CAJ | 학술논문

致病因子一方面诱导肺泡巨噬细胞和上皮细胞产生多种细胞因子和趋化因子,激活中性粒细胞并使其向损伤部位聚集,从而产生炎症因子的瀑布式反应;另一方面激活死亡受体通路Fas-FasL等诱发肺上二皮细胞凋亡,从而引起肺组织损伤.另外,Fas活化后可通过介导肺内炎症介质释放和中性粒细胞聚集进一步加重肺损伤.中性粒细胞活化和上皮细胞凋亡在急性肺损伤的发生过程中起重要作用.
치병인자일방면유도폐포거서세포화상피세포산생다충세포인자화추화인자,격활중성립세포병사기향손상부위취집,종이산생염증인자적폭포식반응;령일방면격활사망수체통로Fas-FasL등유발폐상이피세포조망,종이인기폐조직손상.령외,Fas활화후가통과개도폐내염증개질석방화중성립세포취집진일보가중폐손상.중성립세포활화화상피세포조망재급성폐손상적발생과정중기중요작용.
Causative agents induce alveolar macrophages and epithelial cells to produce cytokines and chemotactic factors, activate neutrophils and make them gather to the injury site, and result in waterfall response of inflammatory factors. On the other hand,causative agents activate the death receptor pathway such as Fas-FasL, induce apoptosis of lung epithelial cells, and cause lung injury. Besides, the activated Fas further aggravate lung injury by mediating the release of lung inflammatory mediators and neutrophil accumulation. Neutrophil activation and epithelial cell apoptosis play an important role in acute lung injury.