Introduction Athough it is widely acknowledged that airway inflammation is a characteristic feature of death from asthma, its relationship to disordered airway function in life is largely speculative. It was not long ago that airway dysfunction in asthma was considered largely in terms of contraction of airway smooth muscle (bronchospasm). However, in his classic textbook, The Principles and Practice of

Medicine (1st edition, 1892), William Osler drew the conclusion that asthma" is a special form of inflammation of the small airway"(1). In retrospect it is hardly surprising that the cellular basis of disordered airway function in asthma has eluded detailed study since the complex dichotomous branching of the airway together with procedural problems encountered with rigid bronchoscopy combined to limit access to the relevant tissues (2). Indeed, over the last half century clinicians and physiologists deserve full credit for the ingenious methods they have devised to obtain indirect information about how the airway functions in health and in disease. The discovery of drugs that increase airway caliber such as f3-agonists, anticholinergics, and xanthines has further served to focus attention on the smooth muscle aspects of asthma without allowing assessment of the other important causes of airway obstruction, namely, mucosal swelling and increased secretion. In the face of overwhelming evidence supporting a role for airway smooth muscle contraction as an important component of asthma, severalclinical observations have provided clues for considering inflammation as the basis of the disease. Among these are included the association of asthma with atopy, the presence of eosinophils and their products in sputum (3) and blood (4) during active asthma, and the well-established beneficial response of asthmatic airway to systemically and locallyadministered corticosteroids (5-8). These observations align with the postmortem findings of evidence for widespread inflammation of the airway in those with severe disease, especially eosinophil infiltration (9, 10). However, there exists an enormous gap in relating these observations to the pattern of reversible airflow obstruction that characterizes day-to-day asthma.