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

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus

Lung morphometry in the mouse model of chronic Pseudomonas aeruginosa infection.Notes: (A) The mean linear intercept (Lm) was measured by previously reported methods to evaluate the emphysematous changes of the lung. The Lm was significantly elevated in club cell secretory protein–deficient (CCSP−/−) mice in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The destructive index (DI) was measured by the previously reported methods to evaluate the destruction of the alveolus wall of the lung. The DI in the CCSP−/− mice was significantly elevated in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (C) The lung compliance in the mouse model of chronic P. aeruginosa infection was measured. Pressure–volume (P–V) curves were drawn using the lung physiology data. Lung compliance was then calculated using the slope of the early phase of P–V curve. The lung compliance of CCSP−/− mice was significantly increased in comparison with wild-type mice. Eight CCSP−/− mice and four wild-type mice were used.Abbreviations: Wt, wild-type; Cst, static lung compliance.
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f5-copd-11-2321: Lung morphometry in the mouse model of chronic Pseudomonas aeruginosa infection.Notes: (A) The mean linear intercept (Lm) was measured by previously reported methods to evaluate the emphysematous changes of the lung. The Lm was significantly elevated in club cell secretory protein–deficient (CCSP−/−) mice in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The destructive index (DI) was measured by the previously reported methods to evaluate the destruction of the alveolus wall of the lung. The DI in the CCSP−/− mice was significantly elevated in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (C) The lung compliance in the mouse model of chronic P. aeruginosa infection was measured. Pressure–volume (P–V) curves were drawn using the lung physiology data. Lung compliance was then calculated using the slope of the early phase of P–V curve. The lung compliance of CCSP−/− mice was significantly increased in comparison with wild-type mice. Eight CCSP−/− mice and four wild-type mice were used.Abbreviations: Wt, wild-type; Cst, static lung compliance.

Mentions: The histologic and physiologic findings of the naïve CCSP−/− mice were also similar to those of the naïve wild-type mice (data not shown). The index of bronchial stenosis was investigated. The bronchus of the CCSP−/− mice showed significantly greater stenotic development in comparison to wild-type mice (Figure 4). The Lm was measured by previously reported methods to evaluate the emphysematous changes of the lung. The Lm in the CCSP−/− mice was significantly higher than in the wild-type mice (Figure 5A). The DI was measured by previously reported methods to evaluate the destruction of the alveolus wall of the lung. The DI in the CCSP−/− mice was significantly higher than in the wild-type mice (Figure 5B). P–V curves were drawn using the lung physiology data. The lung compliance was then calculated using the slope of the early phase of the P–V curve. The CCSP−/− mice showed significantly higher lung compliance than the wild-type mice (Figure 5C).


Chronic Pseudomonas aeruginosa infection-induced chronic bronchitis and emphysematous changes in CCSP-deficient mice
Lung morphometry in the mouse model of chronic Pseudomonas aeruginosa infection.Notes: (A) The mean linear intercept (Lm) was measured by previously reported methods to evaluate the emphysematous changes of the lung. The Lm was significantly elevated in club cell secretory protein–deficient (CCSP−/−) mice in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The destructive index (DI) was measured by the previously reported methods to evaluate the destruction of the alveolus wall of the lung. The DI in the CCSP−/− mice was significantly elevated in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (C) The lung compliance in the mouse model of chronic P. aeruginosa infection was measured. Pressure–volume (P–V) curves were drawn using the lung physiology data. Lung compliance was then calculated using the slope of the early phase of P–V curve. The lung compliance of CCSP−/− mice was significantly increased in comparison with wild-type mice. Eight CCSP−/− mice and four wild-type mice were used.Abbreviations: Wt, wild-type; Cst, static lung compliance.
© Copyright Policy
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5036550&req=5

f5-copd-11-2321: Lung morphometry in the mouse model of chronic Pseudomonas aeruginosa infection.Notes: (A) The mean linear intercept (Lm) was measured by previously reported methods to evaluate the emphysematous changes of the lung. The Lm was significantly elevated in club cell secretory protein–deficient (CCSP−/−) mice in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The destructive index (DI) was measured by the previously reported methods to evaluate the destruction of the alveolus wall of the lung. The DI in the CCSP−/− mice was significantly elevated in comparison with wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (C) The lung compliance in the mouse model of chronic P. aeruginosa infection was measured. Pressure–volume (P–V) curves were drawn using the lung physiology data. Lung compliance was then calculated using the slope of the early phase of P–V curve. The lung compliance of CCSP−/− mice was significantly increased in comparison with wild-type mice. Eight CCSP−/− mice and four wild-type mice were used.Abbreviations: Wt, wild-type; Cst, static lung compliance.
Mentions: The histologic and physiologic findings of the naïve CCSP−/− mice were also similar to those of the naïve wild-type mice (data not shown). The index of bronchial stenosis was investigated. The bronchus of the CCSP−/− mice showed significantly greater stenotic development in comparison to wild-type mice (Figure 4). The Lm was measured by previously reported methods to evaluate the emphysematous changes of the lung. The Lm in the CCSP−/− mice was significantly higher than in the wild-type mice (Figure 5A). The DI was measured by previously reported methods to evaluate the destruction of the alveolus wall of the lung. The DI in the CCSP−/− mice was significantly higher than in the wild-type mice (Figure 5B). P–V curves were drawn using the lung physiology data. The lung compliance was then calculated using the slope of the early phase of the P–V curve. The CCSP−/− mice showed significantly higher lung compliance than the wild-type mice (Figure 5C).

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus