ALLERGEN-IRRITANT INTERACTION AND THE ROLE OF CORTICOSTEROIDS

Studies of exposure to air pollutants, such as ozone and nitrogen diox ide (NO2)+/- sulphur dioxide (SO2), have demonstrated that these agent s, either individually or in combination, increase the airway response of both asthmatics and allergic rhinitics to inhaled allergen. Other studies have demonstrated that exposure to these pollutants significan tly increased the levels of eosinophil cationic protein (ECP) in the n asal secretions of both asthmatics and allergic rhinitics, suggesting that pollutants may prime eosinophils for subsequent activation by all ergen. More recently, our studies have demonstrated that treatment wit h inhaled corticosteroids, such as fluticasone propionate, significant ly attenuated pollution+ allergen-induced release of ECP in allergic r hinitics. Although the mechanisms underlying the potentiating effects of pollutants on allergen-induced changes in the airways of allergic i ndividuals are not fully understood, in vitro studies have suggested t hat airway epithelial cells may play an important role, since they can synthesize a variety of cytokines and adhesion molecules which influe nce the activity of eosinophils and other inflammatory cells. Studies of nasal epithelial cells cultured from biopsies of atopic rhinitic an d atopic non-rhinitic individuals have shown that they constitutively release significantly greater quantities of proinflammatory cytokines than nasal epithelial cells of non-atopic individuals, and that the re lease of these cytokines is greater from cells of atopic rhinitics dur ing the pollen season. Furthermore, exposure of the cells of rhinitics to ozone led to an even greater release of these cytokines, and this effect was attenuated by treatment with fluticasone propionate and bec lomethasone dipropionate.