Interleukin‐6 in synovial fluid and serum of patients with rheumatoid arthritis and other inflammatory arthritides

Houssiau, Frédéric; Devogelaer, Jean‐Pierre; Damme, Jo Van; Deuxchaisnes, C Nagant de; Snick, Jacques Van

doi:10.1002/art.1780310614

Cited by 798 publications

(379 citation statements)

References 16 publications

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“…OA FLS also express BAFF on their membrane and release minute amounts of IL-6 (ref. 32 and Figure 6C in the present study). As a consequence, B cells may expand clonally and hypermutate somatically in the presence of OA FLS (41).…”

Section: Discussionsupporting

confidence: 76%

“…Among these observations are our previous studies showing that IL-6 contributes to the expression of RAG in mature B cells (23,24). Other investigators have shown that the levels of IL-6 are elevated in the synovial fluid and serum of RA patients (32). Both in our present study and in a study reported by other investigators (6), RA FLS were found to produce far more IL-6 than did OA FLS (P Ͻ 0.05) ( Figure 6C).…”

Section: Functionality Of Rag-1 and Rag-2 Proteinsmentioning

confidence: 87%

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Transmembrane BAFF from rheumatoid synoviocytes requires interleukin‐6 to induce the expression of recombination‐activating gene in B lymphocytes

Rochas¹,

Hillion²,

Saraux³

et al. 2009

Arthritis & Rheumatism

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Section: Discussionsupporting

confidence: 76%

Section: Functionality Of Rag-1 and Rag-2 Proteinsmentioning

confidence: 87%

Transmembrane BAFF from rheumatoid synoviocytes requires interleukin‐6 to induce the expression of recombination‐activating gene in B lymphocytes

Rochas¹,

Hillion²,

Saraux³

et al. 2009

Arthritis & Rheumatism

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“…Both clinical observations and studies in transgenic mice have shown a link between IL-6 overexpression and several pathologic conditions, including atherosclerosis [53][54][55], Alzheimer's disease [56][57][58][59], and rheumatoid arthritis [60][61][62]. It is worth mentioning that statins, which have become important in the treatment of patients with coronary artery disease [63,64] and also have been reported to have beneficial effects in POAG [65], are associated with a reduction in serum levels of IL-6.…”

Section: Discussionmentioning

confidence: 99%

Induction of IL-6 expression by mechanical stress in the trabecular meshwork

Liton

Luna

Bodman

et al. 2005

Biochemical and Biophysical Research Communications

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The trabecular meshwork (TM)/Schlemm's canal (SC) outflow pathway is the tissue responsible for maintaining normal levels of intraocular pressure. In the present study, we investigate the effects of mechanical stress on the expression of IL-6 in the TM meshwork, as well as the effects of this cytokine on outflow pathway function. Application of cyclic mechanical stress to human TM primary cultures resulted in a statistically significant increase in both secretion and transcription of IL-6, compared to nonstressed controls. Addition of TGF-β1, which has been reported to be upregulated in TM cells under mechanical stress, also induced a significant activation of both the transcription and secretion of IL-6. Moreover, anti-TGF-b1 antibodies partially blocked the stretch-induced IL-6 production. Injection of IL-6 into perfused porcine anterior segments resulted in a 30% increase in outflow facility, as well as increased permeability through SC cell monolayers. These results suggest a role for IL-6 in the homeostatic modulation of aqueous humor outflow resistance. KeywordsTrabecular meshwork; Interleukin-6; Mechanical stress; TGF-β1; glaucomaThe trabecular meshwork (TM)/Schlemm's canal (SC) outflow pathway system constitutes the main route by which the aqueous humor exits the anterior chamber of the eye [1]. Maintenance of appropriate levels of aqueous humor outflow resistance through this pathway is critical in sustaining normal levels of intraocular pressure (IOP) [2,3]. Although it has been hypothesized that the TM/SC outflow pathway may respond to transient changes in IOP by altering its resistance to aqueous humor [4][5][6], thereby maintaining normal IOP levels, there is little experimental evidence explaining such potential homeostatic mechanisms.As a result of cyclic fluctuations of IOP with each heartbeat, the conventional outflow pathway is subjected to continuous cycles of stretch and relaxation that might be involved in tissue homeostasis and, consequently, in IOP regulation [7]. It has been well described that changes in IOP exert dramatic effects on the morphology of the outflow pathway [8][9][10][11][12]. Increased IOP results in distention and stretching of the outflow pathway and its contained cells, while decreased IOP leads to relaxation of the tissue. It has also been demonstrated that mechanical stress can trigger certain responses in TM cells, including cytoskeletal changes, induction of gene expression, and activation of regulatory pathways [13][14][15][16][17][18][19][20][21] One of the reported responses to increased IOP in perfused human anterior segments observed by gene array analysis is an increase in interleukin-6 (IL-6) mRNA [16]. IL-6 is well known to increase the permeability of vascular endothelium through effects on the paracellular pathway, induction of matrix metalloproteinases (MMPs), and vesicular trafficking [22][23][24]. This array of effects mediated by IL-6 suggests that this cytokine could affect aqueous humor outflow resistance in the outflow pathway by increasing ...

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“…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‐6 in synovial fluid and serum of patients with rheumatoid arthritis and other inflammatory arthritides

Cited by 798 publications

References 16 publications

Transmembrane BAFF from rheumatoid synoviocytes requires interleukin‐6 to induce the expression of recombination‐activating gene in B lymphocytes

Transmembrane BAFF from rheumatoid synoviocytes requires interleukin‐6 to induce the expression of recombination‐activating gene in B lymphocytes

Induction of IL-6 expression by mechanical stress in the trabecular meshwork

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

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