Project title: Investigations into bradykinin-provoked edema and inflammation.

Hereditary angioedema (HAE) is a condition in which a genetic mutation causes a quantitative or qualitative lack of C1 inhibitor (C1Inh). This, in turn, leads to overproduction of bradykinin by means of increased protease activity, mainly that of FXIIa and plasma kallikrein.
We are studying how the lack of C1Inh affects pathways in the immune system including the complement system and also how it affects the coagulation and fibrinolytic systems.