Expression levels of IL-15 and IL-17 in synovial fluid of rheumatoid arthritis animal model

Abstract

The aim of the present study was to investigate the expression levels of interleukin-15 (IL-15) and interleukin-17 (IL-17) in synovial fluid of rheumatoid arthritis (RA) animal model, and to investigate their correlations with RA. A total of 100 Wistar rats were selected, among which 60 rats were used to establish the collagen II-induced arthritis (CIA) model as the model observation group, and the remaining 40 rats were used as blank control group. The levels of IL-15 and IL-17 in synovial fluid were detected via enzyme-linked immunosorbent assay (ELISA) at 1, 7, 14, 21 and 28 days after successful modeling. RA was evaluated by using arthritis index (AI) and pedal swelling volume. The expression levels of IL-15 and IL-17 in synovial fluid of rats in model observation group were higher than those in blank control group (P<0.05), and the levels of IL-15 and IL-17 in model observation group were gradually increased over time. In model observation group at 7 days after modeling, AI and pedal swelling volume began to be increased gradually reaching a peak at 28 days. The pedal swelling volume of CIA model rats was significantly higher than that of the blank control group (P<0.05). The increased expression levels of IL-15 and IL-17 in synovial fluid of rats in the CIA model observation group are correlated with the activity of disease, which can be used as reference indexes for the activity of RA.

Phenotypic and functional characterization of natural killer cells in rheumatoid arthritis-regulation with interleukin-15

“…Higher serum IL-15 levels in RA patients which may contribute to the observed NK cell increase. Jin et al who showed that the level of IL-15 and IL-17 were significantly elevated in synovial fluid of rats and involved in the perpetuation of RA synovitis 13 www.nature.com/scientificreports www.nature.com/scientificreports/ NKp46, a natural cytotoxicity receptor, mediates NK cell-induced cell lysis and provide an innate defense against intracellular pathogens, NKp46 also serve as a key factor in the pathogenesis of type 1 diabetes mellitus by recognition of pancreatic β cells ligands [15][16][17] . We observed NK cells from RA patients expressed lower NKp46 than those from controls, and IL-15 decreased NKp46 expression of NK cells from RA patients, similar to that observed in controls.…”

Secreted Osteoclastogenic Factor of Activated T Cells (SOFAT) Is Associated With Rheumatoid Arthritis and Joint Pain: Initial Evidences of a New Pathway

“…However, around 50% are unresponsive to treatment as well as biologics targeting these cytokines increase the incidence of infection (8,32). IL-15 contributes to RA physiopathology by stimulating T-cell development and survival, delaying the apoptosis of fibroblast-like synoviocytes as well as by recruiting neutrophils and lymphocytes to the inflammatory foci (17,33,34). A phase I-II clinical trial using a human IgG1 monoclonal antibody to target IL-15 reduced the disease activity according to the American College of Rheumatology criteria by 20% (ACR20) in 63% of patients, ACR50 in 38% of patients, and ACR70 in 25% of patients (35).…”

Association between the polymorphism of IL-17A and IL-17F gene with knee osteoarthritis risk: a meta-analysis based on case-control studies

“…IL-17 is one of the most important regulators of innate and adaptive immune responses, and it is expressed in synovial tissues, and could contribute to cartilage degeneration and synovial infiltration in joint by inducing the release of chemokines by chondrocytes [29,30]. Furthermore, studies in animal models suggest that IL-17 knock-out mice contribute to more severe RA than wild-type animals [31]. We have reasons to believe that IL-17 may contribute to the development of knee OA.…”