Translated abstract:
Staphylococcus aureus endocarditis begins with bacterial tissue invasion via endothelial α5β1-integrin. As endothelial cells are able to regulate surface molecules, the present dissertation specifically investigates the regulatory function of endothelial cells in regard to α5β1-integrin. An experimental rabbit model showed different regulatory mechanisms of left and right sided endocardium in response to mechanical and inflammatory stimuli. Studies on human endothelial cell cultures further showed differing interactive properties of arterial and venous endothelium for Staphylococcus aureus. These findings show new important hints towards understanding the important clinical differences of left and right heart endocarditis.