Contribution of interleukin 17 to human cartilage degradation and synovial inflammation in osteoarthritis

Honorati, Maria Cristina; Bovara, M.; Cattini, Luca; Piacentini, A.; Facchini, Andrea

doi:10.1053/joca.2002.0829

Cited by 120 publications

(89 citation statements)

References 36 publications

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“…16,17 In addition, IL-17 has been shown to induce the release of chemokines (such as IL-1b and tumour necrosis factor [TNF]-a) by chondrocytes and synovial fibroblasts, contributing to cartilage breakdown and synovial infiltration in osteoarthritis. 13 Others demonstrated that IL-17 inhibited proteoglycan synthesis in rat cartilage, and increased nitrogen monoxide production. 18 Although the aetiology and pathogenesis of osteoarthritis are poorly understood, it is possible that IL-17 may be among the critical mediators of the disturbed processes implicated in osteoarthritis pathophysiology.…”

Section: Discussionmentioning

confidence: 99%

“…12 Osteoarthritis shares several characteristics with rheumatoid arthritis, including joint destruction and synovitis. 13 In addition, IL-17 has been shown to be present in synovial fluid from patients with osteoarthritis, 14 but the relationship between serum and synovial fluid IL-17 concentrations and severity of primary knee osteoarthritis remains to be clarified.…”

Section: Introductionmentioning

confidence: 99%

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Association between severity of knee osteoarthritis and serum and synovial fluid interleukin 17 concentrations

et al. 2013

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Objective: To determine interleukin (IL)-17 concentrations in serum and synovial fluid from patients with knee osteoarthritis, and evaluate their correlation with disease severity. Methods: Serum and synovial fluid were collected from patients with primary knee osteoarthritis; age-and sex-matched healthy control subjects provided serum samples. This study was conducted retrospectively. IL-17 was quantified by enzyme-linked immunosorbent assay. Osteoarthritis severity and grade were assessed using the Lequesne index and Kellgren and Lawrence (KL) grading system, respectively. Results: Serum IL-17 concentrations were significantly higher in patients (n ¼ 98) than in controls (n ¼ 50). In the patient group, the synovial fluid IL-17 concentration increased significantly with KL grade and was significantly positively correlated with Lequesne index (r ¼ 0.6232). Conclusions: The synovial fluid IL-17 concentration could represent a useful biochemical marker to reflect knee osteoarthritis severity and progression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Association between severity of knee osteoarthritis and serum and synovial fluid interleukin 17 concentrations

et al. 2013

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“…78 il17 also contributes to cartilage inflammation by stimu lating chondrocytes and synovial fibroblasts to release chemokines such as il8 and growthregulated α protein (also known as Groα) that are involved in attracting mononuclear cells and in chondrocyte differentiation. 79 However, although the il17 receptor has been clearly identified in chondrocytes, this cytokine does not seem to be produced locally in most cases of oa. 80 il15, a cytokine produced in innate immune res ponses, could be involved in early oa since higher concentrations of il15 are found in the synovial fluid of patients with early oa than in those with endstage oa.…”

Section: Histopathological Features Of Oa Synovitismentioning

confidence: 99%

The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis

2010

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Osteoarthritis (OA), one of the most common rheumatic disorders, is characterized by cartilage breakdown and by synovial inflammation that is directly linked to clinical symptoms such as joint swelling, synovitis and inflammatory pain. The gold-standard method for detecting synovitis is histological analysis of samples obtained by biopsy, but the noninvasive imaging techniques MRI and ultrasonography might also perform well. The inflammation of the synovial membrane that occurs in both the early and late phases of OA is associated with alterations in the adjacent cartilage that are similar to those seen in rheumatoid arthritis. Catabolic and proinflammatory mediators such as cytokines, nitric oxide, prostaglandin E(2) and neuropeptides are produced by the inflamed synovium and alter the balance of cartilage matrix degradation and repair, leading to excess production of the proteolytic enzymes responsible for cartilage breakdown. Cartilage alteration in turn amplifies synovial inflammation, creating a vicious circle. As synovitis is associated with clinical symptoms and also reflects joint degradation in OA, synovium-targeted therapy could help alleviate the symptoms of the disease and perhaps also prevent structural progression.

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“…IL-17F was reported to employ IL-17R for signaling and IL-17F and IL-17A could induce IL-17R ubiquitination and DN-TRAF6, a dominant-negative mutant, could block IL-17F but not IL-17A triggered ubiquitination of IL-17R [46]. The IL-17R is ubiquitously expressed in virtually all cells and tissue and its expression was shown on synoviocytes, chondrocytes and synovial endothelial cells [47][48][49]. Expression of different IL-17 homologs (IL-17A, C, E and F) was detected in synovial fluid mononuclear cells from RA patients and different IL-17R (IL-17RA, IL-17RB, C and D) expression was noted in fibroblast-like synoviocytes of RA patients [50].…”

Section: What Is the Most Physiologically Relevant Target Of Il-17a Imentioning

confidence: 99%

IL-17/Th17 targeting: On the road to prevent chronic destructive arthritis?

Lubberts¹

2008

Cytokine

274

230

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Interleukin-17A (IL-17A) contributes to the pathogenesis of arthritis. Data from experimental arthritis indicate IL-17 receptor signaling as a critical pathway in turning an acute synovitis into a chronic destructive arthritis. The identification of six IL-17 family members (IL-17A-F) may extend the role of this novel cytokine family in the pathogenesis of chronic destructive joint inflammation. Whether the successful anti-IL-17A cytokine therapy in murine arthritis can be effectively translated to human arthritis need to be tested in clinical trials in humans. Interestingly, IL-17A and IL-17F are secreted by the novel T helper subset named Th17. This novel pathogenic T cell population induces autoimmune inflammation in mice and is far more efficient at inducing Th1-mediated autoimmune inflammation in mice than classical Th1 cells (IFN-c). In addition to IL-17A and IL-17F, Th17 cells are characterized by expression of IL-6, TNF, GM-CSF, IL-21, IL-22 and IL-26. Th17 cells have been established as a separate lineage of T helper cells in mice distinct from conventional Th1 and Th2 cells. Whether this also applies to human Th17 and whether RA is a Th1 or a Th17 mediated disease is still not clear. This review summarizes the findings about the role of IL-17 in arthritis and discusses the impact of the discovery of the novel Th17 cells for arthritis. Further studies are needed to unravel the role of Th17 cells and the interplay of IL-17 and other Th17 cytokines in the pathogenesis of arthritis and whether regulating Th17 cell activity will have additional value compared to neutralizing IL-17A activity alone. This might help to reach the ultimate goal not only to treat RA patients but to prevent the development of this crippling disease.

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Contribution of interleukin 17 to human cartilage degradation and synovial inflammation in osteoarthritis

Abstract: These data suggest that IL-17 could contribute to cartilage breakdown and synovial infiltration in OA by inducing both the release of chemokines by chondrocytes and synovial fibroblasts and, in a less extent, the synthesis of IL-1beta by chondrocytes.

Cited by 120 publications

References 36 publications

Association between severity of knee osteoarthritis and serum and synovial fluid interleukin 17 concentrations

Association between severity of knee osteoarthritis and serum and synovial fluid interleukin 17 concentrations

The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis

IL-17/Th17 targeting: On the road to prevent chronic destructive arthritis?

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