Cellular mechanism of toxicity of Clostridium perfringens iota-toxin
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 |
Section | 一般 |
Research Field |
Bacteriology (including Mycology)
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Research Institution | Tokushima Bunri University |
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)
|
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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Report
(4 results)
Research Products
(50 results)
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[Journal Article] Clostridium perfringens alpha-toxin induces the release of IL-8 through a dual pathway via TrkA in A549 cells2012
Author(s)
Masataka Oda, Ryota Shiihara, Yuka Ohmae, Michiko Kabura, Teruhisa Takagishi, Keiko Kobayashi, Masahiro Nagahama, Masahisa Inoue, Tomomi Abe, Koujun Setsu, Jun Sakurai
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Journal Title
Biochim. Biophys. Acta
Volume: 1822(10)
Pages: 1581-1589
Related Report
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[Journal Article] Clostridium perfringens alpha-toxin recognizes the GM1a-Trk A complex2012
Author(s)
Masataka Oda, Michiko Kabura, Teruhisa Takagishi, Ayaka Suzue, Kaori Tominaga, Shiori Urano, Masahiro Nagahama, Keiko Kobayashi, Keiko Furukawa, Koichi Furukawa, Jun Sakurai
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Journal Title
J . Biol. Chem
Volume: 287(39)
Pages: 33070-33079
Related Report
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[Journal Article] Clostridium perfringens alpha-toxin recognizes the GM1a-TrkA complex2012
Author(s)
Oda M, Kabura M, Takagishi T, Suzue A, Tominaga K, Urano S, Nagahama M, Kobayashi K, Furukawa K, Furukawa K, Sakurai J
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Journal Title
J. Biol. Chem.
Volume: 287
Issue: 39
Pages: 33070-33079
DOI
Related Report
Peer Reviewed
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[Journal Article] Clostridium perfringens alpha-toxin induces the release of IL-8 through a dual pathway via TrkA in A549 cells.2012
Author(s)
Oda M, Shiihara R, Ohmae Y, Kabura M, Takagishi T, Kobayashi K, Nagahama M, Inoue M, Abe T, Setsu K, Sakurai J
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Journal Title
Biochim. Biophys. Acta
Volume: 1822
Issue: 10
Pages: 1581-1589
DOI
Related Report
Peer Reviewed
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[Presentation] ウエルシュ菌イオタIb成分の細胞毒性の検討2011
Author(s)
小林敬子,梅崎真理子,田代遼,小田真隆,櫻井純,永浜政博
Organizer
文科省戦略的研究基盤形成支援事業『有機合成と天然物化学の手法による医薬品素材の開発』,第7回研究発表会
Place of Presentation
徳島
Year and Date
2011-12-22
Related Report
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[Presentation] ボツリヌス菌C2毒素の細胞内侵入機構の検討2011
Author(s)
高田奈央,樋口真美,小田真隆,小林敬子,櫻井純,永浜政博
Organizer
文科省戦略的研究基盤形成支援事業『有機合成と天然物化学の手法による医薬品素材の開発』,第7回研究発表会
Place of Presentation
徳島
Year and Date
2011-12-22
Related Report
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