| Project/Area Number |
13670283
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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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 |
TAGUCHI Haruhiko Kyorin University, School of Medicine, lecturer, 医学部, 講師 (20146541)
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| Co-Investigator(Kenkyū-buntansha) |
OSAKI Takako Kyorin University, School of Medicine, Assistant, 医学部, 助手 (90255406)
KAMIYA Shigeru Kyorin University, School of Medicine, Professor, 医学部, 教授 (10177587)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Mycoplasma pneumoniae / pneumonia / mycoplasmal pneumonia / inflammatory cytokines / sonicated antigen of Mycoplasma pneumoniae / Thl / germ-free mouse / experimental infection / 宿主炎症性サイトカイン / 菌体成分 / Th1 / リンパ球サブセット |
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| Research Abstract |
It is well known that Mycoplasma pneumoniae is one of the pathogenic agents of the respiratory infectious diseases. However, the mechanism by xhich primary atypical pneumonia is induced following M. pneumoniae infection has not been clarified. Therefore, we have attempted to establish the mycoplasmal pneumonia model using germ-free mice.
Germ-free were intranasally inoculated with 10^6-10^7 CFU of M. pneumoniae (strain M129) in 30 μl of PPLO broth under anesthesia. In the mice treated with either primary infection or reinfection, bacteriological histpathological and immunological studies were performed.
M. pneumoniae colonized equally well at 10^6 CFU/lung and antibody titer increased to 1:32 in the mice reinfected with M. pneumoniae. In histopathological observation, the mice reinfected with strain M129 showed pneumonia. The CD4, CD8 and CD25 positive cell ratio of lymphocytes infiltrated in the lung increased in the reinfected with strain M129. The lymphocytes produced inflammatory cytokines under the presence of M. pneumoniae antigen in vitro. In addition sonicated antigen of strain M129 induced IL-4 and IFNγ from MOLT-4 culture cells.
From these results, it was speculated that infection of M. pneumoniae strain M129 induced activation of Thl cells in gnotobiotic mice and caused mycoplasmal pneumonia. We confirmed that the gnotobiotic mouse monoassociated with M. pneumoniae is a useful animal model to examine the pathogenesis of M. pneumoniae infection.
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