Search Results (1,282)

Pancreatic cancer (PC) remains one of the malignancies with the most unfavorable prognosis and limited treatment options. The lack of biomarkers for early diagnosis and the asymptomatic nature of the disease contribute to delays in diagnosis and high mortality rates. In recent years, the role of the human microbiota in cancer biology has become increasingly significant, and the oral microbiota in particular has been found to be involved in the pathogenesis and prognosis of several neoplasms. This review summarizes the current evidence relating the salivary microbiota to PC in three key areas: screening and diagnostic potential, pathophysiology and tumor progression, as well as presenting prognostic implications and potential influence on therapy. With regard to early diagnosis, it has been reported that patients with PC have reduced levels of Neisseria elongata (N. elongata) and Streptococcus mitis (S. mitis) and elevated levels of Granulicatella adiacens. Several studies have shown that bacteria present in the saliva can migrate from the oral cavity to pancreatic tissue via hematogenous or enteric routes, where they may actively contribute to tumor development and progression. In particular, it has been shown that Porphyromonas gingivalis (P. gingivalis) and Veillonella atypica (V. atypica) translocate from the mouth to pancreatic tumors, promoting carcinogenesis by inducing a pro-inflammatory tumor microenvironment. Furthermore, some studies have identified certain species associated with prognosis and response to PC treatment. Despite the encouraging results, differences in study methodology, the lack of standardized methods and the scarcity of longitudinal data currently hinder clinical application. Large-scale, multi-omics prospective studies are needed to clarify causality and validate their clinical utility. Overall, the salivary microbiota represents a promising and non-invasive tool for improving early diagnosis, understanding prognosis and enhancing the management of PC. Full article

This study evaluated the effects of monolaurin intake per finishing feedlot cattle on growth performance, metabolic status, ruminal environment, and meat fatty acid profile. Twenty-four castrated Holstein males (379 ± 8.5 kg; 12 months old) were randomly assigned to two treatments: basal diet (control) or basal diet with α-monolaurin (treated: 0.762 g/kg dry matter intake; ≈6.63 g/animal/day) for 79 days. Feed intake, body weight, and feed efficiency were recorded, and blood and ruminal samples were collected during the trial. Ruminal fermentation parameters, protozoa counts, hematological and biochemical variables, oxidative status biomarkers, ruminal microbiota composition (16S rRNA sequencing), and Longissimus dorsi fatty acid profile were analyzed. Monolaurin feed did not affect dry matter intake or final body weight, but increased total weight gain, average daily gain, and feed efficiency (p ≤ 0.05), indicating improved nutrient utilization. Hematological and serum biochemical variables were largely unchanged, although total leukocyte counts were lower in treated cattle. Animals receiving monolaurin showed reduced reactive oxygen species and lower superoxide dismutase activity, suggesting improved oxidative balance without changes in lipid peroxidation. During the adaptation phase (day 14), treated cattle exhibited lower acetate, propionate, valerate, and total volatile fatty acid concentrations and higher protozoa counts, but these differences disappeared by day 79, indicating ruminal adaptation. Microbiota diversity was not altered overall, although specific genera differed in relative abundance between treatments. In meat, monolaurin increased lauric, linoleic, and arachidonic acids, reduced palmitic and heptadecanoic acids, decreased total saturated fatty acids, and increased polyunsaturated fatty acids (p ≤ 0.05). Overall, dietary monolaurin improved feed efficiency, modulated oxidative status, induced transient ruminal microbial adjustments, and enhanced the nutritional quality of beef lipids without compromising metabolic health. Full article

