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Published online before print September 5, 2007
Eur Respir J 2007, doi:10.1183/09031936.00085907
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ORIGINAL ARTICLE

Expression and role of EGFR ligands induced in airway cells by PM2.5 and its components

M. Rumelhard 1*, K. Ramgolam 1, R. Hamel 1, F. Marano 1, A. Baeza-Squiban 1

1 Laboratoire de Cytophysiologie et de Toxicologie Cellulaire, Université Paris Diderot-Paris 7, Paris, France

* To whom correspondence should be addressed. E-mail: melina.rumelhard{at}univ-diderot-paris.fr.


  Abstract

The aim of this work was to establish the epidermal growth factor receptor (EGFR) ligand expression profile in human airway epithelial cells exposed either to PM2.5 (particulate matter, aerodynamic diameter below 2.5 µm) or its components and the involvement of EGFR ligands in PM2.5-provoked airway inflammation.

EGFR ligand mRNA and protein expression were studied on human epithelial (bronchial 16HBE cell line and normal nasal cells) exposed throughout the time to non-cytotoxic concentrations of PM2.5 or its components. The autocrine role of EGFR ligands in airway epithelial cell proinflammation was determined by adding conditioned media from PM2.5-treated cells onto fresh cells and by measuring the secretion of GM-CSF, a proinflammatory biomarker.

PM2.5 increases amphiregulin, TGF? and HB-EGF mRNA expression and protein secretion, with a slight contribution of aqueous metallic compounds, and a strong participation of organic components putatively attributed to PM polyaromatic hydrocarbon content. PM2.5-induced EGFR ligands are involved in GM-CSF release by cells.

This study reveals the upregulation of several EGFR ligands by airway epithelial cells exposed to PM2.5 and their contribution to bronchial epithelial cell GM-CSF secretion by an autocrine action, suggesting that these ligands could elicit and sustain the PM2.5-induced airway proinflammatory response and contribute to bronchial remodeling.

Keywords:  Ambient particles, EGF receptor ligands, inflammation, organic PM2.5, respiratory epithelial cells




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