Platelet-activating factor (PAF-acether) is a phospholipid mediator formed by different cells including eosinophils, macrophages, platelets, neutrophils and vascular endothelium. Its biosynthesis involves the acetylation of a precursor released from membrane phospholipids by activated phospholipase A2. PAF-acether activates most inflammatory cells and induces a variety of in vivo effects related to inflammation, particularly to immediate hypersensitivity and accordingly, to bronchial asthma. These effects include acute bronchoconstriction and bronchopulmonary hyperreactivity in guinea-pigs, which is accompanied by platelet, eosinophil and macrophage activation and their recruitment into the lung parenchyma and airways. Different PAF-acether antagonists have been synthesized, and some of them reduce experimental allergic bronchoconstriction, at as yet poorly characterised sites. Further development of inhibitors of the biosynthesis of PAF-acether and of antagonists of its effects should lead to useful research tools and may lead to valuable therapeutical agents.
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Vargaftig et al. (1987) studied this question.
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