Document Detail


Aerobic exercise attenuates airway inflammatory responses in a mouse model of atopic asthma.
MedLine Citation:
PMID:  15034069     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Amy Pastva; Kim Estell; Trenton R Schoeb; T Prescott Atkinson; Lisa M Schwiebert
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  172     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2004 Apr 
Date Detail:
Created Date:  2004-03-22     Completed Date:  2004-07-30     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4520-6     Citation Subset:  AIM; IM    
Affiliation:
Departments of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
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MeSH Terms
Descriptor/Qualifier:
Allergens / administration & dosage,  immunology
Animals
Asthma / pathology*,  physiopathology*
Cell Adhesion Molecules / antagonists & inhibitors
Chemokines / antagonists & inhibitors
Disease Models, Animal
Female
Hypersensitivity, Immediate / pathology*,  physiopathology*
Immunoglobulin E / biosynthesis
Inflammation / pathology,  physiopathology
Inflammation Mediators / antagonists & inhibitors
Interleukin-4 / antagonists & inhibitors,  biosynthesis
Interleukin-5 / antagonists & inhibitors,  biosynthesis
Lung / immunology,  pathology*,  physiopathology*
Mice
Mice, Inbred BALB C
Ovalbumin / administration & dosage,  immunology
Physical Conditioning, Animal / physiology*
Th2 Cells / immunology,  metabolism
Grant Support
ID/Acronym/Agency:
R01 HL075465/HL/NHLBI NIH HHS; R01 HL075465-01A2/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Allergens; 0/Cell Adhesion Molecules; 0/Chemokines; 0/Inflammation Mediators; 0/Interleukin-5; 207137-56-2/Interleukin-4; 37341-29-0/Immunoglobulin E; 9006-59-1/Ovalbumin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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