Atherosclerosis is considered a chronic inflammatory condition. The importance of immunopathological mechanisms in these processes has been recognized. Several autoantibodies seem to be implicated in atherogenesis, and anti-endothelial cell antibodies (AECA) are among them. The influence of AECA on endothelial cell function may include endothelial cell activation and/or apoptosis. Atherosclerosis is the main consequence of metabolic syndrome where patients may have hyperleptinaemia which might be associated with accelerated atherosclerosis. Leptin is as an adipokine with multiple metabolic functions, which also influences immune mechanisms. Leptin connects nutritional status and proinflammatory Th1 immune response and changes in leptin plasma concentrations may lead to impaired immune functions including autoimmunity. We proposed that hyperleptinaemia is one of the factors that evoke physiological autoimmune reactions and the onset of pathological autoaggressive processes. Therefore, we assessed the correlation between leptinaemia and the presence of AECA in the sera of 284 patients at risk from accelerated atherosclerosis: 154 with ischemic heart disease, 75 with type 2 diabetes, 38 with a stroke and 17 with primary endogenous hypercortisolism (Cushing syndrome). We evaluated leptin levels in AECA-positive and AECA-negative subjects, but no significant difference was found. Moreover, neither AECA positive nor AECA negative subjects with atherosclerosis differ in leptinaemia compared with the normal population. An associated between AECA production and the immunomodulatory effects of leptin was not confirmed.
Keywords: Antiendothelial antibodies, leptin, leptinaemia, atherosclerosis, autoimmunity
Rights & PermissionsPrintExport