Interleukin‐1‐induced interleukin‐6 is required for the inhibition of proteoglycan synthesis by interleukin‐1 in human articular cartilage

Nietfeld, J. J.; Wilbrink, B.; Helle, M.; Roy, J. L. A. M. Van; Otter, W. Den; Swaak, A. J. G.; Huber-Bruning, O.

doi:10.1002/art.1780331113

Cited by 119 publications

(62 citation statements)

References 22 publications

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“…Furthermore, IL-1 induces IL-6 synthesis by chondrocytes and is a cofactor in the IL-1-induced suppression of proteoglycan (PG) synthesis (Nietfeld et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

Cuzzocrea

Mazzon

Bevilaqua

et al. 2000

British J Pharmacology

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1 The aim of the present study was to investigate the e ects of cloricromene, a coumarine derivative, in rats subjected to collagen-induced arthritis. 2 Collagen-induced arthritis (CIA) was induced in Lewis rats by an intradermal injection of 100 ml of the emulsion (containing 100 mg of bovine type II collagen) (CII) and complete Freund's adjuvant (CFA) at the base of the tail. On day 21, a second injection of CII in CFA was administered. 3 Lewis rats developed an erosive hind paw arthritis when immunized with CII in CFA. Macroscopic clinical evidence of CIA ®rst appeared as peri-articular erythema and oedema in the hind paws. The incidence of CIA was 100% by day 27 in the CII challenged rats and the severity of CIA progressed over a 35-day period with radiographic evaluation revealing focal resorption of bone together with osteophyte formation in the tibiotarsal joint and soft tissue swelling. 4 The histopathology of CIA included erosion of the cartilage at the joint margins. Treatment of rats with cloricromene (10 mg kg 71 i.p. daily) starting at the onset of arthritis (day 23), delayed the development of the clinical signs at days 24 ± 35 and improved histological status in the knee and paw. 5 Immunohistochemical analysis for iNOS, COX-2, nitrotyrosine and for poly (ADP-ribose) synthetase (PARS) revealed a positive staining in in¯amed joints from collagen-treated rats. The degree of staining for iNOS, COX-2, nitrotyrosine and PARS were markedly reduced in tissue sections obtained from collagen-treated rats, which had received cloricromene. 6 Radiographic signs of protection against bone resorption and osteophyte formation were present in the joints of cloricromene-treated rat. 7 This study provides the ®rst evidence that cloricromene, a coumarine derivative, attenuates the degree of chronic in¯ammation and tissue damage associated with collagen-induced arthritis in the rat.

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“…Furthermore, IL-1 induces IL-6 synthesis by chondrocytes and is a cofactor in the IL-1-induced suppression of proteoglycan (PG) synthesis (Nietfeld et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

Cuzzocrea

Mazzon

Bevilaqua

et al. 2000

British J Pharmacology

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“…In fact, IL-1␤, together with TNF␣, induces the release of tissue-damaging enzymes from synovial cells and articular chondrocytes and activates osteoclasts (30,31). IL-6 participates together with IL-1 in the catabolism of connective tissue components at inflammation sites (32,33), and activates osteoclasts, resulting in joint destruction (34). It is likely that a decrease in IL-6 and IL-1␤ is one of the factors involved in the amelioration of articular lesions upon anti-IL-18 treatment in our experimental model.…”

