Epithelial cells infected with Chlamydophila pneumoniae (Chlamydia pneumoniae) are resistant to apoptosis

The obligate intracellular pathogen Chlamydophila pneumoniae (Chlamydia pne umoniae) initiates infections in humans via the mucosal epithelia of the re spiratory tract. Here, we report that epithelial cells infected with C pneu moniae are resistant to apoptosis induced by treatment with drugs or by dea th receptor ligation. The induction of protection from apoptosis depended o n the infection conditions since only cells containing large inclusions wer e protected. The underlying mechanism of infection-induced apoptosis resist ance probably involves mitochondria, the major integrators of apoptotic sig naling. In the infected cells, mitochondria did not respond to apoptotic st imuli by the release of apoptogenic factors required for the activation of caspases. Consequently, active caspase-3 was absent in infected cells. Our data suggest a direct modulation of apoptotic pathways in epithelial cells by C pneumoniae.