Search Results (2,027)

Weissella, a genus of Gram-positive, facultatively anaerobic lactic acid bacteria, has emerged as a significant component of human microbiota with diverse biotechnological and therapeutic applications. This narrative review examines the current state of knowledge regarding Weissella taxonomy, physiological characteristics, and functional properties based on research spanning from 1993 to present. Weissella species demonstrate remarkable versatility, producing bioactive metabolites including exopolysaccharides (EPS), bacteriocins, and organic acids that confer antimicrobial, antioxidant, and anti-inflammatory properties. These bacteria show significant potential in food fermentation, probiotic applications, and therapeutic interventions for gut health, obesity, and inflammatory conditions. However, challenges persist regarding strain-specific pathogenicity, particularly with W. confusa as an opportunistic pathogen, and the need for comprehensive safety evaluations. Current limitations include variability in probiotic efficacy, incomplete understanding of host-microbe interactions, and gaps in metabolic pathway characterization. This review provides a foundation for advancing Weissella research and applications while highlighting critical areas requiring further investigation to fully harness their biotechnological and therapeutic potential. Full article

Fusobacterium nucleatum (Fn) has been increasingly recognized as a crucial mediator of colorectal cancer (CRC) biology, particularly in microsatellite-stable (MSS) tumors, where immune checkpoint inhibitors (ICIs) have shown limited efficacy. Rather than representing a passive microbial passenger, Fn actively shapes tumor behavior by adhering to epithelial cells, activating oncogenic signaling, and promoting epithelial–mesenchymal transition (EMT). At the same time, it remodels the tumor microenvironment, driving immune suppression through inhibitory receptor engagement, accumulation of myeloid-derived cells, and metabolic reprogramming of tumor-associated macrophages. These mechanisms converge to impair cytotoxic immunity and contribute to both intrinsic and acquired resistance to ICIs. Beyond immune escape, Fn interferes with conventional chemotherapy by sustaining autophagy and blocking ferroptosis, thereby linking microbial colonization to multidrug resistance. Most of these mechanisms derive from preclinical in vitro and in vivo models, where causal relationships can be inferred. In contrast, human data are mainly observational and provide correlative evidence without proving causality. No interventional clinical studies directly targeting Fn have yet been conducted. Its enrichment across the adenoma–carcinoma sequence and consistent detection in both tumor and fecal samples highlight its potential as a biomarker for early detection and patient stratification. Importantly, multidimensional stool assays that integrate microbial, genetic, and epigenetic markers are emerging as promising non-invasive tools for CRC screening. Therapeutic strategies targeting Fn are also under exploration, ranging from antibiotics and bacteriophages to multifunctional nanodrugs, dietary modulation, and natural microbiota-derived products. These approaches may not only reduce microbial burden but also restore immune competence and enhance the efficacy of immunotherapy in MSS CRC. Altogether, current evidence positions Fn at the intersection of microbial dysbiosis, tumor progression, and therapy resistance. A deeper understanding of its pathogenic role may support the integration of microbial profiling into precision oncology frameworks, paving the way for innovative diagnostic and therapeutic strategies in CRC. Full article

Nowadays, two major pathways seem to be responsible for the development and progression of atherosclerosis, namely, high levels of low-density lipoprotein-cholesterol (LDL-C) and low-grade vascular inflammation. Indeed, the concentration of C-reactive protein (CRP), mirroring low-grade systemic inflammation, has been recognized as a more powerful determinant of recurrent cardiovascular (CV) events, death, and all-cause mortality than LDL-C levels. Gut microbiota (GM) dysbiosis is a causal factor for the development of different inflammatory-based pathologies, such as CV disease (CVD). In addition, pre/probiotics showed beneficial effects on GM dysbiosis, by influencing both inflammation and immunity. It has been well documented that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) exert triglyceride (TG)-lowering and antithrombotic effects and play a seminal role in the resolution of inflammatory processes. We showed the recent studies indicating the relationship between pharmacological reduction in inflammatory cytokines and CV outcomes. The principal aim of our review is to highlight the anti-inflammatory and immune-modulatory activities of GM, EPA, and DHA. Then, we pointed out how developing patient-specific pre/probiotic and EPA/DHA interventions alongside the standard of care (SOC) is needed in order to answer several of the questions raised, ranging from diminishing drug toxicity to including frailty individuals. Therefore, hypothetical tailored clinical studies are presented, aiming to treat all the patients at high-risk of CV events, as well as aged people. Full article

