Preventing autoimmune and infection triggered atherosclerosis for an enduring healthful lifestyle.
Atherosclerosis is a chronic inflammatory disease of the arteries associated with various risk factors that promote lipid abnormalities (i.e., dyslipidemia), development and progression of atherosclerotic lesions, plaque rupture, and vascular thrombosis. Experimental evidence from biochemical and clinical studies support the idea that arterial thrombosis is an autoimmune process resulting from 'autoantibody'-mediated pro-atherogenic mechanisms now seen in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). In addition, it has been shown that persistent infections of Chlamydia pneumoniae (C. pneumoniae), Porphyromonas gingivalis (P. gingivalis), and Helicobacter pylori (H. pylori) cause immune responses (infectious immunity) in their hosts that promote atherogenesis. In this article, we review recent progress in our understanding of immune- and infection-mediated atherosclerosis.
Matsuura
Eiji
E
Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. eijimatu@md.okayama-u.ac.jp
Kobayashi
Kazuko
K
Lopez
Luis R
LR
D050197:Atherosclerosis / Q000209:etiology / Q000517:prevention & control*; D001327:Autoimmune Diseases / Q000209:etiology / Q000517:prevention & control*; D001424:Bacterial Infections / Q000150:complications; D015438:Health Behavior; D006801:Humans; D008019:Life Style; D008077:Lipoproteins, LDL / Q000502:physiology; D010084:Oxidation-Reduction; D053482:beta 2-Glycoprotein I / Q000502:physiology
D008077:Lipoproteins, LDL; D053482:beta 2-Glycoprotein I