烟雾吸入性损伤血清对PMN粘附的影响

Effects of smoke inhalation injury serum on the adhesion of polymorphonuclear neutrophils

目的：通过大鼠烟雾吸入伤血清体外刺激培养的内皮细胞和中性粒细胞（ＰＭＮ），了解ＰＭＮ粘着的变化，以及抗ＣＤ１１ａ、抗ＣＤ１１ｂ和抗ＩＣＡＭ－１对ＰＭＮ粘着的影响，探讨粘附因子在烟雾吸入性损伤中的作用。方法：在体外实验中用荧光标记ＰＭＮ，测定ＰＭＮ与烟雾吸入性损伤血清刺激的内皮细胞的粘着率，并采用抗体阻断技术，测定了粘附因子ＣＤ１１ａ、ＣＤ１１ｂ和ＩＣＡＭ－１在ＰＭＮ粘着的作用。结果：吸入伤血清能使粘着率增高，１２～２４ｈ是正常时的３倍多，ＰＭＮ的内皮细胞粘附因子抗体（抗ＣＤ１１ａ、抗ＣＤ１１ｂ和抗ＩＣＡＭ－１）减少ＰＭＮ与内皮细胞粘着率（４４％、５５％和５１％）。结论：烟雾吸入伤血清能增加ＰＭＮ的粘着，其可能是ＰＭＮ浸润的病理基础，进一步研究证明，粘附因子ＣＤ１１ａ、ＣＤ１１ｂ和ＩＣＡＭ－１在ＰＭＮ浸润过程中起重要作用，而且浸润的中性粒细胞释放氧自由基和蛋白酶能导致进一步的肺组织损害。

Objective: To investigate the effects of smoke inhalation injury serum (SIIS) on the adhesion of polymorphonuclear neutrophils (PMN), and the effects of anti CD11a, anti CD11b and anti ICAM1 on the adhesion of PMN. Methods: Fluorescent assay and antibody blocking technique were used to determine the adhesion of PMN to cultured endothelial cells (EC) in the presence of the serum from the rats with smoke inhalation injury, and the effects of CD11a, CD11b and ICAM1 on the adhesion. Results: ZSIIS promoted PMN adhesion to cultured EC. After being cultured with the serum for 12 to 24 h, PMN adhesion to cultured EC was 3 times more than that in the control. The antiendothelial adhesion factors (anti CD11a, anti CD11b and anti ICAM1) might reduce the adhesion rate (44%, 55% and 51%). Conclusion: SIIS can promote PMN adhesion, which might be the pathological basis for PMN infiltration. Futher studies suggested that the antiendothelial adhesion factor might play an important role in the PMN infiltration and the infiltrated PMN could release oxygen radicals and protease causing damage to lung tissues.