Search Results (814)

Marine bioactive substances exhibit structural diversity and function-specific properties, attracting considerable interest in their potential applications in targeted nutritional delivery to the gut and microbiota regulation. These bioactive components, sourced from seaweed, marine crustaceans, and microorganisms, including polysaccharides, polyphenols, and lipids, demonstrate exceptional biocompatibility and specific recognition capabilities. They serve as an optimal carrier matrix and functional core for developing an efficient, precision-targeted intestinal nutrition delivery system. Research findings demonstrate that optimization via innovative delivery technologies, including nanoencapsulation and polymer microsphere encapsulation, enables marine bioactive substances to navigate various physiological barriers in the gastrointestinal tract effectively. This facilitates targeted, sustained release of nutritional components and enhances bioavailability. Simultaneously, these substances may relieve dysbiosis by modulating the composition of the gut microbiota and the quantity and activity of specific metabolic products, thereby reinforcing intestinal barrier integrity. This narrative review systematically examines the sources and functional attributes of marine bioactive compounds, emphasizing their application strategies in developing targeted delivery systems for the gut and their regulatory effects on gut microbiota. It concludes by delineating future research directions in this field, particularly in optimizing carrier functionalities and clarifying action mechanisms. Full article

Growing limitations on the use of in-feed antibiotics have accelerated the search for functional feed additives capable of supporting animal health and productivity under antibiotic-free production systems. Postbiotics, defined as non-viable microbial products or metabolic byproducts, and phytogenics, which are plant-derived bioactive compounds, have emerged as promising alternatives due to their stability and biological activity. Recent advances in the application of postbiotics and phytogenics in monogastric and ruminant nutrition are summarized, with emphasis on their mechanisms of action, synergistic effects, and impacts on gut health, immune function, and growth performance. Postbiotics modulate the gut microbiota, enhance epithelial barrier integrity, and regulate immune signaling, whereas phytogenic compounds provide antimicrobial, antioxidant, and digestive-stimulant effects. Available evidence suggests that combined strategies can enhance efficacy, particularly under production-related stress. Key challenges related to formulation, dose–response relationships, stability, and regulatory classification are discussed together with emerging omics-based approaches that support precision formulation. Overall, integration of multi-omics evidence with formulation and regulatory considerations supports the practical use of postbiotics and phytogenics in commercial livestock systems. Full article

Microcin C7 (McC7) is a ribosomally synthesized antimicrobial peptide that has emerged as a promising candidate due to its dual antibacterial and immunomodulatory activities. This study evaluated the preventive effect of McC7 against cyclophosphamide (CTX)-induced immunosuppression and intestinal injury. An immunosuppression model was established by intraperitoneal CTX injection in mice, which were randomly allocated into five groups (n = 15): a negative control, a CTX model group, and three McC7 treatment groups receiving dietary McC7 at 100, 200, or 400 mg/kg both before and during CTX exposure. Body weight and feed intake were monitored throughout the study. Organ indices, serum biochemical parameters, immune and antioxidant markers, and intestinal morphology were assessed. Splenic T-cell subsets were analyzed by flow cytometry, and gut microbiota composition was evaluated by 16S rRNA sequencing. McC7 supplementation significantly attenuated the CTX-induced reduction in body weight, feed intake, and organ indices, ameliorated markers of hepatic and renal injury, and restored the splenic CD4⁺/CD8⁺ T-cell ratio. McC7 enhanced intestinal mucosal barrier integrity, increased the abundance of beneficial bacteria such as Candidatus Arthromitus and ASF356, and reduced the abundance of the potentially pathogenic genus Bilophila. In conclusion, our results demonstrate that McC7 alleviates CTX-induced immunosuppression by regulating T-cell differentiation, maintaining cytokine homeostasis, and modulating gut microbial composition to support intestinal health. Full article

