Lactobacillus casei ATCC 393 and it's metabolites alleviate dextran sulphate sodium-induced ulcerative colitis in mice through the NLRP3-(Caspase-1)/IL-1β pathway.

Inflammatory bowel disease (IBD) represents a broad group of intestinal disorders, including ulcerative colitis (UC) and Crohn's disease (CD). Probiotics are increasingly being recognized as a means of treatment for people suffering from IBD. Our previous studies demonstrated that Lactobacillus casei ATCC 393 (L. casei ATCC 393) effectively alleviated enterotoxigenic Escherichia coli K88-induced intestinal barrier dysfunction. This study was conducted to investigate the protective effects of L. casei ATCC 393 and its metabolites on dextran sulfate sodium (DSS)-induced UC in C57BL/6 mice and the potential mechanism of these effects. The results showed that oral administration of L. casei ATCC 393 and its metabolites both effectively reversed the DSS-induced weight loss, and the reduction in the disease activity index (DAI), colon length, and villus height of colon tissue in mice. Compared to the DSS-induced model group, L. casei ATCC 393 and its metabolites significantly inhibited the infiltration of immune cells into the intestinal mucosa, decreased the production of pro-inflammatory factors, and increased the expression of anti-inflammatory factors in the serum and colon tissue, increased the expression levels of occludin, ZO-1, and claudin-1, and reduced the expression of nucleotide binding oligomeric domain-like receptor protein 3 (NLRP3), cysteine proteinase-1 (Caspase-1), IL-1β, and IL-18. In addition, L. casei ATCC 393 and its metabolites effectively improved DSS-induced gut microbiota dysbiosis. These results suggested that L. casei ATCC 393 and its metabolites alleviated the DSS-induced ulcerative inflammatory response in C57BL/6 mice through the NLRP3-(Caspase-1)/IL-1β signaling pathway.