ABSTRACT
Cellular changes in the conducting airways are now recognized as central to the pathogenesis of bronchial asthma. The application of cell and tissue har vesting methods, facilitated by fiberoptic bronchoscopy, has allowed signifi cant advances to be made in the understanding of the mechanisms of airflow obstruction in bronchial asthma. Inflammatory events were the initial focus of this change in research and clinical emphasis but even in early publications, changes in the extracellular matrix were highlighted (1). Increasing awareness of the long-term loss of airway function in patients with asthma (2) has led to attention being focused on the role of changes in the structure of the airways in the production of the characteristic spirometric abnormalities. Computer modeling has shown that thickening of the airway walls is sufficient to explain the exaggerated provocant response and the loss of the plateau in the provocant dose-response curve in patients with asthma (3).
