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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1421.)
© 2000 American Heart Association, Inc.

Editorials

Oxidized Lipoproteins and Infectious Agents

Are They in Collusion to Accelerate Atherogenesis?

David P. Hajjar

From the Center of Vascular Biology, Cornell University, New York, NY.

Correspondence to David P. Hajjar, Center of Vascular Biology, Cornell University, 1300 York Ave, New York, NY 10021. E-mail dphajjar@mail.med.cornell.edu

Key Words: Editorials • lipoproteins • atherosclerosis • infection • inflammation

Recent epidemiological studies have documented an increased incidence of some forms of coronary artery disease (CAD) in patients who have chronic infections and inflammatory disorders. Chlamydia pneumonia^{1 2 3} and herpes viruses^{4 5 6} have been implicated in the pathogenesis of CAD on the basis of their detection in human atherosclerotic plaques and epidemiological evidence of a higher incidence of CAD in patients infected with these agents. In this regard, many investigative reports have focused on the proatherosclerotic effects of infectious agents on vascular cells in tissue culture and how they may affect the biology of the arterial wall. The panoply of changes induced include those that increase the thrombotic potential of the vessel wall,⁷ increase expression of macrophage scavenger receptors with subsequent enhanced uptake of cholesterol through oxidized lipoproteins,⁸ increase expression of adhesion molecules⁹ and inflammatory cytokines,¹⁰ and increase smooth muscle cell migration¹¹ and proliferation. Moreover, products of certain pathogens can exert proatherosclerotic effects directly in the macrophage, thereby promoting transformation of macrophages into atherosclerotic foam cells and stimulating them to express cytokines that contribute to plaque instability and even rupture. Indeed, many of these pathological features fall within the rubric of an inflammatory response. Interestingly, evidence is now mounting that the acute-phase response (APR) is associated with oxidation of LDL. The hypothesis that increased modification of circulating LDL can lead to enhanced atherogenesis specifically through the oxidation process is not novel; it has been tested in several in vitro and in vivo animal models of atherosclerosis over the last two decades.

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