Entry of microorganisms into the blood stream provokes a decline in the contractile function of the cardiac muscle. Lipopolysaccharide of Gram-negative bacteria sets off production of pro-inflammatory cytokines including bactericidal concentrations of nitric oxide which set up the first defence line against bacteremia. At the same time, however, the performance of the cardiovascular system is negatively affected. The immediate menace resides in the occurrence of septic shock, while chronic infectious diseases that are accompanied by low-grade inflammation have been suspected to take an active part in the initiation and progression of atherosclerosis. This hypothesis, as attractive as it may appear, has not yet been accepted unequivocally. The article offers an up-to-date review of the signalling cascades which permit activation by lipopolysaccharide of the target cells. The same holds true for cellular activation by non-infectious stimuli. An emerging paradigm seems plausible that the same biologic events which serve to combat acute infection might be in the long run involved in the pathogenesis of atherosclerosis.

        Key words: lipopolysaccharide, toll-like receptors, atherosclerosis.