Bone immunity represents a dynamic interface where skeletal homeostasis intersects with systemic immune regulation. We synthesize emerging paradigms by contrasting two functionally distinct microenvironments: the marrow cavity, a hematopoietic and immune cell reservoir, and cancellous bone, a metabolically active hub orchestrating osteoimmune interactions. The marrow cavity not only generates innate and adaptive immune cells but also preserves long-term immune memory through stromal-derived chemokines and survival factors, while cancellous bone regulates bone remodeling via macrophage-osteoclast crosstalk and cytokine gradients. Breakthroughs in lymphatic vasculature identification challenge traditional views, revealing cortical and lymphatic networks in cancellous bone that mediate immune surveillance and pathological processes such as cancer metastasis. Central to bone immunity is the neuro–immune–endocrine axis, where sympathetic and parasympathetic signaling bidirectionally modulate osteoclastogenesis and macrophage polarization. Gut microbiota-derived metabolites, including short-chain fatty acids and polyamines, reshape bone immunity through epigenetic and receptor-mediated pathways, bridging systemic metabolism with local immune responses. In disease contexts, dysregulated immune dynamics drive osteoporosis via RANKL/IL-17 hyperactivity and promote leukemic evasion through microenvironmental immunosuppression. We further propose the “brain–gut–bone axis” as a systemic regulatory framework, wherein vagus nerve-mediated gut signaling enhances osteogenic pathways, while leptin and adipokine circuits link marrow adiposity to inflammatory bone loss. These insights redefine bone as a multidimensional immunometabolic organ, integrating neural, endocrine, and microbial inputs to maintain homeostasis. By elucidating the mechanisms of immune-driven bone pathologies, this work highlights therapeutic opportunities through biomaterial-mediated immunomodulation and microbiota-targeted interventions, paving the way for next-generation treatments in osteoimmune disorders. Full article

Inflammatory bowel disease (IBD) demonstrates chronic relapsing inflammation extending beyond adaptive immunity dysfunction. “Trained immunity”—the reprogramming of innate immune memory in myeloid cells and hematopoietic progenitors—maintains intestinal inflammation; however, the mechanism by which gut microbiome orchestration determines protective versus pathological outcomes remains unclear. Microbial metabolites demonstrate context-dependent dual effects along the gut–bone marrow axis. Short-chain fatty acids typically induce tolerogenic immune memory, whereas metabolites like succinate and polyamines exhibit dual roles: promoting inflammation in certain contexts while enhancing barrier integrity in others, influenced by cell-specific receptors and microenvironmental factors. Interventions include precision probiotics and postbiotics delivering specific metabolites, fecal microbiota transplantation addressing dysbiotic trained immunity, targeted metabolite supplementation, and pharmacologic reprogramming of pathological myeloid training states. Patient stratification based on microbiome composition and host genetics enhances therapeutic precision. Future research requires integration of non-coding RNAs regulating trained immunity, microbiome–immune–neuronal axis interactions, and host genetic variants modulating microbiome–immunity crosstalk. Priorities include developing companion diagnostics, establishing regulatory frameworks for microbiome therapeutics, and defining mechanistic switches for personalized interventions. Full article

Healthcare-associated infections (HAIs) in the elderly represent a growing clinical and public health concern, primarily driven by age-related biological remodeling. Key mechanisms include immunosenescence, inflammaging, gut microbiota dysbiosis, and profound metabolic and epigenetic alterations, all of which progressively weaken host defense and resilience to pathogens. In this review, we delineate the molecular pathways underlying these processes, with particular attention to impaired innate and adaptive immune responses, dysfunctional cellular signaling, and disrupted immunometabolic networks that increase susceptibility to multidrug-resistant organisms and aggravate clinical outcomes in older patients. We also address the synergistic impact of frailty-related factors such as malnutrition, multimorbidity, and polypharmacy on infection risk. Finally, we discuss emerging translational perspectives, including nutritional interventions and microbiota-targeted strategies aimed at restoring immune competence and reducing infection burden. By integrating molecular mechanisms with clinical implications, this review highlights innovative opportunities for personalized prevention and management of HAIs in the aging population. Full article

