Interactions between bacterial lipopolysaccharides and serum lipoproteins and their possible role in coronary heart disease.
It has been proposed for several decades that infections may be responsible for the accelerated development of atherosclerosis. Numerous studies have shown an association between atherosclerosis and both viral and bacterial infections. In this review, we summarize the evidence linking infections with abnormalities in lipid and lipoprotein levels and the role of cytokines in mediating these abnormalities. We have also summarized the effects of the interaction between LDL and lipopolysaccharides (LPS) on lipoprotein metabolism and their possible contributing role to the development of atherosclerosis; the possible role of LPS in inducing endothelial cell damage and in stimulating the oxidative metabolism of monocytes, leading to the release of superoxide anion (O2-) and to the oxidation of LDL. Oxidatively modified LDL has, in recent years, been implicated as a contributing factor in the development of atherosclerosis, due to its ability to induce the transformation of macrophages into foam cells, to promote monocyte binding to the endothelium and to act as a potent chemo-attractant for circulating human monocytes. Furthermore, oxidized-LDL is immunogenic and thus, it can induce the production of antibodies and subsequent formation of immune complexes. These immune complexes, when taken up by macrophages through the Fc receptor, induce a marked accumulation of cholesteryl esters in these cells and also promote their activation and the subsequent release of cytokines, such as interleukin 1 (IL-1) and tumour necrosis factor alpha (TNF alpha). In addition to the effects that IL-1 and TNF alpha seem to have on lipid and lipoprotein levels, they induce adherence of leukocytes to endothelial cells by promoting the expression of several specific cell adhesion molecules; they can also elicit synthesis and cell surface expression of procoagulant activity in endothelial cells and cause an increase in vascular permeability.(ABSTRACT TRUNCATED AT 250 WORDS)
Lopes-Virella
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Ralph H. Johnson Department of Veterans Affairs Medical Center, Charleston, SC 29401.
D001424:Bacterial Infections / Q000150:complications / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000209:etiology / Q000378:metabolism; D003327:Coronary Disease / Q000209:etiology / Q000378:metabolism*; D016207:Cytokines / Q000502:physiology; D006801:Humans; D008070:Lipopolysaccharides / Q000009:adverse effects* / Q000378:metabolism; D008074:Lipoproteins / Q000097:blood / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D010084:Oxidation-Reduction
D016207:Cytokines; D008070:Lipopolysaccharides; D008074:Lipoproteins; D008077:Lipoproteins, LDL