Lactobacillus helveticus R0052 attenuates DSS-induced colitis via modulation of gut microbiota, intestinal metabolites and immunological profiles in a mouse model.

Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) pathologically characterized by intestinal immune dysregulation, and substantial clinical evidence suggests that probiotic supplementation demonstrates efficacy and safety. Our study delineated the protective effect of Lactobacillus helveticus R0052 (LH R0052) on dextran sulfate sodium (DSS)-induced murine colitis model and its prospective mechanism. The results suggested that DSS administration induced significant body weight loss, colon shortening, and elevated disease activity index (DAI). Pathological assessments revealed exacerbated colonic tissue injury, concurrent with intestinal barrier disruption, systemic inflammation, gut microbiota dysbiosis, and metabolic dysregulation compared to controls. The administration of LH R0052 exerted a protective effect against colitis by improving the phenotypic presentation, suppressing the proliferation of harmful bacteria, modulating immune responses, preserving intestinal barrier integrity, and restoring the intestinal microbiota and metabolic homeostasis. In summary, our study demonstrated that LH R0052 exhibited potential efficacy in alleviating DSS-induced UC and hold promise as a probiotic for mitigating intestinal inflammation.