Abstract

The mechanisms by which corticosteroids affect circulating granulocytes are not completely understood. Since granulocyte adherence and chemotaxis are both prerequisite for an exudative response in inflammation, we studied these functions in vitro before and at 4, 24, and 48 hr after administration of 60 mg of prednisone to healthy human volunteers and patients with idiopathic hypereosinophilia. Adherence was determined by the number of eosinophils and neutrophils from heparinized whole blood that remained adherent to nylon-wool colums after a 15-min incubation. Prior to prednisone administration, 68 ± 7% neutrophils and 60 ± 18% eosinophils were adherent; 4 hr after prednisone administration, adherence of both cell types decreased by one-third (p < 0.02); at 24 hr adherence had partially recovered (neutrophils 63 ±10%; eosinophils 60 ± 5%). Chemotaxis was measured with a morphologic Boyden-chamber assay using endotoxinactivated serum as the chemoattractant. Twenty-four hours after prednisone administration eosinophil chemotaxis was reduced by more than 50 %, and it had fully recovered by 48 hr. Neutrophil chemotaxis was never depressed, and at 48 hr it was significantly increased over the baseline value. Hence, these studies show that whereas corticosteroids have similar effects in decreasing both neutrophil and eosinophil adherence, they have differential effects on locomotion, in that eosinophil chemotaxis is significantly suppressed by drug administration while neutrophil chemotaxis is not suppressed. It should be emphasized that the eosinophils used in this study were taken from patients with the hypereosinophilic syndrome, and thus they may not truly represent normal eosinophils. However, these studies still suggest fundamental differences in the mechanisms of modulation of locomotion of different granulocyte populations involved in the inflammatory response.

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