IL-6 secretion in osteoarthritis patients is mediated by chondrocyte-synovial fibroblast cross-talk and is enhanced by obesity
Research output: Contribution to journal › Article
- Department of Immunobiology, Yale School of Medicine
- Royal Orthopaed Hosp
Increasing evidence suggests that inflammation plays a central role in driving jointpathology in certain patients with osteoarthritis (OA). Since many patients with OAare obese and increased adiposity is associated with chronic inflammation, weinvestigated whether obese patients with hip OA exhibited differential proinflammatorycytokine signalling and peripheral and local lymphocyte populations,compared to normal weight hip OA patients.No differences in either peripheral blood or local lymphocyte populations were foundbetween obese and normal-weight hip OA patients. However, synovial fibroblastsfrom obese OA patients were found to secrete greater amounts of the proinflammatorycytokine IL-6, compared to those from normal-weight patients (p<0.05),which reflected the greater levels of IL-6 detected in the synovial fluid of the obeseOA patients. Investigation into the inflammatory mechanism demonstrated that IL-6secretion from synovial fibroblasts was induced by chondrocyte-derived IL-6.Furthermore, this IL-6 inflammatory response, mediated by chondrocyte-synovialfibroblast cross-talk, was enhanced by the obesity-related adipokine leptin. Thisstudy suggests that obesity enhances the cross-talk between chondrocytes andsynovial fibroblasts via raised levels of the pro-inflammatory adipokine leptin, leadingto greater production of IL-6 in OA patients.
|Early online date||14 Jun 2017|
|Publication status||E-pub ahead of print - 14 Jun 2017|
- IL-6 , chondrocytes , fibroblasts, obesity , synovial inflammation , leptin