Diesel Exhaust Particles Increase NF-kappaB DNA Binding Activity and c-FOS Proto-oncogene Expression in Human Bronchial Epithelial Cells.

There is increasing evidence that diesel exhaust particles (DEP) could be incriminated in respiratory diseases. They have been shown to induce an inflammatory response in the lung and are suspected to be carcinogenic because of the presence of polyaromatic hydrocarbons (PAH) on their surface. DEP were tested on a human bronchial epithelial cell line (16HBE) in comparison with carbon black particles (CB) devoid of PAH. DEP and CB at 10mug/cm(2) induced the release of the lactate dehydrogenase (LDH) by 16HBE cells from 48hr of exposure. DEP at 5mug/cm(2) but not CB activated the binding of the nuclear factor kappaB (NF-kappaB) to DNA from 2hr of exposure up to 15hr. NF-kappaB is a transcription factor involved in the expression of some cytokines such as IL-8 and GM-CSF which have been shown to be released by 16HBE cells after DEP exposure. In addition, DEP as well as CB induced the expression of the c-fos proto-oncogene. Taken together, these new data suggest that the activation of NF-kappaB and the expression of c-fos could contribute to the proliferation and chronic inflammation processes induced in lungs after DEP exposure.