Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure.
Autor: | Razvi SS; Division of Critical Care Medicine, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas;, Richards JB; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;, Malik F; Division of Critical Care Medicine, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas;, Cromar KR; Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York;, Price RE; Comparative Pathology Laboratory, Center for Comparative Medicine, Baylor College of Medicine, Houston, Texas;, Bell CS; Division of Nephrology, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas;, Weng T; Department of Biochemistry and Molecular Biology, The University of Texas Medical School at Houston, Houston, Texas;, Atkins CL; Division of Pulmonary Medicine, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas;, Spencer CY; Pediatric Pulmonary Section, Department of Pediatrics, Baylor College of Medicine, Houston, Texas;, Cockerill KJ; Pediatric Research Center, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas;, Alexander AL; Pediatric Research Center, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas;, Blackburn MR; Department of Biochemistry and Molecular Biology, The University of Texas Medical School at Houston, Houston, Texas;, Alcorn JL; Department of Biochemistry and Molecular Biology, The University of Texas Medical School at Houston, Houston, Texas; Pediatric Research Center, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas; Division of Neonatal-Perinatal Medicine, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas; and., Haque IU; Division of Critical Care Medicine, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas;, Johnston RA; Division of Critical Care Medicine, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas; Pediatric Research Center, Department of Pediatrics, The University of Texas Medical School at Houston, Houston, Texas; Department of Integrative Biology and Pharmacology, The University of Texas Medical School at Houston, Houston, Texas Richard.A.Johnston@uth.tmc.edu. |
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Jazyk: | angličtina |
Zdroj: | American journal of physiology. Lung cellular and molecular physiology [Am J Physiol Lung Cell Mol Physiol] 2015 Nov 15; Vol. 309 (10), pp. L1174-85. Date of Electronic Publication: 2015 Sep 18. |
DOI: | 10.1152/ajplung.00270.2015 |
Abstrakt: | Acute exposure to ozone (O3), an air pollutant, causes pulmonary inflammation, airway epithelial desquamation, and airway hyperresponsiveness (AHR). Pro-inflammatory cytokines-including IL-6 and ligands of chemokine (C-X-C motif) receptor 2 [keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-2], TNF receptor 1 and 2 (TNF), and type I IL-1 receptor (IL-1α and IL-1β)-promote these sequelae. Human resistin, a pleiotropic hormone and cytokine, induces expression of IL-1α, IL-1β, IL-6, IL-8 (the human ortholog of murine KC and MIP-2), and TNF. Functional differences exist between human and murine resistin; yet given the aforementioned observations, we hypothesized that murine resistin promotes O3-induced lung pathology by inducing expression of the same inflammatory cytokines as human resistin. Consequently, we examined indexes of O3-induced lung pathology in wild-type and resistin-deficient mice following acute exposure to either filtered room air or O3. In wild-type mice, O3 increased bronchoalveolar lavage fluid (BALF) resistin. Furthermore, O3 increased lung tissue or BALF IL-1α, IL-6, KC, TNF, macrophages, neutrophils, and epithelial cells in wild-type and resistin-deficient mice. With the exception of KC, which was significantly greater in resistin-deficient compared with wild-type mice, no genotype-related differences in the other indexes existed following O3 exposure. O3 caused AHR to acetyl-β-methylcholine chloride (methacholine) in wild-type and resistin-deficient mice. However, genotype-related differences in airway responsiveness to methacholine were nonexistent subsequent to O3 exposure. Taken together, these data demonstrate that murine resistin is increased in the lungs of wild-type mice following acute O3 exposure but does not promote O3-induced lung pathology. (Copyright © 2015 the American Physiological Society.) |
Databáze: | MEDLINE |
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