2004 Fiscal Year Final Research Report Summary
Involvement of intestinal microbiota derived secondary bile acids in the patho-physiology of inflammatory baowel disease and the expression of UGT by intestinal epithelial cells.
| Project/Area Number |
14570462
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
FUJIYAMA Yoshihide Shiga University of Medical Science, Faculty of Medicine, professor, 医学部, 教授 (70111896)
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| Project Period (FY) |
2002 – 2004
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| Keywords | IBD / intestinal micorbiota / bile acid / UGT |
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| Research Abstract |
In this research project, new aspect of intestinal microbiota in patients with inflammatory bowel disease has been demonstrated using t-RFLP analysis, i.e., the t-RFLP profile of patients with ulcerative colitis showed a unique profile which was apparently different from that of normal individuals. The major mechanism of interruption of mucosal barrier induced by secondary bile acids using ransepithelial electrical resistance determination method was depend on the synthesis of radical oxygen species, and it was estimated that XO was involved as upper signaling pathway and ERK1/2,PI3K,p38MAPK and MLCK were involved as down-stream signaling pathway of ROS synthesis. Transfection of UGT1A3 to CaCo-2 cells diminished IL-8 mRNA expression induced by lithocholic acid.
These observations are indicative that alterations of bile acid composition produced by an unique intestinal microbiota profile in ulcerative colits might play a novel pathoetiological role in IBD.
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