Table of Contents
Journal of Signal Transduction
Volume 2011, Article ID 415195, 6 pages
Research Article

Effect of PAR-2 Deficiency in Mice on KC Expression after Intratracheal LPS Administration

1Division of Hematology and Oncology, Department of Medicine, McAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035, USA
2Department of Medicine, Center for Airways Disease, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035, USA

Received 30 June 2011; Accepted 17 August 2011

Academic Editor: Kathryn DeFea

Copyright © 2011 Julie C. Williams et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Protease activated receptors (PAR) have been shown to play a role in inflammation. PAR-2 is expressed by numerous cells in the lung and has either proinflammatory, anti-inflammatory, or no effect depending on the model. Here, we examined the role of PAR-2 in a model of LPS-induced lung inflammation. We found that PAR-2-deficient mice had significantly less KC expression in bronchial lavage fluid compared with wild-type mice but there was no difference in MIP-2 or TNF-α expression. We also found that isolated alveolar and resident peritoneal macrophages lacking PAR-2 showed a similar deficit in KC after LPS stimulation without differences in MIP-2 or TNF-α. Infiltration of neutrophils and macrophages into the lung following LPS administration was not affected by an absence of PAR-2. Our results support the notion that PAR-2 plays a role in LPS activation of TLR4 signaling in macrophages.