2014 Fiscal Year Final Research Report
Role of Th17 cells in pathogenesis of Mycoplasma pneumoniae infection and onset of its complications
| Project/Area Number |
24591175
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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 |
Respiratory organ internal medicine
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| Research Institution | Kyorin University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KAMIYA Shigeru 杏林大学, 医学部, 教授 (10177587)
TAGUCHI Haruhiko 杏林大学, 保健学部, 教授 (20146541)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 肺炎マイコプラズマ / 実験的肺炎モデル / Th17 |
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| Outline of Final Research Achievements |
Mycoplasma pneumoniae is a common respiratory pathogen , and the participation of the excessive host immunoresponse is thought to be involved in M. pneumoniae pneumonia and the pathogenic mechanisms of the complications. Recent studies indicate that Th17 cell has been implicated in the onset of autoimmune diseases. In this report, we established an experimental pneumonia mouse model by the use of M. pneumoniae antigens and performed immunological analyses to examine the induction mechanisms. In addition, we have examined the specificity of Th 17 cell inducibility by mouse splenocytes. These analyses indicated that mRNA expression levels of IL-17A and IL-10 in the lung were increased by M. pneumoniae antigens sensitization in vivo. It was also shown that M. pneumoniae antigens induced IL-17A release from mouse splenocytes in a dose-dependent manner in vitro. These results suggest that murine Th17 response is initiated by M. pneumoniae antigen sensitization.
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| Free Research Field |
感染症学
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