Mechanisms of the Development of Nasal Hyperreactivity in Nasal Allergy

Nasal hyperreactivity in nasal allergy conditions is closely related to allergic inflammation, particularly to infiltration by activated eosinophils in the nasal mucosa, observed 4 to 10 hours after a single antigenic challenge. Repeated antigenic challenge in subjects with nasal allergy enhanced nasal hyperreactivity. On the other hand, various therapies including topical steroids, immunotherapy and antiallergic drugs inhibited the infiltration of eosinophils and basophilic cells in the nasal mucosa, and thus inhibited nasal hyperreactivity. The characteristic features of the nasal mucosa in subjects with nasal allergy were:(1)morphological and functional changes of the nasal epithelium which facilitated the sensory excitation of the nasal reflexes to various stimuli; (2) depressed sympathetic and enhanced parasympathetic activity of the nasal mucosa, with corresponding changes in the density of autonomic nerve receptors; (3)enhanced expression of histamine Hl receptor mRNA in the nasal epithelium; and(4)changes in the number and volume of effector organs in the nasal mucosa. Receptor antagonists of leukotrienes and thromboxane A2 could also effectively depress the reactivity of the nasal mucosa to histamine. The direct and indirect effects of these chemical mediators, together with each patient's constitutional predisposition, were also considered to have an effect on enhanced nasal hyper-reactivity.