The cytokine profile in synovial tissue and synovial fluids from patients with rheumatoid arthritis

• Main Authors: Huang-Chen Chang, 張凰真
• Other Authors: Cheng-Chieh Lin
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/48502727523797651807

碩士 === 中興大學 === 生命科學院碩士在職專班 === 99 === Rheumatoid arthritis (RA) is a chronic inflammatory disease that mainly targets the synovial membrane, cartilage and bone. It affects 1% of the population and is associated with significant morbidity and increased mortality.Cytokines are directly implicated in many of the immune processes that are associated with the pathogenesis of RA. In this study, we measured the sera and synovial fluids cytokine levels including IL-1β, TNF-α, IL-6, IL-17, IL-22 and IFN-γ by enzyme-linked immunosorbent assay (ELISA) from patients with RA, osteoarthritis (OA) and systemic lupus erythematosus (SLE). We demonstrated that RA patients expressed significantly higher levels of IL-1β and TNF-α in sera than OA (p<0.0001), SLE (p<0.0005) and healthy control(HC) (p<0.0001). Sera levels of IL-6 in RA and SLE patients significantly higher than in OA and HC (P <0.01), There are no differences in sera levels of IL-6 between RA patients and SLE patients. There are no statistical differences in the sera levels of IL-17 between RA patients and OA patients. In synovial fluids, RA patients expressed significantly higher levels of IL-1β(p<0.05) and TNF-α(p<0.01) than OA .Besides, we analyzed IL-6, TNF-alpha gene expression in synovial tissues from RA and OA paients by Real time PCR (Real-time Polymerase Chain Reaction). We demonstrated increased expression of TNF-αand IL-6 expression in RA synovial samples compared with osteoarthritis synovium. In conclusion, IL-1β, TNF-α and IL-6 were highly expressed in sera, synovial fluids and synovial tissue in RA patients as compared with OA. Our data indicated that proinflammatory cytokines such as IL-1β, TNF-α, IL-6 may regulate inflammatory processes that were implicated in the pathogenesis of rheumatoid arthritis.