Asthmatics respond with reversible airway narrowing when stimulated in ways that have no effect on non-asthmatic persons. Studies conducted at the turn of this century established that the pathology present in the airways of asthmatics is based on the inflammatory process. Recent work suggests that this inflammatory response may be driven by a particular group of T cells (Th2 response) that cause an overproduction of IL-4, IL-5 and other cytokines that produce an excessive infiltration of eosinophils and overproduction of IgE. The structural changes produced by the inflammatory process result in an overall thickening of the airway wall with changes in the epithelium, an increase in the interstitial matrix particularly the collagen types that contribute to the light microscopic appearance of the basement membrane, the vasculature, smooth muscle and mucous glands. Contraction of airway smooth muscle results in narrowing of the lumen particularly in the bronchioles where smooth muscle surrounds the entire lumen. An increase in wall tissue thickness as a result of asthma amplifies this normal effect producing a greater reduction in the airway lumen. Computer modelling of airway function and direct measurement of airway resistance in patients suggest that the smaller airways are the site of the greatest increase in airway resistance in asthma. These new data have shifted the emphasis away from the concept that abnormal airway smooth muscle function causes asthma toward the hypothesis that inflammatory-based changes in the airway wall act in series with normal smooth shortening to produce disease. The increased understanding of the role of the inflammatory process provides a basis for treatment of asthma with anti-inflammatory agents.