ApoA-1 (apolipoprotein A-1) is the main component of HDL (high-density lipoprotein) and stabilizes PON-1 (paraoxonase-1), which prevents lipid peroxidation and oxLDL (oxidized low-density lipoprotein) formation. Autoantibodies against apoA-1 [anti-(apoA-1) IgG] have been found in antiphospholipid syndrome and systemic lupus erythematosous, two diseases with an increased risk of thrombotic events, as well as in ACS (acute coronary syndrome). OxLDL levels are also elevated in these diseases. Whether anti-(apoA-1) IgGs exist in other prothrombotic conditions, such as APE (acute pulmonary embolism) and stroke, has not been studied and their potential association with oxLDL and PON-1 activity is not known. In the present study, we determined prospectively the prevalence of anti-(apoA-1) IgG in patients with ACS (n=127), APE (n=58) and stroke (n=34), and, when present, we tested their association with oxLDL levels. The prevalance of anti-(apoA-1) IgG was 11% in the ACS group, 2% in the control group and 0% in the APE and stroke groups. The ACS group had significantly higher median anti-(apoA-1) IgG titres than the other groups of patients. Patients with ACS positive for anti-(apoA-1) IgG had significantly higher median oxLDL values than those who tested negative (226.5 compared with 47.7 units/l; P<0.00001) and controls. The Spearman ranked test revealed a significant correlation between anti-(apoA-1) IgG titres and serum oxLDL levels (r=0.28, P<0.05). No association was found between PON-1 activity and oxLDL or anti-(apoA-1) IgG levels. In conclusion, anti-(apoA-1) IgG levels are positive in ACS, but not in stroke or APE. In ACS, their presence is associated with higher levels of oxLDL and is directly proportional to the serum concentration of oxLDL. These results emphasize the role of humoral autoimmunity as a mediator of inflammation and coronary atherogenesis.
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July 2008
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Research Article|
June 02 2008
Anti-(apolipoprotein A-1) IgGs are associated with high levels of oxidized low-density lipoprotein in acute coronary syndrome
Nicolas Vuilleumier;
Nicolas Vuilleumier
*Division of Immunology and Allergy, Department of Internal Medicine, University Hospital, Geneva, Switzerland
†Clinical Chemistry, Department of Genetic and Medicine Laboratory, University Hospital, Geneva, Switzerland
‡Department of Medicine, Karolinska Institutet, Stockholm, Sweden
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Emmanuel Charbonney;
Emmanuel Charbonney
§Adult Intensive Care Unit, Department of Anesthesia, Pharmacology and Intensive Care General Internal Medicine, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Lionel Fontao;
Lionel Fontao
*Division of Immunology and Allergy, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Montserrat Alvarez;
Montserrat Alvarez
*Division of Immunology and Allergy, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Natacha Turck;
Natacha Turck
∥Biomedical Proteomic Research Group, Department of Structural Biology and Bioinformatics, Medical University, Geneva, Switzerland
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Jean-Charles Sanchez;
Jean-Charles Sanchez
∥Biomedical Proteomic Research Group, Department of Structural Biology and Bioinformatics, Medical University, Geneva, Switzerland
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Pierre R. Burkhard;
Pierre R. Burkhard
¶Division of Neurology, Department of Clinical Neurosciences, University Hospital, Geneva, Switzerland
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Noury Mensi;
Noury Mensi
†Clinical Chemistry, Department of Genetic and Medicine Laboratory, University Hospital, Geneva, Switzerland
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Marc Righini;
Marc Righini
**Division of Angiology and Haemostasis, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Guido Reber;
Guido Reber
**Division of Angiology and Haemostasis, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Richard James;
Richard James
††Division of Endocrinology and Diabetes and Nutrition, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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François Mach;
François Mach
‡‡Division of Cardiology, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Jean-Claude Chevrolet;
Jean-Claude Chevrolet
§Adult Intensive Care Unit, Department of Anesthesia, Pharmacology and Intensive Care General Internal Medicine, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Jean-Michel Dayer;
Jean-Michel Dayer
*Division of Immunology and Allergy, Department of Internal Medicine, University Hospital, Geneva, Switzerland
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Johan Frostegard;
Johan Frostegard
‡Department of Medicine, Karolinska Institutet, Stockholm, Sweden
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Pascale Roux-Lombard
*Division of Immunology and Allergy, Department of Internal Medicine, University Hospital, Geneva, Switzerland
Correspondence: Dr Pascale Roux-Lombard (email [email protected]).
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Publisher: Portland Press Ltd
Received:
September 13 2007
Revision Received:
November 13 2007
Accepted:
December 19 2007
Accepted Manuscript online:
December 19 2007
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2008 Biochemical Society
2008
Clin Sci (Lond) (2008) 115 (1): 25–33.
Article history
Received:
September 13 2007
Revision Received:
November 13 2007
Accepted:
December 19 2007
Accepted Manuscript online:
December 19 2007
Citation
Nicolas Vuilleumier, Emmanuel Charbonney, Lionel Fontao, Montserrat Alvarez, Natacha Turck, Jean-Charles Sanchez, Pierre R. Burkhard, Noury Mensi, Marc Righini, Guido Reber, Richard James, François Mach, Jean-Claude Chevrolet, Jean-Michel Dayer, Johan Frostegard, Pascale Roux-Lombard; Anti-(apolipoprotein A-1) IgGs are associated with high levels of oxidized low-density lipoprotein in acute coronary syndrome. Clin Sci (Lond) 1 July 2008; 115 (1): 25–33. doi: https://doi.org/10.1042/CS20070325
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