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Acute Exercise Decreases Airway Inflammation, but Not Responsiveness, in an Allergic Asthma Model

¹ Department of Physiology and Biophysics, ² Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama; and ³ Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio

Correspondence and requests for reprints should be addressed to Lisa M. Schwiebert, Ph.D., Department of Physiology and Biophysics, MCLM, Room 955, University of Alabama at Birmingham, 1918 University Boulevard, Birmingham, AL 35294-0005. E-mail: lschwieb{at}uab.edu

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 NFB 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 PGE₂, 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.

Key Words: asthma • aerobic exercise • airway inflammation • remodeling • hyperresponsiveness

CLINICAL RELEVANCE Using acute aerobic exercise of ovalbumin-treated mice, we report that airway remodeling and airway hyperresponsiveness (AHR) persist in the absence of airway inflammation. These findings indicate that airway inflammation is not required for development of airway remodeling and AHR.