Heart failure (HF) continues to be a major global health burden, with persistent morbidity and mortality despite guideline-directed and device-based therapies. Evidence suggests the gut–heart axis is a critical and underrecognized contributor to HF progression. Alterations in cardiac output and systemic venous congestion in HF lead to intestinal hypoperfusion, mucosal edema, and loss of barrier integrity, increasing intestinal permeability, gut dysbiosis, and translocation of microbial products. This systemic translocation is associated with chronic low-grade inflammation that activates innate immune pathways that correlate with endothelial dysfunction, oxidative stress, fibroblast activation, and adverse cardiac remodeling. Gut-derived metabolites derived by microbial metabolism modulate cardiovascular health by altering the metabolic profiles. Dysbiosis results in loss of protective short-chain fatty acid (SCFA)-producing bacteria and enriches pro-inflammatory taxa such as trimethylamine N-oxide (TMAO)-producing bacteria. Elevated TMAO is associated with increased mortality and hospitalization in HF, whereas SCFAs enhance barrier integrity and immune tolerance. Secondary bile acids and uremic toxins such as indoxyl sulfate and p-cresyl sulfate further link dysbiosis to fibrosis and vascular stiffness. Circulating markers such as TMAO, lipopolysaccharide-binding protein (LBP), and soluble CD14 carry prognostic value beyond traditional cardiac biomarkers. This review highlights current experimental, translational, and clinical evidence describing gut dysbiosis and its molecular links to HF progression. Targeting the gut–heart axis represents a novel therapeutic approach in HF. Dietary modulation, probiotics/prebiotics, fecal microbiota transplantation, and inhibitors of microbial metabolic pathways show promise. Future research should emphasize microbiota-based interventions in HF management. Full article

Gestational diabetes mellitus (GDM), as one of the most common metabolic disorders occurring during pregnancy, represents a significant public health concern due to its rising prevalence and the numerous complications that can affect both the mother and the foetus. In recent years, there has been growing interest in the use of omics technologies, such as metabolomics and proteomics, in research on the pathogenesis and early detection of GDM. The aim of this paper was to summarise the current knowledge on metabolomic and proteomic changes observed in women with GDM and to assess the potential usefulness of these methods in identifying biomarkers of the disease. The narrative review was conducted in accordance with the PRISMA 2020 statement, using PubMed and Web of Science until 23 December 2025. The studies analysed show that GDM is associated with abnormalities in the metabolism of lipids, amino acids, carbohydrates and metabolites associated with the gut microbiota. The most commonly observed changes included: elevated levels of branched-chain amino acids, free fatty acids and purine metabolites, as well as changes in the metabolism of phospholipids and acylcarnitines. Multi-omics studies also indicate significant changes in plasma protein and lipid profiles. The data collected suggest that omics technologies may be a promising tool for identifying early biomarkers of GDM and for developing our understanding of the pathophysiological mechanisms of this condition. Nevertheless, further studies involving larger and more diverse patient populations are needed to confirm their diagnostic and clinical value. Full article

Lung cancer, particularly non-small cell lung cancer (NSCLC), remains the leading cause of cancer mortality worldwide. While immune checkpoint inhibitors (ICIs) have revolutionized treatment, primary and acquired resistance, and immune-related adverse events (irAEs) limit their therapeutic efficacy. Recent evidence highlights the gut and local microbial communities as a modifiable determinant of NSCLC outcomes, especially in the context of ICI use. Emerging data support the concept of a gut–lung-immune axis, a tridirectional communication pathway, in which gut and lung microbial communities influence local and systemic antitumor immunity through immune cell trafficking, cytokine signaling, and microbial-derived metabolites. In this review, we synthesize current clinical and mechanistic studies examining the role of gut, tumor-resident, and circulating microbiota in shaping ICI efficacy and toxicity in NSCLC. Distinct gut and tumor microbial signatures, such as the abundance of Akkermansia muciniphila and Bifidobacterium, correlate with improved ICI response, whereas dysbiosis promotes immune suppression, resistance, and irAEs. Additionally, we highlight emerging microbial-based biomarkers, including fecal microbial profiles, circulating microbial DNA, and composite tools such as TOPOSCORE, which show promise for predicting response, toxicity, and optimal treatment duration. Overall, these findings underscore the gut–lung-immune axis as a key regulator of immunotherapy outcomes in NSCLC and suggest that microbiome-informed strategies may enable more precise, effective, and safer personalization of ICI therapy. Full article

