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Infection and Immunity, June 2007, p. 2853-2863, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01045-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Host Cell Responses to Chlamydia pneumoniae in Gamma Interferon-Induced Persistence Overlap Those of Productive Infection and Are Linked to Genes Involved in Apoptosis, Cell Cycle, and Metabolism ^,

Meike Eickhoff,^1, Jessica Thalmann,^2, Simone Hess,³ Myriam Martin,² Thomas Laue,¹ Joachim Kruppa,⁴ Gudrun Brandes,⁵ and Andreas Klos^2*

Department of Research and Development, QIAGEN Hamburg GmbH, Koenigstrasse 4a, 22767 Hamburg, Germany,¹ Department of Medical Microbiology, Medical School Hannover, 30625 Hannover, Germany,² Department of Molecular Biology, Max Planck Institute for Infection Biology, 10117 Berlin, Germany,³ Center of Experimental Medicine, Institute of Molecular Cell Biology, University Hospital of Hamburg-Eppendorf, Martinistraße 52, 20246 Hamburg, Germany,⁴ Department of Cell Biology, Center of Anatomy, Medical School Hannover, 30625 Hannover, Germany⁵

Received 4 July 2006/ Returned for modification 22 August 2006/ Accepted 27 February 2007

The respiratory pathogen Chlamydia (Chlamydophila) pneumoniae is associated with chronic diseases, including atherosclerosis and giant-cell arteritis, which are accompanied by the occurrence of these obligate intracellular bacteria in blood vessels. There, C. pneumoniae seems to be present in a persistent state. Persistence is characterized by modified bacterial metabolism and morphology, as well as a reversible arrest of chlamydial development. In cell culture, this persistent state can be induced by gamma interferon (IFN-). To elucidate this long-term interaction between chlamydiae and their host cells, microarray screening on epithelial HeLa cells was performed. Transcription of persistently (and productively) infected cells was compared with that of mock-infected cells. Sixty-six host cell genes were regulated at 24 h and/or 96 h of IFN--induced persistence. Subsequently, a set of 17 human host cell genes related to apoptosis, cell cycle, or metabolism was identified as permanently up- or down-regulated by real-time PCR. Some of these chlamydia-dependent host cell responses were diminished or even absent in the presence of rifampin. However, other expression patterns were not altered by the inhibition of bacterial RNA polymerase, suggesting two different modes of host cell activation. Thus, in the IFN- model, the persisting bacteria cause long-lasting changes in the expression of genes coding for functionally important proteins. They might be potential drug targets for the treatment of persistent C. pneumoniae infections.

Published ahead of print on 12 March 2007.

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

Editor: J. B. Bliska

M.E. and J.T. contributed equally to this study.

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