Implication of an infectious factor in the pathogenesis of atherosclerosis

The paper considers the implication of an infectious factor and the interaction of microbial ligand structures with toll-like receptors (TLR) in the pathogenesis of atherosclerosis. Lipopolysaccharides of gram-negative bacteria can interact with TLR4 and activate endothelial and smooth muscle cells and arterial intimal macrophages, by inducing their conversion to cholesterol ester-saturated foam cells, and atheroma formation. Loss-of-function mutation in TLR4 receptor reduces the risk of atherosclerosis. Other bacterial ligands, peptidoglycan in particular, as well as endogenous ligands of microbial TLR synthesized under the influence of stressogenic factors can be involved in the induction of atherogenesis. The receptor theory according to which the reactions triggered through the interaction of TLR with their exogenous and endogenous ligands underlie the pathogenesis of atherosclerosis is formulated.