| Acute exercise decreases airway inflammation, but not responsiveness, in an allergic asthma model. | |
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MedLine Citation:
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PMID: 18635813 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Previous studies have suggested that the asthmatic responses of airway inflammation, remodeling, and hyperresponsiveness (AHR) are interrelated; in this study, we used exercise to examine the nature of this interrelationship. Mice were sensitized and challenged with ovalbumin (OVA); mice were then exercised via running on a motorized treadmill at a moderate intensity. Data indicate that, within the lungs of OVA-treated mice, exercise attenuated the production of inflammatory mediators, including chemokines KC, RANTES, and MCP-1 and IL-12p40/p80. Coordinately, OVA-treated and exercised mice displayed decreases in leukocyte infiltration, including eosinophils, as compared with sedentary controls. Results also show that a single bout of exercise significantly decreased phosphorylation of the NFkappaB p65 subunit, which regulates the gene expression of a wide variety of inflammatory mediators. In addition, OVA-treated and exercised mice exhibited decreases in the levels of Th2-derived cytokines IL-5 and IL-13 and the prostaglandin PGE(2), as compared with sedentary controls. In contrast, results show that a single bout of exercise had no effect on AHR in OVA-treated mice challenged with increasing doses of aerosolized methacholine (0-50 mg/ml) as compared with sedentary mice. Exercise also had no effect on epithelial cell hypertrophy, mucus production, or airway wall thickening in OVA-treated mice as compared with sedentary controls. These findings suggest that a single bout of aerobic exercise at a moderate intensity attenuates airway inflammation but not AHR or airway remodeling in OVA-treated mice. The implication of these findings for the interrelationship between airway inflammation, airway remodeling, and AHR is discussed. |
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Authors:
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Matt Hewitt; Amy Creel; Kim Estell; Ian C Davis; Lisa M Schwiebert |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2008-07-17 |
Journal Detail:
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Title: American journal of respiratory cell and molecular biology Volume: 40 ISSN: 1535-4989 ISO Abbreviation: Am. J. Respir. Cell Mol. Biol. Publication Date: 2009 Jan |
Date Detail:
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Created Date: 2008-12-16 Completed Date: 2009-01-02 Revised Date: 2010-09-21 |
Medline Journal Info:
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Nlm Unique ID: 8917225 Medline TA: Am J Respir Cell Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 83-9 Citation Subset: IM |
Affiliation:
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Department of Physiology and Biophysics, University of Alabama at Birmingham, 1918 University Boulevard, Birmingham, AL 35294-0005, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Asthma / immunology* Bronchial Hyperreactivity / immunology* Chemokines / immunology Chemotactic Factors / metabolism Cytokines / immunology Dinoprostone / immunology Disease Models, Animal* Female Humans Inflammation / immunology* Leukocytes / metabolism Mice Mice, Inbred BALB C Ovalbumin / immunology Physical Conditioning, Animal* Random Allocation Respiratory Hypersensitivity / immunology Th2 Cells / immunology Transcription Factor RelA / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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1R01HL075465/HL/NHLBI NIH HHS; 5T32HL007553/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Chemokines; 0/Chemotactic Factors; 0/Cytokines; 0/Rela protein, mouse; 0/Transcription Factor RelA; 363-24-6/Dinoprostone; 9006-59-1/Ovalbumin |
| Comments/Corrections | |
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