The hemostatic system comprises platelet aggregation, coagulation and fibrinolysis and is a host defense mechanism that prevents bleeding after vessel injury. During systemic infection complications occur because of a dysregulated coagulation system. While this is widely accepted, an important role of the coagulation system in the early host response to infectious diseases has been only recently begun to be appreciated. The induction of coagulation entraps microorganisms in a fibrin clot and inhibits pathogen dissemination and survival, indicating that interaction of bacteria or viruses with the coagulation system may be an integral part of the innate immune response.

Our research is focused on a molecular understanding of strategies that are used by bacteria to subvert immune defense and how the innate immune system responds to bacterial and viral invaders. Such studies will expose fundamental functions of the immune system and identify new targets for the treatment of severe infectious diseases.

The general aim of this project is to identify the function of human contact factors during invasive streptococcal infection and define the relative contributions of the intrinsic and extrinsic coagulation pathway in streptococcal sepsis. The findings of this application will help to identify novel diagnostic tools or targets for the treatment of severe infectious diseases.

S. gallolyticus (Sg) is often associated with colorectal cancer, and patients with Sg infections display a much higher risk of having colorectal cancer compared to the general population. It was recently shown that Sg promotes human colon cancer cell proliferation, pointing to a tumor-promoting role of Sg. Beside this it was described that Sg could be considered so far, the best bacterial cellular factories for tannin degradation. We showed that tannine are toxic against cancer cells and will further investigate whether tannin degradation by Sg play a role in tumor protection.