| Project/Area Number |
16K15051
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Integrative animal science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Goto Yasuyuki 東京大学, 大学院農学生命科学研究科(農学部), 准教授 (50553434)
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| Co-Investigator(Renkei-kenkyūsha) |
FUJII Wataru 東京大学, 大学院農学生命科学研究科, 助教 (40708161)
YAMAGISHI Junya 北海道大学, 人獣共通感染症リサーチセンター, 准教授 (80535328)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | マラリア / 肝障害 / MRP14 / 免疫学 / 感染症 / 病理学 |
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| Outline of Final Research Achievements |
Hepatic dysfunction is one of the clinical features in severe malaria. However, the mechanism of hepatic injury during malaria is still unknown. MRP14 is abundantly expressed by myeloid cells and involved in various inflammatory diseases. In order to verify whether extracellular MRP14 is involved in the pathology of hepatic injury during rodent malaria, we intravenously administrated recombinant MRP14 (rMRP14) to mice infected with Plasmodium berghei. The administration of rMRP14 exacerbated the hepatic injury during the infection, and their serum concentration of hepatic enzymes increased significantly more than PBS-treated controls. More MRP14+ macrophages accumulated in rMRP14-treated mice than PBS-treated controls after infection. The results indicate that MRP14 promotes the accumulation of MRP14+ cells and the up-regulation of pro-inflammatory molecules, which amplify inflammatory cascade leading to hepatic injury.
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