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Infection and Immunity, December 2001, p. 7880-7888, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7880-7888.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Epithelial Cells Infected with Chlamydophila pneumoniae (Chlamydia pneumoniae) Are Resistant to Apoptosis

Krishnaraj Rajalingam, Hesham Al-Younes, Anne Müller, Thomas F. Meyer,* Agnes J. Szczepek, and Thomas Rudel

Department of Molecular Biology, Max Planck Institute for Infection Biology, D-10117 Berlin, Germany

Received 27 February 2001/Returned for modification 5 April 2001/Accepted 19 July 2001

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.

* Corresponding author. Mailing address: Max Planck Institute for Infection Biology, Department of Molecular Biology, Schumannstr. 21/22, D-10117 Berlin, Germany. Phone: 49 30 284 60 402. Fax: 49 30 284 60 401. E-mail: meyer{at}mpiib-berlin.mpg.de.

Infection and Immunity, December 2001, p. 7880-7888, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7880-7888.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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