Ozone Enhances Diesel Exhaust Particles (DEP)-Induced Interleukin-8 (IL-8) Gene Expression in Human Airway Epithelial Cells through Activation of Nuclear Factors- ?B (NF-?B) and IL-6 (NF-IL6)

Ramzi M. Kafoury and James Kelley
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Ramzi M. Kafoury: Center of Environmental Health and Molecular Toxicology Laboratory, College of Science, Engineering and Technology, Jackson State University, Jackson, MS 39217, USA
James Kelley: Center of Environmental Health and Molecular Toxicology Laboratory, College of Science, Engineering and Technology, Jackson State University, Jackson, MS 39217, USA

IJERPH, 2005, vol. 2, issue 3, 1-8

Abstract: Ozone, a highly reactive oxidant gas is a major component of photochemical smog. As an inhaled toxicant, ozone induces its adverse effects mainly on the lung. Inhalation of particulate matter has been reported to cause airway inflammation in humans and animals. Furthermore, epidemiological evidence has indicated that exposure to particulate matter (PM 2.5-10 ), including diesel exhaust particles (DEP) has been correlated with increased acute and chronic respiratory morbidity and exacerbation of asthma. Previously, exposure to ozone or particulate matter and their effect on the lung have been addressed as separate environmental problems. Ozone and particulate matter may be chemically coupled in the ambient air. In the present study we determined whether ozone exposure enhances DEP effect on interleukin-8 (IL-8) gene expression in human airway epithelial cells. We report that ozone exposure (0.5 ppm x 1 hr) significantly increased DEP-induced IL-8 gene expression in A549 cells (117 ± 19 pg/ml, n = 6, p

Keywords: Ozone; diesel exhaust particles; lung inflammation; interleukin-8; airway epithelial cells; transcription factors (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2005
References: View complete reference list from CitEc
Citations: View citations in EconPapers (1)

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