Author(s): Anjali Aggarwal


Background Osteoarthritis (OA) one of the most frequent joint disorders is traditionally believed to be a degenerative disease of articular cartilage. Increased understanding about its pathophysiology suggests its etiology to be multifactorial. Evidences suggest that inflammation precedes structural deterioration and plays a crucial role in its pathogenesis. Since inflammation is strongly implicated during OA disease progression, anti-inflammatory agents to block potent inflammatory cytokines such as TNFα and IL1β have gone into preclinical trials; however, larger controlled trials still need to be established [1, 2]. In addition, CD161, a type II transmembrane glycoprotein, is expressed on the surface of Th17 cells and regulated by the RAR-related orphan receptor C transcription factor [3, 4]. An increased percentage of CD161+CD4+ T cells have been found to be associated with disease severity and inflammation during rheumatoid arthritis [5]. Based on this observation, a role of CD161+ T cells in driving the local inflammation during osteoarthritis could be speculated. No specific drug therapy is available. Unravelling role of inflammatory mediators & their downstream signaling pathways leading to OA progression is a thriving area of research. Increasing evidence suggests a role of inflammation during the pathogenesis of Osteoarthritis (OA). Aim of the present study was to evaluate the local and systemic inflammation during OA disease progression and to identify a potential phenotypic marker to distinguish low and high KL grade patients. Methods The local and systemic inflammation was studied in 33 patients of different KL grades, grade2 (n=11), grade3 (n=6) and grade4 (n=16). The levels of cytokines, adipokines, and matrix metalloproteinases (MMPs) were measured in serum and synovial fluid (SF) by flow cytometry and ELISA respectively. The frequency of T cells and CD161 expression was measured by flow cytometry. The levels of cytokines (IL-1β, IL-6, IL-8, IL-12, TNF-α and IL-10) were determined using BD cytometric bead array system (CBA Human Inflammation Kit, BD Biosciences) in the serum and synovial fluid samples. Briefly, 50 μL of mixed capture beads and 50 μL of serum or synovial fluid samples were added to the assay tubes followed by incubation for 1.5 hours at room temperature. After washing, 50 μL of PE detection reagent was added and tubes incubated for another 1.5 hours. The levels of MMP9 and MMP13 (Qayee-bio) were measured in both serum and SF samples using ELISA. The levels of adiponectin (Calbiotech) and leptin (DRG Diagnostics) in serum and synovial fluid were also measured using ELISA on an Infinite M200 PRO spectrophotometer (Tecan). The levels of IL- 17 were measured in the serum of patients using ELISA (Diaclone), and results were expressed as pg/mL. The expression of CD161 [PE] was analysed on all these cell populations by calculating the median fluorescent intensity (MFI) using FACSDivaTM software (BD Bioscience). Appropriate isotype control (IgG1 κ [PE]) for CD161 was used.

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