Diesel exhaust exposure enhances the expression of IL-13 in the bronchial epithelium of healthy subjects

Respir Med. 2004 Sep;98(9):821-5. doi: 10.1016/j.rmed.2004.02.025.

Abstract

Epidemiological studies have demonstrated adverse health effects of environmental pollution. 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 enhanced epithelial expression of IL-8, and Gro-alpha in healthy subjects. The present investigation was aimed to further characterise the epithelial response to DE in vivo, with particular reference to possible TH2 response, in non-atopic healthy subjects. To determine this response, 15 healthy, non-atopic non-smoking subjects with normal lung function were exposed to DE (PM10 300 microg/m3) and filtered air during 1 h on two separate randomised occasions. Bronchoscopy sampling of bronchial mucosal biopsies was performed 6 h after exposure. Immunohistochemical staining were performed using mAb for IL-10, IL-13 and IL-18 expression. DE exposure induced a significant increase in the expression of IL-13 in the bronchial epithelium cells, 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-10 and IL-18 expression. This finding suggests an TH2-inflammatory response in the airways of non-atopic healthy individuals.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Air Pollutants / toxicity*
  • Bronchi / immunology*
  • Environmental Exposure / adverse effects
  • Epithelium / immunology
  • Female
  • Humans
  • Immunohistochemistry / methods
  • Interleukin-13 / analysis*
  • Male
  • Respiratory Mucosa / immunology
  • T-Lymphocytes, Helper-Inducer / immunology
  • Vehicle Emissions / toxicity*

Substances

  • Air Pollutants
  • Interleukin-13
  • Vehicle Emissions