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Infection and Immunity, November 2001, p. 7039-7045, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.7039-7045.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Survival of Chlamydia pneumoniae-Infected Mono Mac 6 Cells Is Dependent on NF-kappa B Binding Activity

Christian Wahl,1,* Franz Oswald,2 Ulrike Simnacher,1 Sonja Weiss,1 Reinhard Marre,1 and Andreas Essig1

Department of Medical Microbiology and Hygiene1 and Department of Internal Medicine I,2 University of Ulm, D-89081 Ulm, Germany

Received 29 June 2001/Returned for modification 27 July 2001/Accepted 14 August 2001

The respiratory tract pathogen Chlamydia pneumoniae has been associated with atherosclerosis. Monocytes are supposed to serve as a vehicle for systemic dissemination of intracellular C. pneumoniae from the lung to the artery vessel wall. We were therefore interested in pathogen-induced cellular events associated with NF-kappa B, a crucial transcription factor for both inflammatory cytokines and antiapoptotic molecules. In this study we demonstrate by electrophoretic mobility shift assay that C. pneumoniae infection of the human monocytic cell line Mono Mac 6 induces activation of NF-kappa B over 48 h, with a maximum level at 1 h postinfection. As shown by supershift assay, the activated NF-kappa B complex consists of the subunits RelA (p65) and NF-kappa B1 (p50). Apoptotic host cells were not detected during the early stages of the infection when maximal activation of NF-kappa B was detected. Pretreatment of Mono Mac 6 with the antioxidant and NF-kappa B inhibitor PDTC (pyrrolidine dithiocarbamate) induced activation of caspase-3 and led to apoptotic cell death. The C. pneumoniae-induced activation of the NF-kappa B complex was reduced by PDTC, which in parallel resulted in an increased apoptosis, as quantified by annexin V labeling and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling reaction. In the complete absence of activated NF-kappa B, when Mono Mac 6 cells were pretreated with the more potent NF-kappa B inhibitors MG-132 and parthenolide a C. pneumoniae-mediated rescue of cells from induced apoptosis could not be achieved. Our results indicate that activation of NF-kappa B in C. pneumoniae-infected Mono Mac 6 cells is associated with protection of Mono Mac 6 cells against apoptosis and might thereby contribute to systemic spread of the pathogen.

* Corresponding author. Mailing address: Department of Medical Microbiology and Hygiene, University of Ulm, Robert-Koch Str. 8, D-89081 Ulm, Germany. Phone: 0049-731-50024610 or 0049-731-50024601. Fax: 0049-731-50024619. E-mail: christian.wahl{at}medizin.uni-ulm.de.

Infection and Immunity, November 2001, p. 7039-7045, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.7039-7045.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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