limited. This randomised, double-blind crossover trial evaluated the effects of a hydrolysed protein diet supplemented or not with Bacillus velezensis DSM 15544 applied during post-extrusion coating. Thirteen CE dogs were randomly assigned to receive the Diet with Probiotic (DIET+PRO) or the Diet without Probiotic (DIET) during two consecutive 60-day feeding periods, with parameters assessed at baseline (T0) and after 30 (T1) and 60 (T2) days of each dietary treatment. Clinical response was assessed using the Canine Inflammatory Bowel Disease Activity Index (CIBDAI) andfecal core (FS). Gut microbiota was evaluated by the qPCR Dysbiosis Index (DI) and 16S rRNA gene sequencing, including taxonomic composition, alpha and beta diversity analyses. Compared with baseline (CIBDAI: 4.2 ± 1.7; FS: 3.9 ± 1.5), both dietary treatments significantly improved clinical scores (CIBDAI: 1.3–1.5; FS: 2.2–2.3; p < 0.02), irrespective of probiotic supplementation. Neither microbiota composition, alpha diversity, beta diversity, nor the DI (−2.7 ± 2.3 to −2.1 ± 2.3) differed between dietary treatments. Clinical responses to B. velezensis DSM 15544 supplementation varied among dogs. Overall, the hydrolysed diet effectively improved gastrointestinal clinical signs in dogs with CE, whereas the effects of B. velezensis DSM 15544 remain unclear and warrant further investigation, as any additional benefit may have been masked by the marked clinical response to the hydrolysed diet. Full article

Despite the traditional application of Sophora moorcroftiana (Benth.) Baker seeds for liver disorders, the capacity of its 70% ethanol extract (SMS) to alleviate metabolic dysfunction-associated steatotic liver disease (MASLD) and the underlying gut–liver axis mechanisms remain unclear. In this study, a high-fat diet (HFD)-induced MASLD mouse model was established to investigate the protective effects of SMS and its regulatory role in the interplay among gut microbiota, short-chain fatty acids (SCFAs), and inflammation. Serum, intestinal, and hepatic samples were collected to evaluate inflammatory responses, intestinal barrier integrity, and hepatic lipid metabolism. Gut microbiota composition and SCFA profiles were analyzed using 16S rRNA sequencing and metabolomics. In LPS-stimulated Caco-2 cells, SMS reduced inflammatory cytokines and TLR4/MyD88/NF-κB-associated signaling. The results demonstrated that SMS markedly alleviated hepatic steatosis by reducing triglyceride synthesis and hepatocellular lipid accumulation. In addition, SMS promoted the proliferation of beneficial bacteria, including Bifidobacterium and Akkermansia, and increased the production of SCFAs, particularly butyrate. SMS also restored intestinal barrier integrity through upregulation of Occludin and Claudin-1, thereby reducing circulating lipopolysaccharide (LPS) levels. Furthermore, SMS attenuated inflammation by inhibiting activation of the TLR4/NF-κB signaling pathway. Collectively, these findings demonstrate that SMS alleviates MASLD through coordinated modulation of gut microbiota composition, SCFA metabolism, intestinal barrier function, and inflammatory responses, highlighting its potential as a therapeutic strategy targeting the gut–liver axis. Full article

Background: Mare’s milk has gained attention as a functional food due to its bioactive compounds and potential microbiome-modulating properties. This systematic review evaluated the evidence on its potential role in gut microbiome restoration and immune modulation following COVID-19, particularly in pediatric and maternal populations. Methods: PubMed/MEDLINE, Scopus, Web of Science, and Embase were systematically searched for studies investigating mare’s milk or koumiss and their effects on gut microbiota, immune responses, inflammatory markers, or gastrointestinal outcomes. Results: Eight studies were included: five examined COVID-19-associated gut microbiome alterations, and three investigated the biological effects of mare’s milk or fermented mare’s milk. COVID-19 was consistently associated with reduced microbial diversity, depletion of beneficial bacteria, and enrichment of opportunistic pathogens, with some changes persisting after recovery. Conclusions: Koumiss demonstrates biologically plausible microbiome-modulating and immunoregulatory properties that may support recovery from COVID-19-associated gut dysbiosis. However, current evidence remains indirect, and clinical studies are needed before recommendations can be made. Full article

