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Infection and Immunity, November 2006, p. 6057-6066, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00760-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Characterization of Host Cell Death Induced by Chlamydia trachomatis ^,

Songmin Ying,¹ Silke F. Fischer,^1, Matthew Pettengill,² Debye Conte,² Stefan A. Paschen,¹ David M. Ojcius,² and Georg Häcker^1*

Institute for Medical Microbiology, Immunology and Hygiene, Technical University Munich, Munich, Germany,¹ School of Natural Sciences, University of California, Merced, California²

Received 12 May 2006/ Returned for modification 21 June 2006/ Accepted 8 August 2006

Chlamydia are obligate intracellular bacteria that modulate apoptosis of the host cell. Strikingly, chlamydial infection has been reported both to inhibit and to induce apoptosis. Although the ability to inhibit apoptosis has been corroborated by the identification of cellular targets, confirmation of cell death induction has been complicated by a mixture of apoptotic features and atypical cell death during infection, as well as by differences in the experimental techniques used to measure cell death. Here we use a panel of well-established approaches in the study of apoptosis to define the form of cell death induced by Chlamydia trachomatis infection. Infected cells displayed apoptotic features such as nuclear condensation and fragmentation, as well as positive TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) staining. Fragmentation of genomic DNA occurred, but was atypical. Clear evidence against the activation of effector caspases was found. Nuclear changes were measured in fibroblasts lacking one or both of the effectors of mitochondrial apoptosis, Bax and Bak. A slight reduction in nuclear changes was observed in Bax-deficient cells and in Bax/Bak double-deficient cells. Most surprisingly, this reduction was almost complete in Bak-deficient cells. Finally, dying infected cells were efficiently taken up by professional phagocytes, suggesting that Chlamydia-induced host-cell death could play a role in the immune response. In conclusion, chlamydial infection can induce cell death. Although Chlamydia-induced cell death has certain morphological features of apoptosis, it does not result from activation of the apoptotic pathway.

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* Corresponding author. Mailing address: Institute for Medical Microbiology, Trogerstr. 30, D-81675 Munich, Germany. Phone: 49 89 4140 4134. Fax: 49 89 4140 4868. E-mail: hacker{at}lrz.tum.de.

Published ahead of print on 28 August 2006.

Supplemental material for this article may be found at http://iai.asm.org/.

Editor: D. L. Burns

Present address: The Walter and Eliza Hall Institute for Medical Research, Melbourne, Australia.

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Infection and Immunity, November 2006, p. 6057-6066, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00760-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

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• Paschen, S. A., Christian, J. G., Vier, J., Schmidt, F., Walch, A., Ojcius, D. M., Hacker, G. (2008). Cytopathicity of Chlamydia is largely reproduced by expression of a single chlamydial protease. JCB 182: 117-127 [Abstract] [Full Text]