Salivary microbiota constitutes complex microbial assemblages and acts as a source of reliable non-invasive biomarkers for evaluating growth, metabolism, and health status of farm animals. This review explores the research value of saliva and its resident microbes in livestock health monitoring. We summarize saliva composition, physiological functions, and sampling protocols for pigs, cattle, sheep, and goats. Core microbial taxa of monogastric and ruminant species are outlined, together with their roles in digestion, rumen fermentation, growth, and stress responses. We also present classic salivary diagnostic indicators and the impacts of oral bacteria on common livestock diseases. Current research is limited by undefined causal relationships, low diagnostic specificity, and heterogeneous technical standards, and thus fails to support accurate diagnosis at the individual animal level. Future studies should elucidate microbial interaction mechanisms, standardize experimental protocols, and establish multi-index evaluation models. This review advances theoretical research and promotes the practical application of salivary microbiota in precision livestock farming. Full article

Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality, with substantial heterogeneity that is not fully explained by genetic alterations alone. Emerging evidence positions metabolic reprogramming as a central driver of tumor behavior, integrating glycolysis, mitochondrial function, lipid and amino acid metabolism, and autophagy into coordinated networks that extend beyond cancer cells to the tumor microenvironment. Tumor–immune metabolic competition and metabolite-mediated signaling shape immune responses, often promoting immunosuppression and resistance to immunotherapy, particularly in microsatellite-stable (MSS) CRC. Systemic factors, including obesity, insulin resistance, and the diet–microbiota axis, further modulate tumor metabolism and immune function, reinforcing disease progression. Metabolic biomarkers reflecting these multi-level interactions, spanning tumor-intrinsic pathways, immune contexture, and host metabolism, offer promising opportunities for improved patient stratification and therapeutic targeting, although clinical validation remains limited. Current treatments, including chemotherapy, targeted agents, and immune checkpoint inhibitors, are effective in selected subgroups but are constrained by resistance mechanisms. In this review, we propose an integrative immunometabolic framework in which tumor, immune, and systemic metabolic processes co-evolve, defining CRC progression and treatment response. Targeting this interconnected network through combinatorial and metabolism-oriented strategies may enable precision therapies, particularly for immunotherapy-resistant MSS CRC. Full article

The gut microbiota of fish plays a crucial role in nutrition, metabolism and immune regulation, and is highly sensitive to environmental stressors such as pesticide exposure. This study investigated the effects of emamectin benzoate (EMB) exposure on Asian stinging catfish (Heteropneustes fossilis) gut microbiota using an integrated culture-dependent and culture-independent approach to assess functional and taxonomic dysbiosis. Gut smear samples from control and EMB-treated fish at two sublethal concentrations (0.5 µg/L and 5 µg/L) were analyzed for major functional bacterial groups, including heterotrophic, lipid-hydrolysing, starch-hydrolysing, spore-forming, and Gram-negative bacteria and Pseudomonas spp., using standard plate count techniques. In parallel, microbial community composition and diversity were examined through 16S rRNA (V3–V4 region) gene amplicon sequencing followed by bioinformatic analysis. Culture-based results showed a significant decline in total heterotrophic bacteria and key functional groups in EMB-treated fish, indicating suppression of microbial metabolic activity and functional imbalance. Lipid-hydrolysing and starch-hydrolysing bacteria showed pronounced sensitivity to pesticide exposure, while spore-forming bacteria exhibited a marked reduction, suggesting compromised microbial resilience. Although Gram-negative bacteria declined overall, Pseudomonas spp. displayed a non-linear response, with an initial decrease, followed by partial recovery under higher exposure. Culture-independent analysis demonstrated reduced alpha diversity, altered community structure, and taxonomic shifts in EMB-treated fish. Pseudomonadota exhibited a distinct pattern characterized by decline at 0.5 µg/L and partial recovery at 5 µg/L, reflecting adaptive tolerance rather than restoration of microbial homeostasis. Overall, the combined evidence indicates pronounced EMB-induced gut dysbiosis at both functional and compositional levels. This study highlights the fish gut microbiome as a sensitive biomarker of stress and underscores the ecological risks associated with EMB in aquatic environments. Full article

