Inconsequential Role for Chemerin-Like Receptor 1 in a Manifestation of Ozone-Induced Lung Pathophysiology in Male Mice

Chemerin, a non-chemokine chemoattractant, and resolvin E1 (RvE1), a specialized pro-resolving lipid mediator, are endogenous ligands for chemerin-like receptor 1 (CMKLR1), a Gi/o protein-coupled receptor expressed by leukocytes and non-leukocytes. In mice, exogenous administration of chemerin or RvE1 diminishes the severity of lung inflammation and airway hyperresponsiveness (AHR) induced by antigen sensitization and challenge, which mimics phenotypic features of atopic asthma in humans. However, the contribution of chemerin or RvE1 to features of non-atopic asthma is unknown. Therefore, to indirectly assess if chemerin or RvE1 facilitates development of a non-atopic asthma phenotype, which includes AHR to acetyl-β-methylcholine chloride, lung hyperpermeability, airway epithelial cell desquamation, and lung inflammation, we quantified features of these sequelae in wild-type mice and mice failing to express CMKLR1 (CMKLR1-deficient mice) following cessation of acute inhalation exposure to either filtered room air or ozone, a criteria pollutant and non-atopic asthma stimulus.