Search Results (190)

As two representative environmental contaminants, the individual toxic effects of microplastics and triclosan have been extensively studied; however, systematic evidence regarding their combined toxicity in mammals and the underlying mechanisms remains lacking. In this study, mice were orally exposed to triclosan (TCS) or/and polystyrene microplastics (PS), and their toxicity to intestine and liver was evaluated through histopathological examination, biochemical assays, and 16S rRNA sequencing. Results demonstrated that co-exposure to TCS and PS elicited markedly aggravated toxicological effects compared to individual exposures. Histopathological evaluation revealed exacerbated tissue damage, with histological scores substantially higher in co-exposed mice (colon: 7.27; liver: 5.0) than in PS-alone (colon: 6.07; liver: 3.0) or TCS-alone (colon: 3.0; liver: 0.7) groups. Quantitative Integrated Biomarker Response (IBR) analysis confirmed this potential additive or synergistic interaction: co-exposure not only dramatically elevated colonic oxidative stress (R_IB = 12.30 vs. 5.88 in PS and 0.23 in TCS groups) but also exacerbated inflammatory responses (R_IB = 11.69 vs. 3.52 in PS and 0 in TCS). Hepatic assessment demonstrated the most severe compromise in liver function and oxidative homeostasis following co-exposure (R_IB = 16.48), markedly exceeding the effects of individual PS (4.75) or TCS (0.43) exposure. In-depth exploration found that co-exposure to TCS and PS significantly disrupted gut microbiota homeostasis, characterized by enrichment of opportunistic pathogens and depletion of short-chain fatty acid-producing bacteria; these alterations were not only correlated with intestinal barrier impairment but also exacerbated gut–liver axis dysregulation. Together, the findings not only highlight the synergistic toxicity of triclosan and polystyrene microplastics in mice but also identify the gut–liver axis as a mediator of this effect, thereby providing novel evidence for health risk assessment and underscoring a potential concern for human health under co-exposure. Full article

Background: The human microbiome holds promise for identifying biomarkers and therapeutic targets. In obesity, interactions between oral and gut communities are increasingly implicated and end in organ injury. Methods: From the IMAGINE study, we analyzed 418 shotgun metagenomes from three specimen types (dental plaque (n = 143; 65 non-obese, 78 obese), saliva (n = 166; 75 non-obese, 91 obese), and stool (n = 109; 57 non-obese, 52 obese)) to compare site-specific microbial shifts between obese (BMI > 30 kg/m²) and non-obese individuals. Differential abundance was assessed with ANCOM-BC; effect sizes were summarized as Cohen’s d. Results: Across all samples, we detected 240 bacterial species in plaque, 229 in saliva, and 231 in stool, with 46 species present across all three sites. Absolute effect sizes were significantly larger in plaque (mean |d| = 0.26) and saliva (0.25) than in stool (0.21; p = 9 × 10⁻³). Several taxa showed an opposite directionality between oral and gut sites, including Streptococcus salivarius and Bifidobacterium longum, indicating site-specific associations. Notably, Actinomyces sp. and Streptococcus sp. exhibited promising effect sizes as diagnostic markers. Conclusions: The oral and gut microbiomes capture complementary obesity-related signals, with stronger shifts observed in oral sites. We suggest that integrating oral and gut profiling could enhance diagnostic and therapeutic strategies in obesity. Full article

