Yeast β-glucan intervention offers a promising strategy for managing colitis; however, the mechanisms remain unknown. In the present work, the protective effects of yeast β-glucan on DSS-induced colitis in mice was evaluated, focusing on its interaction with gut microbiota. The result showed yeast β-glucan significantly alleviated colitis symptoms, evidenced by reduced weight loss, lower disease activity index (DAI) scores, and minimized intestinal damage. It enhanced intestinal barrier integrity via upregulation of tight junction proteins, suppressed lipopolysaccharide (LPS) release, and decreased pro-inflammatory cytokines production. Additionally, yeast β-glucan boosted short-chain fatty acids (SCFAs) production, and activated their receptors, increased the relative abundances of beneficial microbes like Lactobacillus and Lachnospiraceae_UCG-006. Transcriptomic analyses suggest that yeast β-glucan mitigates inflammation by downregulating gene expression related to IL-17 pathway. Our findings highlight potential of yeast β-glucan as a therapeutic agent for colitis through modulation of gut microbiota and inflammatory responses.
Keywords: Colitis; Gut microbiota; IL-17 pathway; Short-chain fatty acids; Yeast β-glucan.
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