The secretion of proinflammatory cytokines and chemokines in stimulated fibroblast-like synoviocytes of osteoarthritis

Purpose: Currently, fibroblast-like synoviocytes (FLS) have been recognized to play a pivotal role in the pathogenesis and progression of rheumatoid and osteoarthritic joint diseases. In-vitro studies offered insights into the mediated effects of FLS in the inflammatory responses and cartilage degradation of the arthritis. The aim of this study is to identify the secretion profile of proinflammatory cytokines and chemokines of arthritic FLS in the presence of other cytokine stimuli. Methods: Synovial tissues were collected from patients with osteoarthritis (OA) or rheumatoid arthritis (RA) received total knee arthroplasty or synovectomy. The FLS were enriched by using enzymatical digestion of synovial tissue with collagenase and repeated passage in vitro. Subsequently, the FLS were treated with different cytokine stimuli including Interleukin (IL) -1b, tumor necrosis factor (TNF) -a and interferon (IFN) -g at gradient concentration for 24 h. The collected supernatant was applied in the following ELISA for the determination of the secretion level of IL-6, IL-8 and monocyte chemotactic protein 1 (MCP-1). Results: Similar to RA FLS, the FLS enriched from OA synovial tissue could response to the cytokine stimulation. All the cytokine stimuli could induce the release of IL-6, IL-8 and MCP-1 from both OA and RA FLS except IFN-g (Fig. 1). Compared to RA FLS, the OA FLS stimulated by IL-1b could produce more MCP-1 chemokine (p<0.01). Conclusions: The investigation suggested that the cytokines existed in the inflammatory environment of both OA and RA is capable to induce the FLS to release proinflammatory cytokines and chemokines which may dramatically enhance the inflammatory activity. Other supporting experiments are required to further elucidate the mechanism of FLS mediated inflammatory responses in osteoarthritis.Fig.1. The secretion level of IL-6, IL-8 and MCP-1 in FLS stimulated by different cytokines including IL-1b, TNF-a and IFN-g.