Serotonin (5-hydroxytryptamine) is a key neurotransmitter involved in gastrointestinal and central nervous system functions. Given that approximately 90% of serotonin is synthesized in the gut, dietary interventions targeting the gut microbiota have emerged as promising strategies to modulate serotonin homeostasis. Kefir, a fermented milk beverage rich in probiotics and bioactive compounds, has been suggested to influence gut–brain axis signaling, yet its effects in the pediatric period remain insufficiently characterized. This study aimed to investigate the impact of kefir supplementation on serotonin biosynthesis, receptor expression, and metabolic pathways in a pediatric rat model, focusing on molecular markers across brain, jejunum, and serum tissues. Sixteen male Wistar rats (four weeks old) were divided into kefir and control groups. The kefir group received daily oral gavage of kefir (1 mL/100 g) for eight weeks, while controls received saline. Gene and protein expression levels of serotonergic markers (5-HT, TPH1, TPH2, SLC6A4, VMAT2, 5-HTR2B, 5-HTR3A, and 5-HTR4) were analyzed using quantitative PCR, ELISA, and Western blotting. Serotonin turnover was assessed via 5-HIAA levels. Kefir supplementation significantly increased 5-HT and TPH1 expression in both brain and jejunum tissues. In the brain, kefir elevated TPH2 and upregulated 5-HTR3A and 5-HTR2B, while reducing 5-HIAA levels, suggesting decreased serotonin degradation. In the jejunum, 5-HTR4 expression was markedly increased. Serum analyses revealed reduced TPH1/TPH2 expression but elevated 5-HTR4 levels, indicating systemic modulation of serotonergic signaling. Kefir exerts multifaceted effects on the serotonergic system in pediatric rats by enhancing serotonin biosynthesis, modulating receptor expression, and reducing serotonin turnover. These findings highlight kefir as a potential psychobiotic capable of influencing the gut–brain axis during early life, with implications for pediatric neurodevelopment and mental health. Further research, including clinical trials, is warranted to confirm its translational potential. Full article

The oral cavity harbors one of the most diverse microbial ecosystems in the human body, second only to the gut. Periodontitis, a chronic inflammatory disease arising from oral microbiota dysbiosis, has been increasingly associated with systemic disorders such as diabetes mellitus, atherosclerosis, rheumatoid arthritis, inflammatory bowel disease, and neurodegenerative conditions. Although hematogenous dissemination of oral pathogens and inflammatory mediators has long been proposed as a mechanistic link, emerging evidence identifies the oral–gut axis as a novel bidirectional pathway. Swallowed oral pathobionts, such as Porphyromonas gingivalis and Fusobacterium nucleatum, can colonize the gut, disrupt the intestinal barrier, and induce dysbiosis, immune imbalance, and metabolic alterations that aggravate systemic inflammation and disease progression. In contrast, gut dysbiosis, especially in obesity or high-fat-diet models, can exacerbate periodontal tissue destruction through hyperuricemia, altered bone metabolism, and Th17/Treg immune imbalance. Experimental and clinical studies further support this reciprocal relationship, implicating microbial, metabolic, and immune crosstalk in both oral and systemic pathology. Understanding this oral–gut–systemic axis offers a paradigm shift in diagnostics and therapeutics, focusing on precision interventions such as microbiome modulation, probiotics, and integrated oral care to mitigate systemic inflammatory burden and improve overall health outcomes. Full article