Background/Objectives: Whether saponins aid in whey protein supplementation remains unclear. We aimed to investigate the effects of Astragalus and Panax saponins (APS) on whey protein absorption, intestinal permeability, and muscle function in healthy adults across different age groups. Methods: A randomized, double-blind, placebo-controlled crossover trial was conducted with 30 healthy participants equally stratified into three age groups (18–25, 26–59, and 60–80 years), over two phases: a single-dose trial to measure immediate amino acid absorption from whey protein and a 4-week phase combining daily supplementation with resistance training to assess long-term effects on amino acid absorption kinetics, muscle function, and gut health. Results: Immediate APS supplementation resulted in a 6.67% higher area under the curve for valine, 3.62% for leucine, and 0.15% for isoleucine, compared with the placebo. After 4 weeks, APS supplementation significantly increased the absorption of valine (14.07%) and leucine (8.34%) and improved the absorption of isoleucine (6.33%). The effects were most pronounced in older adults (60–80 years), who showed a 12.74% increase in total essential amino acid absorption. APS also caused a substantially greater increase (APS: +5.20% vs. placebo: +2.44%) in grip strength, an increase (APS: +0.85% vs. placebo: +0.68%) in muscle mass, and a reduction in blood zonulin levels (APS: −13.01% vs. placebo: −0.9%), indicating improved muscle function and intestinal barrier integrity, without adverse effects on liver or kidney function. Conclusions: APS supplementation enhances amino acid absorption from whey proteins, muscle function and gut barrier integrity, especially in older adults. These findings highlight its synergistic role in improving protein supplementation efficacy for those with age-related muscle loss. Full article

Background: Exercise-induced fatigue (EIF) impairs performance and recovery and may contribute to overreaching/overtraining and adverse health outcomes. Beyond classical explanations (substrate depletion, metabolite accumulation, oxidative stress), accumulating evidence indicates that the gut microbiota modulates fatigue-related physiology through metabolic, immune, barrier, and neurobehavioral pathways. Methods: We conducted a structured narrative review of PubMed and Web of Science covering 1 January 2015 to 30 November 2025 using predefined keywords related to EIF, gut microbiota, recovery, and nutritional interventions. Human studies, animal experiments, and mechanistic preclinical work (in vivo/in vitro) were included when they linked exercise load, microbial features (taxa/functions/metabolites), and fatigue-relevant outcomes. Results: Across models, high-intensity or prolonged exercise is consistently associated with disrupted gut homeostasis, including altered community structure, reduced abundance of beneficial taxa, increased intestinal permeability, and shifts in microbial metabolites (e.g., short-chain fatty acids). Evidence converges on four interconnected microbiota-mediated pathways relevant to EIF: (1) energy availability and metabolic by-product clearance; (2) redox balance and inflammation; (3) intestinal barrier integrity and endotoxemia risk; and (4) central fatigue and exercise motivation via microbiota–gut–brain signaling. Nutritional strategies—particularly targeted probiotics, prebiotics/plant polysaccharides, and selected bioactive compounds—show potential to improve fatigue biomarkers and endurance-related outcomes, although effects appear context-dependent (exercise modality, baseline fitness, diet, and baseline microbiota). Conclusions: Current evidence supports a mechanistic role of the gut microbiota in EIF and highlights microbiota-targeted nutrition as a promising adjunct for recovery optimization. Future work should prioritize causal validation (e.g., fecal microbiota transplantation and metabolite supplementation), athlete-focused randomized trials with standardized fatigue endpoints, and precision approaches that stratify individuals by baseline microbiome features and training load. Full article

