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Am J Physiol Lung Cell Mol Physiol 276: L604-L613, 1999;
1040-0605/99 $5.00
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Vol. 276, Issue 4, L604-L613, April 1999

Diesel exhaust particles are taken up by human airway epithelial cells in vitro and alter cytokine production

Sonja Boland1, Armelle Baeza-Squiban1, Thierry Fournier2, Odile Houcine1, Marie-Claude Gendron3, Michèle Chévrier4, Gilles Jouvenot4, André Coste5, Michel Aubier2, and Francelyne Marano1

1 Laboratoire de Cytophysiologie et Toxicologie Cellulaire and 3 Laboratoire de Cytométrie, Institut J. Monod, Université Paris VII Denis Diderot, 75251 Paris; 2 Institut National de la Sante et de la Recherche Médicale Unité 408, Faculté X. Bichat, 75018 Paris; 4 Technocentre Renault, 78288 Guyancourt; and 5 Service d'Oto-Rhino-Laryngologie et de Chirurgie Cervico-Faciale, Centre Hospitalier Universitaire Henri Mondor, 94000 Créteil, France

The involvement of diesel exhaust particles (DEPs) in respiratory diseases was evaluated by studying their effects on two in vitro models of human airway epithelial cells. The cytotoxicity of DEPs, their phagocytosis, and the resulting immune response were investigated in a human bronchial epithelial cell line (16HBE14o-) as well as in human nasal epithelial cells in primary culture. DEP exposure induced a time- and dose-dependent membrane damage. Transmission electron microscopy showed that DEPs underwent endocytosis by epithelial cells and translocated through the epithelial cell sheet. Flow cytometric measurements allowed establishment of the time and dose dependency of this phagocytosis and its nonspecificity with different particles (DEPs, carbon black, and latex particles). DEPs also induced a time-dependent increase in interleukin-8, granulocyte-macrophage colony-stimulating factor, and interleukin-1beta release. This inflammatory response occurred later than phagocytosis, and its extent seems to depend on the content of adsorbed organic compounds because carbon black had no effect on cytokine release. Furthermore, exhaust gas posttreatments, which diminished the adsorbed organic compounds, reduced the DEP-induced increase in granulocyte-macrophage colony-stimulating factor release. These results suggest that DEPs could 1) be phagocytosed by airway epithelial cells and 2) induce a specific inflammatory response.

16HBE14o- cells; human nasal turbinates; air pollution; carbon black


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