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Am J Physiol Lung Cell Mol Physiol 275: L551-L558, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 3, L551-L558, September 1998

Activation of MAPKs in human bronchial epithelial cells exposed to metals

James M. Samet1, Lee M. Graves2, Jacqueline Quay3, Lisa A. Dailey3, Robert B. Devlin3, Andrew J. Ghio3, Weidong Wu1, Philip A. Bromberg1, and William Reed1

1 Center for Environmental Medicine and Lung Biology and 2 Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill 27599; and 3 Human Studies Division, National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711

We have previously shown that in vitro exposure to metallic compounds enhances expression of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha in human bronchial epithelial cells. To characterize signaling pathways involved in metal-induced expression of inflammatory mediators and to identify metals that activate them, we studied the effects of As, Cr, Cu, Fe, Ni, V, and Zn on the mitogen-activated protein kinases (MAPK) extracellular receptor kinase (ERK), c-Jun NH2-terminal kinase (JNK), and P38 in BEAS cells. Noncytotoxic concentrations of As, V, and Zn induced a rapid phosphorylation of MAPK in BEAS cells. Activity assays confirmed marked activation of ERK, JNK, and P38 in BEAS cells exposed to As, V, and Zn. Cr and Cu exposure resulted in a relatively small activation of MAPK, whereas Fe and Ni did not activate MAPK under these conditions. Similarly, the transcription factors c-Jun and ATF-2, substrates of JNK and P38, respectively, were markedly phosphorylated in BEAS cells treated with As, Cr, Cu, V, and Zn. The same acute exposure to As, V, or Zn that activated MAPK was sufficient to induce a subsequent increase in IL-8 protein expression in BEAS cells. These data suggest that MAPK may mediate metal-induced expression of inflammatory proteins in human bronchial epithelial cells.

signal transduction; airway epithelial cells; metal toxicology; air pollution; mitogen-activated protein kinases


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