C-reactive protein: possibly not only a marker, but a physiopathologic agent in chronic vascular inflammation

Massive changes in the concentration of C-reactive protein (CRP), a well recognized positive acute phase protein, are known take place rapidly in body fluids during the onset of inflammatory and infective diseases. This process results into the accumulation of CRP at the sites of the lesions and is classically closely linked to protective effects through targeted activation of complement and thereby clearance of bacteria and necrotic cells debris. Data collected during the last couple of years has documented an unexpected role of this protein as a major pathogenetic element in atherosclerosis, which is now considered as an inflammation of the arterial endothelial lining. In this disease, intimal and muscular lesions are accompanied by deposition of CRP, local activation of complement, recruitment of phagocytic cells and opposite effects on the final plate stability depending on the balance between proteolytic processing and collagen deposition. Major efforts are now played to reduce pharmacologically the levels of CRP in the blood stream and to counteract its local activation in order to control the development of this dangerous inflammatory disease.