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

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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.