| Project/Area Number |
23590526
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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 | Tokushima Bunri University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
永浜 政博 徳島文理大学, 薬学部, 教授 (40164462)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | ウエルシュ菌イオタ毒素 / エンドサイトーシス / 初期エンドソーム / リサイクリングエンドソーム / 後期エンドソーム / リソソーム / 結晶化 / リサイクリングエンドゾーム |
|---|
| Research Abstract |
Clostridium perfringens iota-toxin is a binary toxin composed of an enzyme component(Ia) and a binding component(Ib). Each component alone lacks toxic activity, but together they produce cytotoxic effects. This study indicated that an internalized Ia and Ib complex was delivered to early endosomes and that subsequent delivery of Ia to the cytoplasm occured mainly in early endosomes. Then, Ib was transported to late endosomes and lysosomes for degradation. Next, we examined the cytotoxicity of Ib. A431 and A549 cells were susceptible to Ib. Ib bound and formed oligomers in the membranes of A431 cells. Then, Ib caused cell swelling and the rapid depletion of cellular ATP in the cells. Ib also induced permeabilization by propidium iodide without DNA fragmentation in the cells. Ultrastructural studies revealed that A431 cells underwent necrosis after treatment with Ib. We demonstrated that Ib by itself produced cytotoxic activity through necrosis.
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