Quinoa (Chenopodium quinoa Willd.) is an ancient Andean crop renowned for its exceptional nutritional profile and diverse bioactive compounds, including polysaccharides, polyphenols, saponins, and essential fatty acids. As global incidence of colonic diseases such as inflammatory bowel disease (IBD), colorectal cancer (CRC), and celiac disease continues to rise, the therapeutic potential of quinoa has garnered increasing scientific attention. This review systematically examines the role of quinoa, with focus on quinoa polysaccharides (QPs), in maintaining and improving colonic health. It summarizes the molecular structure, functional properties, and gut microbiota-modulating effects of QPs, alongside emerging findings on their anti-inflammatory, antioxidant, immunomodulatory, and anticancer activities. Furthermore, the review explores quinoa’s auxiliary effects in mitigating CRC progression and chemotherapy resistance, alleviating intestinal inflammation, and supporting gastrointestinal integrity in celiac patients. By integrating evidence from multi-omics technologies, cell and animal models, and limited clinical studies with mechanistic insights, this review provides a focused synthesis of quinoa bioactive compounds in relation to colonic health. It highlights how precision nutrition and multi-omics approaches could guide future applications of quinoa as a novel functional food-based intervention for colonic diseases. Full article

Intestinal microbiota populations are constantly shaped by both intrinsic and extrinsic factors, including diet, environment, and host genetics. As a result, understanding how to assess, monitor, and exploit microbiome–host interplay remains an active area of investigation, especially in aquaculture. In this study, we analyzed the taxonomic structure and functional potential of the intestinal microbiota of European sea bass and rainbow trout, incorporating gilthead sea bream as a final reference. The results showed that the identified core microbiota (40 taxa for sea bass and 20 for trout) held a central role in community organization, despite taxonomic variability, and exhibited a predominant number of positive connections (>60% for both species) with the rest of the microbial community in a Bayesian network. From a functional perspective, core-associated bacterial clusters (75% for sea bass and 81% for sea bream) accounted for the majority of predicted metabolic pathways (core contribution: >75% in sea bass and >87% in trout), particularly those involved in carbohydrate, amino acid, and vitamin metabolism. Comparative analysis across ecological phenotypes highlighted distinct microbial biomarkers, with genera such as Vibrio, Pseudoalteromonas, and Paracoccus enriched in saltwater species (Dicentrarchus labrax and Sparus aurata) and Mycoplasma and Clostridium in freshwater (Oncorhynchus mykiss). Overall, this study underscores the value of integrating taxonomic, functional, and network-based approaches as practical tools to monitor intestinal health status, assess welfare, and guide the development of more sustainable production strategies in aquaculture. Full article

Traumatic brain injury (TBI) remains a major global health problem, contributing significantly to morbidity and mortality worldwide. Despite advances in understanding its complex pathophysiology, current therapeutic strategies are insufficient in addressing the long-term cognitive, emotional, and neurological impairments. While the primary mechanical injury is immediate and unavoidable, the secondary phase involves a cascade of biological processes leading to neuroinflammation, blood–brain barrier (BBB) disruption, and systemic immune activation. The heterogeneity of patient responses underscores the urgent need for reliable biomarkers and targeted interventions. Emerging evidence highlights the gut–brain axis as a critical modulator of the secondary phase, with microbiota-derived extracellular vesicles (MEVs) representing a promising avenue for both diagnosis and therapy. MEVs can cross the intestinal barrier and BBB, carrying biomolecules that influence neuronal survival, synaptic plasticity, and inflammatory signaling. These properties make MEVs promising biomarkers for early detection, severity classification, and prognosis in TBI, while also offering therapeutic potential through modulation of neuroinflammation and promotion of neural repair. MEV-based strategies could enable tailored interventions based on the individual’s microbiome profile, immune status, and injury characteristics. The integration of multi-omics with artificial intelligence is expected to fully unlock the diagnostic and therapeutic potential of MEVs. These approaches can identify molecular subtypes, predict outcomes, and facilitate real-time clinical decision-making. By bridging microbiology, neuroscience, and precision medicine, MEVs hold transformative potential to advance TBI diagnosis, monitoring, and treatment. This review also identifies key research gaps and proposes future directions for MEVs in precision diagnostics and gut microbiota-based therapeutics in neurotrauma care. Full article

