title: Aerobic exercise attenuates airway inflammatory responses in a mouse model of atopic asthma.
abstract: Recent reports indicate that aerobic exercise improves the overall physical fitness and health of asthmatic patients. The specific exercise-induced improvements in the pathology of asthma and the mechanisms by which these improvements occur, however, are ill-defined; thus, the therapeutic potential of exercise in the treatment of asthma remains unappreciated. Using an OVA-driven mouse model, we examined the role of aerobic exercise in modulating inflammatory responses associated with atopic asthma. Data demonstrate that moderate intensity aerobic exercise training decreased leukocyte infiltration, cytokine production, adhesion molecule expression, and structural remodeling within the lungs of OVA-sensitized mice (n = 6-10; p < 0.05). Because the transcription factor NF-kappaB regulates the expression of a variety of genes that encode inflammatory mediators, we monitored changes in NF-kappaB activation in the lungs of exercised/sensitized mice. Results show that exercise decreased NF-kappaB nuclear translocation and IkappaBalpha phosphorylation, indicating that exercise decreased NF-kappaB activation in the lungs of sensitized mice (n = 6). Taken together, these results suggest that aerobic exercise attenuates airway inflammation in a mouse model of atopic asthma via modulation of NF-kappaB activation. Potential exists, therefore, for the amelioration of asthma-associated chronic airway inflammation through the use of aerobic exercise training as a non-drug therapeutic modality.
authors.affiliation: Departments of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
authors.forename: Amy
authors.initials: A
authors.lastname: Pastva
authors.forename: Kim
authors.initials: K
authors.lastname: Estell
authors.forename: Trenton R
authors.initials: TR
authors.lastname: Schoeb
authors.forename: T Prescott
authors.initials: TP
authors.lastname: Atkinson
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Schwiebert
mesh_terms: D000485:Allergens / Q000008:administration & dosage / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000473:pathology* / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors; D018925:Chemokines / Q000037:antagonists & inhibitors; D004195:Disease Models, Animal; D005260:Female; D006969:Hypersensitivity, Immediate / Q000473:pathology* / Q000503:physiopathology*; D007073:Immunoglobulin E / Q000096:biosynthesis; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors; D015847:Interleukin-4 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D015848:Interleukin-5 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D008168:Lung / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
chemical_list: D000485:Allergens; D015815:Cell Adhesion Molecules; D018925:Chemokines; D018836:Inflammation Mediators; D015848:Interleukin-5; D015847:Interleukin-4; D007073:Immunoglobulin E; D010047:Ovalbumin