摘要：SummaryClostridium butyricumMIYAIRI 588 (CBM 588) is a probiotic bacterium that has previously been used to prevent antibiotic-associated diarrhea. However, the underlying mechanism by which CBM 588 protects the gut epithelial barrier remains unclear. Here, we show that CBM 588 increased the abundance ofBifidobacterium,Lactobacillus, andLactococcusspecies in the gut microbiome and also enhanced the intestinal barrier function of mice with antibiotic-induced dysbiosis. Additionally, CBM 588 significantly promoted the expansion of IL-17A-producing γδT cells and IL-17A-producing CD4 cells in the colonic lamina propria (cLP), which was closely associated with changes in the intestinal microbial composition. Additionally, CBM 588 plays an important role in controlling antibiotic-induced gut inflammation through upregulation of anti-inflammatory lipid metabolites such as palmitoleic acid, 15d-prostaglandin J2, and protectin D1. This study reveals a previously unrecognized mechanism of CBM 588 and provides new insights into gut epithelial barrier protection with probiotics under conditions of antibiotic-induced dysbiosis.Graphical AbstractDisplay OmittedHighlights•CBM 588 increases the abundance ofBifidobacterium,Lactobacillus,andLactococcus•Microbiota-driven TGF-β1controls the differentiation of lymphocytes to γδT cells•CBM 588 promotes the expansion of IL-17A-producing γδT cells and CD4 cells•CBM 588 upregulates anti-inflammatory lipid metabolitesMicrobiome; Clinical Microbiology
