Thromb Haemost 2007; 98(03): 497-502
DOI: 10.1160/TH07-01-0051
Theme Issue Article
Schattauer GmbH

The dual role of the contact system in bacterial infectious disease

Inga-Maria Frick
1   Section for Clinical and Experimental Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden
,
Lars Björck
1   Section for Clinical and Experimental Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden
,
Heiko Herwald
1   Section for Clinical and Experimental Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden
› Author Affiliations
Financial support: This work was supported in part by the foundations of Åke Wiberg, Alfred Österlund, Crafoord, Tore Nilson, Greta and Johan Kock, the Swedish Foundation for Strategic Research, King Gustaf V’s 80-years fund, the Royal Physiographical Society in Lund, the Medical Faculty of Lund University, the Swedish Research Council (projects 7480 and 13413), the Blood and Defence Network at Lund University, and Hansa Medical AB.
Further Information

Publication History

Received 24 January 2007

Accepted after revision 17 April 2007

Publication Date:
28 November 2017 (online)

Summary

Hemostasis is a sensitive and tightly regulated process, involving the vascular endothelium and blood cells as well as factors of the coagulation and fibrinolytic cascades. Over the last four decades evidence has accumulated that during infection, inflammatory mediators from the microbe and/or host are capable to modulate the equilibrium between the procoagulant and anticoagulant status of the host. Dependent on the mode of activation, these changes can cause either local or systemic inflammatory reactions that may be beneficial or deleterious to the human host. The present review aims to present the state of the art with respect to the role of the contact system (also known as the intrinsic pathway of coagulation or the kallikrein/kinin system) in innate immunity and systemic inflammatory reactions.

 
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