Abstract
Ulcerative colitis (UC) is a non-specific chronic inflammatory disease with lesions located in the colon and rectum. The aim of this study was to evaluate the anti-inflammatory effects of exopolysaccharide-1 (EPS-1) isolated by L. helveticus KLDS1.8701 on UC. The anti-inflammatory effects of EPS-1 were studied using dextran sulphate sodium (DSS)-induced UC model. In vivo results showed that EPS-1 administration significantly ameliorated weight loss, colon shortening, disease activity index (DAI) score, myeloperoxidase (MPO) activity, and colon tissue damage. In addition, EPS-1 administration significantly decreased the levels of pro-inflammatory cytokines and increased levels of anti-inflammatory cytokines. Meanwhile, EPS-1 administration significantly up-regulated the expression of tight junction proteins and mucin. Furthermore, EPS-1 administration modulated gut microbiota composition caused by DSS and increased the short-chain fatty acids (SCFAs) levels. Collectively, our study showed the alleviative effects of EPS- isolated by L. helveticus KLDS1.8701 on DSS-induced UC via alleviating intestinal inflammation, improving mucosal barrier function, and modulating gut microbiota composition.
Highlights
Ulcerative colitis (UC) is a non-specific chronic inflammatory disease with lesions located in the colon and rectum
Gut dysbiosis has been linked with intestinal mucosal changes and mucosal inflammation
These findings suggested that EPS-1 had good anti-colitic effects by adjusting the levels of cytokine levels were significantly regulated by EPS-1 administration; a similar result was cytokines in colonic tissue
Summary
Ulcerative colitis (UC) is a non-specific chronic inflammatory disease with lesions located in the colon and rectum. The etiological mechanism of UC is complex, and current studies suggest that its pathogenesis may be related to environmental factors, genetic susceptibility, epigenetic modifications, intestinal mucosal barrier damage, intestinal microecological disorders, and intestinal immune response abnormalities [2,3,4]. The intestinal barrier has the function of absorbing and digesting nutrients and resisting invasion of foreign harmful substances [5]. Previous studies have shown that excessive apoptosis of intestinal epithelial cells will destroy the intestinal epithelial barrier and lead to the development of ulcerative colitis [6]. Gut dysbiosis has been linked with intestinal mucosal changes and mucosal inflammation. Postulations that the gut microbiome constituents can either improve or worsen UC conditions have been made [7,8]
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