Source: Annual Congress 2002 - Exposure to chemicals
Disease area: Airway diseases

Abstract

Diesel exhaust (DE) is an important contributor to ambient particulate matter pollution. DE exposure has been shown to induce a pronounced inflammatory response in the airways, with an up regulation of IL–8 mRNA, and enhanced epithelial expression of IL–8 and Gro-α in healthy subjects (Salvi et al AM J RCCM 1999,2000).
The present investigation was aimed to further characterize the epithelial response to DE in-vivo, with particular reference to possible TH2 response, in non-atopic healthy subjects.
Method: Fifteen healthy, non-atopic non-smoking subjects with normal lung function were exposed to DE (PM10 300μg/m3) and filtered air during one hour on two separate randomised occasions. Bronchoscopy sampling of bronchial mucosla biopsies was performed 6 hours after exposure. The biopsies were processed in GMA resin and immunohistochemical stainings with DAB were performed using mAb for IL-4, IL-5, IL-10, IL-13 and IL-18.
Results: Computerized image analysis showed a significant increase in the expression of IL-13 in the bronchial epithelium after DE , 2.1 (1.35-4.88)Md (Q1-Q3) vs. air 0.94 (0.53-1.23); p=0.009. No significant changes were seen in IL-4, IL-5, IL-10 and IL-18 expression.
Conclusion: Diesel exhaust exposure caused a significant increase in the bronchial epithelial IL-13 expression. This could represent a TH2-response in the airways of non-atopic healthy individuals.

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J. Pourazar, A. Blomberg, A. J. Frew, R. Helleday, S. T. Holgate, F. J. Kelly, C. Nordenhäll, S. Wilson, T. Sandström (Umeå, Sweden; Southampton, London, United Kingdom). IL-13 expression in the bronchial epithelium of healthy non-atopic subjects is enhanced by diesel exhaust exposure. Eur Respir J 2002; 20: Suppl. 38, 869

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