Clostridium butyricum Modulates the Microbiome to Protect Intestinal Barrier Function in Mice with Antibiotic-Induced Dysbiosis

• Published in: iScience Vol. 23; no. 1; p. 100772
• Main Authors: Hagihara, Mao, Kuroki, Yasutoshi, Ariyoshi, Tadashi, Higashi, Seiya, Fukuda, Kazuo, Yamashita, Rieko, Matsumoto, Asami, Mori, Takeshi, Mimura, Kaoru, Yamaguchi, Naoko, Okada, Shoshiro, Nonogaki, Tsunemasa, Ogawa, Tadashi, Iwasaki, Kenta, Tomono, Susumu, Asai, Nobuhiro, Koizumi, Yusuke, Oka, Kentaro, Yamagishi, Yuka, Takahashi, Motomichi, Mikamo, Hiroshige
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 24.01.2020; Elsevier
• Subjects: Clinical Microbiology; Microbiome; Clinical Microbiology; Microbiome
• ISSN: 2589-0042; 2589-0042
• DOI: 10.1016/j.isci.2019.100772

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 γδT 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 acid, 15d-prostaglandin J2, and protectin D1. 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. [Display omitted] •CBM 588 increases the abundance of Bifidobacterium, Lactobacillus, and Lactococcus•Microbiota-driven TGF-β1 controls the differentiation of lymphocytes to γδT cells•CBM 588 promotes the expansion of IL-17A-producing γδT cells and CD4 cells•CBM 588 upregulates anti-inflammatory lipid metabolites Microbiome; Clinical Microbiology