Background/Objectives: Pancreatic ductal adenocarcinoma (PDAC) is characterized by aggressive tumor biology and profound host vulnerability, including pancreatic exocrine insufficiency (PEI), maldigestion, malnutrition, cachexia, sarcopenia, frailty, systemic inflammation, and poor tolerance to multimodal therapy. Gut and intratumoral microbiota have been implicated in pancreatic carcinogenesis, tumor immunity, chemotherapy response, and postoperative outcomes. However, the clinical readiness of microbiome-informed supportive care in PDAC remains uncertain. Results: Current evidence supports plausible mechanistic links among PEI, maldigestion, dysbiosis, microbial metabolites, barrier dysfunction, systemic inflammation, cachexia, sarcopenia, and treatment intolerance. Nevertheless, PDAC microbiome research is limited by major heterogeneity in sampling sites, sequencing platforms, antibiotic exposure, biliary drainage, diet, treatment timing, tumor stage, and analytic pipelines. Evidence is also discordant, particularly regarding alpha diversity and reproducible microbial signatures. Low-biomass tissue contamination and incomplete consideration of fungal and multi-kingdom microbiota further limit interpretation. Conclusions: Microbiome disturbance should currently be viewed as an investigational modifier of nutritional vulnerability and treatment tolerance rather than as a validated clinical biomarker or therapeutic target in PDAC. A clinically responsible framework should distinguish what is actionable now—nutrition screening, PEI management, inflammation and frailty assessment, body-composition evaluation, and treatment-exposure monitoring—from what remains investigational, including microbiome profiling, microbial signatures, probiotics, prebiotics, fecal microbiota transplantation, and metabolite-guided intervention. Full article

Antibiotic-induced dysbiosis can cause persistent alterations in gut microbial composition and fermentative metabolism, yet the long-term role of mushroom β-glucan-based prebiotics in supporting post-antibiotic microbiota modulation remains poorly defined. To address this gap, the present study evaluated the modulatory effects of ColonX, a mushroom β-glucan-based formulation, during a 60-day in vitro simulation of post-antibiotic gut microbiota modulation. Quantitative PCR (qPCR) was used to monitor key bacterial groups, while UHPLC-DAD analysis was applied to characterize fermentation-derived organic acids. ColonX administration produced a selective, time-dependent increase in Bifidobacterium spp., with limited effects on Lactobacillus spp. and no stimulation of opportunistic bacteria such as Escherichia coli. This response became more evident after prolonged administration, suggesting progressive adaptation of the dysbiotic microbiota. Metabolomic analysis showed increased production of short-chain fatty acids and other fermentation-derived organic acids, indicating enhanced saccharolytic activity and functional metabolic remodeling. The accumulation of succinic acid further suggested ongoing microbial metabolic restructuring during recovery, while comparison with individual excipients indicated that resistant dextrin contributed to the fermentative response. Overall, this study addresses an important gap by linking prolonged mushroom β-glucan administration with both taxonomic modulation and functional metabolic recovery markers in a post-antibiotic dysbiosis model. These findings support ColonX as a promising nutraceutical strategy to promote gut microbiota restoration following antibiotic exposure. Full article

