干酪乳杆菌
炎症性肠病
溃疡性结肠炎
化学
结肠炎
微生物学
产肠毒素大肠杆菌
药理学
免疫学
生物
医学
内科学
大肠杆菌
生物化学
肠毒素
疾病
发酵
基因
作者
Xina Dou,Lei Qiao,Jiajing Chang,Shuqi Yan,Xiao fan Song,Yue Chen,Qinhong Xu,Chunlan Xu
出处
期刊:Food & Function
[The Royal Society of Chemistry]
日期:2021-01-01
卷期号:12 (23): 12022-12035
被引量:16
摘要
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.
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