Mediators and non-specific bronchial hyperreactivity

Bronchial hyperreactivity is a major if not an essential characteristic of bronchial asthma. The relation between mediators and non-specific bronchial reactivity is an essential question in the pathogenesis of bronchial asthma. This is reflected in the different hypotheses on pathogenesis. The bronchial reaction to mediators is determined by the pre-existing degree of non specific bronchial reactivity. Bronchial reactivity to histamine or prostaglandin F2 alfa is related to the bronchial metacholine-reactivity. The bronchial lability to exercise or cold air and the immediate bronchoconstriction after allergen inhalation are also determined by the non specific bronchial reactivity. On the other hand, several observations support the concept that mediators modify the non specific bronchial reactivity. The non specific bronchial reactivity increases during the pollen season. Disodiumcromoglycate, a known inhibitor of mediator release, prevents the seasonal increase in bronchial reactivity. The increased bronchial reactivity in patients with allergic rhinitis may also be related to local mediator release. Exposure to ozone and viral upper respiratory tract infections enhance the bronchial reactivity. Avoidance of house dust mite exposure in mite sensitive asthmatics decreases the bronchial reactivity. The same observation has been made after withdrawal from occupational exposure. In experimentally induced asthma, the late asthmatic reaction after allergen inhalation is followed by an increase in nonspecific bronchial reactivity. Mediator release may enhance non specific bronchial reactivity in several ways. Increase of mucosal permeability, modification of sensory nerve endings, alteration of the efferent vagal motor pathway, enhancement of the effect of other mediators, influx of secondary cells, modification of cell receptors and changes in smooth muscle contractility have all been suggested. Mediator release and non specific bronchial reactivity thus appear to be interrelated characteristics of bronchial asthma. Individual differences in the clinical importance of the two characteristics may have therapeutic significance.