Short- and long-term elevation of autoantibody titers against oxidized LDL in patients with acute coronary syndromes. Role of the lipoprotein-associated phospholipase A2 and the effect of atorvastatin treatment
| Autor: | Papathanasiou, A. I., Lourida, E. S., Tsironis, L. D., Goudevenos, J. A., Tselepis, A. D. |
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| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
paf-acetylhydrolase
Male Heptanoic Acids/*pharmacology oxidation autoantibodies activating factor-acetylhydrolase lipoprotein-associated phospholipase a(2) artery-disease Immunoglobulin G/*drug effects Pyrroles/*pharmacology Humans oxidative modification phospholipids Aged low-density-lipoprotein hypercholesterolemia 1-Alkyl-2-acetylglycerophosphocholine Esterase/drug effects Autoantibodies/*drug effects Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology Middle Aged lipoproteins antioxidants Female atherosclerosis Acute Coronary Syndrome/blood/*immunology Lipoproteins LDL/*immunology atorvastain degrading acetylhydrolase |
| Popis: | Oxidized low-density lipoprotein (oxLDL) is immunogenic while oxidized phospholipids (oxPL) formed on oxLDL and lysophosphatidylcholine (lyso-PC) generated during LDL oxidation through the hydrolysis of oxPL by the lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), significantly contribute to oxLDL immunogenicity. We determined the autoantibody titers against various forms of mildly oxLDL in patients with acute coronary syndromes without persistent elevation of the ST segment (NSTE-ACS) and with undetectable serum levels of lipoprotein (a). Moreover, the effect of early atorvastatin administration on these autoantibody titers was evaluated. From the 133 consecutive NSTE-ACS patients, 55 were eligible for the study. Thirty-four received atorvastatin (group A), whereas 21 did not received any hypolipdemic therapy (group B). Two forms of copper-oxidized LDL were prepared at the end of propagation or decomposition phase (oxLDL(P) or oxLDL(D), respectively). Similar types of oxLDL were prepared after previous inactivation of the endogenous Lp-PLA(2) [oxLDL(-)]. In group B, autoantibody titers of IgG class against oxLDL(P) and oxLDL(D) were elevated at 1 month of follow-up to reach the baseline values 3 months afterwards. By contrast the titers against oxLDL(-)(P) and oxLDL(-)(D) increased at 1 month of follow-up and remained elevated for up to 6 months of follow-up. Atorvastatin treatment prevented the elevation of autoantibody titers against all forms of oxidized LDL. We conclude that a short-term immune response against oxLDL(P) and oxLDLD (enriched in lyso-PC) and a chronic immune response against oxLDL(-)(P) and oxLDL(-)(D) (enriched in oxPL) are observed after an NSTE-ACS, suggesting an important role of the LDL-associated Lp-PLA(2) in modulating these immune responses. Early atorvastatin treatment prevents both immune responses; however, the clinical significance of this effect remains to be established. (C) 2006 Elsevier Ireland Ltd. All rights reserved. Atherosclerosis |
| Databáze: | OpenAIRE |
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