2013 Fiscal Year Final Research Report
Regulation of pathogenicity via envelope stress response in Bordetella pertussis
| Project/Area Number |
23590517
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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 | Kyorin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KAMIYA Shigeru 杏林大学, 医学部, 教授 (10177587)
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| Co-Investigator(Renkei-kenkyūsha) |
YONEZAWA Hideo 杏林大学, 医学部, 講師 (60453528)
YAMAMOTO Tomoko 千葉大学, 薬学研究科, 教授 (60110342)
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| Research Collaborator |
ARMSTRONG Sandra K ミネソタ大学, 医学研究科, 教授
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| Project Period (FY) |
2011 – 2013
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| Keywords | 百日咳菌 / 細胞表層 / ストレス応答 / 病原性 / sigmaE |
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| Research Abstract |
Cell surface has an important role in the functioning of Bordetella pertussis virulence factors. We found cell-free adenylate cyclase toxin (ACT) was increased by the activation of sigma E, which is alternative sigma subunit of RNA polymerase relating to envelope stress response. In the present study, we investigated the mechanism of increase of cell-free ACT by sigma E activation.
Transcriptions of the genes encoding ACT and its secretion machinery did not altered by activation of sigma E. On the other hand, production of outer membrane vesicle (OMV) including ACT was significantly increased. Different manner of release would provide the stability to ACT resulted in the increase of cell-free ACT. ACT inhibits phagocytosis by macrophages. Activation of sigma E by deletion of RseA was decreased the efficiency of phagocytosis. It is suggested that sigma E-dependent envelope stress response would be one of the regulation system of the pathogenicity of B. pertussis.
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