| Project/Area Number |
25860305
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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 |
Experimental pathology
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
OHTSUKI Takahiro 公益財団法人東京都医学総合研究所, ゲノム医科学研究分野, 研究員 (10593642)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | HCV / 慢性肝炎 / ワクチン / マクロファージ / 感染免疫 / C型慢性肝炎 / 組換えワクシニアウイルス / 治療ワクチン |
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| Outline of Final Research Achievements |
Macrophages (Mφ) in liver are widely defined as important inflammatory cells in chronic viral hepatitis due to their pro-inflammatory activity. We reported previously that IL-6 and TNF-α played significant role to cause chronic hepatitis in HCV transgenic mice. In addition, we showed recombinant vaccinia viruses expressing HCV nonstructural protein (rVV-N25) could ameliorate chronic hepatitis. The number of M2-like Mφ (M2Mφ) in the liver of HCV transgenic mice was notably increased compared to that of age-matched control mice. These M2Mφ in the liver produced elevated levels of IL-6 and TNF-α. rVV-N25 infection suppressed the number and activation of M2Mφ in liver tissue. These results suggested that inflammatory cytokines produced by M2Mφ contribute to the induction of chronic liver inflammation in HCV transgenic mice. Collectively, we showed here that the therapeutic effect of rVV-N25 results from suppression of the number and activation of hepatic macrophages.
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