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

Center of Environmental Health and Molecular Toxicology Laboratory, College of Science, Engineering and Technology, Jackson State University, Jackson, MS 39217, USA
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Int. J. Environ. Res. Public Health 2005, 2(3), 403-410; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph2005030004
Received: 11 October 2005 / Accepted: 21 December 2005 / Published: 30 December 2005
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 (PM2.5-10), 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 < 0.05) as compared to cultures treated with DEP (100 μg/ml x 4 hr) alone (31 ± 3 pg/ml, n = 6), or cultures exposed to purified air (24 ± 6 pg/ml, n = 6). The increased DEP-induced IL-8 gene expression following ozone exposure was attributed to ozone-induced increase in the activity of the transcription factors NF-κB and NF-IL6. The results of the present study indicate that ozone exposure enhances the toxicity of DEP in human airway epithelial cells by augmenting IL-8 gene expression, a potent chemoattractant of neutrophils in the lung. View Full-Text
Keywords: Ozone; diesel exhaust particles; lung inflammation; interleukin-8; airway epithelial cells; transcription factors Ozone; diesel exhaust particles; lung inflammation; interleukin-8; airway epithelial cells; transcription factors
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MDPI and ACS Style

Kafoury, R.M.; Kelley, J. Ozone Enhances Diesel Exhaust Particles (DEP)-Induced Interleukin-8 (IL-8) Gene Expression in Human Airway Epithelial Cells through Activation of Nuclear Factors- κB (NF-κB) and IL-6 (NF-IL6). Int. J. Environ. Res. Public Health 2005, 2, 403-410. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph2005030004

AMA Style

Kafoury RM, Kelley J. Ozone Enhances Diesel Exhaust Particles (DEP)-Induced Interleukin-8 (IL-8) Gene Expression in Human Airway Epithelial Cells through Activation of Nuclear Factors- κB (NF-κB) and IL-6 (NF-IL6). International Journal of Environmental Research and Public Health. 2005; 2(3):403-410. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph2005030004

Chicago/Turabian Style

Kafoury, Ramzi M., and James Kelley. 2005. "Ozone Enhances Diesel Exhaust Particles (DEP)-Induced Interleukin-8 (IL-8) Gene Expression in Human Airway Epithelial Cells through Activation of Nuclear Factors- κB (NF-κB) and IL-6 (NF-IL6)" International Journal of Environmental Research and Public Health 2, no. 3: 403-410. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph2005030004

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