| Project/Area Number |
21689048
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
TERAO Yutaka Osaka University, 大学院・歯学研究科, 准教授 (50397717)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥26,520,000 (Direct Cost: ¥20,400,000、Indirect Cost: ¥6,120,000)
Fiscal Year 2010: ¥10,920,000 (Direct Cost: ¥8,400,000、Indirect Cost: ¥2,520,000)
Fiscal Year 2009: ¥15,600,000 (Direct Cost: ¥12,000,000、Indirect Cost: ¥3,600,000)
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| Keywords | 感染症 / 細菌 / 微生物 / 免疫学 / バイオ関連機器 / バイオ関連機 |
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| Research Abstract |
Neutrophils are part of the initial group of immune cells recruited to the site of infection. However, in severe streptococcal infection including streptococcal toxic shock syndrome, few neutrophils have been found near Streptococcus pyogenes, which rapidly infects various organs in STSS patients. S.pyogenes is thought to be equipped with virulence factors to evade the neutrophil immune system. Previously, we found that complement C3b functioned as an opsonin is degraded in sera from patients with streptococcal toxic shock syndrome. Furthermore, it has been revealed that S.pyogenes is able to fragment neutrophil extracellular traps (NETs). In the present study, we investigated the mechanism of S.pyogenes evasion from neutrophils. Biacore analysis demonstrated that rSpeB and wild-type S.pyogenes rapidly degrade C3b. In a mouse model, bacterial survival rate was lower for the ΔspeB mutant than the wild-type strain. Furthermore, histopathological observations showed that neutrophils infiltrated to the site of infection by the ΔspeB mutant, whereas few migrated to the infection site in mice injected with the wild type and S. pyogenes continued to spread along the fascia. Time-lapse microscopic analysis revealed that digestion of NETs was seen by the wild-type strain, but not ΔspeB mutant strain. Our results indicate that SpeB contributes to the escape of S. pyogenes from neutrophil immunity by degrading C3b and NETs at the site of initial infection.
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