| Project/Area Number |
24790673
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Hirosaki University |
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Principal Investigator |
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| Research Collaborator |
HIRAGA Hiroto 弘前大学, 大学院医学研究科, 助教 (80637546)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 炎症性腸疾患 / TGF-beta / 腸管上皮細胞 / アポトーシス / シクロスポリン / 腸上皮アポトーシス / TGF-β / IL-22 |
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| Research Abstract |
Cyclosporine (CsA) showed a rapid improvement in the treatment of ulcerative colitis, but the precise mechanism is still obscure. We hypothesized that CsA would affect the TGF-beta expression of intestinal mucosa. Colitis was induced by feeding of 4% DSS in CD4+CD25+cells-transferred SCID mice. Treatment of CsA ameliorated mucosal destruction through reduction of epithelial apoptosis. CsA up-regulated the TGF-beta in the colon. TGF-beta expression was significantly suppressed and treatment of CsA failed to up-regulate the expression of TGF-beta in SCID mice. On the other hand, treatment of CsA up-regulated TGF-beta expression in CD4+CD25+cells-transferred SCID mice. However, TGF-beta production from separated-CD4+CD25+cells was not increased by treatment of CsA in vitro. These results demonstrate that treatment of CsA can ameliorate epithelial damage through TGF-beta-related pathway. CD4+CD25+T cells would indirectly mediate the protective effect of CsA via TGF-beta-related pathway.
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