Inconsequential role for chemerin ‐like receptor 1 in the manifestation of ozone‐induced lung pathophysiology in male mice

AbstractWe executed this study to determine if chemerin-like receptor 1 (CMKLR1), aGi/o protein-coupled receptor expressed by leukocytes and non-leukocytes, contributes to the development of phenotypic features of non-atopic asthma, including airway hyperresponsiveness (AHR) to acetyl- β-methylcholine chloride, lung hyperpermeability, airway epithelial cell desquamation, and lung inflammation. Accordingly, we quantified sequelae of non-atopic asthma in wild-type mice and mice incapable of expressing CMKLR1 (CMKLR1-deficient mice) following cessation of acute inhalation exposure t o either filtered room air (air) or ozone (O3), a criteria pollutant and non-atopic asthma stimulus. Following exposure to air, lung elastic recoil and airway responsiveness were greater while the quantity of adiponectin, a multi-functional adipocytokine, in bronchoalveolar lavage (BAL) fluid was lower in CMKLR1-deficient as compared to wild-type mice. Regardless of genotype, exposure to O3 caused AHR, lung hyperpermeability, airway epithelial cell desquamation, and lung inflammation. Nevertheless, except for minimal genotype-related effects on lung hyperpermeability and BAL adiponectin, we observed no other genotype-related differences following O3 exposure. In summary, we demonstrate that CMKLR1 limits the severity of innate airway responsiveness and lung elastic recoil but has a nominal effect on lung pathophysiology induced by acute exposure to O3.

Source: Physiological Reports - April 18, 2024 Category: Physiology Authors: Richard A. Johnston, Albert W. Pilkington IV, Constance L. Atkins, Theresa E. Boots, Philip L. Brown, William T. Jackson, Chantal Y. Spencer, Saad R. Siddiqui, Ikram U. Haque Tags: ORIGINAL ARTICLE Source Type: research