Abstract
Ulcerative colitis (UC), a persistent intestinal disorder, is now considered a global disease. The present study was designed to investigate the alleviative effects of a cocktail of lactic acid bacteria (CLAB; Lactobacillus rhamnosus MP108, L. paracasei CCFM2711, Bifidobacterium animalis BB-115, and B. longum BLI-02) on UC and its mechanisms through a UC mouse model triggered by dextran sulfate sodium (DSS). The results indicated that CLAB improved colitis symptoms, intestinal pathologic damage, and intestinal barrier in mice. Moreover, CLAB attenuated colonic inflammatory responses in mice by remodeling the homeostasis between pro-inflammatory and anti-inflammatory cytokines. In addition, CLAB improved the structure of the gut microbiota and augmented the proportion of secondary bile acid-producing bacteria. Untargeted metabolomics analysis revealed that CLAB altered the metabolic profile of colonic contents and, importantly, increased the content of lithocholic acid (LCA). Further, CLAB activated the TGR5/PKA pathway via significantly upregulating the protein expression of TGR5, PKA, and p-CREB. Thus, CLAB alleviated UC, probably by increasing secondary bile acid-producing bacteria, resulting in increased levels of LCA, which in turn activated the TGR5/PKA pathway, thereby reducing the inflammatory response. The present study will offer a theoretical foundation for developing probiotic products to mitigate UC.
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