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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

The BAL fluids of chronic Pseudomonas aeruginosa infection.Notes: (A) Cell counts in the BAL fluids, the neutrophils in the BAL fluids of the club cell secretory protein-deficient (CCSP−/−) mice were significantly increased in comparison to wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The cytokine profile in BAL fluids, cytokines in the BAL fluids were measured by the cytokine ELISA kit. The augmentation of the inflammatory cytokine, KC, was observed in CCSP−/− mice. However, it was not significant in IFN-γ and TNF-α. Seven CCSP−/− mice and four wild-type mice were used.Abbreviations: BAL, bronchoalveolar lavage; Wt, wild-type; ns, no significant difference; ELISA, enzyme-linked immunosorbent assay; KC, keratinocyte-derived chemokine; IFN, interferon; TNF, tumor necrosis factor.
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f3-copd-11-2321: The BAL fluids of chronic Pseudomonas aeruginosa infection.Notes: (A) Cell counts in the BAL fluids, the neutrophils in the BAL fluids of the club cell secretory protein-deficient (CCSP−/−) mice were significantly increased in comparison to wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The cytokine profile in BAL fluids, cytokines in the BAL fluids were measured by the cytokine ELISA kit. The augmentation of the inflammatory cytokine, KC, was observed in CCSP−/− mice. However, it was not significant in IFN-γ and TNF-α. Seven CCSP−/− mice and four wild-type mice were used.Abbreviations: BAL, bronchoalveolar lavage; Wt, wild-type; ns, no significant difference; ELISA, enzyme-linked immunosorbent assay; KC, keratinocyte-derived chemokine; IFN, interferon; TNF, tumor necrosis factor.

Mentions: The cell counts in the BAL fluids were also investigated. The number of neutrophils, but not the macrophages or lymphocytes, was significantly increased in the BAL fluids of the CCSP−/− mice in comparison to the wild-type mice (Figure 3A). Cytokines in the BAL fluids were measured by the cytokine ELISA kit. The augmentation of the inflammatory cytokine, KC, was observed; however, it was not significant in IFN-γ and TNF-α (Figure 3B).


Chronic Pseudomonas aeruginosa infection-induced chronic bronchitis and emphysematous changes in CCSP-deficient mice
The BAL fluids of chronic Pseudomonas aeruginosa infection.Notes: (A) Cell counts in the BAL fluids, the neutrophils in the BAL fluids of the club cell secretory protein-deficient (CCSP−/−) mice were significantly increased in comparison to wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The cytokine profile in BAL fluids, cytokines in the BAL fluids were measured by the cytokine ELISA kit. The augmentation of the inflammatory cytokine, KC, was observed in CCSP−/− mice. However, it was not significant in IFN-γ and TNF-α. Seven CCSP−/− mice and four wild-type mice were used.Abbreviations: BAL, bronchoalveolar lavage; Wt, wild-type; ns, no significant difference; ELISA, enzyme-linked immunosorbent assay; KC, keratinocyte-derived chemokine; IFN, interferon; TNF, tumor necrosis factor.
© Copyright Policy
Related In: Results  -  Collection

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

f3-copd-11-2321: The BAL fluids of chronic Pseudomonas aeruginosa infection.Notes: (A) Cell counts in the BAL fluids, the neutrophils in the BAL fluids of the club cell secretory protein-deficient (CCSP−/−) mice were significantly increased in comparison to wild-type mice. Seven CCSP−/− mice and four wild-type mice were used. (B) The cytokine profile in BAL fluids, cytokines in the BAL fluids were measured by the cytokine ELISA kit. The augmentation of the inflammatory cytokine, KC, was observed in CCSP−/− mice. However, it was not significant in IFN-γ and TNF-α. Seven CCSP−/− mice and four wild-type mice were used.Abbreviations: BAL, bronchoalveolar lavage; Wt, wild-type; ns, no significant difference; ELISA, enzyme-linked immunosorbent assay; KC, keratinocyte-derived chemokine; IFN, interferon; TNF, tumor necrosis factor.
Mentions: The cell counts in the BAL fluids were also investigated. The number of neutrophils, but not the macrophages or lymphocytes, was significantly increased in the BAL fluids of the CCSP−/− mice in comparison to the wild-type mice (Figure 3A). Cytokines in the BAL fluids were measured by the cytokine ELISA kit. The augmentation of the inflammatory cytokine, KC, was observed; however, it was not significant in IFN-γ and TNF-α (Figure 3B).

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