| Project/Area Number |
23590949
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Keio University |
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Principal Investigator |
IWAO Yasushi 慶應義塾大学, 医学部, 教授 (40168547)
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| Co-Investigator(Kenkyū-buntansha) |
KANAI Takanori 慶應義塾大学, 医学部, 教授 (40245478)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 炎症性腸疾患 / alternative Th1 / 腸内細菌 |
|---|
| Research Abstract |
In CD4+CD45RBhigh adoptive transfer colitis model, we demonstrated that RORgt+ Th17 and Th17/Th1 cells become colitogenic alternative Th1 cells in vivo. Treg cells suppressed this pathway and development of intestinal inflammation. In addition, we found that Clostridium butyricum, which produces butyrate, suppress intestinal inflammation in mice colitis models. Interestingly, C. butyricum promoted IL-10 production by intestinal macrophage, but not Treg cells. Fecal 16S rRNA analysis, C. butyricum was decreased in the patients with IBD. Our findings provide the new insight into the mechanism of colitogenic T cell development in vivo and suggests the potential of Clostridium butyricum as a novel probiotics.
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