Find in Library

This study was designed to explore the different intestinal barrier repair mechanisms of <i>Bifidobacterium breve</i> (<i>B. breve</i>) H4-2 and H9-3 with different exopolysaccharide (EPS) production in mice with colitis. The lipopolysaccharide (LPS)-induced IEC-6 cell inflammation model and dextran sulphate sodium (DSS)-induced mice colitis model were used. Histopathological changes, epithelial barrier integrity, short-chain fatty acid (SCFA) content, cytokine levels, NF-κB expression level, and intestinal flora were analyzed to evaluate the role of <i>B. breve</i> in alleviating colitis. Cell experiments indicated that both <i>B. breve</i> strains could regulate cytokine levels. In vivo experiments confirmed that oral administration of <i>B. breve</i> H4-2 and <i>B. breve</i> H9-3 significantly increased the expression of mucin, occludin, claudin-1, ZO-1, decreased the levels of IL-6, TNF-α, IL-1β and increased IL-10. Both strains of <i>B. breve</i> also inhibited the expression of the NF-κB signaling pathway. Moreover, <i>B. breve</i> H4-2 and H9-3 intervention significantly increased the levels of SCFAs, reduced the abundance of <i>Proteobacteria</i> and <i>Bacteroidea</i>, and increased the abundance of <i>Muribaculaceae</i>. These results demonstrate that EPS-producing <i>B. breve</i> strains H4-2 and H9-3 can regulate the physical, immune, and microbial barrier to repair the intestinal damage caused by DSS in mice. Of the two strains, H4-2 had a higher EPS output and was more effective at repair than H9-3. These results will provide insights useful for clinical applications and the development of probiotic products for the treatment of colitis.