| Project/Area Number |
15K19097
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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 |
Bacteriology (including mycology)
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
Suzuki Koichi 帝京大学, 医療技術学部臨床検査学科, 教授 (20206478)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | らい菌 / トリアシルグリセロール / GPAT3 / Mycobacterium leprae / triacylglycerol |
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| Outline of Final Research Achievements |
Mycobacterium leprae (M. leprae), the causative agent of leprosy, parasitizes within host macrophages. M. leprae lives and replicates in foamy or enlarged phagosomes within macrophages that are filled with lipids, which provide essential source to form cell wall of the mycobacteria. In the present study, we tried to identify lipid species accumulated following infection and to elucidate the underlying mechanisms for the lipid accumulation in M. leprae-infected macrophages. Most abundant lipid in M. leprae-infected cells was triacylglycerol (TAG). In addition, a large number of fatty acid-containing molecular species were detected in TAG. Expression of GPAT3, a key enzyme in the fatty acid catalysis, was significantly increased in M. leprae infected cells. Further elucidation of specific lipid components in the host cell during infection will establish the mechanism of intracellular survival of M. leprae.
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