Background: Periodontal dysbiosis contributes to liver injury through systemic inflammation, oral–gut microbial translocation, and endotoxemia. Lipopolysaccharides (LPSs) and virulence factors derived from periodontal pathogens, particularly Porphyromonas gingivalis (P. gingivalis) activate Toll-like receptor (TLR) signaling, trigger NF-κB-mediated cytokine release (e.g., TNF-α, IL-1β, IL-6), and promote oxidative stress and Kupffer cell activation within the liver. The present systematic review summarized clinical evidence supporting these mechanistic links between periodontal pathogens and hepatic outcomes, highlighting the role of microbial crosstalk in liver pathophysiology. Methods: A PRISMA-compliant systematic review was conducted by searching PubMed, Scopus, and the Cochrane library, as well as gray literature. Eligible study designs were observational studies and trials evaluating P. gingivalis and other periodontal pathogens (Aggregatibacter actinomycetemcomitans, Prevotella intermedia, and Tannerella forsythia) for liver phenotypes (Non-Alcoholic Fatty Liver Disease [NAFLD]/Metabolic Dysfunction-Associated Steatotic Liver Disease [MASLD], fibrosis/cirrhosis, acute alcoholic hepatitis [AAH], and Hepatocellular carcinoma [HCC]). Risk of bias was assessed using the Newcastle–Ottawa Scale adapted for cross-sectional studies (NOS-CS) for observational designs and the RoB 2 scale for single randomized controlled trials (RCTs). Due to the heterogeneity of exposures/outcomes, results were summarized narratively. Results: In total, twenty studies (2012–2025; ~34,000 participants) met the inclusion criteria. Population-level evidence was conflicting (no clear association between anti-P. gingivalis serology and NAFLD), while clinical cohorts more frequently linked periodontal exposure, particularly to P. gingivalis, to more advanced liver phenotypes, including fibrosis. Microbiome studies suggested stage-related changes in oral communities rather than the effect of a single pathogen, and direct translocation into ascitic fluid was not observed in decompensated cirrhosis. Signals from interventional and behavioral research (periodontal therapy; toothbrushing frequency) indicate a potential modifiability of liver indices. The overall methodological quality was moderate with substantial heterogeneity, precluding meta-analysis. Conclusions: Current evidence supports a biologically plausible oral–liver axis in which periodontal inflammation, often involving P. gingivalis, is associated with liver damage. Causality has not yet been proven; however, periodontal evaluation and treatment may represent a low-risk option in periodontitis-associated NAFLD. Well-designed, multicenter prospective studies and randomized trials with standardized periodontal and liver measurements are needed. Full article

Background/Objectives: Traumatic brain injury (TBI) disrupts both the intestinal epithelium and blood–brain barrier (BBB), contributing to oxidative stress, neuroinflammation, and behavioral impairments. Vitis vinifera leaf (VVL) extract possesses antioxidant and anti-inflammatory properties, but its protective effects on the brain–gut axis following TBI remain unclear. This study aimed to evaluate whether VVL supplementation preserves barrier integrity and improves neurobehavioral outcomes after TBI. Methods: A murine model of TBI was used, with animals receiving daily oral supplementation of the VVL extract. Neurobehavioral performance was assessed through behavioral testing, while histopathological examinations, biochemical assays, and gene expression profiling were performed to evaluate neuronal and intestinal integrity, antioxidant defense, and inflammatory responses. Results: VVL supplementation significantly alleviated anxiety- and depression-like behaviors and preserved the structural integrity of neuronal and intestinal tissues. Antioxidant defense mechanisms were strengthened, as shown by increased catalase and superoxide dismutase activities, together with upregulation of Nrf2 and HO-1 expression. Tight junction proteins, including ZO-1 and occludin, were upregulated in both brain and gut tissues, reflecting improved barrier integrity. Furthermore, VVL markedly reduced pro-inflammatory cytokine expression. Conclusions: VVL extract confers dual protection of the gut and brain barriers after TBI by enhancing endogenous antioxidant defenses, maintaining tight junction integrity, and suppressing inflammation. These findings suggest that VVL may represent a natural therapeutic strategy to mitigate oxidative stress, neuroinflammation, and behavioral dysfunctions associated with TBI. Full article

The oral cavity contains a diverse group of bacteria in the saliva, as well as structured aggregates of bacterial cells on the mucosal surfaces. Oral microbiota (OM) dysbiosis not only induces local inflammation, it can also trigger systemic inflammation leading to metabolic diseases and neuropsychiatric diseases (NPDs). While primary evidence indicates that oral microbiota dysbiosis induces gut microbiota aberrations, which exacerbate inflammation associated with metabolic diseases (obesity, dyslipidemia, diabetes, nonalcoholic fatty liver disease (NAFLD), and insulin resistance), other studies revealed the contribution of the oral microbiota–brain axis in the pathogenesis of NPDs. GM dysbiosis and inflammation also induce epigenetic alterations in cytokine genes, such as IL-1β, IL-6, TNF-α, NF-kB, BTLA, IL-18R1, TGF-β, P13k/Akt1, Ctnnb1, and Hsp90aa1, as well as DNMTs, HDACs, and DAT1 associated with the development and progression of metabolic disorders and/or NPDs. Therefore, the epigenome could serve as a target for preventive or therapeutic interventions. Here, we (i) review emerging evidence of the potential impact of OM dysbiosis in the pathogenesis of metabolic diseases and NPDs, (ii) highlight the relationship between OM-induced inflammation and epigenetic alterations driving NPDs pathogenesis and interlinked metabolic aberrations, (iii) discuss therapeutic approaches capable of treating metabolic diseases and NPDs through reshaping the microbiota and its epigenetic metabolites, and hence mitigating epigenetic aberrations linked to metabolic diseases and NPDs. Finally, we outline challenges and current research gaps related to investigating the relationship between microbiota, epigenetic aberrations, and metabolic abnormalities associated with NPDs. Full article

