title: Acute exercise decreases airway inflammation, but not responsiveness, in an allergic asthma model.
abstract: 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.
authors.affiliation: Department of Physiology and Biophysics, University of Alabama at Birmingham, 1918 University Boulevard, Birmingham, AL 35294-0005, USA.
authors.forename: Matt
authors.initials: M
authors.lastname: Hewitt
authors.forename: Amy
authors.initials: A
authors.lastname: Creel
authors.forename: Kim
authors.initials: K
authors.lastname: Estell
authors.forename: Ian C
authors.initials: IC
authors.lastname: Davis
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Schwiebert
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000276:immunology*; D018925:Chemokines / Q000276:immunology; D002630:Chemotactic Factors / Q000378:metabolism; D016207:Cytokines / Q000276:immunology; D015232:Dinoprostone / Q000276:immunology; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D007962:Leukocytes / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D010805:Physical Conditioning, Animal; D011897:Random Allocation; D012130:Respiratory Hypersensitivity / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D018925:Chemokines; D002630:Chemotactic Factors; D016207:Cytokines; C498144:Rela protein, mouse; D051996:Transcription Factor RelA; D010047:Ovalbumin; D015232:Dinoprostone