Methods: P. aeruginosa PAO1 strain and CCSP-deficient mice background 129 was used in this study. A tube of 1cm in length soaked in the fluid containing P. aeruginosa (PAO01) at the 1x106 cfu/ml for one week was inserted into trachea. One week later, 5x106 cfu/head of P. aeruginosa was administered into trachea. Five week later, mice were sacrificed. Bacterial growths in lungs and bronchiolo-alveolar lavage (BAL) fluid were collected. Cell count in BAL fluids and histology of the lungs were tested. Also physiology of the lungs (pressure-volume curve) was investigated.
Results: P. aeruginosa was continuously detected in BAL fluids during 5 weeks. Inflammatory cells infiltrates around bronchioles, but not alveoli, were observed. Neutrophils in BAL fluids from the CCSP-deficient mice were increased in comparison with that from wild-type mice. Histologic study demonstrated that chronic inflammation developed more serious obstruction of bronchioles and alveolar enlargement in the CCSP-deficient mice without fibrosis. Lung physiology study demonstrated that lung compliance was elevated in the CCSP-deficient mice.
Conclusion: These results indicated that chronic respiratory infection of P. aeruginosa resulted in chronic obstructive pulmonary disease (COPD)-like pathological condition in CCSP-deficient mice.
R. Hirano, None
J. Uchino, None
K. Watanabe, None