Lack of Wall Teichoic Acids inStaphylococcus aureusLeads to Reduced Interactions with Endothelial Cells and to Attenuated Virulence in a Rabbit Model of Endocarditis

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Abstract
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; P<.05). 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 (P<.05) and proliferate within these vegetations, the kidneys, and the spleen (P<.001). 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

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