Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A randomised study was performed to evaluate the association between some commonly measured acute phase proteins and interleukin-6 after a standard musculoskeletal operation, and to investigate the effect of high doses of corticosteroids on these proteins. Eight men and four women with osteoarthrosis but who were otherwise healthy and who were each to have an uncemented hip prosthesis inserted by the porous coated anatomical technique, were included. Patients were randomised to receive methylprednisolone 30 mg/kg body weight 1 1/2 hours before, and four and 12 hours after, operation (n = 6) and compared to a control group (n = 6). Plasma concentrations of C reactive protein, haptoglobin, orosomucoid and alpha 1-antitrypsin; serum concentration of albumin; packed cell volume; white cell count; and plasma concentration of interleukin-6 were measured. The increases in concentrations of acute phase proteins in plasma were significantly less in the group given steroids, but this did not have any obvious clinical consequences. Increase in the concentration of interleukin-6 preceded the increases in acute phase proteins in both groups, reflecting the role of interleukin-6 in the regulation of expression of acute phase protein genes in hepatic cells. The increase of interleukin-6 in the group receiving steroids was less pronounced than that in the control group, indicating that corticosteroids inhibit the generation of interleukin-6 in vivo.
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PMID:Acute phase reactants and interleukin 6 after total hip replacement. Effects of high dose corticosteroids. 138 23

Interleukin-6 (IL-6) concentrations in knee joint synovial fluids and paired plasma samples of arthritis patients were examined with respect to each other and parameters of the inflammatory response. Synovial fluid and plasma IL-6 concentrations were significantly higher in patients with inflammatory arthritis than those detected in patients with osteoarthritis (P less than 0.001). The IL-6 concentrations in synovial fluids were considerably higher than, but significantly correlated with (r = 0.65; P less than 0.001), those of plasma. Furthermore, synovial fluid IL-6 concentrations in bilaterally inflamed knees were significantly correlated (r = 0.79; P less than 0.001) and there was a significant correlation with the extent of inflammatory cell infiltrate (r = 0.75; P less than 0.001). In unselected rheumatoid arthritis patients there was only a weak correlation between IL-6 and plasma C-reactive protein (CRP) concentration, and no correlation between IL-6 and erythrocyte sedimentation rate (ESR). However, both ESR and CRP concentration were highly correlated with plasma IL-6 concentration in patients with other inflammatory arthritides, particularly psoriatic and HLA B27 positive spondyloarthritis (r = 0.72-0.94; P less than 0.005). These relationships suggest that IL-6 production in inflammed knee joints can be a significant determinant of acute phase protein responses in arthritis patients, although the situation in patients with rheumatoid arthritis is more complex and may be influenced by other disease-related factors.
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PMID:Relationships between local inflammation, interleukin-6 concentration and the acute phase protein response in arthritis patients. 175 86

Polyclonal antibodies were raised in rabbits against Interleukin-6 (IL-6) by immunisation with a synthetic peptide of identical sequence to the amino terminal 12 amino acids of human IL-6. These antibodies reacted with recombinant IL-6 by ELISA and stained the cytoplasm of the IL-6 secreting bladder tumour cell line T24. Staining was abolished by prior incubation of the antibody with the IL-6 peptide. F(ab')2 fragments made by pepsin digestion of the IgG were immunopurified, labelled with biotin and retained activity in the biochemical and histological assays. Sections of synovial membrane from patients with rheumatoid arthritis (RA) were stained with these antibodies, using an immunoperoxidase technique, and cells containing IL-6 were domonstrated in the thickened synovial lining layer and also in a perivascular distribution in the deeper synovium. In osteoarthritis there were fewer cells in the lining layer and hence localisation appeared similar in both the interstitial area and lining layer. Double-staining techniques with mouse monoclonal antibodies against cell subset markers in five RA synovial membranes showed that up to 13% of T-cells and 19% of antibody-producing cells stained for IL-6. However, up to 70% of the macrophages contained IL-6 and these were found in close proximity to Ig-producing plasma cells. This study showed that macrophages were the major cells of the immune system in which IL-6 could be localised in RA, and suggests a role for locally produced IL-6 in the stimulation of rheumatoid factor production.
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PMID:Interleukin-6 localisation in the synovial membrane in rheumatoid arthritis. 194 69

