ABSTRACT
Although the inflammatory changes in asthma involve a number of different cell types, there is increasing evidence that eosinophils play a central role. Eosinophils manufacture several toxic mediators capable of producing many of the pathological features of asthma and are present in large numbers in the airways of patients with both anergic and nona11ergic asthma ( 1 ,2). Increased numbers of eosinophils have been documented in the peripheral blood, bronchoalveolar lavage (BAL) fluid, airway epithelium, and sputum of patients with asthma, and their numbers seem to correlate with disease severity (2-5). Over the past decade, there has been escalating evidence that these cells are not innocent bystanders or terminally differentiated ce1ls causing local abnormality, but may actually play a very active role in the pathogenesis of asthma by generating cytokine signals that help to amplify the inflammatory process (6-8}.
