Limits...
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 histology of chronic Pseudomonas aeruginosa infection.Notes: (A) The macroscopic findings and histology, (a) wild-type (Wt) mice with P. aerugionosa infection, (b) club cell secretory protein deficiency (CCSP−/−) with P. aerugionosa infection, (c) naïve CCSP−/− mice. Inflammatory cell infiltrates were observed in the lung, mainly around the bronchus and slightly around the alveoli. The bronchus of the CCSP−/− mice (b) showed more severe inflammation and greater stenotic development than wild-type mice (a) in response to P. aeruginosa infection. Lung histology of naïve CCSP−/− mice showed similar findings to wild-type mice (c); hematoxylin and eosin (H&E) staining, original magnification: 100×. (B) The bronchus in CCSP−/− mice with P. aeruginosa infection was subjected to H&E staining (a), alcian blue staining (b), and Sirius red staining (c). Although bronchial stenosis and inflammation were apparent, neither mucus deposition nor fibrosis was observed in the bronchus (original magnification: 200×).
© Copyright Policy
Related In: Results  -  Collection

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

f2-copd-11-2321: Lung histology of chronic Pseudomonas aeruginosa infection.Notes: (A) The macroscopic findings and histology, (a) wild-type (Wt) mice with P. aerugionosa infection, (b) club cell secretory protein deficiency (CCSP−/−) with P. aerugionosa infection, (c) naïve CCSP−/− mice. Inflammatory cell infiltrates were observed in the lung, mainly around the bronchus and slightly around the alveoli. The bronchus of the CCSP−/− mice (b) showed more severe inflammation and greater stenotic development than wild-type mice (a) in response to P. aeruginosa infection. Lung histology of naïve CCSP−/− mice showed similar findings to wild-type mice (c); hematoxylin and eosin (H&E) staining, original magnification: 100×. (B) The bronchus in CCSP−/− mice with P. aeruginosa infection was subjected to H&E staining (a), alcian blue staining (b), and Sirius red staining (c). Although bronchial stenosis and inflammation were apparent, neither mucus deposition nor fibrosis was observed in the bronchus (original magnification: 200×).

Mentions: The numbers of P. aeruginosa colony forming units (CFU) in the BAL fluids at 1 and 4 weeks after intranasal administration were 11×104 CFU/mL and 6×104 CFU/mL, respectively. P. aeruginosa was continuously detected in BAL fluids during the 4 weeks (Figure 1B). Inflammatory cell infiltrates were observed in the lung, mainly around the bronchus and small numbers were observed around the alveoli (Figure 2A). Most of the mice in the experiment survived until sacrifice. These results indicated that a consistent chronic respiratory infection model of P. aeruginosa had been established.


Chronic Pseudomonas aeruginosa infection-induced chronic bronchitis and emphysematous changes in CCSP-deficient mice
Lung histology of chronic Pseudomonas aeruginosa infection.Notes: (A) The macroscopic findings and histology, (a) wild-type (Wt) mice with P. aerugionosa infection, (b) club cell secretory protein deficiency (CCSP−/−) with P. aerugionosa infection, (c) naïve CCSP−/− mice. Inflammatory cell infiltrates were observed in the lung, mainly around the bronchus and slightly around the alveoli. The bronchus of the CCSP−/− mice (b) showed more severe inflammation and greater stenotic development than wild-type mice (a) in response to P. aeruginosa infection. Lung histology of naïve CCSP−/− mice showed similar findings to wild-type mice (c); hematoxylin and eosin (H&E) staining, original magnification: 100×. (B) The bronchus in CCSP−/− mice with P. aeruginosa infection was subjected to H&E staining (a), alcian blue staining (b), and Sirius red staining (c). Although bronchial stenosis and inflammation were apparent, neither mucus deposition nor fibrosis was observed in the bronchus (original magnification: 200×).
© Copyright Policy
Related In: Results  -  Collection

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

f2-copd-11-2321: Lung histology of chronic Pseudomonas aeruginosa infection.Notes: (A) The macroscopic findings and histology, (a) wild-type (Wt) mice with P. aerugionosa infection, (b) club cell secretory protein deficiency (CCSP−/−) with P. aerugionosa infection, (c) naïve CCSP−/− mice. Inflammatory cell infiltrates were observed in the lung, mainly around the bronchus and slightly around the alveoli. The bronchus of the CCSP−/− mice (b) showed more severe inflammation and greater stenotic development than wild-type mice (a) in response to P. aeruginosa infection. Lung histology of naïve CCSP−/− mice showed similar findings to wild-type mice (c); hematoxylin and eosin (H&E) staining, original magnification: 100×. (B) The bronchus in CCSP−/− mice with P. aeruginosa infection was subjected to H&E staining (a), alcian blue staining (b), and Sirius red staining (c). Although bronchial stenosis and inflammation were apparent, neither mucus deposition nor fibrosis was observed in the bronchus (original magnification: 200×).
Mentions: The numbers of P. aeruginosa colony forming units (CFU) in the BAL fluids at 1 and 4 weeks after intranasal administration were 11×104 CFU/mL and 6×104 CFU/mL, respectively. P. aeruginosa was continuously detected in BAL fluids during the 4 weeks (Figure 1B). Inflammatory cell infiltrates were observed in the lung, mainly around the bronchus and small numbers were observed around the alveoli (Figure 2A). Most of the mice in the experiment survived until sacrifice. These results indicated that a consistent chronic respiratory infection model of P. aeruginosa had been established.

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