Cartilage from normal controls, patients with osteoarthritis, and patients with rheumatoid arthritis produced no interleukin-6 (IL-6) in culture. However, IL-1 induced massive production of IL-6 (up to 135 ng/ml) in cartilage from all 3 sources, in a dose-dependent manner (in some cases, a peak value was reached). The levels of induced IL-6 were similar to those found in rheumatoid arthritis synovial fluid. At IL-1 concentrations that induced almost complete inhibition of proteoglycan (PG) synthesis, IL-6 production could still be increased considerably. Exogenous IL-6 inhibited PG synthesis by up to 25%. IL-1-induced inhibition of PG synthesis was reversed by antibodies against recombinant human IL-6. These results suggest that IL-6 is required for the IL-1-induced inhibition of PG synthesis.
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PMID:Interleukin-1-induced interleukin-6 is required for the inhibition of proteoglycan synthesis by interleukin-1 in human articular cartilage. 224 66

Increased concentrations of interleukin-6 (IL-6) have been found in the synovial fluid of patients with osteoarthritis, rheumatoid arthritis and crystal-related joint diseases. It is therefore of great interest to identify the cells responsible for the production of IL-6, and to investigate whether IL-6 plays a role in the pathogenesis of degenerative or inflammatory joint diseases. Here we show that human interleukin-1 beta (IL-1 beta) induces IL-6 synthesis and secretion in differentiated human chondrocytes. In organ cultures resembling closely the in vivo system 10(6) chondrocytes incubated with 100 units of interleukin-1 beta per ml of medium led to the release of 6 X 10(3) units of IL-6 within 24 h. Chondrocytes cultured in agarose or as monolayers similarly incubated with IL-1 beta produced even higher amounts of IL-6: 70 X 10(3) units per 10(6) cells within 24 h. The induction of IL-6 synthesis by IL-1 beta was also shown at the mRNA level. IL-6 secreted by stimulated chondrocytes showed heterogeneity upon Western blot analysis.
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PMID:Interleukin-1 beta induces synthesis and secretion of interleukin-6 in human chondrocytes. 233 34

Interleukin-6 (IL-6), also called 26-kd protein, hybridoma plasmacytoma growth factor, beta 2-interferon, or B cell stimulatory factor 2, is a recently described human cytokine with multiple growth and differentiation activities. Using a very sensitive bioassay based on the growth factor activity of this protein for B cell hybridomas, we found that IL-6 activity was significantly elevated in synovial fluid from patients with rheumatoid arthritis (RA) or other inflammatory arthritides, as compared with that in a group of patients with osteoarthritis. Moreover, IL-6 was detected in about one-third of the serum samples from patients with RA. In the latter group, we found a significant correlation between serum IL-6 activity and serum levels of C-reactive protein, alpha 1-acid glycoprotein, alpha 1-antitrypsin, fibrinogen, and haptoglobin, which indicates that IL-6 is related to disease activity in patients with RA.
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PMID:Interleukin-6 in synovial fluid and serum of patients with rheumatoid arthritis and other inflammatory arthritides. 326 Jan 2

B cell differentiation factor (BCDF) activity assayed on SKW6-CL4 cells was found in adherent synovial cell (ASC) conditioned medium. ASC of patients with RA (n = 8) produced significantly larger amounts of BCDF than those of patients with osteoarthritis (n = 5) (219.0 +/- 212.1 vs 25.5 +/- 12.4 units/microgram.DNA, p less than 0.01). ASC clones, established by the limiting dilution technique, also produced this factor. Experiments with several neutralizing antibodies revealed that this BCDF is inhibited by anti-B cell stimulatory factor-2/interleukin 6 antibody (anti-BSF-2/IL-6 ab) up to 90%, but not by antiinterleukin 1, antiinterleukin 2 or antiinterferon-r antibodies. Our data suggest that ASC could participate in the B cell differentiation process in joint space by producing a molecule which has a similar active site to BSF-2/IL-6.
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PMID:Rheumatoid adherent synovial cells produce B cell differentiation factor activity neutralizable by antibody to B cell stimulatory factor-2/interleukin 6. 326 48

