| Project/Area Number |
15390232
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 |
ANDOH Akira Shiga University of Medical Science, Assistant Professor, 医学部, 講師 (90252395)
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| Project Period (FY) |
2003 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥10,900,000 (Direct Cost: ¥10,900,000)
Fiscal Year 2005: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2004: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2003: ¥5,100,000 (Direct Cost: ¥5,100,000)
|
|---|
| Keywords | Cytokine / IL-22 / IL-17 / Inflammatory bowel disease / ZBD / IBD |
|---|
| Research Abstract |
We evaluated the effects of rat anti-mouse IL-17 neutralizing monoclonal antibody (mAb) on the development of dextran sulfate sodium (DSS)-induced colitis. Tissue samples were evaluated by standard immunohistochemical procedure. The mucosal mRNA expression of cytokines was analyzed by reverse transcriptase-polymerase chain reaction. In the mice treated with the anti-IL-17 mAb, the body weight was significantly lower, and anal prolapse and colon shortening were apparent. A histologic analysis indicated that the anti-IL-17 mAb markedly enhanced a severity of colitis. The mucosal infiltration of CD4-positive helper T cells and CD11b-positive granulocytes/monocytes was increased in the anti-IL-17 mAb-treated mice. Treatment with the anti-IL-17 mAb increased the mucosal expression of mRNAs of tumor necrosis factor (TNF)-α, interferon (IFN)-γ, IL-6, RANTES and 1P-10. Blocking of IL-17 activity in vivo using the anti-IL-17 mAb enhanced the development of DSS-colitis in mice. This suggests an inhibitory role for IL-17 in the development of DSS-colitis.
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