title: Effect of PAR-2 Deficiency in Mice on KC Expression after Intratracheal LPS Administration.
abstract: 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.
authors.affiliation: Division of Hematology and Oncology, Department of Medicine, McAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035, USA.
authors.forename: Julie C
authors.initials: JC
authors.lastname: Williams
authors.forename: Rebecca D
authors.initials: RD
authors.lastname: Lee
authors.forename: Claire M
authors.initials: CM
authors.lastname: Doerschuk
authors.forename: Nigel
authors.initials: N
authors.lastname: Mackman