Infectious diseases present persistent and complex challenges to global public health, with conventional antibiotic therapies increasingly limited by antimicrobial resistance, microbiota disruption, and adverse effects. There is a critical need to explore complementary strategies that augment host defense mechanisms without exacerbating these limitations. Accumulating evidence underscores the integral role of the gut microbiota—a diverse microbial ecosystem within the gastrointestinal tract—in regulating systemic immunity and pathogen susceptibility. This review synthesizes recent advances from animal models to delineate the multi-faceted mechanisms by which commensal microbes and their metabolites confer protection against enteric and respiratory infections. Key processes include competitive exclusion for nutrients and ecological niches, production of antimicrobial compounds, reinforcement of intestinal barrier integrity, and orchestration of local and systemic immunity via gut–lung axes. We further discuss the potential of microbiota-targeted interventions to enhance treatment efficacy and patient outcomes. By integrating mechanistic insights with translational applications, this review aims to inform the rational design of next-generation anti-infective strategies grounded in microbial ecology and host immunobiology. Full article

Escherichia coli O157:H7 is a pathogenic bacterium that causes severe intestinal infections characterized by inflammation and disruption of the intestinal barrier. Probiotic lactic acid bacteria (LAB) from milk can support intestinal health and combat enteric pathogens; however, the potential of feline milk-derived LAB against E. coli O157:H7 infection remains unclear. In this study, Pediococcus acidilactici (P. acidilactici) M22, isolated from feline milk, was evaluated for probiotic activity in vitro and in vivo in a C57BL/6 mouse model of Escherichia coli O157:H7 infection. In vitro assays demonstrated that M22 significantly inhibited the adhesion of Escherichia coli O157:H7 to intestinal epithelial cells. For in vivo assessment, C57BL/6 mice were orally administered M22 prior to infection with E. coli O157:H7. Protective effects were evaluated by monitoring body weight loss, colon length, disease activity index (DAI), myeloperoxidase (MPO) activity, cytokine levels, tight junction protein expression, oxidative stress markers, and gut microbiota composition. M22-treated mice exhibited significantly less body weight loss and lower DAI scores than infected controls. M22 also prevented colon shortening, indicating reduced colonic damage. Probiotic treatment attenuated neutrophil infiltration and mucosal inflammation, as evidenced by decreased colonic MPO activity, reduced levels of pro-inflammatory cytokines, and elevated anti-inflammatory IL-10. Additionally, M22 preserved intestinal barrier function by upregulating tight junction proteins and mitigating infection-induced histopathological changes. M22 supplementation enhanced antioxidant defenses in colonic tissue (lower malondialdehyde, higher superoxide dismutase and glutathione), indicating reduced oxidative stress. Furthermore, gut microbiota analysis (16S rRNA sequencing) revealed that M22 counteracted infection-induced dysbiosis, restoring microbial diversity and a healthy composition (enrichment of beneficial commensals and suppression of harmful bacteria). By safeguarding intestinal integrity and homeostasis, M22 emerges as a promising next-generation probiotic for improving intestinal health in companion animals. Full article

Aging is a multifactorial biological process marked by the progressive decline in cellular and physiological functions, increasing susceptibility to chronic diseases and mortality. Recent research has identified the gut microbiome as a key modulator of aging, influencing immune regulation, metabolic homeostasis, and neuroendocrine signaling. A diverse and balanced gut microbiota promotes healthspan by supporting gut barrier integrity, nutrient metabolism, and anti-inflammatory responses, whereas dysbiosis contributes to the onset and progression of age-related diseases, including neurodegeneration, cardiovascular conditions, cancer, and metabolic disorders. Currently, anti-aging interventions targeting key aging pathways, such as insulin/IGF-1 signaling, mTOR, AMPK, and sirtuins, are a major focus in the field of geroscience. Compounds such as metformin, rapamycin, anti-inflammatories, GLP-1 agonists, senolytics, spermidine, SGLT2 inhibitors, and sirtuin activators have shown lifespan extension in animal models. In humans, some of these interventions are associated with improvements in healthspan-related outcomes, including metabolic, cardiovascular, musculoskeletal, respiratory, cognitive and ocular functions. Notably, the gut microbiome may serve as both a mediator and modulator of these interventions, influencing drug metabolism, efficacy, and host responses. This review synthesizes current evidence on the gut microbiome’s role in aging, examining its role as both mediator and modulator of longevity interventions and how microbiome-associated mechanisms intersect with emerging anti-aging therapeutics. Full article

Neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) share key molecular features, including neuroinflammation, oxidative stress, mitochondrial dysfunction, and progressive neuronal loss. Increasing evidence indicates that gut dysbiosis and alterations in microbiota-derived metabolites are involved in these processes through multiple pathways along the gut–brain axis. However, while broad compositional changes are well-documented, a critical knowledge gap remains regarding the specific biochemical signal transduction pathways translating dysbiosis into pathology. This narrative review addresses this gap by synthesizing current human and experimental studies addressing gut microbiota alterations in AD, PD, and ALS, with particular emphasis on the biochemical and molecular mechanisms mediated by gut-derived metabolites. Dysbiosis in neurodegenerative diseases is frequently associated with reduced abundance of short-chain fatty acid (SCFA)-producing bacteria and altered metabolism of SCFAs, bile acids, tryptophan-derived indoles, trimethylamine-N-oxide (TMAO), and lipopolysaccharides (LPS). These microbial metabolites have been shown to modulate intestinal and blood–brain barrier integrity, influence Toll-like receptor- and G protein-coupled receptor-dependent signaling, regulate microglial activation, and affect molecular pathways related to protein aggregation in experimental models. In addition, emerging evidence highlights the involvement of oxidative and nitrosative stress, immune–metabolic crosstalk, and altered xenobiotic metabolism in microbiota–host interactions during neurodegeneration. By integrating microbiological, metabolic, and molecular perspectives, this review underscores the important and emerging role of microbiota-derived molecules in neurodegenerative disorders and outlines key chemical and metabolic pathways that may represent targets for future mechanistic studies and therapeutic strategies. Full article

Background: Antibiotics are essential for treating infections; however, they disrupt the microbiome and key microbiome-dependent functions. Clinical evidence is mixed for probiotic supplementation following antibiotics due to product heterogeneity and inconsistencies in evaluating biological mechanisms that drive clinical consequences. Accordingly, this study investigates the effects of a multi-species synbiotic on gut microbiome composition and function, and gut barrier integrity, during and following antibiotics. Methods: In a randomized, placebo-controlled trial designed to assess proof-of-mechanism, healthy adult participants received a daily synbiotic (53.6 billion AFU multi-species probiotic and 400 mg Indian pomegranate extract; DS-01) or matching placebo for 91 days. All participants also received ciprofloxacin (500 mg orally twice daily) and metronidazole (500 mg orally three times daily) for the first 7 days. Samples were collected at baseline and Days 7, 14, 49, and 91. Endpoints included fecal microbiome composition, fecal acetate and butyrate levels, urinary Urolithin A (UroA), serum p-cresol sulfate (pCS), gut barrier integrity, and safety. Results: The multi-species synbiotic significantly increased the alpha-diversity of Bifidobacterium and Lactobacillus at all timepoints compared to placebo, including short-term (Day 7, p < 0.0001) and end-of-study (Day 91, p < 0.001). The multi-species synbiotic enhanced recovery of native beneficial microbes, including butyrate-producing species and a novel Oscillospiraceae species (UMGS1312 sp900550625, p < 0.001). Beneficial microbiome-dependent metabolites increased, including fecal butyrate (119%, p < 0.05), fecal acetate (62%, p < 0.01), and UroA (13,008%, p < 0.05), whereas detrimental metabolite pCS decreased (68%, p < 0.05) compared to placebo. Functionally, the multi-species synbiotic improved gut barrier integrity rapidly (Day 7; 305%, p < 0.05) and over the long-term (Day 91; 161%, p < 0.05) compared to placebo. Conclusions: During and after antibiotics, this multi-species synbiotic promotes recovery of gut microbiome diversity and native beneficial microbes, microbiome metabolite recovery, and gut barrier function, all of which underpin antibiotic-associated gastrointestinal symptoms. Full article