Background/Objectives: Vitamin D is a nutrient-related secosteroid system with endocrine, paracrine, immunological, and neurodevelopmental actions relevant to nutritional psychiatry. Psychiatric research has often treated vitamin D either as a cross-sectional correlate of depression or as a non-specific supplement expected to act across heterogeneous diagnostic categories. This narrative review aimed to develop a more discriminating framework in which vitamin D is considered a lifespan neuroimmune and immunometabolic signal whose psychiatric relevance depends on developmental timing, biological context, and phenotype. Methods: Evidence was integrated from developmental epidemiology, neonatal dried-blood-spot studies, randomized trials, meta-analyses, Mendelian randomization studies, clinical guidelines, and mechanistic neuroscience. The review focuses on prenatal and neonatal 25-hydroxyvitamin D, vitamin D-binding protein, free and bioavailable vitamin D, vitamin D receptor signaling, immune and microglial pathways, neurotransmitter systems, neurotrophic signaling, mitochondrial function, oxidative stress, hypothalamic–pituitary–adrenal-axis regulation, and the gut–microbiota–immune–brain axis. Results: The available evidence does not support vitamin D as a universal treatment for psychiatric disorders. Instead, vitamin D deficiency and altered vitamin D biology appear most relevant in biologically and clinically defined risk states, including neurodevelopmental vulnerability, inflammatory depression, psychosis liability, severe mental illness with nutritional deprivation, metabolic comorbidity, and cognitive frailty. Mechanistic data support plausible links with cytokine biology, the tryptophan–kynurenine pathway, dopaminergic and serotonergic systems, stress regulation, and neuroimmune homeostasis. Conclusions: Vitamin D should be conceptualized in psychiatry as a context-dependent neuroimmune and immunometabolic signal rather than a generic psychotropic intervention. Future studies should prioritize biomarker-enriched, developmentally timed, nutrition-centered models of precision prevention and adjunctive care. Full article

Inflammatory bowel disease (IBD; Crohn’s disease and ulcerative colitis) arises from convergent dysfunction of the epithelial barrier, mucosal immunity, and gut microbiome on a background of genetic susceptibility and environmental exposures. Diet is among the most modifiable of these exposures, yet much of the diet–microbiome research in IBD remains descriptive and poorly aligned with the molecular pathways linking food to mucosal effects. This comprehensive review reframes the field around functional dysbiosis, in which altered microbial metabolic capacity (rather than taxonomic shifts alone) drives disease-relevant biology. We trace how dietary substrates and additives are converted by gut microbes into bioactive metabolites (short-chain fatty acids, secondary bile acids, tryptophan-derived indoles, sulfur compounds, and polyphenol-derived molecules) and map these to host receptors and signaling pathways governing barrier function, mucus and antimicrobial peptide production, and Treg/Th17 balance. Defined dietary therapies (exclusive enteral nutrition, the Crohn’s disease exclusion diet plus partial enteral nutrition, and Mediterranean-style patterns) are reinterpreted as interventions that reshape microbial metabolic output, and candidate biomarkers for microbiome-informed precision nutrition are evaluated. Microbiota-derived metabolites provide the molecular interface between diet and mucosal immunity in IBD; personalized dietary algorithms remain a research goal, not a validated clinical tool, and diet is best framed as adjunctive to pharmacotherapy and dietitian care. Full article

