Abstract

Atherosclerosis and its clinical complications are now understood to be an inflammatory syndrome in which an ongoing systemic inflammatory response is combined with the accumulation of immune cells in the atherosclerotic plaque. Both arms of the immune system, innate and adaptive, have been implicated in contributing to essentially all stages of atherosclerosis, from initiation to progression and, ultimately, atherothrombotic complications. Innate immunity is the first line of defense against invading microorganisms. The recognition units of the innate immune system are designed to respond to molecular patterns shared by a variety of infectious microorganisms, such as bacterial lipopolysaccharide. Numerous basic and clinical studies have provided evidence that responsiveness to lipopolysaccharide may be correlated to the risk of atherosclerotic disease. The molecular basis of this connection appears to lie in Toll-like receptors that are expressed on cells of the innate immune system, bind to lipopolysaccharide, and thus determine the strength of antibacterial immune responses in the host. Variations in the function of Toll-like receptors and their signaling pathways are now suspected to play a critical role in determining the risk of atherosclerosis. This review summarizes recent research advances exploring the role of innate immunity, particularly lipopolysaccharide, CD14 and Toll-like receptors, in the initiation and development of atherosclerotic disease.

View details for DOI 10.2217/14796678.1.5.657

View details for PubMedID 19804106