Background It was reported that type I interferon (IFN) is involved in the pathogenesis of rheumatoid arthritis (RA) [1–3], while the relevance of the IFN signature to RA disease activity and progression remains unclear. There were few reports about the expression of IFN in synovial fluid and joint cartilage.

Objectives The aim of this study is to investigate the role of IFN in the pathogenesis of RA by means of the analysis of joint tissues of RA patients comparing with those of osteoarthritis (OA) patients.

Methods Synovial fluid, synovia and cartilage were collected from RA and OA patients (n=10 for each) during total knee arthroplasty in our hospital and blood samples were collected just before surgery. As preoperative therapy for RA, Methotrexate (MTX) was administered to 9 patients (dose ranged (4–12mg), DMARDS without MTX to 2, biological DMARDS to 2, Prednisolone (PSL) to 6 (dose 1–5mg). Quantities of IFN alpha or beta of blood and joint fluid were measured with ELISA (PBL Assay Science, USA), and expression of IFN alpha, beta and TNF alpha of synovia and joint cartilage were measured with real time PCR. In RA patients. Serum biomarkers such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), Rheumatoid Factor (RF), hemoglobin and platelet were measured and investigated correlation with the quantities of IFN of blood or joint tissues. Medication for RA were investigated as well.

Results In blood and synovial fluid of RA patients, IFN alpha and beta were highly detected, while they were not detected in those of OA patients. The expression of IFN alpha and beta of RA cartilage were much higher than those of OA whereas they were not expressed in synovium of both RA and OA. Expression of IFN was not correlated with that of TNF alpha in RA patients. Statistical analysis revealed that RF was related with blood and joint IFN and other markers were not. Medications for RA were not correlated with IFN expression.

Conclusions IFN was highly expressed in RA synovial fluid, joint cartilage and blood, not in OA. IFN immunotherapy has been reported to induce RA [4–5], therefore abundant IFN might induce RA and inhibit cure of RA. Our results showed that RF was related with blood and joint IFN. It can be speculated that RF might be an index of IFN regulation in RA patient, however, more samples must be investigated to prove this speculation.

References

1. de Padiila CML and Niewold TB. The Type I Interferons: Basic Concepts and Clinical Relevance in Immune-mediated Inflammatory Diseases. Gene. 2016; 15, 576, 14–21.

2. Carrio JR, de Paz B, et al. IFN alpha Serum Levels Are Associated with Endothelial Progenitor Cells Imbalance and Disease Features in Rheumatoid Arthritis Patients. Plos One, 2014;9, e86069.

3. van Holten J, Smeets TJM, et al. Expression of interferon b in synovial tissue from patients with rheumatoid arthritis: comparison with patients with osteoarthritis and reactive arthritis. Ann Rheum Dis. 2005; 64: 1780–2.

4. Passos SE, Evangelista SPT, et al. Rheumatoid arthritis induced by alpha-interferon therapy. Clin Rheumatol. 2001;20(4):297–9.

5. Cacopardo B, Benanti F, et al. Rheumatoid arthritis following PEG-interferon- alfa-2a plus ribavirin treatment for chronic hepatitis C: a case report and review of the literature. BMC research notes. 2013; 6:437.

References

Disclosure of Interest None declared