Modulation of the Eosinophil Chemotactic Factor (ECF) Release from Various Cells and Their Subcellular Components by Phospholipids

Abstract

An eosinophil chemotactic factor (ECF) can be released from human polymorphonuclear neutrophils (PMN), rat mononuclear and rat mast cells by the calcium ionophore (A23187), during phagocytosis, by arachidonic acid and phospholipase A₂. It has been suggested that stimuli such as the ionophore and the phagocytic event lead to phospholipid turnover with the generation of arachidonic acid which is subsequently transformed by a lipoxygenase-like enzyme into ECF. Addition of phospholipids such as phosphatidylethanolamine and phosphatidvlinositol during ionophore stimulation of various cells increased the ECF release significantly. ECF activity is also enhanced in the presence of indomethacin at concentrations which inhibit prostaglandin synthesis. With bromphenylacylbromide and eicosatetraynoic acid, ECF generation as well as the chemotaxis of eosinophils is inhibited suggesting that the phospholipase A₂-arachidonic acid pathway represents a common link for ECF release as well as for the chemotaxis of eosinophils. From the cytosol of human PMN an ECF-containing enzyme was obtained. Incubation of phospholipase A₂ and phospholipids with the ECF-converting enzyme led to potent ECF indicating that addition of phospholipids provides the soluble ECF-generating system with an additional source of arachidonic acid. The data represent a molecular approach to analyze the mechanisms of ECF release from soluble components after immunological triggering of the cells.

Eosinophils during developing periodontal disease of rats

“…The toluidine blue technique and electron microscopy were used to observe mast cells, but the possibility that mast cells were eventually present and that they could be detected by other methods cannot be excluded. On the other hand, in the rat, chemotactic factors can be generated, not only by mast cells, but also by mononuclear leukocytes (Koenig, Kroegel & Pfeiffer 1982) which might therefore be responsible for the eosinophil inflltrate.…”