Anaerobutyricum is a Gram-positive, obligately anaerobic genus within the family Lachnospiraceae that is widely distributed in the gut microbiota of humans and animals. This genus has attracted increasing attention because of its ability to produce short-chain fatty acids, particularly butyrate, a key microbial metabolite involved in intestinal homeostasis, immune regulation, and host energy metabolism. The genus currently comprises only two validly described species, Anaerobutyricum hallii and Anaerobutyricum soehngenii. Despite this limited taxonomic representation, accumulating evidence has linked variation in Anaerobutyricum abundance to host health and disease. In humans, alterations in Anaerobutyricum abundance have been linked to metabolic, inflammatory, and neurodegenerative disorders. In livestock, especially pigs, limited evidence suggests that this genus may also be associated with growth-related traits, intestinal health, and reproductive performance. In this review, we summarize current knowledge of the taxonomy, physiological characteristics, genomic features, metabolic potential, and major factors influencing the abundance of Anaerobutyricum. We further discuss its reported associations with human health and its possible relevance to animal production, with particular attention to pigs at different developmental stages. Overall, Anaerobutyricum appears to be a promising functional genus; however, most available evidence remains association based rather than causal, livestock studies are still sparse, host interaction mechanisms remain poorly understood, and its utility as a probiotic candidate, biomarker, or microbiome-based intervention target requires further strain-level, mechanistic, and in vivo validation. Full article

Background/Objectives: Orthodontic treatment induces controlled mechanical forces that alter the periodontal environment, including changes in oral microbiota composition and activation of local inflammatory pathways. Despite the widespread and growing use of orthodontic appliances across all age groups, the magnitude, timing, and multi-domain biological impact of these changes have not been comprehensively quantified in a single systematic synthesis. This systematic review and meta-analysis aimed to synthesize the available evidence on periodontal clinical parameters, oral microbiota composition, and local inflammatory biomarkers associated with orthodontic treatment using fixed appliances and clear aligners, and to provide a structured, GRADE-rated evidence base for clinical practice. Methods: A systematic review and meta-analysis was conducted in accordance with PRISMA 2020 guidelines. PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to March 2026. Prospective cohort studies, longitudinal clinical studies, and randomized controlled trials evaluating periodontal parameters, oral microbiota, and inflammatory biomarkers during orthodontic treatment were included. Quantitative synthesis was performed using mean differences or standardized mean differences with 95% confidence intervals, primarily assessing within-group (pre–post) changes. Results: Eighteen studies (n = 812 patients; follow-up 3–12 months) met inclusion criteria. Fixed orthodontic appliances were consistently associated with transient increases in plaque index (MD 0.45, 95% CI 0.32–0.58; I² = 62%), gingival index (MD 0.38, 95% CI 0.25–0.51; I² = 55%), and bleeding on probing (MD 15.2%, 95% CI 10.1–20.3%; I² = 48%), particularly during early treatment phases. Microbiological analyses demonstrated within-group shifts toward increased prevalence of periodontopathogenic species (Streptococcus mutans OR 2.45, 95% CI 1.89–3.18; Porphyromonas spp. OR 2.14, 95% CI 1.67–2.75) in patients treated with fixed appliances. Local inflammatory responses were characterized by elevated IL-1β (MD 1.2, 95% CI 0.8–1.6) and IL-6 (MD 0.9, 95% CI 0.6–1.2) in gingival crevicular fluid. Certainty of evidence was rated moderate for plaque and gingival indices and low for microbiological and inflammatory outcomes (GRADE). Conclusions: Orthodontic treatment—particularly with fixed appliances—is associated with transient, reversible deterioration of periodontal indices, shifts toward a more dysbiotic oral microbiome, and elevation of local inflammatory mediators in gingival crevicular fluid during active treatment phases. These changes are manageable through structured preventive protocols and regular periodontal monitoring. Future prospective studies with concurrent control groups and standardized multi-domain outcome measures are needed to better define the magnitude and reversibility of these biological responses. PROSPERO: CRD420261336117. Full article

