Hemostasis is a sensitive and tightly regulated process, involving vascular endothelium and blood cells as well as factors of the coagulation and fibrinolytic cascades. During infection, inflammatory mediators of the microbe and/or host may induce life-threatening complications by modulating the equilibrium between the procoagulant and anticoagulant status of the host. Over the last few years, evidence has been accumulating that activation of the intrinsic pathway of coagulation (also termed the contact system or kallikrein/kinin system) contributes to the severity of the disease. As described for other factors participating in blood coagulation, the contact system belongs to the typical serine proteinase-triggered cascades, which are initiated by limited proteolysis. Upon activation, the contact system is involved in the regulation of different pro-inflammatory and defense machineries, which can induce symptoms that are also seen in patients with severe infections.We recently found that inhibition of the contact system down-regulates inflammatory reactions in a mouse model of sepsis (1). This project is undertaken to gain more insight into the mechanisms that lead to a bacteria-induced induction of this part of the coagulation cascade and a subsequent activation of clotting factors up-stream of the contact system.
Status | Finished |
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Effective start/end date | 2010/01/01 → 2021/01/01 |
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In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This project contributes towards the following SDG(s):