Bacterial pathogens activate plasminogen to breach tissue barriers and escape from innate immunity

Both coagulation and fibrinolysis are tightly connected with the innate immune system. Infection and inflammation cause profound alterations in the otherwise well-controlled balance between coagulation and fibrinolysis. Many pathogenic bacteria directly exploit the host's hemostatic system to i...

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Bibliographic Details
Published in:Critical reviews in microbiology 2016-11, Vol.42 (6), p.866-882
Main Authors: Peetermans, Marijke, Vanassche, Thomas, Liesenborghs, Laurens, Lijnen, Roger H., Verhamme, Peter
Format: Article
Language:English
Subjects:
Animals
Bacteria - genetics
Bacteria - immunology
Bacterial Infections - enzymology
Bacterial Infections - genetics
Bacterial Infections - immunology
Bacterial Infections - microbiology
Bacterial Proteins - genetics
Bacterial Proteins - immunology
Fibrinolysis
Humans
Immunity, Innate
plasmin
plasminogen
Plasminogen - genetics
Plasminogen - immunology
Plasminogen Activators - genetics
Plasminogen Activators - immunology
proteolysis
staphylokinase
streptokinase
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Summary:Both coagulation and fibrinolysis are tightly connected with the innate immune system. Infection and inflammation cause profound alterations in the otherwise well-controlled balance between coagulation and fibrinolysis. Many pathogenic bacteria directly exploit the host's hemostatic system to increase their virulence. Here, we review the capacity of bacteria to activate plasminogen. The resulting proteolytic activity allows them to breach tissue barriers and evade innate immune defense, thus promoting bacterial spreading. Yersinia pestis, streptococci of group A, C and G and Staphylococcus aureus produce a specific bacterial plasminogen activator. Moreover, surface plasminogen receptors play an established role in pneumococcal, borrelial and group B streptococcal infections. This review summarizes the mechanisms of bacterial activation of host plasminogen and the role of the fibrinolytic system in infections caused by these pathogens.
ISSN:1040-841X
1549-7828
DOI:10.3109/1040841X.2015.1080214