Abstract
There is growing evidence that apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) regulates inflammatory responses. Rheumatoid arthritis (RA) is an autoimmune disease, which is characterized with synovitis and joint destruction. Therefore, this study was planned to investigate the relationship between APE1/Ref-1 and RA. Serum and synovial fluid (SF) were collected from 46 patients with RA, 45 patients with osteoarthritis (OA), and 30 healthy control (HC) patients. The concentration of APE1/Ref-1 in serum or SF was measured using the sandwich enzyme-linked immunosorbent assay (ELISA). The disease activity in RA patients was measured using the 28-joint disease activity score (DAS28). The serum APE1/Ref-1 levels in RA patients were significantly increased compared to HC and OA patients (0.44 ± 0.39 ng/mL for RA group vs. 0.19 ± 0.14 ng/mL for HC group, p < 0.05 and vs. 0.19 ± 0.11 ng/mL for OA group, p < 0.05). Likewise, the APE1/Ref-1 levels of SF in RA patients were also significantly increased compared to OA patients (0.68 ± 0.30 ng/mL for RA group vs. 0.31 ± 0.12 ng/mL for OA group, p < 0.001). The APE1/Ref-1 concentration in SF of RA patients was positively correlated with DAS28. Thus, APE1/Ref-1 may reflect the joint inflammation and be associated with disease activity in RA.
Highlights
Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovitis, joint destruction, and other damage caused by systemic inflammation [1]
Tumor necrosis factor (TNF)-α and interleukin (IL)-1 are key proinflammatory cytokines that are mainly secreted by macrophages and induce the expression of IL-6, IL-8, IL-10, adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), and matrix metalloproteinases (MMPs) [2]
As the healthy control (HC) group was randomly selected in a biobank, we could not obtain information on body mass index (BMI), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP)
Summary
Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovitis, joint destruction, and other damage caused by systemic inflammation [1]. Various cytokines are mainly secreted from these cells, which leads to the recruitment of inflammatory cells and joint destruction Among these cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-1 are key proinflammatory cytokines that are mainly secreted by macrophages and induce the expression of IL-6, IL-8, IL-10, adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), and matrix metalloproteinases (MMPs) [2]. Tumor necrosis factor (TNF)-α and interleukin (IL)-1 are key proinflammatory cytokines that are mainly secreted by macrophages and induce the expression of IL-6, IL-8, IL-10, adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), and matrix metalloproteinases (MMPs) [2] These inflammatory mediators accelerate bone erosion, cartilage destruction, and systemic inflammatory responses (including anemia, fatigue, and cardiovascular disease) [1,2]. Inhibitors of these cytokines (especially TNF-α and IL-6 inhibitors) have already been implicated in the treatment of RA [3,4]
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