Influence of serum amyloid A on the decrease of high density lipoprotein-cholesterol in active sarcoidosis

Salazar, Albert; Mañá, Juan; Fiol, C.; Hurtado, Isabel; Argimón, Josep M.; Pujol, Ramón; Pintó, Xavier

doi:10.1016/s0021-9150(00)00368-3

Cited by 39 publications

(33 citation statements)

References 31 publications

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“…These results are in agreement with a previous study, which found that the mean CRP concentrations in patients with stable or progressing disease (indicating severe disease) did not differ significantly from those in controls, in contrast to sIL2R (16 ). It appears that the acute-phase response, reflected through increased CRP and SAA concentrations, can be expected only in patients with active disease, including Löfgren syndrome (8,10,16 ).…”

Section: Discussion Diagnostic Performance Of the Evaluated Markerssupporting

confidence: 92%

“…High-sensitivity CRP (hs-CRP) methods have recently been introduced to accurately monitor minor increases in serum CRP (9 ), but no studies evaluating hs-CRP in sarcoidosis have been reported. Increased SAA has also been shown to be independently associated with sarcoidosis activity (10 ). SAA appears to be less sensitive to immunosuppressive drugs, such as corticosteroids, and therefore has been recommended in the follow-up of patients to whom such drugs have been administered (6 ).…”

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confidence: 99%

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Potential Usefulness of Inflammatory Markers to Monitor Respiratory Functional Impairment in Sarcoidosis

et al. 2003

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Section: Discussion Diagnostic Performance Of the Evaluated Markerssupporting

confidence: 92%

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confidence: 99%

Potential Usefulness of Inflammatory Markers to Monitor Respiratory Functional Impairment in Sarcoidosis

et al. 2003

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“…Secreted A-SAA associates with high-density lipoprotein (HDL), displacing apolipoprotein AI (Apo-AI) and yielding lipoprotein fractions, including SAA, lipidpoor Apo-AI, and lipoprotein-free SAA (4,5). Persistently high SAA usually indicates reduced Apo-AI and HDL cholesterol as a result of increases in HDL metabolism (5). However, during the acute-phase response, serum levels of A-SAA increase up to 1000-fold, saturating HDL and allowing lipid-free A-SAA to circulate.…”

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confidence: 99%

Acute Serum Amyloid A Induces Migration, Angiogenesis, and Inflammation in Synovial Cells In Vitro and in a Human Rheumatoid Arthritis/SCID Mouse Chimera Model

Connolly

Marrelli

Blades

et al. 2010

The Journal of Immunology

107

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Serum amyloid A (A-SAA), an acute-phase protein with cytokine-like properties, is expressed at sites of inflammation. This study investigated the effects of A-SAA on chemokine-regulated migration and angiogenesis using rheumatoid arthritis (RA) cells and whole-tissue explants in vitro, ex vivo, and in vivo. A-SAA levels were measured by real-time PCR and ELISA. IL-8 and MCP-1 expression was examined in RA synovial fibroblasts, human microvascular endothelial cells, and RA synovial explants by ELISA. Neutrophil transendothelial cell migration, cell adhesion, invasion, and migration were examined using transwell leukocyte/monocyte migration assays, invasion assays, and adhesion assays with or without anti–MCP-1/anti–IL-8. NF-κB was examined using a specific inhibitor and Western blotting. An RA synovial/SCID mouse chimera model was used to examine the effects of A-SAA on cell migration, proliferation, and angiogenesis in vivo. High expression of A-SAA was demonstrated in RA patients (p < 0.05). A-SAA induced chemokine expression in a time- and dose-dependent manner (p < 0.05). Blockade with anti-scavenger receptor class B member 1 and lipoxin A4 (A-SAA receptors) significantly reduced chemokine expression in RA synovial tissue explants (p < 0.05). A-SAA induced cell invasion, neutrophil–transendothelial cell migration, monocyte migration, and adhesion (all p < 0.05), effects that were blocked by anti–IL-8 or anti–MCP-1. A-SAA–induced chemokine expression was mediated through NF-κB in RA explants (p < 0.05). Finally, in the RA synovial/SCID mouse chimera model, we demonstrated for the first time in vivo that A-SAA directly induces monocyte migration from the murine circulation into RA synovial grafts, synovial cell proliferation, and angiogenesis (p < 0.05). A-SAA promotes cell migrational mechanisms and angiogenesis critical to RA pathogenesis.

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“…At elevated concentrations, SAA displaces apoA-I and produces lipoprotein fractions containing predominantly SAA, lipid-poor apoA-I, and lipoprotein-free SAA. Persistently high SAA levels are usually associated with significantly reduced apoA-I and HDL cholesterol levels due to enhanced HDL metabolism (18,19). SAA may also act as a signal for redirecting HDL to the sites of tissue destruction and cholesterol accumulation (20).…”

mentioning

confidence: 99%

Serum Amyloid A Binding to CLA-1 (CD36 and LIMPII Analogous-1) Mediates Serum Amyloid A Protein-induced Activation of ERK1/2 and p38 Mitogen-activated Protein Kinases

Baranova

Vishnyakova

Bocharov

et al. 2005

Journal of Biological Chemistry

161

183

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Influence of serum amyloid A on the decrease of high density lipoprotein-cholesterol in active sarcoidosis

Cited by 39 publications

References 31 publications

Potential Usefulness of Inflammatory Markers to Monitor Respiratory Functional Impairment in Sarcoidosis

Potential Usefulness of Inflammatory Markers to Monitor Respiratory Functional Impairment in Sarcoidosis

Acute Serum Amyloid A Induces Migration, Angiogenesis, and Inflammation in Synovial Cells In Vitro and in a Human Rheumatoid Arthritis/SCID Mouse Chimera Model

Serum Amyloid A Binding to CLA-1 (CD36 and LIMPII Analogous-1) Mediates Serum Amyloid A Protein-induced Activation of ERK1/2 and p38 Mitogen-activated Protein Kinases

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