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The role of staphylothrombin-mediated fibrin deposition in catheter-related Staphylococcus aureus infections.


ABSTRACT: Staphylococcus aureus (S. aureus) is a frequent cause of catheter-related infections. S. aureus secretes the coagulases staphylocoagulase and von Willebrand factor-binding protein, both of which form a staphylothrombin complex upon binding to prothrombin. Although fibrinogen and fibrin facilitate the adhesion of S. aureus to catheters, the contribution of staphylothrombin-mediated fibrin has not been examined. In this study, we use a S. aureus mutant lacking both coagulases (?coa/vwb) and dabigatran, a pharmacological inhibitor of both staphylothrombin and thrombin, to address this question. Genetic absence or chemical inhibition of pathogen-driven coagulation reduced both fibrin deposition and the retention of S. aureus on catheters in vitro. In a mouse model of jugular vein catheter infection, dabigatran reduced bacterial load on jugular vein catheters, as well as metastatic kidney infection. Importantly, inhibition of staphylothrombin improved the efficacy of vancomycin treatment both in vitro and in the mouse model.

SUBMITTER: Vanassche T 

PROVIDER: S-EPMC6281407 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature

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The role of staphylothrombin-mediated fibrin deposition in catheter-related Staphylococcus aureus infections.

Vanassche Thomas T   Peetermans Marijke M   Van Aelst Lucas N L LN   Peetermans Willy E WE   Verhaegen Jan J   Missiakas Dominique M DM   Schneewind Olaf O   Hoylaerts Marc F MF   Verhamme Peter P  

The Journal of infectious diseases 20130326 1


Staphylococcus aureus (S. aureus) is a frequent cause of catheter-related infections. S. aureus secretes the coagulases staphylocoagulase and von Willebrand factor-binding protein, both of which form a staphylothrombin complex upon binding to prothrombin. Although fibrinogen and fibrin facilitate the adhesion of S. aureus to catheters, the contribution of staphylothrombin-mediated fibrin has not been examined. In this study, we use a S. aureus mutant lacking both coagulases (Δcoa/vwb) and dabiga  ...[more]

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