黏附分子CD11b与ICAM-1在PMNs跨内皮移行中的作用机制  

Roles of Adhesion Molecules CD11b and ICAM-1 in PMNs Transmigrating across Endothelium

作　　者：张雪萍 刘新波 任永功 石碧明 李亚丽 姚尚龙[2] 曾邦雄[2] 

机构地区：[1]深圳市人民医院暨南大学医学院附属第二医院麻醉科,深圳518020 [2]华中科技大学同济医学院附属协和医院麻醉科,武汉430022

出　　处：《华中科技大学学报（医学版）》2007年第1期94-96,共3页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：深圳市科技计划资助项目(No.200204004)

摘　　要：目的探讨黏附分子CD11b与ICAM-1在多形核白细胞(PMN)跨内皮移行中的作用。方法培养原代人脐静脉内皮细胞(HUVEC)于3.0μm孔径大小聚碳酸膜上直至其长成单层,然后移入48孔两室趋化板内,脂多糖(LPS)分别刺激PMNs及HUVECs,取其中一部分分别用CD11b单抗I、CAM-1单抗、CD11b+ICAM-1单抗处理,PMN移行率通过计数跨越内皮细胞的PMNs数决定。结果LPS激活PMNs和HUVECs后,PMN跨内皮移行显著增加[(168.77±3.60)%,P<0.01)],CD11b单抗和ICAM-1单抗可分别减少这种移行至(122.90±4.65)%和(114.90±6.06)%。合用两种单抗可使移行率进一步降低至(93.00±5.21)%。结论黏附分子CD11b与ICAM-1的表达影响着中性粒细胞的跨内皮移行作用,且这两种分子有协同作用。Objective To investigate the roles of adhesion molecules CD11b and ICAM-1 in PMN transmigrating across endothelium. Methods HUVECs were cultured on polycarbonate membranes of 3.0 ktm pore size until an endothelial cell monolayer was grown. Then they were moved into a 48-well transwell chambers system. PMNs and HUVECs were stimulated with LPS （100 ng/ml）, then treated with or not with CD11bMoAb, ICAM-1MoAb, CD11bMoAb＋ICAM-1MoAb. The rate of PMNs migration was measured by determining the number of PMNs through endothelial cell monolayers. Results There was an increase in the number of PMN transmigrating across endothelium monolayer following activation of the PMNs and HU- VECs by LPS [-（168.77±3.60） %, P〈0.01]. Pretreatment with anti-ICAM-1 Ab or anti-CD11b Ab resulted in inhibition of transmigration to （122.90± 4.65） % and （ 114. 90± 6. 06） % respectively. Combined use of anti-ICAM-1 Ab and anti-CD11b Ab could result in a further decrease in migration rate to （93.00±5.21） %. Conclusion The expression of adhesion molecules CD11b and ICAM-1 had an effect on PMN transmigrating across endothelium in a synergic fashion.

关 键 词：CD11B ICAM-1 多形核白细胞 人脐静脉内皮细胞 跨内皮移行 

分 类 号：R364.5[医药卫生—病理学]