脂多糖诱导多形核白细胞和肺泡巨噬细胞凋亡异常在急性肺损伤发病中的意义  

Effect and mechanism of dysregulated apoptosis of polymorphonuclear leukocytes and alveolar macrophages by lipopolysaccharide in acute lung injury

作　　者：宋勇[1] 毛宝龄[2] 

机构地区：[1]南京军区南京总医院呼吸内科,南京210002 [2]第三军区大学新桥医院解放军呼吸病研究所

出　　处：《中国病理生理杂志》1999年第12期1103-1105,共3页Chinese Journal of Pathophysiology

摘　　要：目的：探讨ＰＭＮ 和ＡＭ 凋亡异常的机制和意义；为适度调控炎性细胞凋亡防治ＡＬＩ 提供理论依据。方法：通过建立大鼠外周血多形核白细胞（ＰＭＮ） 和肺泡巨噬细胞（ＡＭ） 体外培养，采用流式细胞技术观察ＬＰＳ 对上述细胞凋亡的影响。结果：ＬＰＳ 加入体外培养大鼠外周血ＰＭＮ 中，培养２４ ｈ ，ＰＭＮ 的凋亡率明显降低，ＬＰＳ 可明显促进体外培养的大鼠ＡＭ 凋亡，并呈剂量、时间依赖关系。结论：ＬＰＳ 诱导ＰＭＮ 和ＡＭ 细胞凋亡异常可能是失控性全身炎症反应持续发展和加重的重要机制之一。AIM:To investigate the effect of dysregulated apoptosis of polymorphonuclear leukocytes(PMN) and alveolar macrophages (AM) in acute lung injury (ALI). METHODS:The methods of isolation and cultured of PMN and AM. To study the effects of lipopolysaccharide (LPS) on apoptosis of PMN and AM by using cytometrice techniques.RESULTS:LPS delayed apoptosis of PMNs after 24 hours in vitro. LPS also induced apoptosis of AMs in vitro in a time-dose-dependent fashion.CONCLUSION:Dysregulated expression of PMNs and AMs programmed cell death may represent an important mechanism for the development of clinically important consequences of overwhelming inflammation such as ALI of its more generalized expression, multiple organ dysfunction syndrome.

关 键 词：中性白细胞 巨噬细胞 肺泡 肺损伤 脂多糖 

分 类 号：R563.02[医药卫生—呼吸系统]