Official websites use. Share sensitive information only on official, secure websites. Vanassche, P. Verhamme, M. Hoylaerts, and R. Heying designed the research, analyzed the data, and wrote the manuscript; J.
Claes designed and performed the research, analyzed the data, and wrote the manuscript; L. Liesenborghs, M. Peetermans, and T. Veloso performed experiments and helped interpret data; D.
Missiakas, O. Schneewind, S. Mancini, and J. Entenza designed the research, contributed vital new agents, and contributed to writing the manuscript. When establishing endovascular infections, Staphylococcus aureus S. Staphylococcal VWF-binding protein vWbp interacts with VWF, but it is unknown how this secreted protein binds to the bacterial cell wall. We hypothesized that vWbp interacts with a staphylococcal surface protein, mediating the adhesion of S. We studied the binding of S. In vivo adhesion of bacteria was evaluated in the murine mesenteric circulation using real-time intravital vascular microscopy.
Selective overexpression of ClfA in the membrane of Lactococcus lactis enabled these bacteria to bind to VWF and activated endothelial cells but only in the presence of vWbp. Absence of ClfA abolished bacterial adhesion to the activated murine vessel wall. Keywords: endothelium, infection, shear stress, Staphylococcus aureus, von Willebrand factor.
Staphylococcus aureus S. One of the most feared complications of invasive S. Compared with other pathogens, infective endocarditis caused by S. Once S. The dramatic morbidity and mortality of S. This stresses the need for new therapeutic strategies to prevent and treat infective endocarditis. To cause endocarditis, bacteria first need to adhere to the endothelium of the heart valve. However, binding to endothelial cells in flowing blood requires mechanisms to withstand shear stress.
