[Inflammation and atherosclerosis]

Inflammation is the reaction of a vascularized living tissue to local injury. Acute and chronic inflammation result from complex interactions between leukocytes, mesenchymal cells and various components of plasma. The aim of inflammation is reparation, but persisting chronic inflammation is a source of disease. Atherosclerosis can be viewed as an impairment of the normal relationships between blood and arterial wall. As proposed by pathologists of the last century, inflammation may provide a physiopathologic frame for atherosclerosis. Human atherosclerotic lesions at any step of their evolution, as well as the pathogenic models that have been developed to explain atherogenesis, share many features of an inflammatory reaction of arterial intima: increased penetration of plasma components, proliferation of smooth muscle cells, infiltration by monocytes/macrophages and by lymphocytes, building up of a sclerotic extracellular matrix and of a rich neovascularization. The inflammatory model neither contradicts nor jeopardizes the established knowledge on the roles of lipids and thrombosis in atherosclerosis. Rather, introducing the numerous cellular and molecular mediators of inflammation into the pathogenesis of atherosclerosis widens our field of investigations, and may open new avenues for prevention and treatment. There remains the major question of identifying the cause(s) which initiate(s) and perpetuate(s) arterial inflammation that lead to complicated atherosclerosis with ischemic manifestations.