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), formylmethi onylleucylphenylalanine (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% increas e in Mac-1 expression in neutrophils (P < 0.05). PAF also caused a dec rease in L-selectin expression in eosinophils (-37.0 +/- 8.1%, P < 0.0 01) 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 < 0.0 1). In contrast to the effects of PAF and FMLP, IL-5 affected selectiv ely the surface expression of adhesion molecules in eosinophils but no t neutrophils. Expression of Mac-1 increased by 44.3 +/- 7.5% in eosin ophils (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 ca used a 49.5 +/- 4.2% decrease in eosinophil L-selectin expression (P < 0.001) but had no effect on L-selectin expression in neutrophils. Eos inophil VLA-4 expression was not altered by any stimulus. We demonstra te for the first time a concomitant increase in expression of the beta 2 integrin molecule Mac-1 and decrease in expression of L-selectin aft er ex vivo exposure to PAF and FMLP in eosinophils. We further demonst rate that IL-5 causes comparable changes in the expression of these mo lecules that are selective for eosinophils. Our data suggest a potenti al mechanism for selective endothelial adhesion of eosinophilic granul ocytes in inflammatory states such as human asthma.