| Summary: | <p>Abstract</p> <p>Background</p> <p>It has been reported that <it>Chlamydophila (C.) pneumoniae </it>is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of <it>C. pneumoniae </it>on airway function has never been investigated.</p> <p>Methods</p> <p>In this study, mice were inoculated intranasally with <it>C. pneumoniae </it>(strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21.</p> <p>Results</p> <p>We found that from day 7, <it>C. pneumoniae </it>infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness.</p> <p>Conclusion</p> <p>Our study demonstrates for the first time that <it>C. pneumoniae </it>infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD.</p>
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