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Am. J. Respir. Cell Mol. Biol., Volume 25, Number 4, October, 2001 515-521

Organic Compounds from Diesel Exhaust Particles Elicit a Proinflammatory Response in Human Airway Epithelial Cells and Induce Cytochrome p450 1A1 Expression

Véronique Bonvallot, Armelle Baeza-Squiban, Augustin Baulig, Stéphanie Brulant, Sonja Boland, Françoise Muzeau, Robert Barouki, and Frauvelyne Marano

Laboratoire de Cytophysiologie et Toxicologie Cellulaire, Université Paris VII, Paris; and INSERM U490, Centre Universitaire des Saints-Pères, Paris, France

Diesel exhaust particles (DEP) are known to enhance inflammatory responses in human volunteers. In cultured human bronchial epithelial (16HBE) cells, they induce the release of proinflammatory cytokines after triggering transduction pathways, including nuclear factor (NF)-kappa B activation and mitogen-activated protein kinase (MAPK) phosphorylation. This study compares the effects of native DEP (nDEP), organic extracts of DEP (OE-DEP), and carbonaceous particles, represented by stripped DEP (sDEP) and carbon black particles (CB), in order to clarify their respective roles. OE-DEP and nDEP induce granulocyte macrophage colony-stimulating factor (GM-CSF) release, NF-kappa B activation, and MAPK phosphorylation. The carbonaceous core generally induces less intense effects. Reactive oxygen species are produced in 16HBE cells and are involved in GM-CSF release and in the stimulation of NF-kappa B DNA binding by nDEP and OE-DEP. We demonstrate, for the first time, in airway epithelial cells in vitro that nDEP induce the expression of the CYP1A1, a cytochrome P450 specifically involved in polycyclic aromatic hydrocarbons metabolism, thereby demonstrating the critical role of organic compounds in the DEP-induced proinflammatory response. Understanding the respective contributions of DEP components in these effects is important for vehicle manufacturers in order to improve their exhaust gas post-treatment technologies. In conclusion, the DEP-induced inflammatory response in airway epithelial cells mainly involves organic compounds such as PAH, which induce CYP1A1 gene expression.

Abbreviations: aryl hydrocarbon receptor, AhR; carbon black particles, CB; benzo(a)pyrene, BaP; dichlorofluorescein, DCF; dichlorofluorescein diacetate, DCFH-DA; diesel exhaust particles, DEP; dimethylsulfoxide, DMSO; dimethylthiourea, DMTU; dipalmitoylphosphatidylcholine, DPPC; electrophoresis mobility shift assay, EMSA; granulocyte macrophage colony-stimulating factor, GM-CSF; Hanks' balanced salt solution, HBSS; human bronchial epithelial, HBE; inhibitor kappa B, Ikappa B; messenger RNA, mRNA; mitogen-activated protein kinase, MAPK; N-acetylcysteine, NAC; native diesel exhaust particles, nDEP; nuclear factor kappa B, NF-kappa B; organic extract of diesel exhaust particles, OE-DEP; phenylmethylsulfonylfluoride, PMSF; polycyclic aromatic hydrocarbons, PAH; reactive oxygen species, ROS; stripped diesel exhaust particles, sDEP; sodium dodecyl sulfate, SDS; standard error, SE; saline sodium citrate, SSC; Tris-buffered saline, TBS.




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