期刊
MOLECULAR NUTRITION & FOOD RESEARCH
卷 67, 期 11, 页码 -出版社
WILEY
DOI: 10.1002/mnfr.202200340
关键词
colitis; intestinal barrier; intestinal immune response; intestinal microbiota; Lactobacillus
Changes in intestinal microbial composition may lead to the development of inflammatory bowel disease (IBD) by disrupting the balance of their interaction with the host. This study evaluated the effect of a combination treatment with two Lactobacillus strains on a mouse model of colitis and found that it ameliorated the symptoms by altering intestinal microbial composition and suppressing inflammatory response. The treatment also had additional beneficial effects such as maintaining goblet cell numbers, improving intestinal barrier damage, and reducing pro-inflammatory lipopolysaccharides.
ScopeChanges in composition of intestinal microbes may disrupt the balance of their interaction with a susceptible host, resulting in development of inflammatory bowel disease (IBD). Methods and resultsThe study applied in combination two Lactobacillus strains (L. rhamnosus BY-02, L. plantarum BY-05) (LS treatment), previously isolates from feces of healthy human infants, in a mouse model of dextran sodium sulfate (DSS)-induced colitis, and evaluates their ameliorative effect and its possible mechanism. LS treatment suppresses weight loss and colon shortening, and reduces disease activity index in the mice. It also has several additional beneficial effects: i) maintains goblet cell numbers and ameliorates intestinal barrier damage in colonic tissue; ii) alters intestinal microbial composition close to normal by increasing abundances of Muribaculaceae, Akkermansia, Clostridia, Oscillospiraceae, and Lachnospiraceae, and decreasing abundance of Escherichia-Shigella; iii) increases content of short-chain fatty acids; iv) reduces content of pro-inflammatory lipopolysaccharides; v) suppresses overactivation of TLR4/NF-kappa B inflammatory signaling pathway. ConclusionCombination treatment with two Lactobacillus strains strongly ameliorates colitis symptoms in the mouse model by favorably altering intestinal microbial composition and suppressing inflammatory response.
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