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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

¹ University of Southampton, Southampton, UK
² University of N. Sweden, Umeå, Sweden
³ The Rayne Institute, St Thomas’ Hospital, London, UK

Correspondence to:
Correspondence to:
Dr M T Krishna
Medical Specialties (RCMB Division), Mail Point 810, Level D, Centre Block, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK; mtkrishna{at}yahoo.com

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-B, 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-B, TNF-, eotaxin, Gro-, 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.

Keywords: nitrogen dioxide; bronchial epithelium; cytokines; ICAM-1; Th2 response

Abbreviations: 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

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