Abstract
This brief summary of several studies relating to allergic mucociliary dysfunction suggests that (1) mucociliary transport in the lower airways (and possibly in the nose) is impaired in subjects with allergic airway disease, (2) acute antigen challenge causes a further impairment of mucociliary transport that is related to chemical mediators, and (3) the elaboration of abnormal respiratory secretions is, at least in part, responsible for acute allergic mucociliary dysfunction. It is apparent from the currently available information that some of the in vivo and in vitro studies carried out in patients with allergic asthma would have to be applied to patients with allergic rhinitis. With respect to the management of patients with allergic rhinitis and asthma, the use of antiallergic agents such as cromolyn sodium or specific mediator antagonists (as they become available) seems to be justified when considering the important role of mucociliary dysfunction in the manifestations of allergic airway disease.
