2017 Fiscal Year Final Research Report
Analysisi of EGFR-signaling pathway in Mycoplasma pneumoniae infection
| Project/Area Number |
15K09589
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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 |
Infectious disease medicine
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| Research Institution | Kurume University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山本 武司 久留米大学, 医学部, 助教 (20632566)
木田 豊 久留米大学, 医学部, 准教授 (30309752)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | マイコプラズマ肺炎 / EGFR / 細胞死 |
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| Outline of Final Research Achievements |
The excessive immune responses are thought to be responsible for the pathophysiology of Mycoplasma pneumoniae(Mp) pneumonia. Although TLR2 plays a predominant role in the inflammatory responses against Mp, the inflammatory responses still observed in TLR2-deficient mice. In this study, we investigated the involvement of EGFR in the TLR2-independent immune responses.
Since the membrane fraction of Mp induces EGFR activation, we first examined the mycoplasmal protein binding to EGFR. We found that Mpn573 binds to EGFR, but unfortunately the protein was unable to activate EGFR. Moreover, cytoadherence that is thought to be important for the progression of Mp pneumonia was not essential for the activation of EGFR. On the other hand, we found that Mp has an ability to regulate the infected cell death, and the ability may allow the EGFR activating factor of Mp to act on the infected cells for a long time.
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| Free Research Field |
感染症
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