Selective Regulation of Expression of Surface Adhesion Molecules Mac-1, L-selectin, and VLA-4 on Human Eosinophils and Neutrophils

We studied the differential expression of cellular adhesion molecules on the surface of purified human eosinophils and neutrophils caused by ex vivo activation with platelet-activating factor (PAF), formylmethionylleucylphenylalanine (FMLP), or recombinant human interleukin-5 (IL-5). PAF (10−7 M) caused a 42.8 ± 5.7% (mean ± SEM) increase in Mac-1 expression in eosinophils (P < 0.01) and a 34.6 ± 9.2% increase in Mac-1 expression in neutrophils (P < 0.05). PAF also caused a decrease in L-selectin expression in eosinophils (−37.0 ± 8.1%, P < 0.001) and neutrophils (−14.1 ± 3.2%, P < 0.05). FMLP (10−6 M) caused a similar increase in Mac-1 expression in both eosinophils (P < 0.001 versus controls) and neutrophils (P < 0.01) and a comparable decrease in L-selectin expression in both eosinophils and neutrophils (P < 0.01). In contrast to the effects of PAF and FMLP, IL-5 affected selectively the surface expression of adhesion molecules in eosinophils but not neutrophils. Expression of Mac-1 increased by 44.3 ± 7.5 % in eosinophils (P < 0.001 versus controls) and by 0.7 ± 1.2% in neutrophils (P = NS versus controls) after exposure to 10−9 M IL-5. IL-5 also caused a 49.5 ± 4.2% decrease in eosinophil L-selectin expression (P < 0.001) but had no effect on L-selectin expression in neutrophils. Eosinophil VLA-4 expression was not altered by any stimulus. We demonstrate for the first time a concomitant increase in expression of the β2 integrin molecule Mac-1 and decrease in expression of L-selectin after ex vivo exposure to PAF and FMLP in eosinophils. We further demonstrate that IL-5 causes comparable changes in the expression of these molecules that are selective for eosinophils. Our data suggest a potential mechanism for selective endothelial adhesion of eosinophilic granulocytes in inflammatory states such as human asthma.