肺炎支原体致病机制的研究进展

The research progress of mycoplasma pneumoniae pathogenesis

肺炎支原体是社区获得性肺炎的常见病原体,致病机制主要包括其对气道上皮细胞的黏附作用,产生氧化应激;释放CARDS毒素,导致气道损伤;通过细胞免疫和体液免疫,引起长期感染或自身免疫反应。肺炎支原体还可导致多脏器的损伤,然而其致病机制尚未明确。肺炎支原体感染后可通过血液、淋巴液向远处传播,直接损伤器官;或者形成循环或原位免疫复合物,诱发机体免疫反应,伴或不伴有血液高凝状态。文章系统综述了目前肺炎支原体致病机制的研究结果。

Mycoplasma pneumoniae is a common pathogen of community-acquired pneumonia, and its pathogenesis mainly includes three aspects. Mycoplasma pneumoniae attaches to ciliated cells of the respiratory epithelium and then produces oxidative stress. It also releases the CARDS toxin, leading to airway damage. Through immunomodulation of the host immune response it enables establishment of persistent infections and causes autoimmune phenomena. My-coplasma pneumoniae can also lead to multiple organs damage, which pathogenic mechanism is not yet clear. Many clinical manifestations of acute infection as well as extrapulmonary complications are due to immunopathologic and in-flmmatory effects produced by the host, with or without blood clotting. This paper systematically reviewed the results of the current Mycoplasma pneumoniae pathogenic mechanisms.