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Infection and Immunity, December 2000, p. 6704-6711, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Infection of Human Monocyte-Derived Macrophages with Chlamydia trachomatis Induces Apoptosis of T Cells: a Potential Mechanism for Persistent Infection

Michael C. Jendro,1,* Tobias Deutsch,1 Britta Körber,1 Lars Köhler,1 Jens G. Kuipers,1 Birgit Krausse-Opatz,1 Jürgen Westermann,2 Elke Raum,3 and Henning Zeidler1

Departments of Rheumatology,1 Anatomy,2 and Epidemiology, Social Medicine, and Health System Research,3 Medical School Hannover, Hannover, Germany

Received 18 January 2000/Returned for modification 29 February 2000/Accepted 8 September 2000

Viruses can escape T-cell surveillance by infecting macrophages and thereby induce apoptosis of noninfected T cells. This ability had not been demonstrated for bacteria. We investigated whether infection of macrophages with the important human pathogen Chlamydia trachomatis can induce T-cell apoptosis. Because Chlamydia-Mycoplasma coinfection is a frequent event, the ability of Mycoplasma fermentans-infected macrophages to induce T-cell apoptosis was also studied. Infected macrophages were cocultivated with autologous T cells in different activation states. Propidium iodide-based fluorescence-activated cell sorter analysis demonstrated that macrophages infected with viable chlamydiae induced T-cell death. Apoptosis was identified as the mode of death induction by using a terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling assay. Induction of T-cell death was macrophage dependent. Incubation of T cells with infectious chlamydiae in the absence of macrophages did not lead to T-cell apoptosis. UV irradiation of chlamydiae diminished the ability to induce death. T-cell death was induced by a cell-free supernatant of infected macrophages. Not only phytohemagglutinin-preactivated T cells but also non-mitogen-preactivated T cells were susceptible to C. trachomatis-induced apoptosis. In contrast, M. fermentans infection of macrophages did not induce T-cell death. Coinfection had no additional effect. In summary, intracellular chlamydial infection of macrophages can induce T-cell apoptosis. Apoptosis induction by chlamydiae possibly explains how persistently infected macrophages escape T-cell surveillance and why the Chlamydia-specific T-cell response is diminished during persistent chlamydial infection.


* Corresponding author. Mailing address: Department of Rheumatology, Medical School Hannover, Carl-Neuberg-Str. 1, 30625 Hannover, Germany. Phone: (49) 511-532-2190. Fax: (49) 511-532-5841. E-mail: Jendro.Michael{at}Mh-Hannover.de.


Infection and Immunity, December 2000, p. 6704-6711, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.



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