Background and Objectives: Endometriosis is associated with chronic inflammation, immune dysregulation, oestrogen-dependent growth, oxidative stress, altered steroid hormone metabolism, compromised epithelial barrier integrity, and the production of bioactive microbial metabolites. These interconnected alterations have been proposed to create, in principle, a permissive local microenvironment for malignant transformation. This narrative review examines whether endometriosis-associated dysregulation of the gut and reproductive tract microbiota may act as a hypothetical biological modulator linking these multi-axis changes to endometrial carcinogenesis, with attention to immunological, endocrine, metabolic, microbial–metabolite, oxidative, and barrier-related pathways. Material and Methods: We narratively integrated current evidence on gut and reproductive tract microbiota alterations relevant to endometrial homeostasis, with emphasis on the estrobolome, low-biomass uterine microbial communities, inflammatory and immune signaling, microbial metabolites, and pathways implicated in carcinogenesis. Results: Available data suggest that dysbiosis may influence endometrial carcinogenesis through interconnected endocrine, inflammatory, metabolic, and immune mechanisms. Attention has been given to loss of Lactobacillus dominance, enrichment of anaerobic and pro-inflammatory taxa, altered estrogen recirculation, progesterone resistance, Toll-like receptor activation, NF-κB/STAT3 signaling, COX-2/PGE2 activity, PI3K/AKT/mTOR pathway activation, oxidative stress, macrophage polarization, and impaired natural killer cell surveillance. These alterations may contribute to a permissive microenvironment characterized by persistent inflammation, defective immune control, and disrupted endometrial homeostasis. However, the current literature remains limited by small and heterogeneous cohorts, predominantly cross-sectional designs, contamination risk, and marked methodological variability, particularly in low-biomass uterine samples. Conclusions: Current evidence supports the view that microbiome dysregulation is a context-dependent biological modulator that intersects with endocrine, inflammatory, metabolic, immune, oxidative, and barrier-related pathways relevant to endometrial carcinogenesis. Microbiome dysbiosis should be regarded as a hypothetical contributory factor rather than as an established causal driver. Its near-term translational relevance appears greater for biomarker development and risk stratification than for immediate microbiome-directed therapy. Longitudinal, standardized, and functionally integrated studies are needed to clarify whether microbiome-associated signatures can be translated into clinically meaningful prevention and management strategies in endometrial cancer. Full article

Background: Gut microbiota plays a key role in the aging process, with age-related microbial shifts contributing to chronic inflammation, metabolic dysfunction, frailty, and cognitive decline. Despite growing interest, an integrated synthesis of how diet and lifestyle modifications influence gut microbiota remains limited. This overview of reviews summarizes the current evidence on how dietary and lifestyle interventions shape microbial composition and affect aging outcomes. Methods: Following the PRISMA guidelines, we searched PubMed and Scopus for English-language reviews (January 2023–October 2025) including human adults aged ≥ 18 years, evaluating dietary or lifestyle interventions, and reporting gut microbiota with healthy-aging outcomes. Quality of the reviews was appraised using the SANRA tool. Results: Mediterranean and plant-based diets, calorie restriction, and microbiota-targeted approaches such as probiotics, prebiotics, symbiotics, and fecal microbiota transplantation were associated with increases in short-chain fatty acid-producing bacteria, including Faecalibacterium, Bifidobacterium, Lactobacillus, and Akkermansia muciniphila, while reducing pro-inflammatory taxa. These changes were linked to improved metabolic and immune function, reduced inflammaging, lower frailty, and greater physical resilience. Cognitive benefits included decreased neuroinflammation and a lower risk of Alzheimer’s and Parkinson’s diseases. Conclusions: Maintaining microbial balance through targeted dietary strategies may support healthier, more resilient aging, offering practical insights for public health and clinical nutrition planning. Full article

Depression is a prevalent and complex neuropsychiatric disorder that substantially impairs quality of life worldwide. Current pharmacological and psychotherapeutic interventions are often limited by inadequate efficacy and restricted accessibility. Exercise has emerged as a potent non-pharmacological alternative, exhibiting antidepressant effects comparable to conventional treatments, with the microbiota–gut–brain (MGB) axis increasingly recognized as a key mediator. Despite growing interest, existing research articles largely describe associations without mapping the molecular pathways from exercise-altered microbes to neurobiological changes in depression. This review addresses these gaps by comprehensively dissecting the molecular cascades from microbial remodeling to synaptic and systemic adaptations, thereby providing a mechanistic roadmap absent in current syntheses. We first delineate how gut dysbiosis contributes to depression via endocrine, neural, and immune pathways. Subsequently, we highlight the ability of exercise to reverse these pathological states by restoring microbial diversity, reinforcing intestinal barrier function, and modulating the production of microbial metabolites. These exercise-driven changes collectively attenuate systemic and neuroinflammation, enhance brain-derived neurotrophic factor signaling, augment serotonin synthesis, and dampen hypothalamic–pituitary–adrenal axis hyperactivity. By reinstating intestinal homeostasis, exercise acts as a central regulator of the MGB axis and represents a promising therapeutic strategy. This integrative framework offers novel insights into depression pathogenesis and opens avenues for multifaceted intervention. Full article

