肺炎支原体感染引起气道黏液高分泌的机制研究进展

Progress on mechanism of airway mucus hypersecretion induced by mycoplasma pneumoniae infection

肺炎支原体(mycoplasma pneumoniae,MP)感染引起气道黏液高分泌所致的气道阻塞的发病率逐年增高,并增加慢性气道炎症性疾病的风险。MP可通过黏附、迁移、分泌社区获得性呼吸窘迫综合征毒素(community acquired respiratory distress syndrome toxin,CARDS Tx)等毒力因子对气道黏膜造成损伤,直接破坏气道上皮的结构和功能,影响纤毛细胞功能及代谢等。MP感染气道后使促炎细胞因子增多及Toll样受体上调,引起气道黏液分泌增多。此外,当MP感染气道上皮细胞后,通过信号传导途径使黏蛋白(mucin,MUC)产生增加,使MUC5AC分泌增多,进而导致气道黏液高分泌。探讨调控MP感染后气道黏液高分泌的机制,有可能对难治性MP感染的治疗及降低气道慢性炎症的发生率有一定帮助。

The incidence rate of chronic airway inflammatory diseases caused by airway mucus hypersecretion caused by mycoplasma pneumoniae(MP)infection is increasing year by year.In this paper,the damage of MP on airway mucosa through its adhesion,migration,community acquired respiratory distress syndrome toxin(CARDS Tx)and other virulence factors is described,which directly damages the structure and function of airway epithelium and affects the metabolism of ciated cells.It can also cause the increase of airway pro-inflammatory cytokines and the up regulation of toll-like receptor,resulting in the increase of airway mucus secretion.In addition,when MP infects airway epithelial cells,it will increase mucin(MUC)production through signal transduction pathway,which will increase the secretion of MUC5AC and lead to airway mucus hypersecretion.Controling airway mucus hypersecretion caused by MP infection can reduce the occurrence of chronic airway inflammation and helpful to the treatment of refractory MP infection.