Allergen‐irritant interaction and the role of corticosteroids
Authors: R. J. DAVIES, C. RUSZNAK, M. A. CALDERON, J. H. WANG, M. M. ABDELAZIZ, J. L. DEVALIA
Journal: Allergy (1997)

Davies RJ, Rusznak C, Calderón MA, Wang JH, Abdelaziz MM, Devalia JL. Allergen‐irritant interaction and the role of corticosteroids. Studies of exposure to air pollutants, such as ozone and nitrogen dioxide (NO 2 )± sulphur dioxide (SO 2 ), 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 eosinophls 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. Taken together, the results described above provide evidence to suggest that atmospheric pollutants, such as ozone or the combination of NO 2 and SO 2 , increase the bronchial response of mild asthmatic subjects to inhaled allergen, and that this may persist for a period of 24–48 h after exposure. Acute exposure to ozone or NO 2 ‘primes’ the eosinophils for subsequent activation by allergen, and pretreatment with FP attenuates both the pollution‐induced eosinophil priming and allergen‐induced increase in the number of EGZstaining cells in the bronchial mucosa, suggesting that FP treatment may modulate airway inflammation by influencing the activity of eosinophils, and perhaps other inflammatory cell types. At the cellular level, airway epithelial cells probably play an important role in the initiation and maintenance of airway inflammation, since these cells express and release pro‐inflammatory mediators which influence the recruitment and activation of inflammatory cells, such as neutrophils and eosinophils, in the airways. Nasal epithelial cells from both atopic non‐rhinitics and atopic rhinitics release sigmficantly greater amounts of IL‐8, GM‐CSF and TNFα, than cells from non‐atopic non‐rhinitics. The cells of atopic rhinitics release significantly greater quantities of these cytokines during the pollen season, compared with outside of the pollen season, and exposure of these cells to ozone further enhances the release of these cytokines, an effect which can be attenuated by incubating the cells with FP or BDI ?