Objective:To observe and analyze the influence of deoxycholic acid (DCA) on intestinal microbiota and bile acid metabolism during the process of enteritis induced by DCA in mice.Methods:Twenty C57BL/6J mice were randomly and equally divided into DCA group and control group. The mice in DCA group were developed by feeding the feed with 0.2% DCA and the mice in control group were developed with routine feed for 24 weeks. The degree of intestinal tissue inflammation was evaluated by HE staining and scored, the change of intestinal microbiota was analyzed by pyrosequencing, bile acid levels of all grades in faeces were detected by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS) , the expressions of bile acid-related genes were detected by quantitive real-time PCR.Results:The intestinal histology scores in DCA group was significantly higher than that of the control group (both P<0.05) . The diversity of fecal microbiota in the DCA group was significantly reduced, the percentage of Firmicutes at the phylum level and the percentage of Clostridium XIVa at the genus level were significantly decreased (both P<0.05) . The total bile acid, secondary bile acid, unconjugated bile acid and tauro-α-muricholic acid (T-α-MCA) of mice faeces in DCA group were significant higher than those in control group (all P<0.05) . The expression of biliary acid transporter gene organic solute transporter β ( Ost- β) , farnesoid X receptor ( FXR) and fibroblast growth factor 15 ( FGF15) in DCA group decreased significantly (all P<0.05) , while the expressions of liver bile synthesis rate-limiting enzymes Cyp7a1, Cyp7b1 and Cyp27a1 increased obviously (all P<0.05) . Conclusions:DCA can induce the progress of enteritis, which may be related to its destruction of intestinal microbiota in mice and the promotion of liver bile acid synthesis through FXR-FGF15 signaling pathway.

Intestinal microbiota plays key roles in nutrient absorption, metabolism and immune defense, and is regarded as the cornerstone of maintaining the health status of human host. After entering the intestine, the bile acids synthesized in the liver can not only promote the absorption of fat-soluble substances but also directly or indirectly affect the structure and function of intestinal microbiota. Intestinal microbiota can change primary bile acids into secondary bile acids, and help it to be reabsorbed back to the liver through the enterohepatic circulation. The complex mechanism of microbiota-bile acids crosstalk is involved in the development of intestinal inflammation including inflammatory bowel disease (IBD) . This article reviews the influence of intestinal microbiota, bile acids and their interaction on the pathogenesis of IBD and the related progress of therapeutic application.

Objective:To observe and analyze the influence of deoxycholic acid (DCA) on intestinal microbiota and bile acid metabolism during the process of enteritis induced by DCA in mice.Methods:Twenty C57BL/6J mice were randomly and equally divided into DCA group and control group. The mice in DCA group were developed by feeding the feed with 0.2% DCA and the mice in control group were developed with routine feed for 24 weeks. The degree of intestinal tissue inflammation was evaluated by HE staining and scored, the change of intestinal microbiota was analyzed by pyrosequencing, bile acid levels of all grades in faeces were detected by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS) , the expressions of bile acid-related genes were detected by quantitive real-time PCR.Results:The intestinal histology scores in DCA group was significantly higher than that of the control group (both P<0.05) . The diversity of fecal microbiota in the DCA group was significantly reduced, the percentage of Firmicutes at the phylum level and the percentage of Clostridium XIVa at the genus level were significantly decreased (both P<0.05) . The total bile acid, secondary bile acid, unconjugated bile acid and tauro-α-muricholic acid (T-α-MCA) of mice faeces in DCA group were significant higher than those in control group (all P<0.05) . The expression of biliary acid transporter gene organic solute transporter β ( Ost- β) , farnesoid X receptor ( FXR) and fibroblast growth factor 15 ( FGF15) in DCA group decreased significantly (all P<0.05) , while the expressions of liver bile synthesis rate-limiting enzymes Cyp7a1, Cyp7b1 and Cyp27a1 increased obviously (all P<0.05) . Conclusions:DCA can induce the progress of enteritis, which may be related to its destruction of intestinal microbiota in mice and the promotion of liver bile acid synthesis through FXR-FGF15 signaling pathway.

Intestinal microbiota plays key roles in nutrient absorption, metabolism and immune defense, and is regarded as the cornerstone of maintaining the health status of human host. After entering the intestine, the bile acids synthesized in the liver can not only promote the absorption of fat-soluble substances but also directly or indirectly affect the structure and function of intestinal microbiota. Intestinal microbiota can change primary bile acids into secondary bile acids, and help it to be reabsorbed back to the liver through the enterohepatic circulation. The complex mechanism of microbiota-bile acids crosstalk is involved in the development of intestinal inflammation including inflammatory bowel disease (IBD) . This article reviews the influence of intestinal microbiota, bile acids and their interaction on the pathogenesis of IBD and the related progress of therapeutic application.