Pharmacology of interleukin-1-induced neutrophil migration

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Abstract
Neutrophil (PMN) accumulation induced by interleukin-1β (IL-1β, 5–20 ng) into the mouse air pouch was inhibited in a dose-dependent manner (2–200 μg) by concomitant injection of IL-1 receptor antagonist (IL-1RA). Similarly, co-administration of the neuropeptideα-melanocyte-stimulating hormone (α-MSH) resulted in a reduction of the number of migrated PMN but only at the highest dose tested (200 μg). Although IL-1RA does not select between the two types of receptor so far described for IL-1, the effectiveness ofα-MSH suggests that this property of the cytokine may occur through IL-1 type I receptor. This observation was confirmed by using a specific monoclonal antibody (mAb) raised against this receptor type, and which strongly inhibited (87%) IL-1-induced PMN recruitment.