| Project/Area Number |
22591108
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Infectious disease medicine
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SHOBUIKE Takeo 佐賀大学, 医学部, 助教 (70336113)
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| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 感染症防御学 / 自然免疫 / レジオネラ / 微生物学 / 感染症 / 肺炎 |
|---|
| Research Abstract |
Macrophages from C57BL/6 mice restrict growth of Legionella pneumophila. Restriction of bacterial growth is dependent on cell death which requires caspase-1 and Naip5. On the other hand, A/J mouse strain carries a defective Naip5allele, whose macrophages resultin permissiveness to L. pneumophilareplication. We found murine RAW264 macrophage cells exceptionally supported bacterial growth and failed to induce caspase-1-mediated cell death. C57BL/6 Naip5 restored susceptibility to L. pneumophilaand impaired induction of cell death,indicating RAW264 harbors a defect in endogenous Naip5 function. Human NAIP, structural homolog of Naip5, also restored Naip5-deficiency in RAW264 cells. A/J mice expressing human NAIP in macrophages exhibited improved bacterial clearance and decreased mortality when challenged with L. pneumophilaat lung. These results suggest that human NAIP is a functional homolog of murine Naip5 and contributes host's defense against L. pneumophilaby inducing caspase-1-dependent cell death.
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