Does airway smooth muscle care about platelet-activating factor?

In 1966, BARBARO and ZvAIFLER [l] demonstrated the release of histamine from rabbit platelets during an acute allergic response. Five years later, it was shown that a soluble factor from leucocytes, capable of inducing platelet activation, was responsible for this effect [2, 3). In subsequent years, the factor was recognized for its potent ability to s timulate platelet aggregation and secretion and was consequently named "platelet-activating factor" (PAF) [4]. By the end of the decade, three independent groups had elucidated its chemical structure as 1-alkyi-2(R)-acetyl-glycerol-3phosphocholine. On the basis of its structural and physiological properties, the lipid was subsequently termed as P AF-acether ("ace" for acetate and "ether" for the alkyl bond) [5], acetylglyceryletherphosphorylcholine (AGEPC) [6], or antihypertensive polar renomedullary lipid (APRL) [7]. P AF is an unique phosphoglyceride, which possesses many potent biological acti vi ties relevant for various physiological ~111d pathophysiological conditions [ 810 J. Although originally described as an activator of platelets 14), PAF is now known to have a wide range of biological activities, acting on a long list of inflammatory cells that includes mast cells, mononuclear cells, neutrophils and eosinophils. In addition, PAF has potent biological effects on noninflammatory cells, such as smooth muscle cells, fibroblasts, endothelial cells, type II alveolar cells, and some neurologically derived cell lines. Two principal pathways for the biosythesis of PAF have been discovered [11]. In the deacylationreacylation pathway, PAF is derived from l-0-alkyl-2acyl.-glycerophosphocholine cellular pools through lhe action of a phospholipase A,. The resulling 1-0-alkyl2-lyso-glycerophosphocbolirie is then acylated by an acetyi-CoA-requiring enzyme to form PAF [12J. Alternatively, PAF can be synthesized via a de novo pathway [13], which involves the transfer of phosphocholine from CDP-choline to 1-0-alkyl -2acetylglycerol. The former pathway predominates in activated inflammatory cells, whereas the latter has been shown to be particularly important in a number of noninflammatory cells and isolated tissues. Metabolic degradation of PAF occurs via an acetyl hydrolase, which removes the acetyl group leaving the