title: Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
abstract: Patients with systemic lupus erythematosus (SLE) have a high risk of developing cardiovascular disease; however, the mechanisms involved in the early onset of atherosclerosis in these patients are not clear. Scavenger receptors, CD36 and CD163 are expressed by mononuclear phagocytes and participate in the binding and uptake of oxidized low-density lipoproteins (Ox-LDL), contributing to foam-cells formation and atherosclerosis development. The aim of the present study was to evaluate CD36(+) and CD163(+) expression and Ox-LDL removal by monocytes from SLE and atherosclerotic patients, compared to similar age-range healthy controls. Healthy controls, SLE, and atherosclerotic patients were evaluated for carotid intima media thickness (CIMT), lipid profile, and native LDL (N-LDL) and Ox-LDL binding/endocytosis. SLE patients presented decreased high-density lipoproteins (HDL) and increased Triglyceride levels, and half of the SLE patients had increased CIMT, compared to their healthy controls (HC(SLE)). The number of CD14(+)CD163(+) cells was increased in atherosclerosis healthy controls (HC(Atheros)) compared to HC(SLE), but there were no differences between SLE or atherosclerotic patients and their respective healthy controls. Clearance assays revealed a similar capacity to bind/endocytose Ox-LDL by monocytes from SLE patients and HC(SLE), and an increased binding and endocytosis of Ox-LDL by monocytes from atherosclerotic patients, compared to HC(Atheros). The decreased CD36 and CD163 expression observed in atherosclerotic and SLE patients, respectively, suggest that these inflammatory conditions modulate these receptors differentially. The increased CIMT observed in SLE patients cannot be explained by Ox-LDL binding/endocytosis, which was comparable to their controls.
authors.affiliation: Grupo de Inmunología Celular e Inmunogenética, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
authors.forename: Lina M
authors.initials: LM
authors.lastname: Yassin
authors.forename: Julián
authors.initials: J
authors.lastname: Londoño
authors.forename: Guillermo
authors.initials: G
authors.lastname: Montoya
authors.forename: Juan B
authors.initials: JB
authors.lastname: De Sanctis
authors.forename: Mauricio
authors.initials: M
authors.lastname: Rojas
authors.forename: Luis A
authors.initials: LA
authors.lastname: Ramírez
authors.forename: Luis F
authors.initials: LF
authors.lastname: García
authors.forename: Gloria
authors.initials: G
authors.lastname: Vásquez
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D050197:Atherosclerosis / Q000150:complications* / Q000276:immunology*; D018955:CD36 Antigens / Q000276:immunology; D004705:Endocytosis / Q000276:immunology*; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000276:immunology*; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D010084:Oxidation-Reduction; D011485:Protein Binding / Q000276:immunology; D011956:Receptors, Cell Surface / Q000276:immunology; D055815:Young Adult; D000098902:CD163 Antigen
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D018955:CD36 Antigens; D018950:Lipopolysaccharide Receptors; D008077:Lipoproteins, LDL; D011956:Receptors, Cell Surface; C099252:oxidized low density lipoprotein