Study on mycoplasmal pneumonia using Mycoplasma pneumoniae infection model

众所周知，肺炎支原体是呼吸道感染性疾病的病原体之一。而原发性非典型肺炎的发病机制是由M.肺炎感染尚未明确。因此，我们尝试用无菌小鼠鼻内接种10^6-10^7 CFU的支原体肺炎模型。在麻醉下，在30 μl PPLO肉汤中接种肺炎链球菌（菌株M129）。对初次感染和再感染的小鼠进行了细菌学、组织病理学和免疫学研究。肺炎支原体以10^6 CFU/肺同样良好地定殖，并且抗体滴度在再次感染肺炎支原体的小鼠中增加至1：32。肺炎。病理组织学观察显示M129再感染小鼠出现肺炎。M129再感染组肺内浸润淋巴细胞中CD 4、CD 8、CD 25阳性细胞比例增加。淋巴细胞在M. pneumoniae抗原。另外，M129菌株的抗原经超声处理后，可诱导MOLT-4培养细胞产生IL-4和IFNγ。肺炎支原体菌株M129在无菌小鼠中诱导Th 1细胞活化并引起支原体肺炎。我们证实了与M.肺炎支原体是研究其致病机制的一种有用的动物模型。肺炎感染。

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.