Abstract
Synovial fibroblasts contribute to the inflammatory temporomandibular joint under pathogenic stimuli. Synovial fibroblasts and T cells participate in the perpetuation of joint inflammation in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. IL-17 is an inflammatory cytokine produced primarily by Th17 cells which plays critical role in the pathogenesis of numerous autoimmune and inflammatory diseases. Here, we investigated the roles of IL-17A in temporomandibular joint disorders (TMD) using genome-wide analysis of synovial fibroblasts isolated from patients with TMD. IL-17 receptors were expressed in synovial fibroblasts as assessed using real-time PCR. Microarray analysis indicated that IL-17A treatment of synovial fibroblasts upregulated the expression of IL-6 and chemokines. Real-time PCR analysis showed that the gene expression of IL-6, CXCL1, IL-8, and CCL20 was significantly higher in IL-17A-treated synovial fibroblasts compared to nontreated controls. IL-6 protein production was increased by IL-17A in a time- and a dose-dependent manner. Additionally, IL-17A simulated IL-6 protein production in synovial fibroblasts samples isolated from three patients. Furthermore, signal inhibitor experiments indicated that IL-17-mediated induction of IL-6 was transduced via activation of NFκB and phosphatidylinositol 3-kinase/Akt. These results suggest that IL-17A is associated with the inflammatory progression of TMD.
Highlights
The temporomandibular joint (TMJ) is one of the most complex and active joints in the human body, playing an important role in functions such as jaw motion speaking, chewing, and swallowing
Before examination of the functional effects of IL-17A in synovial fibroblasts, we first analyzed the expression of IL-17 receptor (IL-17R) family members A-E in synovial fibroblasts using real-time PCR
These data suggested that IL-17A signaling is transduced in synovial fibroblasts
Summary
The temporomandibular joint (TMJ) is one of the most complex and active joints in the human body, playing an important role in functions such as jaw motion speaking, chewing, and swallowing. Patients with temporomandibular disorders (TMD) most frequently present with pain, limited mandibular motion, and TMJ sounds. Inflammatory factors contribute to both inflammatory and degradative pathways associated with the progression of the pathological condition in the joints [1,2,3]. These inflammatory factors have been detected in the synovial fluids and/or tissues from patients with intracapsular pathological conditions of TMJ such as disc displacement (DD), internal derangement (ID), and/or osteoarthritis (OA) [1, 2]. An understanding of the molecular mechanisms that underlie the activities of these factors may contribute to an understanding of the pathogenesis of TMD; little is known about the molecular mechanisms that underlie the development of the pathological condition in TMJ
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