Prior exercise training alleviates the lung inflammation induced by subsequent exposure to environmental cigarette smoke

• Published in: Acta Physiologica Vol. 205; no. 4; pp. 532 - 540
• Main Authors: Yu, Y.-B., Liao, Y.-W., Su, K.-H., Chang, T.-M., Shyue, S.-K., Kou, Y. R., Lee, T.-S.
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell Publishing Ltd 01-08-2012; Wiley-Blackwell; Wiley Subscription Services, Inc
• Subjects: Animal subjects; Animals; Biological and medical sciences; Bronchoalveolar Lavage Fluid - chemistry; Bronchoalveolar Lavage Fluid - cytology; Cell adhesion molecules; Chemokines; Chronic diseases; Cigarette smoke; Cytokines; exercise; Exercise (effects); Exercise (programs); Fundamental and applied biological sciences. Psychology; Inflammation; Inflammation - chemically induced; Lung diseases; Lung Diseases - chemically induced; Lungs; Mice; mucin; Mucus - secretion; NF- Kappa B protein; Permeability; Physical Conditioning, Animal; Physical training; Proliferating cell nuclear antigen; proliferation; Respiratory Mucosa - drug effects; Respiratory Mucosa - pathology; Respiratory system; Smoking; Tobacco; Tobacco Smoke Pollution - adverse effects; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Physical exercise; Cell proliferation; Vertebrata; Tobacco smoke; Mammalia; Mucin; proliferation; Lung; exercise; Inflammation; cigarette smoke; Respiratory system
• DOI: 10.1111/j.1748-1716.2012.02433.x
• EISSN: 1748-1716
• ISSN: 1748-1708

Aim
Environmental cigarette smoke (CS) contains many compounds that are harmful to the respiratory system and lead to chronic lung inflammation and other lung diseases. Exercise training is known to confer protection against diseases with chronic inflammation by reducing inflammatory response in human or experimental animals. In this study, we investigated the preventive effect of exercise training against lung inflammation induced by environmental CS.
Methods and results
In this study, two groups of mice received air exposure with (the exercise group) or without (the control group) exercise training for 8 weeks and another two groups received air exposure for the first 4 weeks and CS exposure for the following 4 weeks with (the exercise+CS group) or without (the CS group) exercise training for 8 weeks. As compared with lung tissues of control and exercise groups, those of the CS group showed significantly increased bronchoalveolar‐capillary permeability, inflammatory cell infiltration, epithelial thickening, expression of proliferating cell nuclear antigen, mucin 2, cytokines, chemokines, adhesion molecules and activation of NF‐κB. These CS‐induced pathophysiologic consequences were largely prevented in the exercise + CS group.
Conclusion
Collectively, prior exercise training may protect against lung inflammation induced by environmental CS in mice by attenuating the activation of NF‐κB and the production of inflammatory mediators.