Table 1:
Cytokine | Role in OA | Reference |
---|---|---|
IL-1β | Increased in OA joint synovial fluid, cartilage, synovial membrane and subchondral bone. It increases the production of iNOS, COX-2, IL-6, TNF-α IL-8, MCP1, RANTES and the levels of PGE2 and NO in chondrocytes and in cartilage explants. Increases the levels of matrix degrading proteases MMP-1, MMP-3, MMP-9, MMP-13, ADAMTS-4 and ADAMTS-5 and matrix degradation. Suppresses the synthesis of type II collagen and aggrecan and proteoglycan. |
[52, 74, 86] |
TNF-α | Increased in OA joint synovial fluid, cartilage, synovial membrane and subchondral bone. It increases the production of iNOS, COX-2, IL-6, IL-8, MCP1, RANTES and the levels of PGE2 and NO in chondrocytes and in cartilage explants. Increases the levels of matrix degrading proteases MMP-1, MMP-3, MMP-9, MMP-13, ADAMTS-4 and ADAMTS-5 and matrix degradation. Suppresses the synthesis of type II collagen and aggrecan. |
[61] |
IL-6 | Increased in OA joint synovial fluid, cartilage, synovial membrane and serum of OA patients. Upregulates MMP-13 expression in chondrocytes. Downregulates the expression of type II collagen. |
[66, 70] |
IL-15 | Increased in the synovial fluids of OA joints. Is associated with joint pain. |
[48] |
IL-17 | Increased in the synovial fluids of OA joints. Induces IL-1β, TNF-α and IL-6 expression and suppresses proteoglycan synthesis. |
[14, 46] |
IL-18 | Increased in the OA joints cartilage and synovial fluid. Increases the production of MMP-1, MMP-3, MMP-13. |
[47] |
LIF | Increased in the synovial fluids of OA joint. Enhances cartilage extracellular matrix degradation. Increases matrix degrading proteases expression and nitric oxide levels. |
[49, 139] |
MCP1 | Increased in OA joint tissue and in chondrocytes under pathological conditions | [54] |
RANTES | Increased in OA joint tissue and in chondrocytes under pathological conditions | [54] |
IL-8 | Increased in OA joint tissue and in chondrocytes under pathological conditions | [54, 70] |
IL-4 and IL-10 | Anti-inflammatory. Increase the expression of IL-IRa and TIMP and decrease IL-1β, TNF-α expression. |
[46, 54] |