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Infection and Immunity, December 2004, p. 7045-7054, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.7045-7054.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Yersinia enterocolitica Induces Apoptosis and Inhibits Surface Molecule Expression and Cytokine Production in Murine Dendritic Cells

Stella E. Erfurth,1 Sabine Gröbner,1 Uwe Kramer,1 Dani S. J. Gunst,1 Irena Soldanova,1 Martin Schaller,2 Ingo B. Autenrieth,1 and Stefan Borgmann1*

Institute of Medical Microbiology and Hygiene,1 Department of Dermatology, University of Tübingen, Tübingen, Germany2

Received 28 May 2004/ Returned for modification 6 July 2004/ Accepted 20 August 2004

Yersinia enterocolitica evades innate immunity by expression of a variety of pathogenicity factors. Therefore, adaptive immunity including CD4+ T cells plays an important role in defense against Y. enterocolitica. We investigated whether Y. enterocolitica might target dendritic cells (DC) involved in adaptive T-cell responses. For this purpose, murine DC were infected with Y. enterocolitica wild-type and mutant strains prior to incubation with ovalbumin (OVA) as antigen and 5-(6)-carboxyfluorescein diacetate N-succinimidyl ester-labeled OVA-specific T cells from DO11.10 mice. While T-cell proliferation was partially affected by infection of DC with plasmid-cured and YopP-deficient Yersinia mutant strains, no T-cell proliferation occurred after infection of DC with wild-type Y. enterocolitica. Infection of DC with Y. enterocolitica wild type resulted in decreased up-regulation of major histocompatibility complex class II, CD54 (intercellular adhesion molecule 1), CD 80, and CD86 expression. Experiments with plasmid-cured Y. enterocolitica or a YopP-deficient mutant strain revealed that YopP accounts for inhibition of surface molecule expression. Wild-type Y. enterocolitica suppressed the release of KC, tumor necrosis factor alpha, interleukin-10 (IL-10), and IL-12 by DC, while infection of DC with plasmid-cured Y. enterocolitica or with the YopP-deficient mutant resulted in the production of these cytokines. Moreover, infection with wild-type Y. enterocolitica induced apoptosis in DC mediated by YopP. Apoptosis occurred despite translocation of NF-{kappa}B to the nucleus, as demonstrated by electromobility shift assays. Together, these data demonstrate that Y. enterocolitica targets functions of murine DC that are required for T-cell activation. This might contribute to evasion of adaptive immune responses by Y. enterocolitica.

* Corresponding author. Mailing address: Dept. of Medical Microbiology and Hygiene, University of Tübingen, Elfriede-Aulhorn-Str. 6, D-72076 Tübingen, Germany. Phone: 49 7071 29 82072. Fax: 49 7071 29 3435. E-mail: stefan.borgmann{at}med.uni-tuebingen.de.

Editor: J. B. Bliska

Infection and Immunity, December 2004, p. 7045-7054, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.7045-7054.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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