| Project/Area Number |
25461596
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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 |
Pediatrics
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| Research Institution | The University of Tokushima |
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Principal Investigator |
CHIDA Junji 徳島大学, 疾患酵素学研究センター, 助教 (20437651)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | インフルエンザ / プリオン蛋白質 / 抗プリオン抗体 / 脳症 / 多臓器不全 / プリオン / 抗PrP抗体 / インフルエンザウイルス / インフルエンザ脳症 / サイトカイン / SFKs / ミトコンドリア / 重症化 / エネルギー代謝 |
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| Outline of Final Research Achievements |
The cellular prion protein, designated PrPC, is a membrane glycoprotein expressed the most abundantly in brain and to a lesser extent in other non-neuronal tissues. Conformational conversion of PrPC into the amyloidogenic isoform, PrPSc , is a key event in the pathogenesis of prion disease. However, the physiologyical functions of PrPC remain largely unknown, particularly in non-neuronal tissues. Here we show that, compared with wild-type (WT) mice, mice devoid of PrPC (Prnp0/0) were highly susceptible to various strains of influenza A virus (IAV). Prnp0/0 mice displayed higher mortality after intranasal infection with IAVs, with higher virus titers and more severe inflammatory responses in their lungs, indicating that PrPC has a protective role against IAV infection.
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