Effect of ozone and nitrogen dioxide on the release of proinflammatory mediators from bronchial epithelial cells of nonatopic nonasthmatic subjects and atopic asthmatic patients in vitro.

摘要: Abstract Background: Although studies have suggested that ozone (O 3 ) and nitrogen dioxide (NO 2 may play a role in the pathogenesis of asthma, underlying mechanisms are not clear. Objective: We aimed to investigate effects O NO on release IL-8, GM-CSF, RANTES, soluble intercellular adhesion molecule 1 (sICAM-1) from human bronchial epithelial cells (HBECs) nonatopic nonasthmatic subjects (nonasthmatic subjects) atopic with mild asthma (asthmatic vitro. Methods: cultured HBECs biopsy specimens asthmatic subjects; exposed these for 6 hours air, 10 100 ppb , or 400 ; analyzed sICAM-1 after 24 hours' incubation. Results: There was no significant difference between constitutive subjects. RANTES detected only derived Exposure both 50 200 significantly increased However, led increase IL-8 A comparison pollutant-induced mediators demonstrated -induced GM-CSF greater (medians, 0.59 27.4 pg/μg cellular protein, respectively) than 0.27 14.4 respectively; P Conclusion: These results suggest modulate airway diseases, such as by increasing inflammatory be more susceptible adverse pollutants. (J Allergy Clin Immunol 2001;107:287-94.)