Mechanisms of airflow limitation in the nose and lungs.

The main differences in the anatomies of the upper and lower airways are the vascular characteristics and bony surroundings of the upper airways compared with the smooth muscle component and the loose-lying situation of the lower airways. Both allergic asthma and rhinitis involve a similar process of mucosal inflammation in response to allergen exposure, characterized by inflammatory cell infiltration and local release of mediators. In addition, both the upper and lower airways are under similar influences from local neuronal reflexes, exercise, posture and cyclic variations. Challenge tests have been able to demonstrate the roles of the various influences and components in the inflammatory processes of asthma and allergic rhinitis. A particular difference in the response in asthma compared with rhinitis is the degree of non-specific hyperresponsiveness, which is a characteristic of the late response or response to repeated or prolonged exposure to allergen. Responsiveness of the bronchial mucosa in asthma patients is approximately 50 times that of normal (non-allergic or non-asthmatic) subjects, whereas that of the nasal mucosa in allergic rhinitis is only 2-8 times that of control subjects. The inflammatory process involved in hyperresponsiveness is similar in both conditions, involving increased infiltration of eosinophils and subsequent increased mediator release. The greater degree of hyperresponsiveness seen in asthma appears to be a consequence of the anatomical differences between the upper vs the lower airways. Evidence is presented for the contribution of increased airway wall thickness to the hyperresponsiveness in asthma, together with other possible factors, such as decoupling of responder tissue from surrounding tissue, increased smooth muscle contractility, and smooth muscle hypertrophy.