Abstract
Rheumatoid arthritis is a severe chronic autoimmune disorder that results from pathological activation of immune cells and altered cytokine/chemokine network. The aim of our study was to evaluate concentrations of chosen cytokines and chemokines in blood sera and synovial fluid samples isolated from low disease activity rheumatoid arthritis (RA) patients and osteoarthritis (OA) sufferers. Blood sera and synovial fluid samples have been obtained from 24 OA and 14 RA patients. Cytokines/chemokines levels have been determined using a Milliplex® Map 38-plex human cytokine/chemokine magnetic bead-based panel (Merck Millipore, Germany) and Luminex® MAGPIX® platform (Luminex USA). Low disease activity RA patients showed altered concentration of numerous cytokine/chemokine when compared to OA controls—they were characterized by, inter alia, increased: eotaxin/CCL11 (p = 0.037), GRO/CXCL1 (p = 0.037), IL-2 (p = 0.013), IL-4 (p = 0.017), IL-7 (p = 0.003), IL-8 (p = 0.0007) and GM-CSF (p = 0.037) serum levels, whilst MDC/CCL22 concentration was decreased in this group (p = 0.034). Eotaxin/CCL11 (p = 0.001), GRO/CXCL1 (p = 0.041), IL-10 (p = 0.003), GM-CSF (p = 0.01), IL-1RA (p = 0.0005) and VEGF (p = 0.01) concentrations in synovial fluid of RA females were also increased. Even with low disease activity score, RA patients exhibited increased concentrations of cytokines with pro- and anti-inflammatory activities, as well as numerous chemokines, growth factors and regulators of angiogenesis. Surprisingly, RA subjects also shown decreased concentration of CCL22 chemokine. The attempt to restore cytokine balance and tolerogenic environment is ineffective in RA sufferers even with good disease management. Distinguished factors could serve as possible indicators of disease progression even in low disease activity patients.
Highlights
Rheumatoid arthritis (RA) is a severe chronic autoimmune disorder that is believed to affect approximately 1% of world’s population
Numerous cytokines have been indicated as playing pivotal role in RA including: TNF, IL-1, IL-6, or IL-12 to name just a few [4]
Disturbed interleukin 2 (IL-2) pathway has been described in various autoimmune disorders [13], e.g., RA sufferers display heightened titer of anti-IL-2 antibodies that may affect cytokine bioavailability for Tregs [14]
Summary
Rheumatoid arthritis (RA) is a severe chronic autoimmune disorder that is believed to affect approximately 1% of world’s population. It develops as a consequence of lack of proper inflammation resolution that lasts throughout patients’ lifetime [1]. Specific and non-specific leukocytes that migrate into joints interact with synovial tissue-resident cells as well as each other, creating continual highly destructive synovitis [2, 3]. This sophisticated communication between cells is heavily dependent on cytokines and chemokines. Despite successful TNF- or IL-6-targeted biological therapies, the frequency of refractory RA creates growing need to better understand cytokine hierarchy and seek for additional cytokine-focused therapeutic approaches [5]
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