炎症及细胞自噬与急性肺损伤关系的研究进展

Research progress on relationship between inflammation and autophagy with acute lung injury

肺内炎症细胞的过度活化、募集,失控性地释放炎症因子,是急性肺损伤(ALI)的根本原因。IL-1β等具有进一步触发其他促炎细胞因子分泌的作用,是ALI形成过程中的关键促炎因子之一。研究显示,NLRP3炎性体是调控IL-1β成熟和分泌的关键分子平台。而细胞自噬能抑制NLRP3炎性体的效应蛋白caspase-1的活化,减少IL-1β的成熟及释放。由此提示,针对炎性体及自噬的治疗有可能成为防治ALI的靶点之一。本文就炎症及自噬对ALI作用的研究进展做一综述。

Excessive activation and recruitment of inflammatory cell in lung and uncontrolled release of cytokines and chemokines was considered as the key reason of acute lung injury (ALI).Interleukin-1β(IL-1β),which further triggered the secretion of other proinflammatory cytokines,was one of the key proinflammatory cytokine in the formation of ALI.It has been reported that NLRP3 inflammasome is a key molecular platform for regulating IL-1β maturation and secretion.Autophagy can inhibit the activation of caspase-1,which is the key effector protein of NLRP3 inflammasome,and reduce the maturation and release of IL-1β.It suggests that NLRP3 inflammasome and autophagy may be one of the targets for ALI prevention.This article reviews the research progress of the role of inflammation and autophagy in ALI.