Clostridium butyricum Modulates the Microbiome to Protect Intestinal Barrier Function in Mice with Antibiotic-Induced Dysbiosis
Clostridium butyricum Modulates the Microbiome to Protect Intestinal Barrier Function in Mice with Antibiotic-Induced Dysbiosis
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DOI：
10.1016/j.isci.2019.100772
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发表时间：
2020-01-24
期刊：
影响因子：
5.8
通讯作者：
Mikamo, Hiroshige
中科院分区：
文献类型：
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作者：
Hagihara, Mao;Kuroki, Yasutoshi;Mikamo, Hiroshige
丁酸梭菌MIYAIRI 588（CBM 588）是一种益生菌，以前曾用于预防腹泻。然而，CBM 588保护肠道上皮屏障的潜在机制仍不清楚。在这里，我们表明，CBM 588增加了肠道微生物组中双歧杆菌，乳杆菌和乳球菌的丰度，并增强了肠道屏障功能的小鼠与益生菌诱导的生态失调。此外，CBM 588显著促进结肠固有层（cLP）中产生IL-17 A的γ δ T细胞和产生IL-17 A的CD 4细胞的扩增，这与肠道微生物组成的变化密切相关。此外，CBM 588通过上调抗炎脂质代谢物如棕榈油酸，15 d-前列腺素J（2）和保护素D-1。这项研究揭示了CBM 588以前未被认识的机制，并为益生菌在益生菌诱导的生态失调条件下保护肠道上皮屏障提供了新的见解。
Clostridium butyricum MIYAIRI 588 (CBM 588) is a probiotic bacterium that has previously been used to prevent antibiotic-associated diarrhea. However, the underlying mechanism by which CBM 588 protects the gut epithelial barrier remains unclear. Here, we show that CBM 588 increased the abundance of Bifidobacterium, Lactobacillus, and Lactococcus species in the gut microbiome and also enhanced the intestinal barrier function of mice with antibiotic-induced dysbiosis. Additionally, CBM 588 significantly promoted the expansion of IL-17A-producing gamma delta T cells and IL-17A-producing CD4 cells in the colonic lamina propria (cLP), which was closely associated with changes in the intestinal microbial composition, Additionally, CBM 588 plays an important role in controlling antibiotic-induced gut inflammation through upregulation of anti-inflammatory lipid metabolites such as palmitoleic add, 15d-prostaglandin J(2), and protectin D-1. This study reveals a previously unrecognized mechanism of CBM 588 and provides new insights into gut epithelial barrier protection with probiotics under conditions of antibiotic-induced dysbiosis.