Abstract
Atherosclerosis, the major cause of cardiovascular disease (CVD), is a chronic inflammatory condition with immune competent cells in lesions producing mainly pro-inflammatory cytokines. Dead cells and oxidized forms of low density lipoproteins (oxLDL) are abundant. The major direct cause of CVD appears to be rupture of atherosclerotic plaques. oxLDL has proinflammatory and immune-stimulatory properties, causes cell death at higher concentrations and contains inflammatory phospholipids with phosphorylcholine (PC) as an interesting epitope. Antibodies against PC (anti-PC) may be atheroprotective, one mechanism being anti-inflammatory. Bacteria and virus have been discussed, but it has been difficult to find direct evidence, and antibiotic trials have not been successful. Heat shock proteins could be one major target for atherogenic immune reactions. More direct causes of plaque rupture include pro-inflammatory cytokines, chemokines, and lipid mediators. To prove that inflammation is a cause of atherosclerosis and CVD, clinical studies with anti-inflammatory and/or immune-modulatory treatment are needed. The potential causes of immune reactions and inflammation in atherosclerosis and how inflammation can be targeted therapeutically to provide novel treatments for CVD are reviewed.
Highlights
Atherosclerosis is the dominant cause of cardiovascular disease (CVD) including myocardial infarction (MI), heart failure, stroke and claudication
We have reported in several papers that immunoglobulin M (IgM) Antibodies against phosphorylcholine (anti-PC) is negatively associated with atherosclerosis development and risk of CVD
We suggested in previous studies that hypertension could cause inflammation by induction of immunogenic HSP60/65, which is induced by Oxidized low density lipoprotein (oxLDL) [56,57]
Summary
Atherosclerosis is the dominant cause of cardiovascular disease (CVD) including myocardial infarction (MI), heart failure, stroke and claudication. While much evidence from epidemiological studies indicates that smoking is associated with atherosclerosis and CVD [18,19], the exact mechanisms by which smoking could cause inflammation in the arteries are not fully elucidated, increased oxidation of lipids is one interesting possibility [20]. Other infectious agents that have been discussed and reported as potential causes of CVD and atherosclerosis include HIV, Epstein-Barr virus (EBV), influenza, Mycoplasma pneumoniae and Streptococcus pneumoniae Another interesting case, in which there is evidence from human studies, is Borrelia [73], experimental data or plaque data are not available to the best of my knowledge. In another interesting study immunization with human HSP60 (with or without combination with apoB peptides) led to decreased atherosclerosis [124] It is presently not clear how HSP-immunization could work as therapy against atherosclerosis development even in animal models. Competing interests JF is named as inventor on patent applications relating to phospholipids and antibodies
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