|
|
||||||||
1Research Service, Department of Veterans Affairs Medical Center, Omaha 68105; and 2Pulmonary and Critical Care Medicine Section, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska 68198
Submitted 17 April 2003 ; accepted in final form 6 January 2004
The dust of hog confinement facilities induces airway inflammation. Mechanisms by which this dust modulates inflammation are not completely defined, although it is clear that exposure to dust can modulate both epithelial cell and inflammatory cell function. In this work, we demonstrate that airway epithelial cell (BEAS-2B) treatment with hog barn dust extract (HDE) results in augmentation of peripheral blood lymphocyte adhesion to epithelial cell cultures in vitro. The augmentation of lymphocyte adhesion to epithelial cells is dependent on the concentration of HDE and time of HDE exposure, with twofold increases observed by 3 h and maintained at 24 h. Similar results are seen with primary human bronchial epithelial cells in culture. Lymphocyte adhesion to epithelial cells is inhibited in a concentration-dependent fashion by the treatment of epithelial cells with antibody to intercellular adhesion molecule-1 (ICAM-1). In addition, HDE exposure of epithelial cells results in an approximate twofold increase in ICAM-1 expression as determined by flow cytometry analysis. Pretreatment of epithelial cells with a protein kinase C-
(PKC-
) inhibitor, Gö-6976, also inhibited subsequent lymphocyte adhesion to HDE-exposed epithelial cells. These data suggest that airway epithelial cell HDE exposure enhances subsequent lymphocyte adhesion to epithelial cells that is mediated in part by HDE modulation of ICAM-1 expression and PKC-
.
lung; lipopolysaccharide; interferon-gamma; swine confinement workers
This article has been cited by other articles:
![]() |
J. A. Poole, T. A. Wyatt, P. J. Oldenburg, M. K. Elliott, W. W. West, J. H. Sisson, S. G. Von Essen, and D. J. Romberger Intranasal organic dust exposure-induced airway adaptation response marked by persistent lung inflammation and pathology in mice Am J Physiol Lung Cell Mol Physiol, June 1, 2009; 296(6): L1085 - L1095. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. L. Bailey, J. A. Poole, T. L. Mathisen, T. A. Wyatt, S. G. Von Essen, and D. J. Romberger Toll-like receptor 2 is upregulated by hog confinement dust in an IL-6-dependent manner in the airway epithelium Am J Physiol Lung Cell Mol Physiol, June 1, 2008; 294(6): L1049 - L1054. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. E. Slager, D. S. Allen-Gipson, A. Sammut, A. Heires, J. DeVasure, S. Von Essen, D. J. Romberger, and T. A. Wyatt Hog barn dust slows airway epithelial cell migration in vitro through a PKC{alpha}-dependent mechanism Am J Physiol Lung Cell Mol Physiol, December 1, 2007; 293(6): L1469 - L1474. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. A. Wyatt, R. E. Slager, J. DeVasure, B. W. Auvermann, M. L. Mulhern, S. Von Essen, T. Mathisen, A. A. Floreani, and D. J. Romberger Feedlot dust stimulation of interleukin-6 and -8 requires protein kinase C{varepsilon} in human bronchial epithelial cells Am J Physiol Lung Cell Mol Physiol, November 1, 2007; 293(5): L1163 - L1170. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Rubinstein and S. G. Von Essen Hog barn dust extract increases macromolecular efflux from the hamster cheek pouch J Appl Physiol, July 1, 2006; 101(1): 128 - 134. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |