Allergen-irritant interaction and the role of corticosteroids

Studies of exposure to air pollutants, such as ozone and nitrogen dioxide (NO2) +/- sulphur dioxide (SO2), have demonstrated that these agents, 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 significantly increased the levels of eosinophil cationic protein (ECP) in the nasal secretions of both asthmatics and allergic rhinitics, suggesting that pollutants may prime eosinophils for subsequent activation by allergen. More recently, our studies have demonstrated that treatment with inhaled corticosteroids, such as fluticasone propionate, significantly attenuated pollution+ allergen-induced release of ECP in allergic rhinitics. Although the mechanisms underlying the potentiating effects of pollutants on allergen-induced changes in the airways of allergic individuals are not fully understood, in vitro studies have suggested that airway epithelial cells may play an important role, since they can synthesize a variety of cytokines and adhesion molecules which influence the activity of eosinophils and other inflammatory cells. Studies of nasal epithelial cells cultured from biopsies of atopic rhinitic and atopic non-rhinitic individuals have shown that they constitutively release significantly greater quantities of pro-inflammatory cytokines than nasal epithelial cells of non-atopic individuals, and that the release of these cytokines is greater from cells of atopic rhinitics during 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 beclomethasone dipropionate.