The escalating challenge of antimicrobial resistance has spurred interest in probiotics as alternatives for combating bacterial infections. This study aimed to isolate and characterize probiotic Lactobacillus johnsonii (L. johnsonii) from yak feces with protective efficacy against acute Escherichia coli (E. coli) infection. In vitro, DY2 supernatant inhibited the growth of E. coli. In vivo, mice pretreated orally with DY2 (1 × 10⁹ CFU/mL) for 21 days before E. coli challenge exhibited significantly reduced weight loss (p < 0.001), lower bacterial translocation in the intestines (p < 0.001), and normalized organ indices (p < 0.05) compared to untreated infected controls. DY2 modulated host immune and oxidative responses by significantly lowering serum levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6; p < 0.001 to p < 0.05) and malondialdehyde (MDA; p < 0.001), while elevating levels of the anti-inflammatory IL-10 (p < 0.05) and antioxidant enzymes (SOD, GSH-Px, T-AOC; p < 0.001 to p < 0.01). Histologically, DY2 preserved intestinal mucosal integrity, with reduced villus shortening and inflammatory infiltration (p < 0.001 for villus length in key segments). 16S rRNA sequencing of intestinal microbiota revealed enhanced α-diversity (p < 0.05 to p < 0.001), community stability, and enrichment of beneficial genera such as Butyricimonas in DY2-treated mice. Conclusively, Lactobacillus johnsonii DY2 protects against acute E. coli infection via anti-inflammatory, antioxidant, gut barrier strengthening, and microbiota-modulating activities. Yak-derived lactobacilli are promising probiotics with excellent antibacterial properties. Full article

This review examines how distinct gut microbial community configurations—characterized by differential enrichment of Bacteroides, Prevotella, Ruminococcus, Bifidobacterium, and Lachnospira—may be associated with variations in host redox homeostasis through microbiota-derived metabolites, including short-chain fatty acids, secondary bile acids, and tryptophan derivatives. These compositional patterns represent reproducible features across populations and correlate with differential disease susceptibility in metabolic disorders. While microbial communities exist along compositional continua rather than discrete clusters, stratification based on dominant patterns offers a pragmatic framework for interpreting large-scale microbiome datasets and guiding precision nutrition interventions. Observational evidence suggests Bacteroides-enriched communities may associate with pro-inflammatory signatures, whereas Prevotella- Ruminococcus, Proteobacteria, Bifidobacterium, and Lachnospira-enriched configurations may exhibit anti-inflammatory or antioxidant characteristics in certain populations. However, inter-population variability and species- and strain-level heterogeneity limit generalization. Condition-dependent effects are exemplified by Prevotella copri, which demonstrates pro-inflammatory responses in specific settings despite beneficial profiles in others. When dysbiosis compromises intestinal barrier integrity, microbial translocation may amplify chronic oxidative stress and immune activation. We evaluate therapeutic potential of beneficial genera including Lactobacillus and Bifidobacterium while examining the dose-dependent, context-specific, and sometimes paradoxical effects of key metabolites. Microbiota-stratified therapeutic strategies—personalizing dietary, probiotic, or prebiotic interventions to baseline community composition—show promise but remain at proof-of-concept stage. Current evidence derives predominantly from cross-sectional and preclinical studies; prospective interventional trials linking community stratification with oxidative stress biomarkers remain scarce. The community–redox relationships presented constitute a hypothesis-generating framework supported by mechanistic plausibility and observational associations, rather than established causal pathways. Future research should prioritize intervention studies assessing whether aligning therapeutic approaches with baseline microbial configurations improves outcomes in oxidative stress-related metabolic disorders. Full article