Background: The biliary and pancreatic tract is increasingly recognized as a microbial ecosystem rather than a sterile environment. Dysbiosis contributes to inflammation, bile acid alterations, and carcinogenesis, with distinct microbiota profiles linked to progression from benign to malignant conditions. Clinical factors, including gut–liver axis disruption and biliary stenting, may further exacerbate microbial imbalance. Objective: The objective of this study is to synthesize current evidence and identify knowledge gaps on the role of biliary microbiota in pancreaticobiliary carcinogenesis and its implications for diagnosis, prognosis, and therapy. Methods: This scoping review was conducted following PRISMA-ScR guidelines. A systematic search of PubMed, Web of Science, and Scopus was performed for studies published between January 2015 and December 2025, guided by the PICo framework. Results: Included studies primarily characterized changes in microbiota composition to identify microbial biomarkers associated with pancreaticobiliary diseases. Predictive bioinformatics analyses suggest that dysbiosis may promote carcinogenesis through metabolic and inflammatory pathways. Machine learning approaches identified microbiota-based signatures with potential diagnostic value for precancerous lesions, although discrimination remains limited. Biliary dysbiosis was also associated with outcomes related to biliary stenting, chemoprophylaxis, postoperative complications, and responses to chemotherapy or surgery. Conclusions: Integration of microbiota profiling with predictive bioinformatics and machine learning may improve understanding of pancreaticobiliary carcinogenesis. Identifying microbial and functional biomarkers could enable personalized diagnostic and therapeutic strategies, ultimately improving patient outcomes. Full article

Type 2 diabetes mellitus is a systemic metabolic disorder with an extensive spectrum of complications, which still persist despite improvements in glycemic control. Emerging evidence suggests that gut dysbiosis may be an underpinning factor in the pathogenesis of both microvascular and macrovascular complications associated with diabetes. This narrative review explores the relationship between gut microbiota and the development of diabetes complications, including nephropathy, retinopathy, neuropathy, cardiovascular, cerebrovascular, peripheral vascular, and reproductive system disorders. First, existing evidence regarding the nature of shared and organ-specific microbial patterns is summarized. Next, key mechanistic pathways of inflammation and metabolism underlying tissue damage induced by dysbiosis are illustrated. Lastly, the role of gut microbiota and inflammaging as modifiers of these processes is described. Emerging clinical and translational implications are finally discussed, underscoring the promises of microbiota-based diagnostics as well as therapeutics that could serve as add-on approaches to the management of diabetic complications, alongside the application of artificial intelligence-based approaches to microbiome data analysis which may enhance biomarker discovery and risk stratification. Overall, although most evidence remains associative, increasing data support that gut microbiota dysbiosis may represent a potential disease modifier in the development of various diabetic complications. Further longitudinal and mechanistic studies are needed to clarify causality and to evaluate the clinical utility of microbiome-targeted interventions, including AI-assisted predictive models, in preventing or mitigating diabetic complications. Full article

The bovine gut microbiota is crucial for many physiological functions, but how microbial interactions and related metabolic processes shift during pregnancy and lactation remains poorly understood. This study utilized fecal samples from 18 Bunaji (White Fulani) cows as a model to examine the gut microbial composition and structure across lactation, pregnancy, and the dry phase using 16S rRNA gene sequencing. Community composition analysis, alpha and beta diversity, LEfSe and correlation analyses were performed to explore the relationship between these reproductive stages, gut microbiota, and concentrations of short-chain fatty acids (SCFAs). Based on the Shannon and Simpson alpha diversity indices, no significant differences among the groups were found. However, beta diversity analysis revealed clear distinctions in microbial community structures between the groups. The most abundant microbial phyla across all three groups were the Bacillota (55–60%) and Bacteroidota (25–33%). At both the family and genus levels, cellulose-degrading bacteria such as Oscillospiraceae, Bacteroidaceae, Sphingobacteriaceae, Intestinimonas, Bacteroides, and Acetivibrio were prevalent across lactating, pregnant, and dry cows. Fifteen genera, including Intestinimonas, Bacteroides, Aristaeella, and Acinetobacter, were identified as potential biomarkers due to their significantly different abundances (p < 0.05) among the groups based on LEfSe. Notably, Spearman’s correlation analysis (p < 0.05) showed significant associations between the levels of specific microbial taxa and SCFA concentrations. In conclusion, although the core gut microbiota was similar across the groups, significant variations in microbial composition were detected. Additionally, these microbial profiles were associated with variations in fecal SCFA levels, indicating a potential interaction between them. Full article