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Papers In Press, published online ahead of print October 17, 2003
Department of Internal Medicine, University of Iowa, Iowa City, IA 52242
Corresponding Author: martha-monick{at}uiowa.edu
Airway epithelial cells are unresponsive to endotoxin (LPS) exposure under normal conditions. This study demonstrates that respiratory syncytial virus (RSV) infection results in increased sensitivity to this environmental exposure. Infection with RSV results in increased expression of Toll-like receptor (TLR) 4 mRNA, protein, and increased TLR4 membrane localization. This permits significantly enhanced LPS binding to the epithelial monolayer that is blocked by disruption of the golgi. The increased TLR4 results in an LPS-induced inflammatory response as demonstrated by increased MAP kinase activity, IL-8 production and TNFa production. RSV infection also allowed for TNFa production subsequent to TLR4 cross-linking with an immobilized antibody. These data suggest that RSV infection sensitizes airway epithelium to a subsequent environmental exposure (LPS) by altered expression and membrane localization of TLR4. The increased interaction between airway epithelial cells and LPS has the potential to profoundly alter airway inflammation.
J. Biol. Chem, 10.1074/jbc.M308093200
Submitted on July 25, 2003
Revised on October 17, 2003
Accepted on October 16, 2003
Respiratory syncytial virus upregulates TLR4 and sensitizes airway epithelial cells to endotoxin
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