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，研究了过氧化氢（H_20_2）和白三烯C4对嗜酸性粒细胞粘附性和内皮粘附分子表达的影响。0.1-luM h_20_2显著增强了嗜酸性粒细胞对内皮细胞的粘附。用luM白三烯C4也有类似的效果。抗β 2整合素单克隆抗体可阻断h_20_2活化的增强粘附，而抗α 4抗体则不能。抗cd11a抗体对H_20_2的抑制作用较弱，但对H_20_2的抑制作用较弱。H_20_2增强了ODlib和CD18的表达，表明H_20_2通过对这些粘附蛋白的作用增强了细胞的粘附能力。另一方面，H_20_2对内皮细胞VCAM-1和icam -1的表达有调节作用。我们接下来询问嗜酸性粒细胞主要碱性蛋白（MBP）是否会改变嗜酸性粒细胞粘附分子的表达。3uM MBP可增强CDIIc和CD54 （ICAM-1）的表达。MBP还增强了嗜酸性粒细胞与内皮细胞的粘附。然而，抗粘附分子抗体并没有改变这种增强的粘附，这表明MBP效应的发展可能涉及未知的机制。

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.