内毒素急性肺损伤与中性粒细胞凋亡研究现状

摘要

内毒素(endotoxin)是革兰阴性菌细胞壁的脂多糖(lipopolysaccharide,LPS)成分,细菌死后细胞壁崩解时释出.内毒素可诱导肺泡巨噬细胞和上皮细胞产生多种细胞因子、趋化因子和激活中性粒细胞(polymorphonucler neu trophil,PMN)并使其向损伤部位聚集,导致急性肺损伤(acute lung injury,ALI)和急性呼吸窘迫综合征(acute respira-tory distress syndrome,ARDS).现有资料表明PMN 凋亡延迟在急性肺损伤的发生过程中起到重要作用,了解PMN凋亡调控有利于调节机体炎症反应,可为ALI 开辟新的治疗路径.%Endotoxin releases from the death of the bacteria when the cell wall collapsed, which is (LPS) the component of the cell wall of gram-negative bacteria. LPS can induce alveolar macrophages and epithelial cells to produce multiple cytokines, chemokines and activate polymorphonucler neutrophils (PMN), and make them gather to the injury site, leading to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Available informations have indicated that delayed apoptosis of PMN played an important role in ALI. Understanding of apoptosis regulation will be conducive to regu -late PMN inflammatory response, expecting to find a new way for the treatment of ALI.