Section: Discussionmentioning

confidence: 92%

Role of interleukin‐18 in experimental group B streptococcal arthritis

Tissi¹,

McRae²,

Ghayur³

et al. 2004

Arthritis & Rheumatism

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Objective. To assess the role of interleukin-18 (IL-18) in the evolution of septic arthritis induced by group B streptococci (GBS) in mice.Methods. CD1 mice were inoculated intravenously with 8 ؋ 10 6 colony-forming units (CFU) of type IV GBS (strain 1/82), and administered intraperitoneally 1 hour before infection with anti-IL-18 monoclonal antibodies (0.25 mg/mouse). In a subsequent set of experiments, mice infected with a suboptimal arthritogenic dose of GBS (4 ؋ 10 6 CFU/mouse) were administered different doses of recombinant IL-18 for 4 days, starting 1 hour after infection. Mortality, evolution of arthritis, bacterial clearance, joint histopathology, and cytokine production were examined in infected mice that did or did not receive treatment with anti-IL-18 antibodies or IL-18.Results. IL-18 was produced during GBS infection. Neutralization of IL-18 resulted in a decrease in mortality rates, and in the incidence and severity of arthritis. Amelioration of arthritis was accompanied by a dramatic reduction in local IL-1␤, IL-6, macrophage inflammatory protein 1␣ (MIP-1␣) and MIP-2 production, and reduced bacterial burden. Administration of exogenous IL-18 resulted in increased mortality rates and increased incidence and severity of GBS arthritis, concomitant with a higher number of GBS and increased levels of IL-6, IL-1␤, MIP-1␤, and MIP-2 production in the joints.Conclusion. The present study indicated some involvement of IL-18 in the pathogenesis of GBSinduced arthritis. The role of IL-18 in joint pathology is shown by a regulatory effect on inflammatory mediator levels and local cell influx. Thus, IL-18 should be regarded as a potential therapeutic target in GBS infection and arthritis.

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“…It is reported to be produced constitutively by both synoviocytes (22) and chondrocytes (23), as well as by T cells and B cells (24). Its production by synoviocytes and chondrocytes is markedly up-regulated by cytokines, such as IL-1 and TNF (22,23,25), and by transforming growth factor P (TGFP) (23). IL-6 synthesis by peripheral blood mononuclear cells can also be induced by TNFa (26) and TGFP (27).…”

Section: Discussionmentioning

confidence: 99%

“…IL-6 synthesis by peripheral blood mononuclear cells can also be induced by TNFa (26) and TGFP (27). Production of IL-6 by the higher proportion of activated mononuclear cells in the rheumatoid joint may partly account for the generally higher levels of IL-6 found in the synovial fluid of patients with rheumatoid arthritis (RA) compared with those with osteoarthritis (22,25,28,29).…”

Section: Discussionmentioning

confidence: 99%

Elevated synovial fluid levels of interleukin‐6 and tumor necrosis factor associated with early experimental canine osteoarthritis

Venn

Nietfeld

Duits

et al. 1993

Arthritis & Rheumatism

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Objective. To measure levels of cytokines, proteases, and glycosaminoglycans (GAG) in synovial fluid (SF) From the knees of animals with experimental osteoarthritis (OA) and from their contralateral (control) knees, and to compare and correlate these values with each other as well as with measures of proteoglycan synthesis in the corresponding articular cartilage. This study will help to identify cytokines of potential importance in the early stages of the development of OA.Methods. OA was induced in 12 mature animals by sectioning the anterior cruciate ligament. After 3 months, SF From the operated and contralateral (control) knee joints was assayed for interleukind (IL-6), tumor necrosis Factor (TNF), IL-1, latent metalloproteinase, and sulfated GAG. Proteoglycan synthesis in the corresponding articular cartilage was also measured.Results. IL-6 levels in SF from the operated joint compared with the control joint were significantly ele- Submitted for publication July 9, 1992; accepted in revised form January 6, 1993. vated in 11 of 12 animals. TNF levels were also elevated in 10 of 11 SF samples from operated joints, but to a lesser extent than those of IL-6. IL-1 and IL-1 inhibitors were undetectable in either the operated or control joint SF. The GAG concentration was elevated in SF from experimental OA joints. This elevation correlated with that of TNF, but not IL-6. There was no significant difference in the concentration of APMA-activatable metalloproteinase. The rate of proteoglycan synthesis was higher in the cartilage from the operated joint in 8 of 12 animals, and the mean rate of synthesis was significantly higher than in the control joint. There was a positive correlation between this increase in cartilage proteoglycan synthesis (operated versus control) and the increase in SF IL-6, but there was no correlation with the levels of TNF or GAG.Conclusion. This is the first study of SF levels of cytokines in early experimental OA. Our results show surprisingly high levels of IL-6 in operated joints, where the cytokine could act directly on the chondrocytes, and thus play a role in mediating their responses to cartilage injury.

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Interleukin‐1‐induced interleukin‐6 is required for the inhibition of proteoglycan synthesis by interleukin‐1 in human articular cartilage

Cited by 119 publications

References 22 publications

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

Role of interleukin‐18 in experimental group B streptococcal arthritis

Elevated synovial fluid levels of interleukin‐6 and tumor necrosis factor associated with early experimental canine osteoarthritis

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