Alleviating Effect of Bifidobacterium animalis subsp. lactis XLTG11 on Ulcerative Colitis Induced by Sodium Dextran Sulfate in Mice

To investigate the relieving effect of Bifidobacterium animalis subsp. lactis XLTG11 on ulcerative colitis induced by dextran sulfate sodium (DSS) in mice.

Forty-five eight-week-old C57BL/6N male mice were randomly divided into three groups: normal, model and bifidobacterium treatment. To induce ulcerative colitis, the mice were allowed free access to 3% DSS in water. B. animalis subsp. lactis XLTG11 was gavaged to the animals at a dose of 1 × 10⁷ CFU/d. The percentage change of body mass, colon length, disease activity index (DAI) and intestinal myeloperoxidase (MPO) activity were measured. Hstopathological changes were observed in the colon. Tumor necrosis factor (TNF)-α, interleukin 6 (IL-6), IL-1β, and IL-10 contents in the colon tissue were determined. The gut microbiota composition and the contents of fecal short-chain fatty acids were evaluated. The relative expression levels of genes related to intestinal barrier and the nuclear transcription factor (NF)-κB signaling pathway were detected.

Compared to the model group, B. animalis subsp. lactis XLTG11 significantly increased the percentage change of body mass (P < 0.05) and colon length (P < 0.01), and decreased DAI, MPO activity and proinflammatory cytokine levels (P < 0.01) in mice with DSS-induced ulcerative colitis. Moreover, it decreased the relative abundance of pathogenic bacteria, increased the relative abundance of short-chain fat acid-producing bacteria in the gut, significantly increased the contents of short-chain fat acids and the expression of genes related to intestinal barrier function (P < 0.01), and inhibited the activation of the NF-κB signaling pathway.

B. animalis subsp. lactis XLTG11 could increase the percentage change of body mass and colon length, decrease DAI, MPO activity, and proinflammatory cytokine levels, regulate the gut microbiota composition, increase fecal short-chain fatty acid contents and the expression of intestinal barrier-related genes and inhibit the NF-κB signaling pathway, thereby effectively relieving DSS-induced ulcerative colitis in mice.