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

Details

• Personal Author:
  Atkins CL ; Boots TE ; Brown PL ; Haque IU ; Jackson WT ; Johnston RA ; Pilkington AW IV ; Siddiqui SR ; Spencer CY
• Description:
  We executed this study to determine if chemerin-like receptor 1 (CMKLR1), a Gi/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 to 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. [Description provided by NIOSH]
• Subjects:
  Animals Asthma Asthma, Occupational Blood Immune System Lung Macrophages Occupational Health Ozone Respiratory System Safety

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• Keywords:
  Airway Resistance Animal Studies Author Keywords: Airway Hyperresponsiveness Chemerin-like Receptor 1 Elastic Recoil Immune Reaction Inhalation Studies Leukocytes Lung Lung Irritants Physiopathology

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• ISSN:
  2051-817X
• Document Type:
  Text
• Genre:
  Journal Article
• Place as Subject:
  OSHA Region 3 ; OSHA Region 6 ; Texas ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  12
• Issue:
  8
• NIOSHTIC Number:
  nn:20069587
• Citation:
  Physiol Rep 2024 Apr; 12(8):e16008
• Contact Point Address:
  Richard A. Johnston, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, 1000 Frederick Lane, Morgantown, WV 26508-5402, USA
• Email:
  rfj1@cdc.gov
• CAS Registry Number:
  Ozone (CAS RN 10028-15-6)
• Federal Fiscal Year:
  2024
• NORA Priority Area:
  Manufacturing
• Peer Reviewed:
  True
• Source Full Name:
  Physiological Reports
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:7bbc538afcc048f3f82bb8866ab4864c21a51ab72523c20bce123c1293a4826bcdbef5345b7b95ca64a5dd000ecaecfc4bf3fbc10bc2977272d2f16976a51ad4
• Download URL:
  https://stacks.cdc.gov/view/cdc/207991/cdc_207991_DS1.pdf
• File Type:
  [PDF - 841.14 KB ]