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Chronic Pseudomonas aeruginosa infection-induced chronic bronchitis and emphysematous changes in CCSP-deficient mice

Authors Matsumoto T, Fujita M, Hirano R, Uchino J, Tajiri Y, Fukuyama S, Morimoto Y, Watanabe K

Received 27 May 2016

Accepted for publication 4 July 2016

Published 20 September 2016 Volume 2016:11(1) Pages 2321—2327

DOI https://doi.org/10.2147/COPD.S113707

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Professor Hsiao-Chi Chuang

Peer reviewer comments 3

Editor who approved publication: Dr Richard Russell


Takemasa Matsumoto,1 Masaki Fujita,1 Ryosuke Hirano,1 Junji Uchino,1 Yukari Tajiri,2 Satoru Fukuyama,2 Yasuo Morimoto,3 Kentaro Watanabe1

1Department of Respiratory Medicine, Faculty of Medicine, Fukuoka University, 2Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 3Department of Occupational Pneumology, Institute of Industrial and Ecological Sciences, University of Occupational and Environmental Health, Kitakyushu, Japan

Abstract: The club cell secretory protein (CCSP) is a regulator of lung inflammation following acute respiratory infection or lung injury. Recently, the relationship between CCSP and COPD has been reported. Since COPD results from an abnormal inflammatory response, we hypothesized that CCSP could have a protective role against chronic inflammation-induced lung damage. To address this issue, the pathophysiology of chronic lung inflammation induced by Pseudomonas aeruginosa in CCSP-deficient mice was determined. A tube of 5 mm in length was soaked in a fluid containing P. aeruginosa (PAO01 strain) for 1 week and inserted into the trachea of CCSP-deficient mice. One week later, P. aeruginosa was administered into the trachea. Five weeks after insertion of tube, the mice were sacrificed. Bronchoalveolar lavage fluids were collected to determine the bacterial growth, and the lung histology and physiology were also examined. P. aeruginosa was continuously detected in bronchoalveolar lavage fluids during the study. Neutrophils were increased in the bronchoalveolar lavage fluids from the CCSP-deficient mice in comparison to wild-type mice. A histological study demonstrated chronic inflammation around bronchus, serious bronchial stenosis, and alveolar enlargement in the CCSP-deficient mice. The lung physiology study demonstrated an increase in the lung compliance of the CCSP-deficient mice. Chronic P. aeruginosa inflammation resulted in chronic bronchitis and emphysematous changes in the CCSP-deficient mice. CCSP could play an important role in protecting the host from the chronic inflammation-induced lung damage.

Keywords: chronic bronchitis, animal models, emphysema, inflammation
 

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