烧伤后CD11b/CD18介导的中性多形核白细胞粘附对肺微血管内皮细胞单层通透性的影响

The effect of PMN adhesion mediated by CD11b/CD18 on the increasing permeability of microvascular endothelial monolayer after severe burn injury

目的观察烧伤后中性多形核白细胞（ＰＭＮ）对肺微血管内皮细胞单层通透性的影响，以及ＰＭＮ粘附及其粘附分子ＣＤ１１ｂ／ＣＤ１８在该影响中的介导作用。方法用培养血管内皮细胞单层模型，建立培养肺微血管内皮细胞（ＰＭＥＣ）单层通透性测定的方法，根据处理内皮细胞单层的不同成份，将实验分为７组，用含荧光素异硫氰酸酯白蛋白的灌流液灌流后，测定液体滤过系数（ｋｆ）和渗透压反射系数（δ）。结果烧伤后ＰＭＮ能使反映小分子物质通透性的ｋｆ值明显增加，使渗透压反射系数（δ）显著下降。用单抗封闭ＰＭＮ膜上ＣＤ１１ｂ／ＣＤ１８能使δ值的变化得到纠正；用孔径０２μｍ的滤膜阻断ＰＭＮ与内皮细胞单层的粘附则使ｋｆ值和δ值均接近正常水平。结论白细胞与内皮细胞的粘附是介质类物质发生作用的前提条件，这些物质主要影响肺血管对小分子物质的通透性。粘附分子ＣＤ１１ｂ／ＣＤ１８本身可能具有着生物学信号调控的作用。

Objective To detect the effect of burn activated PMN adhesion and its adhesion molecule CD11b/CD18 on microvascular endothelial permeability using an experimental model of endothelial monolayer on polycarbonate microporous filters.Methods An experimental model for in vitro study of endothelal monolayer for permeability analysis was established. Seven groups were divided into according to the treatment of microvascular endothelial monolayer. Fluid filtration coeffecient(Kf) and albumin reflection coeffecient(δ) were measured after endothelial monolayer was perfused with albumin labelled by FITC. Results Burn activated PMN could increase the level of fluid filtration coeffecient(Kf) and decrease the albumin reflection coeffecient(δ). Monoclonal antibody sealing off CD11b/CD18 on PMN provented the change of δ induced by burn activated PMN. Another microporous filter interposed between PMNs and endothelial monolayer corrected the changes of Kf and δ. Conclusion The permeability enhancing effect of PMNs may be attributed mainly to the PMN EC adhesion mediated by CD11b/CD18. Blocking the PMN EC over adhesion in moderation may be helpful in reducing the lung injury due to severe burn injury.