Methylphenidate (MPH) and its active enantiomer, dexmethylphenidate, are widely prescribed as first-line therapies for attention deficit hyperactivity disorder (ADHD), yet their increasing non-medical use highlights significant clinical and toxicological challenges. MPH blocks dopamine (DAT) and norepinephrine (NET) transporters, thereby elevating synaptic catecholamine levels. While this underpins therapeutic efficacy, prolonged or abusive exposure has been associated with mitochondrial impairment, disrupted bioenergetics, and excessive reactive oxygen species (ROS) production, which collectively contribute to neuronal stress and long-term neurotoxicity. Growing evidence suggests that the gut–brain axis may critically influence MPH outcomes: diet-induced shifts in microbiome composition appear to regulate oxidative stress, neuroinflammation, and drug metabolism, opening potential avenues for dietary or probiotic interventions. From a forensic perspective, the detection and monitoring of MPH misuse require advanced methodologies, including enantioselective LC–MS/MS and analysis of alternative matrices such as hair or oral fluids, which enable retrospective exposure assessment and improves abuse surveillance. Despite its established therapeutic profile, MPH remains a compound with a narrow balance between clinical benefit and toxicological risk. Future directions should prioritize longitudinal human studies, biomarker identification for abuse monitoring, and the development of mitochondria-targeted therapies to minimize adverse outcomes and enhance safety in long-term treatment. 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

Aging is the result of the accumulation of a great variety of molecular and cellular damage over time. During aging, the brain undergoes changes and diseases such as depression, dementia, anxiety, Alzheimer’s, delirium, behavioral disorders and aggression, and prolonged mourning, among others, appear. The gut–brain axis suggests that the gut and the brain have a bidirectional communication, so it is important to maintain proper intestinal health to strengthen the neurological changes of this age group. The intestinal microbiota is a dynamic and highly complex ecosystem of microorganisms residing in the gastrointestinal tract. The bidirectional and dynamic communication between the homeostatic systems, such as the endocrine and immune systems, as well as the nervous system, allow us to face problems associated with several diseases. Probiotics are defined as non-pathogenic live microorganisms that provide beneficial effects to the organism and participate in the prevention and treatment of diseases, which is the reason why it is important to promote interventions that keep intestinal microbiota in eubiosis (microbiota balance). The concentration and balance of the intestinal microbiota depend on several conditions, such as diet, antibiotic consumption, and lifestyle, to mentioned a few. However, interventions with probiotics have shown improvements in both cognitive function and processes that promote neurodegeneration. It is such that the research has been directed on designing strategies that improve not only oral bioavailability but also intestinal adhesion and retention, to clarify the frequency and dosage that should be consumed. Full article

Bone health is critically influenced by the oral and gut microbiota, which are among the largest microbial reservoirs in the human body. These microbiota play essential roles in maintaining bone mass through immune modulation, metabolite production, and nutrient resorption. Recent observations have underscored that extracellular vesicles (EVs) derived from oral and gut microbiota may circulate to the brain and bone marrow, suggesting their integral roles in the gut–brain–bone axis and oral–brain–bone axis. This review outlines the current research status of bacterial extracellular vesicles (BEVs), including their biogenesis, classification, structural features, and cargo composition, with emphasis on factors influencing cargo heterogeneity and the consequences of cellular uptake and presentation. Oral-microbiota-derived BEVs and their cargo associated with bone health are highlighted, along with recent evidence linking BEVs to systemic dis-eases and the potential integration into the oral–gut–bone axis. Preclinical animal studies on BEV dosage, routes of administration, and disease models are summarized, together with the limitations of current approaches and strategies for engineering BEVs. Finally, an overview of translational applications and future therapeutic prospects is provided, aiming to advance the understanding of BEVs as innovative tools for the treatment and prevention of bone-related diseases. Full article

