Excessive respiratory glycoprotein secretion occurs in a variety of inflammatory states. A variety of lipid inflammatory mediators have been demonstrated to have a stimulatory effect on secretion in human and experimental animal studies in an in vitro airway organ culture system. The role of Platelet Activating Factor (PAF) on respiratory glycoprotein secretion and the mechanism of its effect have not been well described. PAF stimulates glycoprotein secretion in a dose response fashion. This response is inhibited by a specific PAF receptor antagonist and is also inhibitable by inhibitors of the lipoxygenase pathway of eicosanoid metabolism. Studies of specific eicosanoid metabolites suggests that PAF induces selective production of lipoxgenase pathway metabolites and that the effect of PAF on airway secretion is mediated by the production of these metabolites. The importance of these studies is that they lay the groundwork for the development of new therapies for inflammatory diseases of the lung.