Persistent racial and ethnic disparities in type 2 diabetes mellitus (T2DM) are incompletely explained by genetic susceptibility, obesity, lifestyle, and socioeconomic factors, suggesting that additional biological mechanisms may link environmental exposures to metabolic disease risk. Increasing evidence indicates that the exposome, encompassing environmental exposures across the life course, may influence long-term metabolic health through molecular mechanisms that integrate environmental signals with host biology. This Review synthesizes epidemiological, experimental, and mechanistic evidence on the gut microbiota–host epigenetic axis and its potential role in linking environmental exposures to population differences in T2DM susceptibility. Gut microbial dysbiosis alters the production and metabolism of short-chain fatty acids, bile acids, and tryptophan-derived metabolites. These microbial metabolites can modulate host signaling and epigenetic processes, including DNA methylation, histone modifications, and non-coding RNA activity, which may influence the expression of genes involved in glucose homeostasis, inflammation, and insulin sensitivity. Conversely, host epigenetic programs may influence intestinal barrier integrity and immune responses, thereby potentially affecting the gut microbial ecosystem, highlighting the reciprocal nature of host–microbiota interactions. We further examine how diet, psychosocial stress, environmental pollutants, and socioeconomic conditions may shape the microbiota–epigenetic axis across diverse populations, providing a framework for understanding differences in metabolic susceptibility without attributing disparities to intrinsic biological variation. However, direct human evidence linking the gut microbiota–host epigenetic axis to racial and ethnic disparities in T2DM risk remains limited, and much of the current framework is based on mechanistic studies, animal models, and associative human data rather than direct causal evidence. Further research in diverse human populations is needed to validate these pathways and establish their contribution to T2DM disparities. This framework may inform biomarker discovery, stratification, precision nutrition, and microbiome-targeted interventions and generate hypotheses for equitable prevention and personalized management of T2DM across diverse populations. Full article

Ruminal acidosis, particularly subacute ruminal acidosis, remains a major metabolic disorder that compromises animal health, production efficiency, and the sustainability of intensive ruminant systems. Although traditionally defined by reduced ruminal pH, it is increasingly recognized as a multidimensional disorder involving microbial ecological destabilization, disrupted metabolic cross-feeding, impaired epithelial barrier function, and dysregulated host inflammatory responses. This review synthesizes current knowledge of the microbial and metabolic mechanisms underlying acute and subacute ruminal acidosis and highlights processes that extend beyond pH depression alone. High-concentrate feeding shifts the balance among amylolytic and lactate-producing microorganisms, lactate-utilizing populations, and fibrolytic guilds, thereby promoting organic acid accumulation, reducing functional redundancy, and weakening microbial resilience. Concurrent increases in volatile fatty acids, lactate, lipopolysaccharide, histamine, and other microbially derived bioactive compounds increase epithelial acid load, disrupt tight-junction integrity, and facilitate inflammatory signaling. The principal novelty of this review is the integration of microbial functional guilds, metabolic cross-feeding, ecological resilience, epithelial barrier dysfunction, and host inflammation into a unified microbiota–metabolism–barrier–inflammation framework linking dietary perturbation with microbial dysfunction and host pathology. We further critically evaluate nutritional regulation, buffering agents, probiotics, yeast-derived products, postbiotics, and plant bioactive compounds according to their capacity to restore microbial function rather than merely correct ruminal pH. Additionally, this review may support multidimensional risk assessment, guide targeted intervention, and facilitate the integration of continuous ruminal monitoring with precision nutrition for earlier prediction and individualized prevention of ruminal acidosis. Full article

