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Current status of PAF antagonists

The evidence that PAF may be involved in the pathophysiology of asthma was initially derived from its ability to induce bronchoconstriction [ 1 ] at very low doses as well as its properties as an inflammatory mediator [2]. The bronchoconstrictive action [1] as well as the inflammatory action [2] of PAF is shared by other putative mediators of inflammation like histamine, thromboxane and leukotrienes; but in contrast PAF is so far unique as PAF concomitantly and in addition increases mucus secretion [3] and recruits platelets and eosinophils [4] from the extravascular space into the lungs. Since an important role is attributed to eosinophils in the pathogenesis of asthma [5], it is of particular interest, that PAF is one of the most potent chemotactic factors so far discovered for eosinophils [6]. Furthermore PAF seems to be involved in the late-phase response [7,8] of asthma and may induce bronchial hyperreactivity [9,10] in different species including man (Fig. I). In addition there is support that PAF may be involved in down-regulation of betareceptors in human lung tissue [11]. With respect to increased level of PAF in asthma and allergies the short half-life of PAF has to be taken into account. The limitations from available methods for determination of PAF in tissue and the compartmentation of PAF-mediated processes in disease may explain the paucity of reports on measurements of PAF in lung disease. In relation to asthma both increased levels of PAF-like activity in the bronchoalveolar lavage fluid and in saliva [12] as well as increased levels of lyso-PAF after allergen provocation in plasma in patients with late phase response [13], have been reported. The antigen-induced release of PAF from sensitized lung tissue has been described [14].