Emerging evidence suggests a key role of gut microbiota in maintaining liver functions through modulating the gut–liver axis. In this study, we investigated whether microbiota alteration mediated by probiotic Bacillus was involved in alleviating oxidative stress- induced liver injury. Sprague–Dawley rats were orally administered Bacillus SC06 or SC08 for a 24-day period and thereafter intraperitoneally injected diquat (DQ) to induce oxidative stress. Results showed that Bacillus, particularly SC06 significantly inhibited hepatic injuries, as evidenced by the alleviated damaged liver structure, the decreased levels of ALT, AST, ALP and LDH, and the suppressed mitochondrial dysfunction. SC06 pretreatment markedly enhanced the liver antioxidant capacity by decreasing MDA and p47, and increasing T-AOC, SOD and HO-1.16S rRNA sequencing analysis revealed that DQ significantly changed the diversities and composition of gut microbiota, whereas Bacillus pretreatments could attenuate gut dysbiosis. Pearson’s correlation analysis showed that AST and MDA exerted a positive correlation with the opportunistic pathogenic genera and species (Escherichia and Shigella), and negatively correlated with the potential probiotics (Lactobacillus), while SOD exerted a reverse trend. The microbial metagenomic analysis demonstrated that Bacillus, particularly SC06 markedly suppress the metabolic pathways such as carbohydrate metabolism, lipid metabolism, amino acid metabolism and metabolism of cofactors and vitamins. Furthermore, SC06 decreased the gene abundance of the pathways mediating bacterial replication, secretion and pathogenicity. Taken together, Bacillus SC06 alleviates oxidative stress-induced liver injuries via optimizing the composition, metabolic pathways and pathogenic replication and secretion of gut microbiota. These findings elucidate the mechanisms of probiotics in alleviating oxidative stress and provide a promising strategy for preventing liver diseases by targeting gut microbiota.

This study aims to explore the effects of modified montmorillonite (MMT, copper loading) on the growth performance, gut microbiota, intestinal barrier, antioxidative capacity and immune function of broilers. Yellow-feathered broilers were randomly divided into control (CTR), modified montmorillonite (MMT), and antibiotic (ANTI) groups. Results revealed that MMT supplementation increased the BW and ADG and decreased the F/R during the 63-day experiment period. 16S rRNA sequencing showed that MMT modulated the cecal microbiota composition of broilers by increasing the relative abundance of two phyla (Firmicutes and Bacteroidetes) and two genera (Bacteroides and Faecalibacterium) and decreasing the abundance of genus Olsenella. MMT also improved the intestinal epithelial barrier indicated by the up-regulated mRNA expression of claudin-1, occludin, and ZO-1 and the increased length of microvilli in jejunum and the decreased levels of DAO and D-LA in serum. In addition, MMT enhanced the immune function indicated by the increased levels of immunoglobulins, the decreased levels of MPO and NO, the down-regulated mRNA expression of IL-1β, IL-6, and TNF-α, and the up-regulated mRNA expression of IL-4 and IL-10. Moreover, MMT down-regulated the expression of jejunal TLRs/MAPK/NF-κB signaling pathway-related genes (TLR2, TLR4, Myd88, TRAF6, NF-κB, and iNOS) and related proteins (TRAF6, p38, ERK, NF-κB, and iNOS). In addition, MMT increased the antioxidant enzyme activities and the expression of Nrf2/HO-1 signaling pathway-related genes and thereby decreased the apoptosis-related genes expression. Spearman’s correlation analysis revealed that Bacteroides, Faecalibacterium, and Olsenella were related to the inflammatory index (MPO and NO), oxidative stress (T-AOC, T-SOD, and CAT) and intestinal integrity (D-LA and DAO). Taken together, MMT supplementation improved the growth performance of broilers by modulating intestinal microbiota, enhancing the intestinal barrier function, and improving inflammatory response, which might be mediated by inhibiting the TLRs/MAPK/NF-κB signaling pathway, and antioxidative capacity mediated by the Nrf2/HO-1 signaling pathway.

Large-scale use of antimicrobials in agriculture and medicine contributes to antibiotic residues in raw foods, the spread of antimicrobial resistance (AMR) and drug pollution, which seriously threatens human health and imposes significant economic burdens on society, suggesting the need for novel therapeutic options that prevent or control zoonoses. In this study, four probiotics were selected to assess their capability to alleviate pathogen-induced damage. Results showed that a simulated gastrointestinal juice and bile tolerated L. plantarum Lac16 with high lactic acid secretion can significantly inhibit the growth of multiple zoonotic pathogens. Lac16 also significantly inhibited the biofilm formation and mRNA expression of virulence traits (genes related to virulence, toxins, flagella biogenesis and motility, antibiotic resistance, biofilm formation and AI-2 quorum sensing) of enterohemorrhagic E. coli O157:H7 (EHEC). Furthermore, Lac16 and Lac26 significantly protected C. elegans against zoonotic pathogen-induced (EHEC, S. typhimurium, C. perfringens) deaths. Moreover, Lac16 significantly promoted epithelial repair and ameliorated lipopolysaccharide (LPS)-induced intestinal epithelial apoptosis and barrier dysfunction by activating the Wnt/β-catenin signaling pathway, and markedly reduced LPS-induced inflammatory responses by inhibiting the TLR4/MyD88 signaling pathway. The present results indicate that Lac16 attenuates enterohemorrhagic E. coli infection-induced damage by inhibiting key virulence traits of E. coli, promoting epithelial repair and improving intestinal epithelial barrier function, which may be mediated by the activated Wnt/β-catenin signaling pathway and the inhibited TLR4/MyD88 signaling pathway of the intestinal epithelium.