Modulating effects of eosinophil-derived mediators in the development of eosinophil infiltration in the asthmatic airways.

在活化的嗜酸性粒细胞产生的炎症介质中，检测了过氧化氢(H_2O_2)和白三烯C4对嗜酸性粒细胞黏附和内皮黏附分子表达的影响。0.1-Lum H_20_2可显著增加嗜酸性粒细胞与内皮细胞的黏附。Lum白三烯C4也获得了类似的效果。抗β2整合素的单抗可阻断细胞与H_2O_2活化的粘附性增强，而抗α4抗体则不能阻断这一过程。抗CD Lib抗体对H_2O_2效应也有部分抑制作用，但抗CD11a抗体对H_2O_2效应无明显抑制作用。H_2O_2促进了ODlib和CD18的表达，提示这种增强的黏附作用至少部分是通过影响这些黏附蛋白来实现的。而H_2O_2对血管内皮细胞表面血管细胞间黏附分子-1或细胞间黏附分子-L的表达有一定的调节作用。接下来，我们询问嗜酸性粒细胞主要碱性蛋白(MBP)是否能改变嗜酸性粒细胞表面黏附分子的表达。3uM MBP促进CDIIc和CD54(ICAM-1)的表达。MBP还能增强嗜酸性粒细胞与内皮细胞的黏附。然而，抗黏附分子抗体不能改变这种增强的黏附，这表明MBP效应的发生涉及未知的机制。

Among inflammatory mediators generated from activated eosinophils, hydrogen peroxide (H_20_2) and leukotriene C4 were examined for their ability to modify eosinophil adhesiveness and expression of endothelial adhesion molecules. 0.1-luM H_20_2significaxitly augmented eosinophil adhesion to endothelial cells. Similar effect was also obtained with luM leukotriene C4. The augmented adhesion with H_20_2activation was blocked by a monoclonal antibody against beta2 integrin, but not by anti- alpha4 antibody. The H_20_2 effect was also partially but significantly inhibited by anti-CD lib antibody, but not by anti-CD11a. H_20_2 enhanced the expression of ODlib and CD18 suggesting that the augmented adhesion occurred, at least in part, via the effects on these adhesion proteins. On the other hand, H_20_2 did modify the expression of VCAM-1 or ICAM-l on endothelial cells. We next asked whether eosinophil major basic protein (MBP) modify the expression of adhesion molecules on eosinophilla. 3uM MBP enhanced the expression of CDIIc and CD54 (ICAM-1). MBP also augmented eosinophil adhesion to endothelial cells. However, the enhanced adhesion was not modified by anti- adhesion molecule antibodies suggesting the involvement of unknown mechanisms in the development of MBP effect.