PAR-2-deficient mice had significantly less KC expression in bronchial lavage fluid compared with wild-type mice after LPS administration, with no difference in MIP-2 or TNF-α.
Does PAR-2 deficiency reduce inflammatory cytokine expression in a mouse model of LPS-induced lung inflammation?
PAR-2 deficiency reduces KC expression in response to LPS, suggesting PAR-2 plays a role in LPS activation of TLR4 signaling in macrophages.
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.
Williams et al. (2011) studied LPS-induced lung inflammation. PAR-2 deficiency vs. Wild-type mice was evaluated on KC expression in bronchial lavage fluid. PAR-2-deficient mice had significantly less KC expression in bronchial lavage fluid compared with wild-type mice after LPS administration, with no difference in MIP-2 or TNF-α.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: