| Project/Area Number |
22590404
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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 |
Bacteriology (including Mycology)
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
SHINJI Hitomi 東京慈恵会医科大学, 医学部, 講師 (30287247)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2011: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2010: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 黄色ブドウ球菌 / 感染 / フィブロネクチン結合たんぱく質 / FnBP / FnBPA / FnBPB / 感染症 / 病原性 |
|---|
| Research Abstract |
The fibronectin-binding proteins, FnBPA and FnBPB, are important adhesins for S. aureusinfection. We constructed fnbA and/or fnbBmutant strains from S. aureusSH1000, which possesses intact rsbU, and the role of these adhesins in in vitroand in vivoinfections was studied. In intravenous infection, all fnbmutants caused a remarkable reduction in the colonization rate in kidneys and the mortality of mice. fnbB mutant caused a more severe decrease in body weightthan that caused byfnbAmutant. Serum levels of IL-6 and NF-κB activation in spleen cells were remarkably reduced in fnbAor fnbA/fnbB mutant infections; however, there was no significant reduction in fnbBmutant. In in vitrocellular infection, FnBPA was shown to be indispensable in adhesion and internalization into non-professional phagocytic cells, upon ingestion by inflammatory macrophages and NF-κB activation. However, both FnBPs were required for efficient cellular responses. The results showed that FnBPA is more important for in vitroand in vivoinfections; however, the cooperation between FnBPA and FnBPB is indispensable for the induction of severe infection resulting in septic death.
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