Bacterial pathogens under high-tension: Staphylococcus aureus adhesion to von Willebrand factor is activated by force
Authors:Felipe Viela1, Pietro Speziale2,3, Giampiero Pietrocola2 and Yves F. Dufrêne1,4
doi: 10.15698/mic2019.07.684
Volume 6, pp. 321 to 323, published 11/06/2019.
1 Institute of Life Sciences, Université catholique de Louvain, Croix du Sud, 4-5, bte L7.07.06, B-1348 Louvain-la-Neuve, Belgium.
2 Department of Molecular Medicine, Unit of Biochemistry, University of Pavia, Viale Taramelli 3/b, 27100 Pavia, Italy.
3 Department of Industrial and Information Engineering, University of Pavia, Italy.
4 Walloon Excellence in Life sciences and Biotechnology (WELBIO), Belgium.
Keywords:
Staphylococcus aureus, protein A, von Willebrand factor, endothelial cells, adhesion, mechanical force.
Corresponding Author(s):
Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Felipe Viela, Pietro Speziale, Giampiero Pietrocola and Yves F. Dufrêne (2019). Bacterial pathogens under high-tension:Staphylococcus aureus adhesion to von Willebrand factor is activated by force. Microbial Cell 6(7): 321-323. doi: 10.15698/mic2019.07.684
© 2019 Viela et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.
Abstract:
Attachment of Staphylococcus aureus to platelets and endothelial cells involves binding of bacterial cell surface protein A (SpA) to the large plasma glycoprotein von Willebrand factor (vWF). SpA-mediated bacterial adhesion to vWF is controlled by fluid shear stress, yet little is currently known about the underlying molecular mechanism. In a recent publication, we showed that the SpA-vWF interaction is tightly regulated by mechanical force. By means of single-molecule pulling experiments, we found that the SpA-vWF bond is extremely strong, being able to resist forces which largely outperform the strength of typical receptor-ligand bonds. In line with flow experiments, strong adhesion is activated by mechanical tension. These results suggest that force induces conformational changes in the vWF molecule, from a globular to an extended state, leading to the exposure of cryptic binding sites to which SpA strongly binds. This force-sensitive mechanism may largely contribute to help S. aureus bacteria to resist shear stress of flowing blood during infection.