Objectives: The higher incidence of atherosclerosis and cardiovascular disease (CVD) in patients with systemic autoimmune diseases cannot be attributed exclusively to traditional risk factors for CVD. Antibodies to oxidised Low Density Lipoprotein (ox-LDL) seem to have a crucial role in atherogenesis.
Methods: Sera from 63 consecutive patients with primary Sjögren's syndrome (pSS), 121 with systemic lupus erythematosus (SLE), 79 with rheumatoid arthritis (RA) and 26 apparently healthy individuals were evaluated for the presence of antibodies to ox-LDL by ELISA. The femoral and/or carotid intima media thickness (IMT) and plaque formation as well as traditional CVD risk factors and disease-related features were recorded for all study participants.
Resukts: Anti-ox-LDL antibody levels were significantly reduced in SS and RA patients, but not in SLE patients, compared to their healthy counterparts. Subsequently, SS patients were divided into two groups according to antibody levels to ox-LDL, using as cut off the median of each group studied. SS patients with high titres of antibodies to ox-LDL displayed higher rates of autoantibodies to Ro/SSA and La/SSB antigens, purpura, low complement levels and increased SS activity index. On the other hand, the high anti-ox-LDL group was characterised by reduced rates of carotid and/or femoral plaque after adjusting for potential confounders (OR [95%CI]: 0.14 [0.03-0.72]). Such associations were not shown in all other groups included in the study.
Conclusions: These findings suggest that antibodies to ox-LDL, possibly resulting from B cell hyperactivity, might exert a protective role in the development of atherosclerosis among primary SS patients.
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Antioxidants (Basel)
December 2024
Otto Loewi Research Center, Division of Medicinal Chemistry, Medical University of Graz, 8010 Graz, Styria, Austria.
One of the most prominent actions of oxidative stress is the attack of free radicals on poylyunsaturated fatty acids (PUFAs), initiating a chain reaction to modify these PUFAs and generate oxidized modifications on all biomolecules. In the last quarter of the 20th century, intensive research was carried out to identify antibodies against such modifications. In the mid-1990s, the first enzyme-linked immunosorbent assay (ELISA) was introduced to the market, significantly accelerating research activities and knowledge gain.
View Article and Find Full Text PDFJACC Adv
November 2024
Units of Immunology and chronic disease, and Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Background: Antibodies against phosphorylcholine (anti-PC) have been reported as associated with protection against atherosclerosis, cardiovascular disease (CVD), and other chronic inflammatory diseases. Underlying potential mechanisms have been demonstrated and include anti-inflammatory, clearance of dead cells, and inhibition of oxidized low-density lipoprotein effects.
Objectives: This study examined the role of IgM anti-PC and incident CVD among women, where less is known than among men in the general population.
Thromb Res
December 2024
Department of Bioengineering, College of Engineering and Computing, George Mason University, Manassas, VA 20110, United States of America. Electronic address:
Introduction: Acute respiratory distress syndrome (ARDS) patients are at risk of thrombosis through mechanisms implicating oxidized low-density lipoprotein (oxLDL). Endothelial cells, immune cells and platelets were reported to express scavenger receptors for oxLDL: Lox-1 and CD36. We hypothesized that platelets shed a soluble Lox-1 ectodomain (sLox-1) and release CD36-bearing procoagulant microparticles (MPs), that both become elevated in subjects with ARDS-induced coagulopathy.
View Article and Find Full Text PDFImmun Inflamm Dis
November 2024
Department of Clinical Laboratory and Hematology, School of Medicine, Jiangsu University, Zhenjiang, China.
Background: Previous research has established that the oxidized low-density lipoprotein/β2-glycoprotein I/anti-β2-glycoprotein I antibody (oxLDL/β2GPI/anti-β2GPI) complex can stimulate macrophages to secrete molecules associated with atherosclerosis (AS), such as monocyte chemotactic protein 1 (MCP-1), tissue factor (TF), and tumor necrosis factor-α (TNF-α). This complex also enhances the uptake of oxLDL, thereby accelerating foam cell formation through the Toll-like receptor-4/nuclear factor kappa B (TLR4/NF-κB) pathway. Given the critical role of macrophage autophagy in the instability of vulnerable atherosclerotic plaques, it is imperative to investigate whether the oxLDL/β2GPI/anti-β2GPI complex influences macrophage autophagy in AS.
View Article and Find Full Text PDFGlob Cardiol Sci Pract
August 2024
Department of Cardiology, GB Pant hospital, Raj Ghat, New Delhi, India.
Objective: Atherosclerosis is a chronic condition characterized by impaired lipid homeostasis and chronic inflammatory pathology in large and mid-sized arteries. Myocardial infarction is caused by coronary artery thrombosis in a ruptured or unstable atherosclerotic plaque. Despite the emphasis on known triggering factors, such as hypertension and dyslipidemia, adverse events following MI, such as recurrence and mortality, are still high.
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