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This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: jimmunol.0900937v1 183/4/2697    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Zenk, S. F. Articles by Hensel, M. PubMed PubMed Citation Articles by Zenk, S. F. Articles by Hensel, M.

Role of Salmonella enterica Lipopolysaccharide in Activation of Dendritic Cell Functions and Bacterial Containment¹

Sebastian F. Zenk^*, Jonathan Jantsch and Michael Hensel^2,*

^* Infektionsbiologische Abteilung and Mikrobiologisches Institut, Universitätsklinikum Erlangen, Erlangen, Germany

In contrast to nonpathogenic bacteria, the Gram-negative pathogen Salmonella enterica is not eradicated, but persists in murine dendritic cells (DC). The molecular basis of this phenotype is unknown. We set out to characterize bacterial and DC functions that are involved in Salmonella persistence. Our data prove that neither bacterial nor host cell de novo protein biosynthesis is required for Salmonella persistence in DC. We identified the Salmonella O-Ag of the LPS of Salmonella as an important factor for controlling the intracellular fate of Salmonella in DC. A Salmonella strain with entirely absent O-Ag showed an increased rate of uptake by DC, altered intracellular processing, and increased degradation, and also boosted the activation of immune functions of DC. These novel findings demonstrate that in addition to the multiple functions of the bacterial LPS in adaptation to the intestinal environment and protection against innate immune function, this molecule also has an important role in interaction of Salmonella with DC.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grant HE1964/8-3 of the Deutsche Forschungsgemeinschaft (to M.H.) and by the Interdisciplinary Center for Clinical Research at the University Hospital of the University of Erlangen-Nuremberg (to J.J. and M.H.). The support of S.F.Z. by a fellowship of the Universität Bayern as per BayEFG is gratefully acknowledged.

² Address correspondence and reprint requests to Dr. Michael Hensel, Infektionsbiologische Abteilung, Universitätsklinikum Erlangen, Wasserturmstr. 3-5, D-91054 Erlangen. E-mail address: Michael.Hensel{at}uk-erlangen.de

³ Abbreviations used in this paper: DC, dendritic cell; BM, bone marrow; LB, Luria-Bertani; MOI, multiplicity of infection; SP, spacious phagosome; SPI2, Salmonella pathogenicity island 2; T3SS, type III secretion system; WT, wild type.

⁴ The online version of this article contains supplemental material.