Chemokine (C‐C Motif) Receptor‐Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone

Details

• Alternative Title:
  Physiol Rep
• Personal Author:
  Malik, Farhan ; Cromar, Kevin R. ; Atkins, Constance L. ; Price, Roger E. ; Jackson, William T. ; Siddiqui, Saad R. ; Spencer, Chantal Y. ; Mitchell, Nicholas C. ; Haque, Ikram U. ; Johnston, Richard A.
• Description:
  Inhalation of ozone (O|), 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|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|-induced lung pathology and that chemerin, a Ccrl2 ligand, is increased in bronchoalveolar lavage fluid (BALF) by O|, we hypothesized that Ccrl2 contributes to the development of lung injury, lung inflammation, and airway hyperresponsiveness induced by O|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-|-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|In air-exposed mice, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O|increased BALF chemerin in mice of both genotypes, yet following O|exposure, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O|increased indices of lung injury, lung inflammation, and airway responsiveness. Nevertheless, no indices were different between genotypes following O|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|-induced lung pathology.
• Subjects:
  Chemerin Cmklr1 CXCR2 Gpr1 Immunology Lung Methacholine Original Research Osteopontin Respiratory Conditions Disorder And Diseases Toxins, Pollutants And Chemical Agents

  More +
• Source:
  Physiol Rep. 5(24).
• Pubmed ID:
  29242308
• Pubmed Central ID:
  PMC5742705
• Document Type:
  Journal Article
• Volume:
  5
• Issue:
  24
• Collection(s):
  CDC Public Access
• Main Document Checksum:
  urn:sha256:902eebeb6fff74a5ba28c87abc85c224f841c474f576055d62f4870436d06302
• Download URL:
  https://stacks.cdc.gov/view/cdc/50703/cdc_50703_DS1.pdf
• File Type:
  [PDF - 1.20 MB ]