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Infection and Immunity, November 2006, p. 6365-6376, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00974-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Discordance in the Effects of Yersinia pestis on the Dendritic Cell Functions Manifested by Induction of Maturation and Paralysis of Migration{triangledown}

Baruch Velan,* Erez Bar-Haim, Ayelet Zauberman, Emanuelle Mamroud, Avigdor Shafferman, and Sara Cohen

Department of Biochemistry and Molecular Genetics, Israel Institute for Biological Research, P.O. Box 19, Ness-Ziona 74100, Israel

Received 18 June 2006/ Returned for modification 31 July 2006/ Accepted 10 August 2006

The encounter between invading microorganisms and dendritic cells (DC) triggers a series of events which include uptake and degradation of the microorganism, induction of a maturation process, and enhancement of DC migration to the draining lymph nodes. Various pathogens have developed strategies to counteract these events as a measure to evade the host defense. In the present study we found that interaction of the Yersinia pestis EV76 strain with DC has no effect on cell viability and is characterized by compliance with effective maturation, which is manifested by surface display of major histocompatibility complex class II, of costimulatory markers, and of the chemokine receptor CCR7. This is in contrast to maturation inhibition and cell death induction exerted by the related species Yersinia enterocolitica WA O:8. Y. pestis interactions with DC were found, however, to impair functions related to cytoskeleton rearrangement. DC pulsed with Y. pestis failed to adhere to solid surfaces and to migrate toward the chemokine CCL19 in an in vitro transmembrane assay. Both effects were dependent on the presence of the pCD1 virulence plasmid and on a bacterial growth shift to 37°C prior to infection. Moreover, while instillation of a pCD1-cured Y. pestis strain into mouse airways triggered effective transport of alveolar DC to the mediastinal lymph node, instillation of Y. pestis harboring the plasmid failed to do so. Taken together, these results suggest that virulence plasmid-dependent impairment of DC migration is the major mechanism utilized by Y. pestis to subvert DC function.


* Corresponding author. Mailing address: Department of Biochemistry and Molecular Genetics, Israel Institute for Biological Research, P.O. Box 19, Ness-Ziona 74100, Israel. Phone: 972-8-9381518. Fax: 972-8-9401404. E-mail: baruch{at}iibr.gov.il.

{triangledown} Published ahead of print on 21 August 2006.

Editor: D. L. Burns


Infection and Immunity, November 2006, p. 6365-6376, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00974-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




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