抄録
Platelet activating factor, PAF, was originally identified as a product released by antigen-stimulated, IgE-sensitized rabbit basophils. The chemical structure of PAF is 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine. PAF has a wide spectrum of potent biological activities. In addition to the platelet activation, PAF produces constraction of smooth muscle, cardiac effects, or increase of vascular permeability. PAF induces aggregation, chemotaxis, and active oxygen generation in neutrophils. It also induces monocytes aggregation, eosinophil chemotaxis, and macrophage activation. PAF has a strong hypotenive action. PAF is generated, by an appropriate stimulation, from basohils, monocytes-macrophages, polymorphonuclear leukocytes, platelets, or endothelial cells. Several organs including lung and kidney were also demonstrated to produce PAF.
PAF is present as a precursor; alkylacyl GPC in cell membrane, and synthesized upon stimulation. So far two routes of PAF biosynthesis have been considered; acetylation of lyso PAF catalyzed by “acetyltransferase” and cholinephosphorylation of alkylacetylglycerol by “cholinephosphotransferase”. Inactivation of PAF is mainly catalyzed by “acetylhydrolase”, to yield lyso PAF, which is often converted to alkylacyl GPC.
Although the precise role of PAF in vivo has not yet been fully understood, it is becoming increasingly evident that PAF is important in some physiological and pathological reaction, such as gram-negative septic shock, inflammation, asthma, and nephritis. In the present review, we describe the outline of development of PAF research based on biological, physiological, and pathological aspects.
