Cell Biology and Toxicology

, Volume 18, Issue 5, pp 315–320 | Cite as

Human airway epithelial cells in culture for studying the molecular mechanisms of the inflammatory response triggered by diesel exhaust particles

  • F. Marano
  • S. Boland
  • V. Bonvallot
  • A. Baulig
  • A. Baeza-Squiban


Epidemiological studies have shown that particulate air pollution is linked to the increase of morbidity and mortality due to respiratory diseases. Diesel exhaust particles (DEPs), which are the most important part of PM2.5 in Western European and Japanese urban areas, have been suspected. The mechanisms of proinflammatory response induced by DEPS were elucidated using a human epithelial cell line (16-HBE). It has been shown that DEPs can be phagocytosed by HBE cells, inducing the release of cytokines. MAP kinase pathways (i.e., ERK1/2 and P38) were triggered as well as the activation of the nuclear factor NF-κB. Reactive oxygen species (ROS) were strongly incriminated in this response because DEPs induce the increase of intracellular hydroperoxides and antioxidants inhibit the release of DEP-induced cytokines, the activation of MAP kinases and NF-κB. Organic compounds adsorbed on DEPs seemed to be involved in the response and the production of ROS. Moreover, we have demonstrated that DEPs can activate CYP1A1 in HBE cells. These experimental results give biological plausibility to the epidemiological findings.

DEP 16-HBE14o- cells signal transduction ROS proinflammatory cytokines metabolization enzymes inflammation 


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Copyright information

© Kluwer Academic Publishers 2002

Authors and Affiliations

  • F. Marano
    • 1
  • S. Boland
    • 1
  • V. Bonvallot
    • 1
  • A. Baulig
    • 1
  • A. Baeza-Squiban
    • 1
  1. 1.Laboratoire de Cytophysiologie et Toxicologie cellulaireUniversité Paris 7 – Denis DiderotParisFrance

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