J Pharm Pharmacogn Res 2(Suppl. 1): S42, 2014
Special supplement with the abstract book of LATINFARMA 2013
CO 069: LEVELS OF SOLUBLE IL-15, IL-6, TNFΑ AND IL-15RΑ IN SYNOVIAL FLUID AND MEMBRANE BOUND IL-15 ON SYNOVIAL CELLS FROM PATIENTS WITH RHEUMATOID ARTHRITIS AND OSTEOARTHRITIS
Machado-Díaz AC1, Arrieta-Aguero C1, Chico-Capote A2, RodriguezAlvarez Y1, García-del Barco Herrera D1, Raices-Cruz I1, Falcón-Cama V1, Chacón-Quintero Y1, Guillen-Nieto G1, Santos-Savio A1.
Introduction: Cytokines are a family of proteins involved in regulation of the immune system and the intercellular communication. Many autoimmune diseases such as Rheumatoid arthritis (RA) are related to deregulation of cytokine expression. High levels of pro-inflammatory cytokines IL-15, IL-6 and TNF-α have been described in synovial fluid from RA patients.
Material and methods: In this study we quantified these cytokines levels in synovial fluid from 18 RA and 17 osteoarthritis (OA) patients, from Rheumatology service at B. Ameijeiras hospital, who presented inflammation and abundant synovial fluid in damaged joints. We also quantified levels of soluble IL-15Rα, a private receptor for IL-15, using an ELISA designed by our group. We also studied expression of membrane-bound IL-15 on synovial cells by FACS and EM.
Results: Current study confirmed presence of soluble IL-15Rα in synovial fluids from RA and OA patients. Although we detected expression of membrane IL-15 on cells from synovial fluids of RA patients. Also we determined that IL-15 is present as a membrane bound ligand. Acidic treatment produced a slight decrease in the amount of membrane-bound IL-15. Indicating that, in addition to transmembrane IL-15, a certain number of IL-15 molecules are bound to membrane IL-15Rα. Interestingly, we found a positive correlation between high levels of IL-6 and high levels of IL-15Rα in RA but not in OA.
Conclusions: The presence of soluble IL-15Rα and membrane IL-15 suggested that soluble IL-15Rα could induce IL-6 through a reverse signaling pathway and then contributing to a proinflammatory medium in RA.