Pathobiology of platelet-activating factors.

Throughout the evolution of knowledge about inflammation, a primary goal has been to understand this important biological response in sufficient depth to prevent the unwanted tissue injury that may spontaneously occur or that may coevolve to produce disease. That is, although the host defense systems normally function in a protective manner, excessive activation or alterations of the homeostatic regulation of the inflammatory responses often results in overt tissue injury and organ dysfunction. Thus, significant attention has been focused upon precise definition of the interactions of the myriad of involved cells and mediators so that interventions may be developed to block these events to prevent and control inflammatory tissue injury. PAF, as a relative newcomer to the investigative eye of experimental pathologists, is a potent proinflammatory mediator of many aspects of the complex host defense system. No doubt, its role in the initiation and maintenance of tissue injury or disease will be conclusively documented with additional research and forthcoming advances in biomedical technology. At present, however, we must be content to accept the conclusion that, while it is tempting to speculate that this unique phospholipid is involved in many different disease processes, unequivocal details to this end are lacking. Nonetheless, the spectrum of antagonists of PAF action which are currently evolving [cf. 95-100] will undoubtedly permit assessment of the putative contributions of PAF to many biological conditions associated with disease. At that time, meaningful conclusions as to the biological role of PAF in human tissue injury and disease may be provided.