8A2 and acetyltransferase on membrane alkylacyl phospholipids. PAF was found to possess many properties that made it well suited as a proinflammatory mediator of inflammation in many inflammatory diseases. 1 Interest in Degradation of PAF its potential role as a mediator of asthma was fuelled Being a potent bioactive mediator, it makes sense that PAF by the observations that it induced airway microvascular can be degraded rapidly by PAF acetylhydrolase which leakage, bronchconstriction, and bronchial hyper- would therefore limit the activity of PAF. A decrease in PAF responsiveness. In addition, PAF could activate a wide acetylhydrolase activity would lead to greater inflammatory variety of cells including neutrophils, eosinophils, and responses induced by endogenously released PAF. Recent endothelial cells, and was also found to have potent chemo- studies in Japan have examined the presence of respiratory attractant properties for eosinophils. With the discovery of symptoms in asthmatic children and the activity of serum PAF receptor antagonists, the hypothesis that PAF was PAF acetylhydrolase. 9 These investigators found that 4% involved in chronic asthma was tested. In two studies of of a healthy Japanese population had a deficiency of this moderate to severe asthmatic patients no positive clinical enzyme and that, amongst asthmatic children, the severity benefit was demonstrated with two diVerent PAF receptor of symptoms was greater in those with PAF acetylhydrolase antagonists, 23 casting doubt on the contribution of PAF to deficiency. More recently, the inherited serum PAF acetylthe pathophysiology of chronic asthma despite the fact that hydrolase deficiency was found to be the result of a point PAF or its metabolite or precursor, lyso-PAF, is released mutation in exon 9 which leads to complete abolition of in the airways of patients with asthma. It has been argued enzymatic activity. 10 Whether these individuals are more that the potency of the receptor antagonists may not have prone to inflammatory conditions such as asthma can only been adequate in the in vivo situation, or these antagonists be determined by prospective studies. Perhaps of more may not be blocking the eVects of other bioactive PAF relevance is whether this deficiency could lead to more homologues acting perhaps at diVerent PAF receptor sub- severe asthma in asthmatic patients. types. A preliminary study performed in Japan indicated that a higher dose of one of the two antagonists used, WEB 2086, provided some benefit in steroid-dependent asthmatic patients. 4