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Staphylokinase controls Staphylococcus aureus biofilm formation and detachment through host plasminogen activation.

Journal article
Authors Jakub Kwiecinski
Marijke Peetermans
Laurens Liesenborghs
Manli Na
Halla Björnsdottir
Xuefeng Zhu
Gunnar Jacobsson
Bengt R Johansson
Joan A Geoghegan
Timothy J Foster
Elisabet Josefsson
Johan Bylund
Peter Verhamme
Tao Jin
Published in The Journal of infectious diseases
Volume 213
Issue 1
Pages 139-148
ISSN 0022-1899
Publication year 2016
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Biomedicine
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Odontology, Section 3
Pages 139-148
Language en
Links dx.doi.org/10.1093/infdis/jiv360
Subject categories Infectious Medicine

Abstract

Staphylococcus aureus biofilms, a leading cause of persistent infections, are highly resistant to immune defenses and antimicrobial therapies. In this study, we investigated the contribution of fibrin and staphylokinase to biofilm formation. Both in clinical S. aureus isolates and in laboratory strains, high staphylokinase-producing strains formed less biofilm than strains that lacked staphylokinase, suggesting that staphylokinase prevents biofilm formation. Additionally, staphylokinase induced detachment of mature biofilms. This effect depended on plasminogen activation by staphylokinase. Host-derived fibrin, the main substrate cleaved by staphylokinase-activated plasminogen, was a major component of biofilm matrix and dissolution of this fibrin scaffold greatly increased susceptibility of biofilms to antibiotics and neutrophil phagocytosis. Staphylokinase also attenuated biofilm-associated catheter infections in mouse models. In conclusion, our results reveal a novel role for staphylokinase-induced plasminogen activation that prevents S. aureus biofilm formation and induces detachment of existing biofilms through proteolytic cleavage of biofilm matrix components.

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