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

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