Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 191, Issue 10, Pages 1771-1777Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/429692
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- NCRR NIH HHS [RR-13304] Funding Source: Medline
- NIAID NIH HHS [AI-39108] Funding Source: Medline
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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 (Delta tagO). There were no significant differences detected between the isogenic parental strain (SA113) and the Delta tagO 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 Delta tagO 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 DtagO mutant was compared with the parental strain. Clearances of staphylococcus from the bloodstream were equivalent, but the DtagO 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 < .0001). 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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