Repeated daily exposure to 2 ppm nitrogen dioxide upregulates the expression of IL-5, IL-10, IL-13, and ICAM-1 in the bronchial epithelium of healthy human airways. Issue 11 (22nd October 2003)

• Record Type: Journal Article
• Authors: Pathmanathan, S; Krishna, M T; Blomberg, A; Helleday, R; Kelly, F J; Sandström, T; Holgate, S T; Wilson, S J; Frew, A J
• Is Part Of: Occupational and environmental medicine. Volume 60:Issue 11(2003)
• Page Start: 892
• Page End: 896
• Publication Date: 2003-10-22
• Subjects: nitrogen dioxide -- bronchial epithelium -- cytokines -- ICAM-1 -- Th2 response; BHR, bronchial hyperresponsiveness -- CV, coefficient of variation -- FEV, forced expiratory volume -- GMA, glycol methacrylate -- ICAM, intercellular adhesion molecule -- IL, interleukin -- NF, nuclear factor -- TNF, tumour necrosis factor -- ROI, reactive oxygen intermediates; Medicine, Industrial -- Periodicals; Environmental health -- Periodicals; 616.980305
• DOI: 10.1136/oem.60.11.892
• Languages: English
• ISSNs: 1351-0711

Abstract

Abstract : Background: Repeated daily exposure of healthy human subjects to NO2 induces an acute airway inflammatory response characterised by neutrophil influx in the bronchial mucosa Aims: To assess the expression of NF-κB, cytokines, and ICAM-1 in the bronchial epithelium. Methods: Twelve healthy, young non-smoking volunteers were exposed to 2 ppm of NO2 /filtered air (four hours/day) for four successive days on separate occasions. Fibreoptic bronchoscopy was performed one hour after air and final NO2 exposures. Bronchial biopsy specimens were immunostained for NF-κB, TNF-α, eotaxin, Gro-α, GM-CSF, IL-5, -6, -8, -10, -13, and ICAM-1 and their expression was quantified using computerised image analysis. Results: Expression of IL-5, IL-10, IL-13, and ICAM-1 increased following NO2 exposure. Conclusion: Upregulation of the Th2 cytokines suggests that repeated exposure to NO2 has the potential to exert a "pro-allergic" effect on the bronchial epithelium. Upregulation of ICAM-1 highlights an underlying mechanism for leucocyte influx, and could also explain the predisposition to respiratory tract viral infections following NO2 exposure since ICAM-1 is a major receptor for rhino and respiratory syncytial viruses.