The increasing and global distribution of microplastics and nanoplastics (MPs/NPs) in the environment has led to concern about their potential influence on human health, especially on the gastrointestinal tract, as well as the brain. MPs/NPs could traverse epithelial and endothelial barriers, disrupt the gut microbiota, and perturb the microbiota–gut–brain axis, leading to systemic inflammation and possibly extending neurodegenerative processes. Experimental models now demonstrate that MPs/NPs reprogram nuclear and mitochondrial epigenetics—DNA methylation, histone modifications, non-coding RNAs, and mitochondrial DNA regulation—in gut, immune, and neural cells with downstream effects on synaptic function, neuronal survival, and protein aggregation. This mechanistic narrative review integrates preclinical and emerging human evidence of how MPs/NPs compromise intestinal barrier integrity, modulate gut microbiota composition, affect the blood–brain barrier, and converge on oxidative stress, neuroinflammatory signaling, and cell death pathways within the central nervous system across key neurodegenerative diseases. Overall, the review offers an integrated model in which environmental exposure to chronic MPs/NPs disrupts the microbiota–gut–brain axis and drives concurrent nuclear and mitochondrial epigenetic remodeling, lowering the threshold for neurodegeneration in susceptible individuals, while outlining candidate mechanistic readouts that require exposure-specific validation in human-relevant models and longitudinal cohorts. Full article

Sepsis is a life-threatening condition characterized by a dysregulated host response to infection, often resulting in multiorgan dysfunction. Among affected systems, the gastrointestinal tract plays a central role in sepsis progression by promoting systemic inflammation through impaired barrier function, immune imbalance, and microbiome alterations. Recent research has identified selected medical gases and gasotransmitters as promising therapeutic candidates for preserving gut integrity in sepsis. In particular, hydrogen, carbon monoxide, and hydrogen sulfide exhibit antioxidative, anti-inflammatory, and cytoprotective properties. These gases act through defined molecular pathways, including activation of Nrf2, inhibition of NF-κB, and preservation of tight junction integrity, thereby supporting intestinal barrier function. In addition, they influence immune cell phenotypes and autophagy, with indirect effects on the gut microbiome. Although most supporting evidence derives from preclinical models, translational findings and emerging safety data highlight the potential of gut-targeted gas-based strategies. This review summarizes current mechanistic and translational evidence for gut-protective medical gases in sepsis and discusses their integration into future organ-specific and mechanism-based therapeutic approaches. Full article

Objective: The study aims to evaluate the diagnostic and prognostic efficacy of gut-derived trimethylamine N-oxide (TMAO) as a molecular biomarker for heart failure (HF) in comparison to the N-terminal pro-B-type natriuretic peptide. Background: The clinical value of N-terminal pro-B-type natriuretic peptide (NT-proBNP) is frequently affected by non-cardiac physiological variables, including adiposity, advanced age, and renal clearance rates. Consequently, there is a compelling need for additional biomarkers. This analysis investigates TMAO as a critical mediator within the gut–heart axis, reflecting systemic inflammation and myocardial fibrosis secondary to intestinal dysbiosis. Methods: A comprehensive literature search was conducted using PubMed. Keywords such as “trimethylamine N-oxide”, “heart failure”, “heart failure with preserved ejection fraction” and “N-terminal pro-B-type natriuretic peptide” were used. The inclusion criteria comprised original research and literature reviews describing the pathophysiological mechanisms and clinical utility of TMAO in the context of HF diagnosis and prognosis. Results: The analyzed literature suggests that TMAO functions as an independent predictor of major adverse cardiovascular events, correlating with all-cause mortality and rehospitalization risk across all HF phenotypes. Furthermore, data indicate that using TMAO alongside NT-proBNP measurements may predict patient risk more accurately, particularly in patients where natriuretic peptide interpretation is traditionally obscured by comorbidities such as diabetes mellitus and chronic kidney disease. Conclusions: Although NT-proBNP remains the gold standard for acute diagnosis, TMAO provides significant value for long-term clinical management. By serving as a metabolic–inflammatory indicator, TMAO complements standard diagnostic panels, offering deeper insights into the prognostic trajectory and the underlying intestinal barrier integrity of patients with HF. Full article