ABSTRACT
Over a decade of research and clinical efforts in the immunopathogenesis of asthma (1,2) have substantiated the critical role of airway inflammation and identified key mediators and mechanisms. Because information on the pathological features of asthma was first obtained from postmortem examination of severe asthmatics, airway inflammation was believed to be a feature of advanced, terminal disease (3). Those airways showed infiltration by granulocytes (neutrophils, eosinophils), increased numbers of lymphocytes, activated mast cells, collagen deposition beneath the basement membrane, and occlusion of the bronchial lumen by mucus produced from hyperplastic goblet cells. The finding of hypertrophied bronchial smooth muscle supported the widely held belief that asthma was primarily a disease of airway smooth muscle.
