| Project/Area Number |
24590545
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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 |
Bacteriology (including Mycology)
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
YANAGISAWA Tatsuo 理化学研究所, 横山構造生物学教室, 研究員 (10450420)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 髄膜炎菌 / Neisseria meningitidis / グルタミン酸 / トランスポーター / 細胞侵入 / 宿主細胞侵入 / 転写後制御 / ヒト内皮細胞 / 感染 / 侵入 |
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| Outline of Final Research Achievements |
We found that, 1) the ΔgltT-ΔgltM invasion defect in assay medium (AM) was alleviated in AM without 10% FBS [AM(-S)], 2) the alleviation disappeared again in AM(-S) supplemented with 500 μM glutamate, 3) glutamate uptake by the ΔgltT-ΔgltM mutant was less efficient than that by the wild type strain, 4) both the GltT-GltM-dependent invasion and accumulation of ezrin were more pronounced when N. meningitidis formed larger colonies on human brain microvasocular endothelial cells (HBMEC). These results suggested that GltT-GltM-dependent meningococcal internalization into HBMEC might be induced by the reduced environmental glutamate concentration upon infection. We also found that the amount of glutathione within the ΔgltT-ΔgltM mutant was much lower than that within the wild type Ν. meningitidis strain only upon HBMEC infection, and was correlated with intracellular survival, showing that L-glutamate uptake via GltT-GltM plays multiple roles.
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