Role of inflammation in the hyperreactivity of the airways in asthma.

Although asthma is usually diagnosed because of spontaneous and reversible attacks of bronchoconstriction, its most characteristic feature is the increased bronchial reactivity to a large variety of pharmacological and physical agents, such as histamine, methacholine, leukotrienes, prostaglandins, cold air, and dust. Thus asthmatic subjects develop a greater degree of bronchoconstriction from exposure to these stimuli than do subjects with normal bronchial reactivity. That this feature of asthmatic airways appears to have a fundamental role in the pathophysiology of asthma is supported by the observation that the severity of the disease correlates closely with the degree of hyperreactivity.' The precise mechanism underlying the hyperreactivity of asthma is unknown. Whether this abnormality is inherent in the intrinsic property of airway smooth muscle or is at the level of its neural control remains unclear. The possibility that airways inflammation could be related to the development and maintenance of the bronchial hyperreactivity of asthma has been the subject of increasing research in recent years. Indeed, inflammation of the airways may create conditions that have themselves been proposed as possible mechanisms of hyperreactivity, such as bronchial oedema, mucosal hyperpermeability, exposure of epithelial sensory nerve endings, and release of inflammatory mediators.2 This article will review (a) the recent experimental data linking the development of airways inflammation to the induction of airways hyperreactivity and (b) the interactions between inflammatory cells and mediators that may be crucial in the pathophysiology of airways hyperreactivity.