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Infection and Immunity, October 2003, p. 5814-5822, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5814-5822.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Chlamydia pneumoniae Activates Epithelial Cell Proliferation via NF-B and the Glucocorticoid Receptor

Department of Research, Pulmonary Cell Research, University Hospital Basel, Switzerland,¹ Heart and Lung Transplant Unit, St. Vincent's Hospital,² The Woolcock Institute for Medical Research, University of Sydney, Sydney, Australia³

Received 24 January 2003/ Returned for modification 2 April 2003/ Accepted 17 June 2003

Chlamydia pneumoniae is an obligate intracellular eubacterium and a common cause of acute and chronic respiratory tract infections. This study was designed to show the effect of C. pneumoniae on transcription factor activation in epithelial cells. The activation of transcription factors by C. pneumoniae was determined in human epithelial cell lines (HL and Calu3) by electrophoretic DNA mobility shift assay, Western blotting, and luciferase reporter gene assay. The activation of transcription factors was further confirmed by immunostaining of C. pneumoniae-infected HL cells and mock-infected controls. The effect of transcription factors on C. pneumoniae-induced host cell proliferation was assessed by [³H]thymidine incorporation and direct cell counting in the presence and absence of antisense oligonucleotides targeting transcription factors or the glucocorticoid receptor (GR) antagonist RU486. The activation of the GR, CCAAT-enhancer binding protein (C/EBP), and NF-B was induced within 1 to 6 h by C. pneumoniae. While the interleukin-6 promoter was not activated by C. pneumoniae, the GR-driven p21^(Waf1/Cip1) promoter was increased 2.5- to 3-fold over controls 24 h after infection. C. pneumoniae dose-dependently increased the DNA synthesis of the host cells 2.5- to 2.9-fold, which was partly inhibited either by RU486 or by NF-B antisense oligonucleotides. Furthermore, we provide evidence that heat-inactivated C. pneumoniae does not cause a significant increase in cell proliferation. Our results demonstrate that C. pneumoniae activates C/EBP-ß, NF-B, and the GR in infected cells. However, only NF-B and the GR were involved in C. pneumoniae-induced proliferation of epithelial cells.

Editor: J. N. Weiser

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