Study on mycoplasmal pneumonia using Mycoplasma pneumoniae infection model

众所周知，肺炎支原体是呼吸道传染病的病原之一。然而，肺炎支原体感染后诱发原发性非典型肺炎的机制尚不清楚。因此，我们尝试用无菌小鼠建立支原体肺炎模型。将10^6 ~ 10^7 CFU的肺炎支原体（M129株）在麻醉条件下用30 μl的PPLO肉汤经鼻接种。对原发感染和再感染小鼠进行细菌学、组织学和免疫学研究。肺炎支原体在10^6 CFU/肺时定植良好，抗体滴度增加到1:32。组织病理学观察，M129株再感染小鼠出现肺炎。M129再感染组肺浸润淋巴细胞CD4、CD8、CD25阳性细胞比例升高。在体外肺炎支原体抗原存在下，淋巴细胞产生炎性细胞因子。此外，菌株M129的超声抗原诱导MOLT-4培养细胞产生IL-4和IFNγ。从这些结果推测，感染肺炎支原体菌株M129可诱导小鼠体内Thl细胞活化，引起支原体肺炎。我们证实肺炎支原体单抗小鼠是研究肺炎支原体感染发病机制的一种有用的动物模型。

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.