2013
DOI: 10.1161/circulationaha.113.002008
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Ultralarge von Willebrand Factor Fibers Mediate Luminal Staphylococcus aureus Adhesion to an Intact Endothelial Cell Layer Under Shear Stress

Abstract: 50S taphylococcus aureus is a major pathogen responsible for various infections in humans and is the most frequent cause of infective endocarditis in industrialized countries. 1 Prerequisite for the pathogenesis of infective endocarditis is infection of the endocardium.2 Therefore, one of the first and essential steps is bacterial adhesion to the endothelium. In contrast to other pathogens causing infective endocarditis, S. aureus appears to be able to bind not only to damaged but also to intact endothelium. [… Show more

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Cited by 78 publications
(96 citation statements)
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“…It is tempting to speculate that this mechanism could be relevant for other pathophysiological conditions, such as autoinflammatory diseases and sepsis, known to support the formation of ULVWF fibers and attenuate ADAMTS13 activity. 31,33,[62][63][64] Thus, our data provide essential information delineating thrombotic mechanisms and highlight EC activation or microthrombi formation as new therapeutic targets in cancer treatment ( Figure 7H). …”
Section: Discussionmentioning
confidence: 81%
“…It is tempting to speculate that this mechanism could be relevant for other pathophysiological conditions, such as autoinflammatory diseases and sepsis, known to support the formation of ULVWF fibers and attenuate ADAMTS13 activity. 31,33,[62][63][64] Thus, our data provide essential information delineating thrombotic mechanisms and highlight EC activation or microthrombi formation as new therapeutic targets in cancer treatment ( Figure 7H). …”
Section: Discussionmentioning
confidence: 81%
“…These findings have been demonstrated in studies involving the knockout of genes encoding these proteins in S. aureus as well as experiments where the expression of these proteins in the normally nonpathogenic bacterium Lactococcus lactis results in the ability to cause IE (161,162). More recent studies have determined the importance of host-derived ultralarge von Willebrand factor fibers in mediating adhesion (probably via cell wall teichoic acids) of S. aureus to intact endothelial cells (163) and the role of the prothrombin-activating proteins staphylocoagulase and von Willebrand factor-binding protein in binding prothrombin and converting fibrinogen into fibrin (164). Staphylococcal superantigens have also been shown to be critical to the formation of vegetations, probably through a combined effect of systemic hypotension and direct toxicity to endothelial cells (165).…”
Section: Pathophysiologymentioning
confidence: 87%
“…23,24 What is more, we previously showed that S. aureus itself binds to the VWF A1-and A3-domains, which supports S. aureus adhesion to the vessel wall and, in turn, can be blocked using heparin. 25 Besides this process, DNA release by leukocytes can be induced by S. aureus infection. Hence one may imagine a scenario where S. aureus-induced NET formation leads to DNA-VWF-Staphylococcus binding, followed by leukocyte adhesion to the vessel wall and consecutive extravasation.…”
Section: Discussionmentioning
confidence: 99%