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Infect. Immun. doi:10.1128/IAI.00974-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Discordance in the Effects of Yersinia pestis on Dendritic Cell Functions: Induction of Maturation and Paralysis of Migration

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

^* To whom correspondence should be addressed. Email: baruch{at}iibr.gov.il,

	Abstract

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, as well as enhancement of DC migration to the draining lymph nodes. Various pathogens have developed strategies to counteract these events as a measure to evade 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 MHC class II, of co-stimulatory 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 was 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 presence of the pCD1 virulence plasmid, and on bacterial growth shift to 37°C, prior to infection. Moreover, while instillation of a pCD1-cured Y. pestis strain into mice 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.

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