Epithelial cells infected with Chlamydophila pneumoniae (Chlamydia pneumoniae) are resistant to apoptosis.
The obligate intracellular pathogen Chlamydophila pneumoniae (Chlamydia pneumoniae) initiates infections in humans via the mucosal epithelia of the respiratory tract. Here, we report that epithelial cells infected with C. pneumoniae are resistant to apoptosis induced by treatment with drugs or by death receptor ligation. The induction of protection from apoptosis depended on the infection conditions since only cells containing large inclusions were protected. The underlying mechanism of infection-induced apoptosis resistance probably involves mitochondria, the major integrators of apoptotic signaling. In the infected cells, mitochondria did not respond to apoptotic stimuli 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.
Rajalingam
K
K
Department of Molecular Biology, Max Planck Institute for Infection Biology, D-10117 Berlin, Germany.
Al-Younes
H
H
Müller
A
A
Meyer
T F
TF
Szczepek
A J
AJ
Rudel
T
T
D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D016993:Chlamydophila pneumoniae / Q000254:growth & development*; D003574:Cytochrome c Group / Q000378:metabolism; D004789:Enzyme Activation; D004847:Epithelial Cells / Q000382:microbiology*; D006801:Humans; D008928:Mitochondria / Q000187:drug effects; D019311:Staurosporine / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D003574:Cytochrome c Group; D014409:Tumor Necrosis Factor-alpha; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases; D019311:Staurosporine