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Regulation of COX-2 expression and IL-6 release by particulate matter in airway epithelial cells

Yutong Zhao1, Peter V Usatyuk, Irina A Gorshkova

  • 1Department of Medicine, University of Chicago, Chicago, IL 60637, USA.

American Journal of Respiratory Cell and Molecular Biology
|July 12, 2008
PubMed

Insights

Particulate matter (PM) exposure triggers inflammation in airway cells via reactive oxygen species (ROS) and other pathways. Antioxidants reduce PM-induced inflammatory responses, suggesting therapeutic targets for respiratory diseases.

Area of Science:

  • Environmental Health
  • Cell Biology
  • Toxicology

Background:

  • Ambient particulate matter (PM) is a known risk factor for respiratory and cardiovascular diseases.
  • Mechanisms underlying PM-induced inflammatory responses in airway epithelial cells are not fully understood.

Purpose of the Study:

  • To elucidate the molecular pathways involved in particulate matter-induced inflammation in human bronchial epithelial cells (HBEpCs).
  • To investigate the role of reactive oxygen species (ROS) and specific signaling pathways (NF-kappaB, C/EBPbeta) in PM-induced inflammatory responses.

Main Methods:

  • HBEpCs were treated with Baltimore PM, and inflammatory markers (ROS, COX-2, IL-6) were measured.
  • Cells were pretreated with antioxidants (NAC, EUK-134), NF-kappaB inhibitor (Bay11-7082), or C/EBPbeta siRNA.
  • Mitochondrial ROS production was assessed using mitochondrially targeted hydroethidine.

Main Results:

  • PM exposure induced ROS production, COX-2 expression, and IL-6 release in HBEpCs.
  • Antioxidant pretreatment dose-dependently attenuated PM-induced ROS, COX-2, and IL-6.
  • PM-induced ROS was primarily of mitochondrial origin.
  • PM stimulated NF-kappaB and C/EBPbeta phosphorylation; inhibitors/siRNA attenuated PM-induced COX-2 and IL-6.
  • Antioxidants inhibited NF-kappaB activation but not C/EBPbeta phosphorylation.
  • COX-2 inhibition partially reduced PM-induced Prostaglandin E2 and IL-6 release.

Conclusions:

  • PM induces inflammation in HBEpCs via both ROS-dependent NF-kappaB and ROS-independent C/EBPbeta pathways.
  • Mitochondrial ROS plays a significant role in PM-induced inflammatory signaling.
  • Targeting ROS and these specific pathways may offer therapeutic strategies for PM-related respiratory diseases.

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