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.

To investigate the relieving effect of Bifidobacterium animalis subsp. lactis XLTG11 on antibiotic-associated diarrhea (AAD) in mice using clindamycin-induced AAD model.

Forty-eight 6-week-old C57BL/6N male mice were randomly divided into four groups: normal control, model, low-dose and high-dose XLTG11. All mice except for the control group were administered with clindamycin orally daily for 14 days to induce AAD, The low-dose and high-dose groups were given 0.2 mL of the bacterial suspensions with viable count of 5×10⁶ and 1×10⁷ CFU, respectively. Body mass gain, cecum mass, fecal water content and fecal consistency score were measured. The levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-1β, and IL-10 in cecum tissue and the serum levels of lipopolysaccharide (LPS) and D-lactic acid were determined. The gut microbiota composition and the fecal contents of short-chain fatty acids were detected. The expression levels of genes related to the intestinal barrier and the nuclear factor kappa-B (NF-kB) pathway were determined.

The high dose of Bifidobacterium animalis subsp. lactis XLTG11 significantly increased the body mass gain and anti-inflammatory cytokine levels (P < 0.05), and significantly decreased cecum mass, fecal water content, fecal consistency score and proinflammatory cytokine levels in the mouse model mice of AAD. Moreover, it significantly up-regulated the gene expression levels of ZO-1, occludin, claudin-1 and MUC2, regulated the composition of the gut microbiota, evidently increased the fecal contents of acetate, propanoate, and butanoate, and significantly down-regulated the expression levels of genes related to the Toll like receptor 4 (TLR4), myeloid differentiation factor (MYD88) and NF-κB signaling pathway.

Bifidobacterium animalis subsp. lactis XLTG11 can effectively alleviate AAD symptoms in mice by regulating cytokines and the gut microbiota, increasing fecal short-chain fatty acid contents, increasing the expression levels of intestinal barrier related genes and inhibiting the activation of the TLR4/MyD88/NF-kB signaling pathway.