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Chemokine (C-C Motif) Receptor-Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone.
- Source :
-
Physiological reports [Physiol Rep] 2017 Dec; Vol. 5 (24). - Publication Year :
- 2017
-
Abstract
- Inhalation of ozone (O <subscript>3</subscript> ), a gaseous air pollutant, causes lung injury, lung inflammation, and airway hyperresponsiveness. Macrophages, mast cells, and neutrophils contribute to one or more of these sequelae induced by O <subscript>3</subscript> Furthermore, each of these aforementioned cells express chemokine (C-C motif) receptor-like 2 (Ccrl2), an atypical chemokine receptor that facilitates leukocyte chemotaxis. Given that Ccrl2 is expressed by cells essential to the development of O <subscript>3</subscript> -induced lung pathology and that chemerin, a Ccrl2 ligand, is increased in bronchoalveolar lavage fluid (BALF) by O <subscript>3</subscript> , we hypothesized that Ccrl2 contributes to the development of lung injury, lung inflammation, and airway hyperresponsiveness induced by O <subscript>3</subscript> To that end, we measured indices of lung injury (BALF protein, BALF epithelial cells, and bronchiolar epithelial injury), lung inflammation (BALF cytokines and BALF leukocytes), and airway responsiveness to acetyl- β -methylcholine chloride (respiratory system resistance) in wild-type and mice genetically deficient in Ccrl2 (Ccrl2-deficient mice) 4 and/or 24 hours following cessation of acute exposure to either filtered room air (air) or O <subscript>3</subscript> In air-exposed mice, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O <subscript>3</subscript> increased BALF chemerin in mice of both genotypes, yet following O <subscript>3</subscript> exposure, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O <subscript>3</subscript> increased indices of lung injury, lung inflammation, and airway responsiveness. Nevertheless, no indices were different between genotypes following O <subscript>3</subscript> exposure. In conclusion, we demonstrate that Ccrl2 modulates chemerin levels in the epithelial lining fluid of the lungs but does not contribute to the development of O <subscript>3</subscript> -induced lung pathology.<br /> (© 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)
- Subjects :
- Animals
Asthma etiology
Asthma genetics
Bronchoalveolar Lavage Fluid cytology
Chemokines genetics
Chemokines metabolism
Female
Genotype
Intercellular Signaling Peptides and Proteins genetics
Intercellular Signaling Peptides and Proteins metabolism
Lung Injury etiology
Lung Injury genetics
Male
Mice
Mice, Inbred C57BL
Receptors, CCR
Receptors, Chemokine metabolism
Respiratory Mucosa metabolism
Asthma metabolism
Lung Injury metabolism
Ozone adverse effects
Receptors, Chemokine genetics
Subjects
Details
- Language :
- English
- ISSN :
- 2051-817X
- Volume :
- 5
- Issue :
- 24
- Database :
- MEDLINE
- Journal :
- Physiological reports
- Publication Type :
- Academic Journal
- Accession number :
- 29242308
- Full Text :
- https://doi.org/10.14814/phy2.13545