Background Rheumatoid arthritis is characterized by painful joint swelling, cartilage and bone destruction, chronic inflammation of the synovium (synovitis) with the accumulation of synovial fluid into the joint cavity. Within the synovial fluid the number of MSC-like cells (SYF-MSC) is increasing during the active phase of the disease. MSC are able to mediate immunosuppression via cell-cell contact and secreted factors respectively.
Objectives Our goal was to screen the secreted proteins by SYF-MSCs under pro-inflammatory conditions.
Methods Synovial fluid was harvested from patients with active RA (according to the Guidelines of the Helsinki Declaration). The isolated fluid/cells were cultured in vitro, their expression of well-known MSC markers as well as their differentiation potential was tested. SYF-MSCs were treated with human recombinant TNF alpha (TNFa) for 24 hour than the secreted cytokines were determined by high throughput protein array.
Results SYF-MSCs secreted aggrecan, angiogenin, chitinase 3 like-1, Dkk-1, DPPIV, EMMPRIN, FGF-19, GM-CSF, IGFBP-3, IL-6, IL-17A, MCP-1, PDGF-AA, Pentraxin-3, Resistin, SDF-1α and Thrombospondin-1 under normal condition. Treatment by TNFa decreased the level of the secreted chitinase 3 like-1 (544003±56200.85; Pixel density, Mean±SD) and Dkk-1 (388062.5±10488.51) compared to untreated controls (721671.5±10434.77 and 705830±16013.14). Beside this phenomenon the pro-inflammatory provocation increased the secretion of IL-6 (from 79140±6940.96 to 615191±73256.26), MCP-1 (283985.5±25964.25 to 846348±81354.05), furthermore induced the release of IL-(8743315±71580.42) IL-24 (32189±29555.65) and RANTES (641698±26383.57). Unlike untreated cells no resistin, empirin and SDF-1 could be detected after TNFa exposure.
Conclusions The in vitro data suggest that TNFa is able to turn SYF-MSCs to a pro-inflammatory phenotype, which may play a role in the inflammatory processes of RA prolonging the active phase of the disease.
Disclosure of Interest None declared