The interaction between PAF, platelets and eosinophils in bronchial asthma.

Many mediators have been proposed to be important in the pathogenesis of bronchial asthma based solely on their ability to elicit airway smooth muscle contraction. However, such an approach fails to appreciate the underlying pathological changes as being central to the aetiology of the disease. Platelet activating factor (PAF) has been demonstrated to mimic many of the features of asthma including bronchial hyperreactivity, eosinophil recruitment, mucus secretion and smooth muscle hyperplasia. The recent availability of selective PAF antagonists has demonstrated the central role of PAF in allergic responses in experimental animals and at least in the skin of man. The precise mechanism by which PAF and antigen induce BHR is not completely understood but may involve an interaction between platelets and eosinophils. It is anticipated that further investigation into the relationship between PAF, platelets and eosinophils may provide a greater insight into the pathogenesis of the disease.