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1Department of Environmental Sciences and Engineering, School of Public Health and 2Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina, Chapel Hill; and 5Human Studies Division, National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, Chapel Hill, North Carolina; 4Department of Neurosciences, College of Medicine, University of Florida, Gainesville, Florida; and 3Institute for Inhalation Biology, National Research Center for Environment and Health, Munich, Germany
Submitted 26 July 2004 ; accepted in final form 11 October 2004
Epidemiological studies suggest that ultrafine particles contribute to particulate matter-induced adverse health effects. Interleukin (IL)-8 is an important proinflammatory cytokine in the human lung that is induced in respiratory cells exposed to a variety of environmental insults, including ambient air ultrafine particles. In this study, we examined the effect of a model ultrafine particle on IL-8 expression and the cellular mechanisms responsible for this event. Here, we report that carbonaceous ultrafine particles consisting of synthetic elemental carbon particles (UfCP) markedly increase the expression of IL-8 mRNA and protein in normal human bronchial epithelial (NHBE) cells. IL-8 promoter activity was increased by UfCP exposure in NHBE cells, indicating UfCP-induced IL-8 expression is transcriptionally regulated. IL-8 expression in NHBE is known to be regulated by nuclear factor (NF)-
B activation. However, UfCP did not induce inhibitory factor B
degradation, NF-B-DNA binding, or NF-B-dependent promoter activity in NHBE cells, indicating that UfCP induces IL-8 expression through a mechanism that is independent of NF-B activation. Additionally, we observed that UfCP exposure induces the phosphorylation and activation of p38 mitogen-activated protein kinase (MAPK) in a biphasic manner and that the inhibition of p38 MAPK activity can block IL-8 mRNA expression induced by UfCP in NHBE cells. These results demonstrate that UfCP-induced expression of IL-8 involves a transcriptional mechanism and activation of p38 MAPK in NHBE cells.
human bronchial epithelial cell; p38 mitogen-activated protein kinase; particulate matter; ultrafine particles; nuclear factor-B
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