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Plasminogen activation by staphylokinase enhances local spreading of S. aureus in skin infections.

Journal article
Authors Marijke Peetermans
Thomas Vanassche
Laurens Liesenborghs
Jorien Claes
Greetje Vande Velde
Jakub Kwiecinski
Tao Jin
Bart De Geest
Marc F Hoylaerts
Roger H Lijnen
Peter Verhamme
Published in BMC microbiology
Volume 14
Issue 1
Pages Article. nr. 310
ISSN 1471-2180
Publication year 2014
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages Article. nr. 310
Language en
Links dx.doi.org/10.1186/s12866-014-0310-...
https://gup.ub.gu.se/file/149454
Subject categories Clinical bacteriology, Infectious Medicine

Abstract

Background Staphylococcus aureus (S. aureus) is a frequent cause of skin and soft tissue infections. A unique feature of S. aureus is the combined presence of coagulases that trigger fibrin formation and of the plasminogen activator staphylokinase (SAK). Whereas the importance of fibrin generation for S. aureus virulence has been established, the role of SAK remains unclear.We studied the role of plasminogen activation by SAK in a skin infection model in mice and evaluated the impact of alpha-2-antiplasmin (¿2AP) deficiency on the spreading and proteolytic activity of S. aureus skin infections. The species-selectivity of SAK was overcome by adenoviral expression of human plasminogen. Bacterial spread and density was assessed non-invasively by imaging the bioluminescence of S. aureus Xen36.ResultsSAK-mediated plasmin activity increased the local invasiveness of S. aureus, leading to larger lesions with skin disruption as well as decreased bacterial clearance by the host. Even though fibrin and bacterial surfaces protected SAK-mediated plasmin activity from inhibition by ¿2AP, the deficiency of ¿2AP resulted in increased bacterial spreading. SAK-mediated plasmin also induced secondary activation of gelatinases, shown both in vitro and in lesions from the in vivo model.ConclusionSAK contributes to the phenotype of S. aureus skin infections by enhancing bacterial spreading as a result of fibrinolytic and proteolytic activation.

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