ABSTRACT
Eosinophilia is associated with a number of disease processes, including helminthic parasitic infections, allergic diseases, and a variety of other diseases with less defined causes. This chapter discusses the regulatory effect of platelet-activating factor (PAF) on human eosinophils. PAF is a potent phospholipid mediator, secreted by many cells involved in inflammatory processes. Serum-treated zymosan (STZ) can activate the NADPH oxidase, resulting in enhanced oxygen consumption and production of toxic oxygen metabolites. The PAF-primed response induced by STZ is accompanied by changes in signal transduction. In untreated eosinophils, the accumulation of diglycerides occurs rather late after stimulation with STZ and the cytosolic free calcium ion concentration remains unchanged. The STZ-induced respiratory burst in eosinophils is almost completely blocked by monoclonal antibody B2. STZ-induced responses in human eosinophils are primed not only by PAF, but also the cytokines granulocyte-macrophage colony-stimulating factor, interleukin-3 and interleukin-5 enhance the percentage of eosinophils binding STZ. These cytokines greatly potentiate the STZ-induced PAF synthesis and release.
