Dysbiosis leads to continuous progress of inflammatory bowel disease (IBD). However, current therapeutic approaches for IBD have limited efficacy and are associated with various side effects. This study focused on exploring the positive effect of a new Bacillus cereus (B. cereus) strain (HMPM18123) in a colitis mouse model and elucidate the underlying molecular mechanisms. The colitis symptoms were alleviated by the B. cereus administration as evidenced by decreased body weight loss, colon length shortening, disease activity index score, and histopathological score. The B. cereus mitigated intestinal epithelial barrier damage by upregulating tight junction protein expression. Moreover, B. cereus exerted anti-inflammatory effects by regulating macrophage polarization and suppressing the TLR4-NF-κB-NLRP3 inflammasome signaling pathways. B. cereus also rebalanced the damaged gut microbiota. Thus, the molecular mechanism of alleviating colitis by B. cereus treatment involved the regulation of the TLR4-NF-κB-NLRP3 inflammasome signaling pathways in intestinal mucosal barriers by modulating gut microbiota composition.
Keywords: Bacillus cereus; NLRP3; colitis; gut microbiota; inflammation; intestinal mucosal barriers.