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Analysis of the Mechanisms of Exercise-Induced Bronchoconstriction Using Mouse Model
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A1910 - Analysis of the Mechanisms of Exercise-Induced Bronchoconstriction Using Mouse Model
Author Block: T. Koya1, H. Ueno1, T. Hasegawa2, K. Yoshizawa1, T. Sakagami1, M. Hayashi1, T. Kikuchi1; 1Department of Respiratory Medicine and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan, 2Department of General Medicine, Niigata University Medical and Dental Hospital, Niigata, Japan.
Introduction: It is well known that the prevalence of asthma is higher in athlete population such as Olympic athletes than in general population. Airway epithelial injury induced by intense exercise is considered as one of the mechanisms of asthma in athlete population but the precise mechanisms are not fully determined. In this study, we analyzed the mechanism of exercise induced bronchoconstriction (EIB) by using animal model Methods: We used the treadmill for mice (TM54, MELQUEST, Japan) to load exercise training. The speed set at approximately 1.3 km/h for 45min and mice received exercises once a day, 5 days/week for 5 consecutive weeks. The duration of exercise stimulation was changed to 1seek, 3weeks, and 5week. We analyzed airway hyperresponsiveness (AHR), bronchoalveolar lavage fluid (BALF) and the immunohistological analysis in each point. Results: AHR to methacholine was enhanced with repeated exercise stimulation but cell composition in BALF did not change compared to sedentary group. Exercise induced hypertrophy of airway smooth muscle and subepithelial collagen deposition. In regard to the growth factor, epidermal growth factor (EGF) and amphiregulin (AREG) are significantly increased both mRNA and protein in BALF. Conclusion: These data suggested that AHR and progress of airway remodeling were confirmed by repeated and strenuous exercise stimulation in mouse model. Inflammatory cells were not found in BALF and histological analysis, so the possibility was occurred that airway inflammation was hardly involved with EIB in this model. EGF and AREG may play important roles for EIB and further analysis are required to elucidate detailed mechanism.
Author Block: T. Koya1, H. Ueno1, T. Hasegawa2, K. Yoshizawa1, T. Sakagami1, M. Hayashi1, T. Kikuchi1; 1Department of Respiratory Medicine and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan, 2Department of General Medicine, Niigata University Medical and Dental Hospital, Niigata, Japan.
Introduction: It is well known that the prevalence of asthma is higher in athlete population such as Olympic athletes than in general population. Airway epithelial injury induced by intense exercise is considered as one of the mechanisms of asthma in athlete population but the precise mechanisms are not fully determined. In this study, we analyzed the mechanism of exercise induced bronchoconstriction (EIB) by using animal model Methods: We used the treadmill for mice (TM54, MELQUEST, Japan) to load exercise training. The speed set at approximately 1.3 km/h for 45min and mice received exercises once a day, 5 days/week for 5 consecutive weeks. The duration of exercise stimulation was changed to 1seek, 3weeks, and 5week. We analyzed airway hyperresponsiveness (AHR), bronchoalveolar lavage fluid (BALF) and the immunohistological analysis in each point. Results: AHR to methacholine was enhanced with repeated exercise stimulation but cell composition in BALF did not change compared to sedentary group. Exercise induced hypertrophy of airway smooth muscle and subepithelial collagen deposition. In regard to the growth factor, epidermal growth factor (EGF) and amphiregulin (AREG) are significantly increased both mRNA and protein in BALF. Conclusion: These data suggested that AHR and progress of airway remodeling were confirmed by repeated and strenuous exercise stimulation in mouse model. Inflammatory cells were not found in BALF and histological analysis, so the possibility was occurred that airway inflammation was hardly involved with EIB in this model. EGF and AREG may play important roles for EIB and further analysis are required to elucidate detailed mechanism.
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