动物双歧杆菌乳亚种XLTG11对克林霉素诱导的抗生素相关性腹泻的改善作用

目的：通过克林霉素诱导抗生素相关性腹泻(antibiotic-associated diarrhea,AAD)模型，探究动物双歧杆菌乳亚种XLTG11缓解小鼠AAD的作用。方法：将48只6周龄C57BL/6N雄鼠随机分为4组：对照组、模型组、低剂量组和高剂量组，除对照组外，各组小鼠连续14 d灌胃克林霉素(250 mg/(kg m_b·d))诱导AAD模型，然后低剂量组和高剂量组灌胃不同剂量(0.2 mL,5×10⁶、1×10⁷ CFU)动物双歧杆菌乳亚种XLTG11，测定小鼠体质量增长量、盲肠质量、粪便含水量和粪便稠度，测定结肠肿瘤坏死因子α、白细胞介素6(interleukin 6,IL-6)、IL-1β、IL-10水平，血清脂多糖(lipopolysaccharide,LPS)和D-乳酸质量浓度，测定肠道菌群组成及短链脂肪酸含量，以及肠道屏障和核因子κB(nuclear factor kappa-B,NF-κB)信号通路相关基因表达水平。结果：高剂量动物双歧杆菌乳亚种XLTG11显著提高AAD模型小鼠的体质量增长量和...

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

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