Shear-Resistant Binding to von Willebrand Factor Allows<i>Staphylococcus lugdunensis</i>to Adhere to the Cardiac Valves and Initiate Endocarditis

Liesenborghs, Laurens; Peetermans, Marijke; Claes, Jorien; Veloso, Tiago Rafael; Vandenbriele, Christophe; Criel, Maarten; Lox, Marleen; Peetermans, Willy; Heilbronner, Simon; Groot, Philip G. de; Vanassche, Thomas; Hoylaerts, Marc; Verhamme, Peter

doi:10.1093/infdis/jiv773

Cited by 44 publications

(38 citation statements)

References 25 publications

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“…VWF circulates in a compact globular form, but is progressively unfolded in a flow field or when bound to collagen, thereby exposing VWF A1, A2 and A3‐domain . It has been described that bacteria can bind to endothelial cells via VWF . Similar to our findings, Pappelbaum et al .…”

Section: Discussionsupporting

confidence: 90%

Clumping factor A, von Willebrand factor‐binding protein and von Willebrand factor anchor Staphylococcus aureus to the vessel wall

Claes

Liesenborghs

Peetermans

et al. 2017

Journal of Thrombosis and Haemostasis

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Summary. Objective: When establishing endovascular infections, Staphylococcus aureus (S. aureus) overcomes shear forces of flowing blood by binding to von Willebrand factor (VWF). 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. aureus to VWF and vascular endothelium under shear stress. Methods: We studied the binding of S. aureus to vWbp, VWF and endothelial cells in a micro-parallel flow chamber using various mutants deficient in Sortase A (SrtA) and SrtA-dependent surface proteins, and Lactococcus lactis expressing single staphylococcal surface proteins. In vivo adhesion of bacteria was evaluated in the murine mesenteric circulation using real-time intravital vascular microscopy. Results: vWbp bridges the bacterial cell wall and VWF, allowing shear-resistant binding of S. aureus to inflamed or damaged endothelium. Absence of SrtA and Clumping factor A (ClfA) reduced adhesion of S. aureus to vWbp, VWF and activated endothelial cells. ADAMTS-13 and an anti-VWF A1 domain antibody, when combined, reduced S. aureus adhesion to activated endothelial cells by 90%. 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. Conclusions: vWbp interacts with VWF and with the SrtA-dependent staphylococcal surface protein ClfA. The complex formed by VWF, secreted vWbp and bacterial ClfA anchors S. aureus to vascular endothelium under shear stress.

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Section: Discussionsupporting

confidence: 90%

Clumping factor A, von Willebrand factor‐binding protein and von Willebrand factor anchor Staphylococcus aureus to the vessel wall

Claes

Liesenborghs

Peetermans

et al. 2017

Journal of Thrombosis and Haemostasis

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“…Platelets play a pivotal role in the progression and development of IE, but their role can be likened to a double-edged sword (185)(186)(187)(188). Platelets display both haemostatic and host defence properties.…”

Section: Innate Host Responsementioning

confidence: 99%

Biofilms and host response – helpful or harmful

Moser

Pedersen

Lerche

et al. 2017

APMIS

127

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host response -helpful or harmful. APMIS 2017; 125: 320-338.Biofilm infections are one of the modern medical world's greatest challenges. Probably, all non-obligate intracellular bacteria and fungi can establish biofilms. In addition, there are numerous biofilm-related infections, both foreign bodyrelated and non-foreign body-related. Although biofilm infections can present in numerous ways, one common feature is involvement of the host response with significant impact on the course. A special characteristic is the synergy of the innate and the acquired immune responses for the induced pathology. Here, we review the impact of the host response for the course of biofilm infections, with special focus on cystic fibrosis, chronic wounds and infective endocarditis.

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“…Staphylococcus lugdunensis expresses various adhesion factors that are possibly involved in endocarditis, including von Willebrand and fibrinogen adhesion proteins as well as cytotoxic factors, i.e. a d-like haemolysin, b-haemolysin and haemolysin III [6]. It is also able to produce a biofilm that is mainly proteinaceous and is the only CoNS carrying an ESAT-6 system [7].…”

Section: Introductionmentioning

confidence: 99%

VISLISI trial, a prospective clinical study allowing identification of a new metalloprotease and putative virulence factor from Staphylococcus lugdunensis

Argemi

Prévost

Riegel

et al. 2017

Clinical Microbiology and Infection

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Shear-Resistant Binding to von Willebrand Factor AllowsStaphylococcus lugdunensisto Adhere to the Cardiac Valves and Initiate Endocarditis

Cited by 44 publications

References 25 publications

Clumping factor A, von Willebrand factor‐binding protein and von Willebrand factor anchor Staphylococcus aureus to the vessel wall

Clumping factor A, von Willebrand factor‐binding protein and von Willebrand factor anchor Staphylococcus aureus to the vessel wall

Biofilms and host response – helpful or harmful

VISLISI trial, a prospective clinical study allowing identification of a new metalloprotease and putative virulence factor from Staphylococcus lugdunensis

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