Background: The gut-liver axis is essential for maintaining liver physiology, with the gut microbiota playing a central role in this bidirectional communication. Recent studies have identified microbiota-derived extracellular vesicles (EVs) as key mediators of inter-organ signaling. This study explored the impact of EVs from two beneficial Escherichia coli strains, the probiotic EcN and the commensal EcoR12, on hepatic metabolism and oxidative stress in healthy neonatal rats. Methods: EVs were administered orally during the first 16 days of life, and blood and liver samples were collected on days 8 and 16. Results: The results demonstrated that EVs significantly reduced intestinal permeability, as evidenced by decreased plasma zonulin levels. In the liver, EVs enhanced redox homeostasis by downregulating CYP2E1 and upregulating key antioxidant genes (SOD1, CAT, GPX). Furthermore, the treatment shifted liver metabolism toward an anti-lipogenic profile by inducing fatty acid oxidation genes (PPARA, CPT1A) and suppressing genes involved in de novo lipogenesis (SREBP1C, ACC1, FASN, CNR1). Importantly, markers of hepatic inflammation remained unchanged, indicating the safety of the intervention. In vitro experiments using human HepG2 cells supported these findings, further validating the antioxidant and metabolic effects of the EVs. Conclusions: Our results underscore the role of microbiota-derived EVs as important mediators of hepatic metabolic programming in healthy individuals via the gut-liver axis and highlight their potential as therapeutic postbiotic agents for management of fatty liver diseases. Full article

Background/Objectives: Emerging evidence suggests a role for oral microbiota in mood disorders, particularly bipolar disorder (BD), complementing established links between gut dysbiosis and psychiatric symptoms. This study investigates the composition of oral microbial taxa and the expression of inflammation-related pri-miRNAs (146a and 155) in individuals with BD, aiming to explore their potential as biomarkers in the oral–gut–brain axis. Methods: A matched case–control design was implemented, recruiting 25 BD patients and 46 controls matched by age and sex. Salivary samples were collected, and microbial profiling was conducted via real-time qPCR targeting major bacterial phyla and genera. Pri-miRNA 146a and 155 expression was evaluated through RT-qPCR using validated primers. Statistical comparisons between groups were performed using Fisher’s exact test and non-parametric tests for continuous variables. Results: Microbial analysis revealed significant reductions (p < 0.01) in α-Proteobacteria, γ-Proteobacteria, and Actinobacteria in BD patients versus controls. A shift toward a higher Firmicutes/Bacteroidetes ratio was observed in the BD cohort, suggesting differences in the oral biotic status between the two groups. However, pri-miRNA 146a and 155 expression levels did not differ significantly between the groups and exhibited high inter-individual variability. Conclusions: The findings indicate that oral microbiota composition differs in BD patients, potentially influencing systemic homeostasis through interactions with gut microbial communities and SCFA pathways. These findings should be interpreted as preliminary and hypothesis-generating given the modest sample size. While pri-miRNAs 146a and 155 did not distinguish BD status, the observed microbial taxa alterations should be regarded as exploratory and hypothesis-generating. Larger, longitudinal studies are required to clarify their potential role in BD pathogenesis and risk assessment. Full article

