Infective endocarditis is an illness that usually afflicts persons who have either had previous damage to their heart or who have congenital heart disease. At times, however, endocarditis occurs In otherwise normal hearts. Endocarditis results from colonization of cardiac tissues by micro-organisms, typically oral streptococci, that gain access to the blood stream and cause brief bacteremias. An important aspect of the pathophysiology of infective endocarditis is the marked propensity of the cardiac valve to bind and allow proliferation of micro-organisms. There Is evidence that this peculiar propensity could be related to the development on the cardiac valve of nonbacterial thrombotic endocarditis (NBTE) following injury; other vascular tissues do not form NBTE. This application will continue our work on the cell biology of the porcine cardiac valve, proposing four specific aims of potential relevance to the understanding of the cellular basis of infective endocarditis: 1) what properties of cardiac valvular cells may affect their interaction with platelets or bacteria; 2) host bacteria interact with platelets; 3) do valve endothelial cells possess unique surface markers; 4) that procoagulant properties are present in cardiac valve cells. The experiments use isolated cell culture systems of porcine vascular endothelial and smooth muscle cells, and compare then to porcine aortic valvular endothelial and subendothelial cells. These comparisons Include binding of bacteria and platelets and coagulation of the coagulation system on cellular monolayers. In addition, bacterial- platelet interactions will be assessed. The ultimate aim is to explore unique attributes of valvular cells that might explain the propensity of that tissue to develop infective endocarditis. Such knowledge could be crucial toward understanding how to intervene to prevent this illness.
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