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Am J Physiol Lung Cell Mol Physiol 293: L1469-L1474, 2007. First published October 12, 2007; doi:10.1152/ajplung.00274.2007
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Hog barn dust slows airway epithelial cell migration in vitro through a PKC{alpha}-dependent mechanism

Rebecca E. Slager,1 Diane S. Allen-Gipson,1 Alexi Sammut,1 Art Heires,1 Jane DeVasure,1 Susanna Von Essen,1,2 Debra J. Romberger,1,3 and Todd A. Wyatt1,3

1Pulmonary and Critical Care Medicine Section, Department of Internal Medicine and 2College of Public Health, University of Nebraska Medical Center, Omaha; and 3Research Service, Department of Veterans Affairs Medical Center, Omaha, Nebraska

Submitted 16 July 2007 ; accepted in final form 7 October 2007

Agricultural work and other occupational exposures are responsible for ~15% of chronic obstructive pulmonary disease (COPD). COPD involves airway remodeling in response to chronic lung inflammatory events and altered airway repair mechanisms. However, the effect of agricultural dust exposure on signaling pathways that regulate airway injury and repair has not been well characterized. A key step in this process is migration of airway cells to restore epithelial integrity. We have previously shown that agents that activate the critical regulatory enzyme protein kinase C (PKC) slow cell migration during wound repair. Based on this observation and direct kinase measurements that demonstrate that dust extract from hog confinement barns (HDE) specifically activates the PKC isoforms PKC{alpha} and PKC{varepsilon}, we hypothesized that HDE would slow wound closure time in airway epithelial cells. We utilized the human bronchial epithelial cell line BEAS-2B and transfected BEAS-2B cell lines that express dominant negative (DN) forms of PKC isoforms to demonstrate that HDE slows wound closure in BEAS-2B and PKC{varepsilon} DN cell lines. However, in PKC{alpha} DN cells, wound closure following HDE treatment is not significantly different than media-treated cells. These results suggest that the PKC{alpha} isoform is an important regulator of cell migration in response to agricultural dust exposure.

protein kinase C; chronic obstructive pulmonary disease


Address for reprint requests and other correspondence: T. A. Wyatt, Dept. of Internal Medicine, Pulmonary and Critical Care Medicine Section, Univ. of Nebraska Medical Center, 985300 Nebraska Medical Center, Omaha, NE 68198-5300 (e-mail: twyatt{at}unmc.edu)






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