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Infection and Immunity, November 2001, p. 7121-7129, Vol. 69, No. 11
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.11.7121-7129.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Characterization of Antiapoptotic Activities of
Chlamydia pneumoniae in Human Cells
Silke F.
Fischer,
Claudia
Schwarz,
Juliane
Vier, and
Georg
Häcker*
Institute for Medical Microbiology,
Technische Universität München, D-81675 Munich,
Germany
Received 23 May 2001/Returned for modification 17 July
2001/Accepted 3 August 2001
Chlamydia pneumoniae is an obligate intracellular
bacterium which frequently causes airway infection in humans and has
been implicated in atherosclerosis. Here we show that infection with C. pneumoniae protects HeLa human epithelioid cells
against apoptosis induced by external stimuli. In infected HeLa cells,
apoptosis induced by staurosporine and CD95-death-receptor signaling
was strongly reduced. Upon treatment with staurosporine, generation of
effector caspase activity, processing of caspase-3 and caspase-9 and
cytochrome c redistribution were all profoundly
inhibited in cells infected with C. pneumoniae.
Bacterial protein synthesis during early infection was required for
this inhibition. Furthermore, cytochrome c-induced
processing and activation of caspases were inhibited in cytosolic
extracts from infected cells, suggesting that a C.
pneumoniae-dependent antiapoptotic factor was generated in the
cytosol upon infection. Infection with C. pneumoniae
failed to induce significant NF-
B activation in HeLa cells,
indicating that no NF-
B-dependent cellular factors were involved in
the protection against apoptosis. These results show that C.
pneumoniae is capable of interfering with the host cell's
apoptotic apparatus at probably at least two steps in signal
transduction and might explain the propensity of these bacteria to
cause chronic infections in humans.
*
Corresponding author. Mailing address: Georg
Häcker, Institute for Medical Microbiology, Technische
Universität München, Trogerstr. 9, D-81675 Munich, Germany.
Phone: 49 89 4140 4121. Fax: 49 89 4140 4868. E-mail:
hacker{at}lrz.tum.de.
Infection and Immunity, November 2001, p. 7121-7129, Vol. 69, No. 11
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.11.7121-7129.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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