Bacterial vaginosis (BV) and aerobic vaginitis (AV) are usually described as distinct forms of vaginal dysbiosis. BV is characterized by depletion of lactobacilli, overgrowth of anaerobic microorganisms, and biofilm formation, whereas AV is associated with inflammatory changes, epithelial disruption, and predominance of aerobic bacteria. Over the past two decades, this distinction has profoundly influenced the understanding, diagnosis, and management of vaginal disorders. Despite their apparent differences, the relationship between BV and AV remains incompletely understood. Growing evidence indicates that many women exhibit microbiological and microscopic patterns that cannot be readily classified within existing diagnostic frameworks. Intermediate Nugent scores, mixed vaginitis, transitional ecological states, post-treatment microbiota reconstitution, physiological hypoestrogenic conditions, and uncommon inflammatory patterns all challenge the traditional view of BV and AV as strictly separate entities. This narrative review examines the historical evolution of BV and AV concepts, compares their microbiological, immunological, and epithelial characteristics, and evaluates the diagnostic paradigms currently used to identify vaginal dysbiosis. The strengths and limitations of clinical and diagnostic approaches are discussed together with the extent to which contemporary international guidelines reflect current biological knowledge. Particular emphasis is placed on intermediate, mixed, and overlapping states that blur the boundaries between established diagnostic categories. The available evidence supports the clinical usefulness of distinguishing BV and AV as separate clinicopathological entities. However, it also indicates that vaginal ecosystem disturbances frequently extend beyond rigid dichotomous classifications. Current diagnostic categories remain valuable tools for clinical practice, yet they may only partially capture the complexity and dynamic nature of vaginal dysbiosis. Understanding how microbial communities, host responses, epithelial integrity, and physiological factors interact remains a major challenge for future research and clinical interpretation. Full article

Background/Objectives: The oral microbiome plays a central role in maintaining oral health from early life, with childhood representing a critical period for its establishment and long-term stability. While many environmental factors influence this dynamic microbial ecosystem, diet is distinct in being both universal and highly modifiable. This systematic review aims to evaluate and synthesize current evidence regarding the impact and mechanisms of distinct dietary habits, food matrices, and nutritional components on the composition, diversity, and ecological resilience of the pediatric oral microbiome. Methods: A literature review aligned with PRISMA guidelines was conducted via digital searches on PubMed, ScienceDirect, and Cochrane databases (January 2015–December 2025). Search strategies combined MeSH terms and keywords targeting “Microbiota”, “Mouth”, “Child”, “Diet”, and “Oral health”. Results: From 1068 records identified, 16 relevant articles met the inclusion criteria. Dietary habits may influence taxonomic and functional profiles. Frequent consumption of sugar-sweetened beverages, sucrose-rich sodas, and sweet treats induces notable dysbiosis and enriches acidogenic/aciduric taxa. Conversely, protective food matrices, including probiotic-fortified dairy products, polyol-based sugar-free chewing gums (xylitol and maltitol), bovine milk, and bioactive-rich agents like green tea, actively suppress cariogenic pathways (specifically Streptococcus mutans) and support commensal, health-associated genera without disrupting overall microbial structures. Conclusions: Diet represents an important modifiable factor shaping the pediatric oral microbiome, capable of either driving dysbiosis or reinforcing symbiosis. Cultivating a microbiome-informed dietary approach early in childhood supports a resilient microbial architecture, offering a non-invasive, public health framework for long-term oral and systemic disease prevention. Full article

Hemodialysis (HD) is the most widely used renal replacement therapy for patients with end-stage renal disease (ESRD) and is frequently accompanied by long-term complications that impair quality of life, including metabolic and inflammatory disturbances. Growing evidence suggests that these complications may be linked to alterations in the gut microbiota; however, microbial composition and interaction patterns in HD patients remain incompletely characterized. In this exploratory, cross-sectional study, high throughput 16S rRNA gene sequencing was used to profile the fecal microbiota of patients undergoing hemodialysis and of healthy controls. The objective was to characterize associations between hemodialysis and gut microbial composition, ecological network organization, and predicted functional potential. Comparative analyses revealed significant differences in bacterial community structure and microbial networks in the HD cohort. Both gender and dialysis vintage were associated with variation in specific taxa, including increased detection of the Synergistetes phylum, particularly among male patients and those undergoing long-term HD. Associations were also observed between clinical and demographic factors and the relative abundance of several short-chain fatty acid-associated taxa, including members of the Lachnospiraceae and Ruminococcaceae families and the genus Bifidobacterium. Predicted functional potential (PICRUSt2) indicated distinct microbial metabolic profiles in HD patients compared with controls, particularly in pathways related to carbohydrate, nucleotide, and amino acid metabolism, with additional variation according to dialysis vintage. Overall, these findings provide an exploratory characterization of structural, compositional, and predicted functional alterations of the gut microbiota associated with hemodialysis. Although the modest cohort size precludes definitive conclusions, the results support the rationale for larger, longitudinal studies investigating microbiota-derived biomarkers and host–microbiome interactions in ESRD. Full article