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15 May 2005

Volume 191, Number 10
The Journal of Infectious Diseases 2005;191:1771–1777
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19110-0025$15.00
DOI: 10.1086/429692
MAJOR ARTICLE

Lack of Wall Teichoic Acids in Staphylococcus aureus Leads to Reduced Interactions with Endothelial Cells and to Attenuated Virulence in a Rabbit Model of Endocarditis

Christopher Weidenmaier,1

Andreas Peschel,1

Yan‐Qiong Xiong,3,5

Sascha A. Kristian,4

Klaus Dietz,2

Michael R. Yeaman,3,5 and

Arnold S. Bayer3,5

1Cellular and Molecular Microbiology Division, Medical Microbiology and Hygiene Department, and 2Department of Medical Biometry, University of Tübingen, Tübingen, Germany; 3Geffen School of Medicine at UCLA, University of California at Los Angeles, Los Angeles, 4Department of Pediatrics, Division of Infectious Diseases, University of California at San Diego, La Jolla, and 5Department of Medicine, Division of Infectious Diseases, LA Biomedical Research Institute, St. John’s Cardiovascular Research Center, Harbor‐UCLA Medical Center, Torrance

Wall teichoic acids (WTAs) are major surface components of gram‐positive bacteria that have recently been shown to play a key role in nasal colonization by Staphylococcus aureus. In the present study, we assessed the impact that WTAs have on endovascular infections by using a WTA‐deficient S. aureus mutant (ΔtagO). There were no significant differences detected between the isogenic parental strain (SA113) and the ΔtagO mutant in polymorphonuclear leukocyte–mediated opsonophagocytosis; killing by a prototypic platelet microbicidal protein; or binding to platelets, fibronectin, or fibrinogen. However, compared with the parental strain, the ΔtagO mutant adhered considerably less well to human endothelial cells, especially under flow conditions (70.3% reduction; ). Beads coated with WTA bound to endothelium in a dose‐dependent manner, suggesting that WTA contributes specifically to this interaction. These in vitro data closely paralleled those from a rabbit model of infective endocarditis in which the ΔtagO mutant was compared with the parental strain. Clearances of staphylococcus from the bloodstream were equivalent, but the ΔtagO mutant showed a significantly reduced capacity to both colonize sterile cardiac vegetations ( ) and proliferate within these vegetations, the kidneys, and the spleen ( ). We conclude that WTA is an important factor in the induction and progression of endovascular S. aureus infection, likely through a specific interaction with endothelial cells.

Received 15 June 2004; accepted 17 December 2004; electronically published 11 April 2005.

Reprints or correspondence: Dr. Andreas Peschel, Cellular and Molecular Microbiology Div., Medical Microbiology and Hygiene Dept., University of Tübingen, 72076 Tübingen, Germany ().

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  • Presented in part: Status seminar of Priority Program SPP1130 of the German Research Council, Dresden, Germany, 9–11 September 2003.

    Financial support: German Research Council (grants SPP1130 and FOR 449/T2 to A.P.); National Institutes of Health (grant AI‐39108 to A.S.B. and grants AI‐48031 and RR‐13004 to M.R.Y.); American Heart Association (Western Affiliate) (grant 0265054Y to Y.‐Q.X.).

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