Interleukin-6-dependent mouse hybridoma cell line KD83 was used to test the biologic activity of interleukin-6 in synovial fluid from 37 patients with temporomandibular disorders. The results showed that the interleukin-6 level was greater than 100 U/mL in 13 of 18 patients with degenerative joint disease and in five of 12 patients with temporomandibular disc displacement. However, the interleukin-6 level was less than 100 U/mL (range, 20 to 75 U/mL) in all patients with masticatory muscle disorder. It has been found that degenerative joint disease tends to have acute and chronic stages, and interleukin-6 activity was probably related to the acute stage in the patients. Histologic studies of the synovium from seven patients with degenerative joint disease showed a variable degree of hyperplasia of the synovial lining cells and chronic inflammation in five of eight specimens. Immunostaining studies clearly showed the presence of significantly more HLA-DR-expressing cells (human leukocyte antigen-D-related) in synovium. Although it is unlikely that immune responses play an important primary role in initiating synovial inflammation and cartilage destruction, immune reactions may be one important factor in the maintenance and severity of some patients with temporomandibular disorders.
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PMID:Interleukin-6 in synovial fluid and HLA-DR expression in synovium from patients with temporomandibular disorders. 748 82

Plasma and synovial fluid concentrations of interleukin-6 (IL-6), using an enzyme-linked immunosorbent assay, as well as immunoreactive levels of calcitonin gene-related peptide (CGRP), substance P and vasoactive intestinal peptide (VIP) were measured in 18 patients with rheumatoid arthritis and 20 with osteoarthritis of the knee. The concentrations of IL-6 were elevated in both plasma and synovial fluids from patients with rheumatoid arthritis whereas higher levels of substance P-, CGRP- and VIP-like immunoreactivities were found in the synovial fluid, but not in plasma, from patients with rheumatoid arthritis when compared with those in osteoarthritis. Furthermore, IL-6 and substance P levels in synovial fluid were significantly correlated both in rheumatoid arthritis and osteoarthritis patients. Our data seem to support the idea of an important role shared by neuropeptides and IL-6 in the pathogenesis of human inflammatory joint disease.
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PMID:Neuropeptides and interleukin-6 in human joint inflammation relationship between intraarticular substance P and interleukin-6 concentrations. 752 Jan 39

Most of the previous studies dealing with the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on the synthesis of inflammatory mediators involved in joint damage have been done in cells cultured in vitro or in blood cells from patients treated for short periods of time. In this work we have evaluated the long-term effect of aceclofenac, a new NSAID, and diclofenac on the production of a series of inflammatory mediators by blood cells from 30 patients with severe knee osteoarthritis. Both aceclofenac and diclofenac significantly inhibited prostaglandin E2 (PGE2) synthesis by blood mononuclear and polymorphonuclear cells after 180 days of treatment. However, no clear effect was noted on leukotriene B4 (LTB4) and platelet activating factor (PAF) production. The generation of O-2 by polymorphonuclear cells, stimulated with FMLP, was decreased after 15 days of treatment with both drugs, but reached normal values after 180 days. Interleukin-1 beta (IL-1 beta) production decreased significantly at 180 days with both drugs in the group of high producer patients. In a few (n = 3) patients with high basal mononuclear cell tumor necrosis factor alpha (TNF alpha) production, this also decreased on treatment for 180 days with the NSAIDs. In the remaining low TNF alpha-producing patients, TNF alpha production tended to increase. Interleukin-6 (IL-6) synthesis was not affected by aceclofenac while it was diminished by diclofenac. The decrease in IL-6 in all treated patients was significantly correlated with a worsening of the clinical condition. On the whole, these data could afford a pathogenetic basis for the long-term employment of these drugs in patients with inflammatory conditions.
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PMID:Long-term effect of nonsteroidal anti-inflammatory drugs on the production of cytokines and other inflammatory mediators by blood cells of patients with osteoarthritis. 794 25


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