| Project/Area Number |
15K19099
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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 | Tokushima Bunri University |
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Principal Investigator |
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| Research Collaborator |
NAGAHAMA Masahiro
KOBAYASHI Keiko
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 毒素 / エフェクター / 免疫回避 / 好中球 / 分化 / ウエルシュ菌α毒素 / 細菌感染 / 細胞分化 |
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| Outline of Final Research Achievements |
Granulopoiesis is accelerated to suppress bacteria during infection, but some bacteria can still cause life-threatening infections. The mechanism behind this remains unclear. In this study, we found that mature neutrophils in bone marrow cells (BMCs) were decreased in Clostridium perfringens-infected and virulence factor α-toxin-injected mice. C. perfringens infection interfered with the replenishment of mature neutrophils into peripheral circulation. Treatment of BMCs with α-toxin (phospholipase C) blocked neutrophil differentiation accompanied by modification of lipid rafts. Since treatment with methyl-β-cyclodextrin, a lipid raft-disrupting agent, impaired neutrophil differentiation, the alteration of lipid rafts by α-toxin might be involved in the impairment of granulopoiesis. These results suggest that C. perfringens α-toxin impairs neutrophil differentiation, which provides new insight to understand how pathogenic bacteria evade the host immune system.
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