| Project/Area Number |
26461499
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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 |
Infectious disease medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
ISO-O Naoyuki 東京大学, 医科学研究所, 助教 (80420214)
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| Co-Investigator(Renkei-kenkyūsha) |
KITA Kiyoshi 長崎大学, 熱帯医学グローバルヘルス研究科, 教授 (90134444)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | マラリア / リポ蛋白 / スカベンジャー受容体 / エクソソーム |
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| Outline of Final Research Achievements |
In this study, we found a novel feeding pathway for cholesteryl esters by Plasmodium erythrocyte-stage parasites in a form of high density lipoprotein (HDL). Addition of fluorescently-labelled HDL into in vitro culture resulted in an internalization of HDL signal to both parasitized erythrocyte membrane and parasite body. BLT-1, an antagonist for class B scavenger receptors, blocked HDL uptake, and Plasmodium growth in vitro significantly reduced. Reaction with anti-CD36 antibody was positive only with parasitized host erythrocyte membranes and the apical membrane of internal parasites, but not in a CD36-deficient mouse or a mouse with bone marrow transplanted from the CD36-deficient mouse. We also found that double positive exosomes for CD36 and platelet-specific CD41 were detected from infected mouse plasma. In addition, anti-CD41 antibody reacted with parasite membrane, suggesting that CD36 is delivered from host platelets via exosomes.
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