Objectives: Emerging evidence suggests that propolis possesses significant anti-obesity properties. While gut hormones and microbiota are known to play crucial roles in obesity development, the specific mechanisms through which propolis exerts its effects via the gut hormone axis remain poorly characterized. Methods: A high-fat diet (HFD) rat model was established to investigate the regulatory effects of propolis. After 10 weeks of intervention, blood serum, liver, colon tissues, and luminal contents were analyzed for metabolic parameters, gene expression of gut hormones and AMPK pathway markers, microbial community structure, and short-chain fatty acid production. Results: Propolis effectively mitigated HFD-induced metabolic disturbances, including excessive weight gain, adipose tissue accumulation, hyperlipidemia, and hepatic dysfunction. These improvements were associated with significant upregulation of the AMPK pathway. Importantly, propolis enhanced intestinal barrier integrity and differentially modulated gut hormone expression by increasing the mRNA levels of Cck, Gip, and Ghrl, and decreasing Lep and Gcg levels. 16S rRNA sequencing analysis revealed that propolis administration selectively enriched butyrate- and propionate-producing bacterial species. Correlation analysis further identified the Eubacterium brachy group as a pivotal microbial mediator in the propolis-modulated gut microbiota–gut hormone–liver AMPK axis. Conclusions: Our findings establish that propolis ameliorates obesity-related metabolic disorders by orchestrating crosstalk among gut microbiota, enteroendocrine hormones, and hepatic AMPK signaling. These results elucidate a novel mechanistic pathway in rodents; however, their direct translatability to humans requires further clinical investigation. This tripartite axis offers a mechanistic foundation for developing microbiota-targeted anti-obesity therapies. Full article

Gut microbiota has increasingly been shown to exert effects beyond the gastrointestinal tract, some of which are mediated through its metabolites, such as trimethylamine N-oxide (TMAO)—a compound converted by gut bacteria from dietary choline found predominantly in animal products that is associated with cardiovascular disease (CVD). However, a significant gap persists in human clinical trials assessing its potential causal role. This narrative review aims to present the current understanding of the gut microbiome, TMAO, and their relationship with CVD, while proposing future directions that may support the use of TMAO as a biomarker and guide potential interventions to reduce its harmful impact. Both animal and human studies have demonstrated a link between TMAO and CVD, with animal studies also indicating a causal effect—showing increased cardiovascular risk following TMAO administration and reduced risk when TMAO is eliminated. While direct extrapolation from animal models to humans is limited due to biological differences, these findings offer a foundation for the development of well-designed clinical trials in human populations. Although direct approaches to target TMAO—such as trimethylamine (TMA) lyase inhibitors and antisense oligonucleotide (ASO) therapy—have shown promising results in animal studies, they have yet to be investigated in human trials, leaving indirect strategies such as dietary changes and probiotics as the only currently available options. Full article

Background/Objectives: Infant diarrhea is a major global cause of morbidity and mortality. While Bifidobacterium is linked to diarrhea, its preventive effects, underlying mechanisms, and potential synergistic benefits with prebiotics remain unclear. The objective of this study was to explore the efficacy of a synbiotic composed of Bifidobacterium animalis subsp. lactis BB-12 (BB-12) and 2′-fucosyllactose (2′-FL) in alleviating infant diarrhea. Methods: One-week-old C57BL/6J mice were used to construct a model of infant diarrhea via infection with enteropathogenic Escherichia coli (EPEC) O127. Mice were administered BB-12 (10⁸ CFU per mouse), 2′-FL (1 g/kg), or their combination (synbiotic) for three consecutive weeks. Results: Administration of the synbiotic not only markedly improved diarrhea, anxiety-like behavior, colon inflammation, and gut barrier function but also positively reshaped the microbial community. This was achieved through a significant rise in short-chain fatty acid (SCFA)-producing bacteria (e.g., Akkermansia and Paraprevotella), a rise in fecal SCFAs, and a reduction in harmful bacteria such as Escherichia. Conclusions: The synbiotic effectively relieves EPEC-induced infant diarrhea by regulating gut microbiota composition and metabolic functions. These findings highlight its potential as a dietary intervention in infant diarrhea and provide new insights into infant health applications. Full article

Background/Objectives: With increasing knowledge of the role of the microbiota in health and disease, the need for the reliable simulation of its behavior in response to various factors, such as diet and probiotic administration in in vitro conditions, has emerged. Although many studies utilize developed systems, data on how accurately these systems represent individual microbiota responses are scarce. Methods: In the present study, the Simulator of Human Intestinal Microbial Ecosystem (SHIME^®) was exposed to experimental conditions mimicking the application of probiotics and dietary changes in the study participant. Next-generation 16S rRNA sequencing was used to reveal the structure of the microbial communities in the analyzed samples. Results: Analysis of 17 samples revealed that predominantly diet and, to a lesser extent, probiotics had a divergent effect on the microbiota’s fluctuations dependent on the culture environment. Despite this, results from both in vitro and in vivo conditions aligned well with previously published data on the expected impact of dietary changes on the intestinal microbial community. Conclusions: The anecdotal evidence presented in this study suggested that current in vitro technology enables the reproduction of some of the microbiota responses that are well known from in vivo research. However, further work is required to enable simulations of an individual microbiota. Full article

