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Originally published In Press as doi:10.1074/jbc.C700181200 on October 1, 2007

J. Biol. Chem., Vol. 282, Issue 47, 33897-33901, November 23, 2007
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Injection of Flagellin into the Host Cell Cytosol by Salmonella enterica Serotype Typhimurium*

Yao-Hui Sun, Hortensia García Rolán, and Renée M. Tsolis1

From the Department of Medical Microbiology and Immunology, University of California at Davis, Davis, California, 95616

Bacterial flagellins are potent inducers of innate immunity. Three signaling pathways have been implicated in the sensing of flagellins; these involve toll-like receptor 5 (TLR5) and the cytosolic proteins Birc1e/Naip5 and Ipaf. Although the structural basis of TLR5-flagellin interaction is known, little is known about how flagellin enters the host cell cytosol to induce signaling via Birc1e/Naip5 and Ipaf. Here we demonstrate for the first time the translocation of bacterial flagellin into the cytosol of host macrophages by the vacuolar pathogen, Salmonella enterica serotype Typhimurium. Translocation of flagellin into the host cell cytosol was directly demonstrated using beta-lactamase reporter constructs. Flagellin translocation required the Salmonella Pathogenicity Island 1 Type III secretion system (SPI-1 T3SS) but not the flagellar T3SS.


Received for publication, September 13, 2007

* This work was supported by U.S. Public Health Service Grants AI50553 and AI065739. 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 To whom correspondence should be addressed: Dept. of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave., Davis, CA 95616. Fax: 530-754-7240; E-mail: rmtsolis{at}ucdavis.edu.


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