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Published ahead of print on December 30, 2003, doi:10.1165/rcmb.2003-0281RC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 4, April 2004, 421-427

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Submitted on July 28, 2003
Revised on December 30, 2003

FINE PARTICULATE MATTER INDUCES AMPHIREGULIN SECRETION BY BRONCHIAL EPITHELIAL CELLS

Sophie BLANCHET, Kiran RANGOLAM, Augustin BAULIG, Francelyne MARANO, and Armelle BAEZA-SQUIBAN*

* To whom correspondence should be addressed. E-mail: baeza{at}paris7.jussieu.fr.

Particulate matter (PM) is thought to be responsible for respiratory health problems. Epithelial cells exposed to particles release pro-inflammatory cytokines leading to inflammation of airways. However, the signalling cascades triggered by particles are poorly understood. We demonstrate that PM2.5 (PM with an aerodynamic diameter <2.5µm) or diesel exhaust particles (DEP) upregulate the expression of amphiregulin (AR), a ligand of the epidermal growth factor receptor (EGFR), in human bronchial epithelial cells. AR secretion was blocked by an inhibitor of the EGFR tyrosine kinase (AG1478), or a selective mitogen-activated protein (MAP) kinase/Extracellular regulated kinase (Erk) inhibitor (PD98059), but not by the p38 MAP kinase inhibitor (SB203580). Thus, AR secretion is mediated through the activation of the EGFR and Erk MAP kinase pathway. In addition, AR secretion was inhibited by the antioxidant N-acetyl cysteine, but not by a neutralizing anti-EGFR, suggesting an EGFR transactivation via oxidative stress. AR may be involved in cytokines secretion as AR can induce GM-CSF release and a neutralizing anti-EGFR reduces the particles-induced GM-CSF release. This study indicates that PM2.5 induces the expression and secretion of AR, an EGFR ligand contributing to GM-CSF release which may reflect an important mechanism for sustaining the pro-inflammatory response.




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