Abstract
Osteoarthritis (OA) is a chronic systemic musculoskeletal disorder involving inflammation, immunity, and metabolic alterations. OA is commonly regarded as non-inflammatory disease; still inflammation is recognized as contributing to the symptoms and progression of OA. New evidence suggests that adipokines are involved in the pathophysiology of OA and might modulate the production of inflammatory mediators including in immune cells. However, the role of immune component in osteoarthritis is still poorly investigated. To gain further insights into the interaction of immune cells in OA and the role of adipokines on these cells, we performed experiments aimed to determine the cytokine profile in activated CD4+ T cells from OA patients. For completeness, we also explored the cross talk between T lymphocytes and chondrocytes in OA by co-culturing human primary chondrocytes with activated CD4+ T cells in two ways: the first by incubating the cells by direct contact (D.C.) or by transwell system. Our results show that the exposure of activated CD4+ T cells to adipokines modulates IL-6, IL-8, and CCL-3 production. In addition, the production of key macromolecules of ECM (aggrecan and collagen-2) and matrix metalloproteinase 13 (MMP-13) in co-cultured chondrocytes with activated CD4+ T cells was altered. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1299-1303, 2017.
Highlights
Osteoarthritis (OA) is a complex disease influenced by multiple risk factors that has been conventionally regarded as a non- inflammatory arthropathy.OA cannot be considered anymore as a simple degenerative disease driven by mechanical events
MRNA expression of COL2A1 (Figure 2 B) was significantly decreased in chondrocytes seeded in direct contact (D.C.) with activated CD4+ T cells and in the transwell system when compared with chondrocytes alone
We observed that MMP-13 mRNA expression was significantly increased in D.C. and transwell system when compared with chondrocytes alone Figure 2 D)
Summary
Osteoarthritis (OA) is a complex disease influenced by multiple risk factors that has been conventionally regarded as a non- inflammatory arthropathy.OA cannot be considered anymore as a simple degenerative disease driven by mechanical events. Osteoarthritis (OA) is a complex disease influenced by multiple risk factors that has been conventionally regarded as a non- inflammatory arthropathy. A growing body of evidence supports the notion of a leading role of immunometabolic alterations and inflammatory processes, both at local as well as systemic levels in inducing cellular and tissue damage[1,2,3]. Activated T cells can stimulate monocytes to produce cytokines through cell contact–dependent interaction or through soluble mediators[6,7] such as TNF-α and IL-1β. CD4+ T cells were activated during the onset of OA and induced MIP-1γ expression and subsequent osteoclast formation[9].
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