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Platelets and the complement system can influence each other. As early as 10 years ago, prolonged bleeding times were described in mice deficient in certain complement factors. However, the more precise mechanisms were not understood. Our research group has been able to elucidate these mechanisms and show that the platelet C3a receptor plays an essential role in platelet function and connects the systems of blood clotting and innate immunity. We were able to publish these results in Circulation® in 2018.
The results of this work raise further questions, the answer to which is the goal of this project. In recent years there has been a significant gain in knowledge about the role of platelets in the inflammatory disease of atherosclerosis. Now the complement system as a system of innate immunity plays a crucial role in the immune defense of bacteria. Bacteremia leads to massive activation of the complement system. Platelets also play an important role in the pathogenesis of endocarditis. Typical conglomerates of bacteria and thrombocytes are found on affected heart valves. Therefore, the aim of this work is to investigate the role of the platelet C3a receptor in these diseases in order to learn more about the underlying molecular mechanisms and (patho)physiological processes.