Background: Engineered nanoparticles (NPs)—titanium dioxide, silver, zinc oxide and silica—are widely used in cosmetics for UV protection, antimicrobial activity and texturising effects. Chronic consumer-level exposure may impair skin-barrier integrity, disturb microbiome composition and dysregulate immune signalling via the gut–skin axis. Current regulatory frameworks typically omit chronic- or microbiome-focused safety assessments, leaving potential gaps. Objectives: This study aimed to evaluate the long-term effects of cosmetic-relevant NPs (titanium dioxide, silver, zinc oxide, silica) on skin and gut microbiota, epithelial-barrier integrity and immune signalling—including telocyte- and exosome-mediated pathways—and to identify regulatory shortcomings, particularly the absence of microbiome endpoints, validated chronic models and consideration of vulnerable populations. Methods: Following PRISMA 2020, PubMed, Scopus and Web of Science were searched for English-language in vivo animal or human studies (December 2014–April 2025) meeting chronic-exposure criteria (≥90 days in rodents or >10% of lifespan in other species; for humans, prolonged, repetitive application over months to years consistent with cosmetic use). Although not registered in PROSPERO, the review adhered to a pre-specified protocol. Two independent reviewers screened studies; risk of bias was assessed using a modified SYRCLE tool (animal) or adapted NIH guidance (zebrafish). Owing to heterogeneity, findings were synthesised narratively. Results: Of 600 records, 450 unique articles were screened, 50 full texts were assessed and 12 studies were included. Oral exposure predominated and was associated with dysbiosis, barrier impairment, immune modulation and metabolic effects. Dermal models showed outcomes from minimal change to pronounced immune activation, contingent on host susceptibility. Comparative human–animal findings are summarised; telocyte and exosome pathways were largely unexplored. Regulatory reviews (EU SCCS, US FDA and selected Asian frameworks) revealed no requirements for chronic microbiome endpoints. Limitations: Evidence is limited by the small number of eligible studies, heterogeneity in NP characteristics and exposure routes, predominance of animal models and a scarcity of longitudinal human data. Conclusions: Cosmetic nanoparticles may disrupt the microbiome, compromise barrier integrity and trigger immune dysregulation—risks amplified in vulnerable users. Existing regulations lack requirements for chronic exposure, microbiome endpoints and testing in vulnerable groups, and neglect mechanistic pathways involving telocytes and exosomes. Long-term, real-world exposure studies integrating gut–skin microbiome and immune outcomes, and harmonised global nanomaterial-safety standards, are needed to ensure safer cosmetic innovation. Full article

Background: Cardiovascular diseases (CVDs) represent a major global health burden, and cholesterol reduction is a key strategy for their prevention and management. This study investigated the mechanism by which bile salt hydrolase (BSH) from Lactobacilli reduces cholesterol levels by modulating the growth of Bifidobacterium pseudolongum. Methods: The BSH-recombinant strain YB334 was administered to high-cholesterol-diet mice, and the cholesterol-lowering function of the strain was evaluated by assessing serum cholesterol parameters, including total cholesterol (TC), low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Metagenomic sequencing was used to analyze the gut microbiota, leading to the screening and acquisition of the “responsive” strains affected by BSH. Subsequent investigations were conducted into their cholesterol-lowering effects and mechanisms of action. Results: Oral administration of the BSH-recombinant strain YB334 can effectively reduce serum cholesterol levels in hypercholesterolemic mice while simultaneously leading to a significant increase in the abundance of B. pseudolongum within the gut microbiota. In vitro experiments indicated that this increased abundance might be closely associated with the strain’s high tolerance to CA, the catalytic product of the BSH enzyme. The BPL-4 strain, obtained through screening, demonstrated cholesterol-lowering efficacy. Mechanistically, BPL-4 altered bile acid pool composition and modulated the farnesoid X receptor (FXR) signaling axis: it suppressed ileal FXR-fibroblast growth factor 15 (FGF15) expression, thereby de-repressing hepatic cholesterol 7α-hydroxylase (CYP7A1) and accelerating cholesterol catabolism into bile acids. Conclusions: This study provides the first evidence that BSH from lactobacilli can shape the signature gut microbiota by modulating bile acid metabolism via the FXR-CYP7A1 axis, thereby demonstrating a mechanism for its cholesterol-lowering effects. Full article