MECHANISMS FOR EOSINOPHIL DE-GRANULATION - RELEASE OF THE EOSINOPHIL CATIONIC PROTEIN

Abstract

Mechanisms for degranulation in human eosinophils were evaluated. Release of eosinophil cationic protein (ECP), a unique eosinophil granule constituent, was measured upon exposure of purified eosinophils to a large surface consisting of Sephadex beads coated with serum, which leads to complement activation. Extracellular release of .apprx. 15% of the cellular ECP occurred both with eosinophils from patients with eosinophila and normal people. Almost all eosinophils isolated from patients with eosinophila and normal people adhered to serum-treated Sephadex. Interaction through C3 [complement component 3] receptors is probably a prerequisite for ECP release from eosinophils when exposed to serum-treated Sephadex. Both cytochalasin B, cytochalasin D and hydrocortisone reduced the release of ECP. Neither the cytochalasins nor hydrocortisone inhibited the adherence of eosinophils to the Sephadex beads. The inhibitory effect of these agents on ECP release is a direct effect on the degranulation process. ECF-A [eosinophil chemotactic factor-A], histamine and colchicine did not affect the release mechanism. No direct relationship was found between degranulation and oxidative burst inasmuch as some soluble mediators induced a high respiratory burst without a concomitant ECP release. Mechanisms for degranulation are not fully identical in eosinophils and neutrophils.