This study was designed to first investigate the effects of zinc phytate (ZnPA) from wheat bran in alleviating high-fat diet (HFD)-induced hepatic inflammation and metabolic disorders and its underlying mechanism. C57BL/6J mice were randomly assigned to five groups including normal diet (ND), HFD, HFD+low-dose ZnPA (100 mg/kg), HFD+high-dose ZnPA (200 mg/kg), and HFD+wheat bran (100 mg/kg). All interventions were administered orally for 12 weeks. The results indicated that ZnPA significantly mitigated HFD-induced weight gain, dyslipidemia, pathoglycemia, hepatic steatosis and inflammation (p < 0.05). ZnPA effectively corrected HFD-induced microbial dysbiosis, in which the relative abundance of the Ruminococcus torques group decreased from 11.0% to 0.75%, and Coriobacteriaceae_UCG-002 dropped from 2.47% to 0.087% (p < 0.05). Conversely, ZnPA increased the abundance of Ileibacterium from 0.32% to 17.76% and Dubosiella from 1.03% to 4.24% (p < 0.05). Meanwhile, ZnPA could be metabolized by the gut microbiota to release IP6, which was further converted into secondary inositol phosphates (InsP_3–5), resulting in increases of 52.1%, 83.3%, 62.5%, and 96.2% in the colonic contents of InsP₆, InsP₅, InsP₄, and InsP₃ (p < 0.05), respectively. In addition, ZnPA increased levels of secondary bile acids and short-chain fatty acids, especially deoxycholic acid and taurocholic acid, which were elevated by 1.95-fold and 1.88-fold (p < 0.05), respectively. Interestingly, ZnPA enhanced hepatic expressions of histone deacetylase 3, bile acid receptor FXR, and lipid metabolism coactivator PGC-1α (p < 0.05). Collectively, these results indicated that ZnPA might alleviate obesity-related hepatic inflammation and metabolic disorders by reshaping microbial composition and increasing the production of microbial metabolism such as secondary bile acids, thereby triggering FXR–PGC1α axis activation. Full article

Background: Alterations of the gut microbiota have been increasingly implicated in the pathogenesis of dementia through mechanisms involving systemic inflammation, immune dysregulation, and gut–brain axis disruption. Clinical evidence, however, remains fragmented. Objectives: This systematic review aimed to characterize gut microbiota profiles in individuals with mild cognitive impairment (MCI) or Alzheimer’s dementia (AD), explore mechanistic associations with neurodegeneration, and evaluate the impact of microbiota-targeted interventions on cognitive outcomes. Methods: Following PRISMA 2020 guidelines and a registered protocol (PROSPERO CRD420251074832), PubMed/Medline was searched through May 2025. Eligible studies included randomized controlled trials (RCTs) and cohort and case–control studies assessing microbiota composition or interventions in participants with MCI or AD. Results: Twenty-one studies were included (1 RCT, 20 observational; sample size 22–302). Most used 16S rRNA sequencing; one used shotgun metagenomics. Across cohorts, MCI and AD patients consistently showed reduced short-chain fatty acid-producing bacteria (Faecalibacterium, Ruminococcaceae, Lachnospiraceae) and increased pro-inflammatory taxa (Escherichia/Shigella, Enterobacteriaceae, Bacteroides). Several studies reported reduced microbial diversity. Specific taxa, including Akkermansia muciniphila and Faecalibacterium, were associated with amyloid burden, hippocampal atrophy, and cognitive decline. Environmental and dietary factors influenced microbial composition and cognition. The RCT reported that probiotic supplementation improved inflammatory markers and BDNF levels, although changes in microbiota composition were inconsistent. Conclusions: Gut dysbiosis is strongly associated with cognitive impairment and markers of neurodegeneration. Modulation of the microbiota through diet and probiotics emerges as a promising avenue for dementia prevention and management, though robust longitudinal and interventional studies are needed to confirm causality and therapeutic efficacy. Full article