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

Abstract

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.

• Fibrinolysis
• plasmin
• plasminogen
• proteolysis
• staphylokinase
• streptokinase

Declaration of interest

This work was supported by grants of the Research Foundation Flanders (FWO-Vlaanderen, 11I0113N and 11S5416N). Marijke Peetermans and Laurens Liesenborghs are fellows of the FWO, Peter Verhamme is a senior clinical investigator of the FWO.

The authors have no competing interests to declare in relation to this work.