Diesel exhaust particles activate human bronchial epithelial cells to express inflammatory mediators in the airways: a review

Respirology. 2000 Jun;5(2):197-203. doi: 10.1046/j.1440-1843.2000.00245.x.


Objective: Epidemiological as well as experimental studies suggest that particulate air pollutants, including diesel exhaust particles (DEP), may play a role in the recent increase of respiratory morbidity and mortality. We studied the effect of DEP on the production of inflammatory cytokines and mediators including IL-8 and granulocyte macrophage colony stimulating factor (GM-CSF) by human airway epithelial cells in vitro.

Methodology: Suspended DEP were added to cultured normal human bronchial epithelial cells or transformed BEAS-2B cells. The release of cytokines and mediators was evaluated by enzyme-linked immunosorbent assay. The transcriptional levels of IL-8 mRNA was studied by northern blot analysis and run-on transcription assay. Activation of transcription factors was assessed by electrophoretic mobility shift assay.

Results: Non-toxic doses of suspended DEP showed a significant stimulatory effect on IL-8 and GM-CSF production by airway epithelial cells. Diesel exhaust particles increased the steady-state levels of IL-8 mRNA, which was suggested to be largely due to increased transcriptional rates. Electrophoretic mobility shift assay demonstrated that DEP induced increased binding to the specific motif of nuclear factor (NF)-kappaB, but not of transcription factor AP-1. Both N-acetylcysteine and pyrrolidine dithiocarbamate attenuated the action of DEP on IL-8 mRNA expression, suggesting that oxidant-mediated pathway might be involved in its processes. Transient transfection of airway epithelial cells with wild and NF-kappaB binding motifs indicated that the activation of NF-kappaB was essential for IL-8 gene upregulation by reporter gene assay.

Conclusions: These results suggested that DEP activate NF-kappaB, which might be an important pathway for the expression of inflammatory cytokines in vitro.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Bronchi / immunology*
  • Cells, Cultured
  • Cytokines / biosynthesis*
  • Epithelial Cells / immunology*
  • Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis*
  • Humans
  • In Vitro Techniques
  • Inflammation / immunology*
  • Interleukin-8 / biosynthesis*
  • Respiratory Hypersensitivity / immunology*
  • Vehicle Emissions / adverse effects*


  • Cytokines
  • Interleukin-8
  • Vehicle Emissions
  • Granulocyte-Macrophage Colony-Stimulating Factor