Alleviative Effect of Bifidobacterium animalis subsp. lactis XLTG11 on Antibiotic-Associated Diarrhea Induced by Clindamycin

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.