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

• 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-α 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 μg/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.

Keyword

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

Publication and Content Type

ref (subject category)

art (subject category)