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At least 1,027 records · Page 57Linked to original sources
PubMed1999

Determination of interleukin-1 receptor antagonist, interleukin-10, and transforming growth factor-beta1 in synovial fluid aspirates of patients with temporomandibular disorders.

PURPOSE: This study was undertaken to examine the presence of interleukin-1 receptor antagonist (IL-1ra), IL-10, and transforming growth factor-beta1 (TGF-beta1) in the synovial fluid (SF) lavage specimens of patients with temporomandibular disorders (TMDs). PATIENTS AND METHODS: Synovial fluid lavage specimens were obtained from 14 temporomandibular joints (TMJs) of 12 patients with TMJ internal derangement (ID) and 17 TMJs of 15 patients with TMJ osteoarthritis (OA). Seven synovial fluid lavage samples of TMJs of four asymptomatic donors served as normal controls. The concentrations of IL-1ra, IL-10, and TGF-beta1 were detected with sensitive and specific sandwich enzyme-linked immunosorbent assay (sandwich-ELISA). RESULTS: IL-1ra, IL-10, and TGF-beta1 in all the normal controls were undetectable. IL-1ra concentrations were 175.78 +/- 52.43 pg/mL in the patients with TMJ ID and 187.85 +/- 59.51 pg/mL in those with TMJ OA. IL-10 was undetectable in all the TMJ ID and OA samples. The concentration of TGF-beta1 in TMJ ID patients (47.93 +/- 88.25 pg/mL) was significantly less than in patients with TMJ OA (143.61 +/- 108.00 pg/mL) (P < .01). CONCLUSION: The results suggest that deficiencies of IL-1ra, IL-10, and TGF-beta1 probably play an important role in the cause and pathogenesis of TMJ ID and OA.

Adolescent↗
PubMed1989

Determination of synovial fluid hyaluronate concentration and polymerisation by high performance liquid chromatography.

High performance liquid chromatography (HPLC) with a size exclusion column and ultraviolet monitoring was used to study the effect of synovial fluid hyaluronate concentration and degree of polymerisation on viscosity and mucin clot formation. Rotational viscometry measurements showed an exponential relation between the synovial fluid hyaluronate concentration and relative viscosity, the viscosity increasing particularly steeply with hyaluronate concentrations exceeding 2-2.5 mg/ml. The scattering of individual values observed around the expected curve was eliminated when both the hyaluronate concentration and its degree of polymerisation were taken into account. Hyaluronate concentration and degree of polymerisation also correlated with the quality of mucin clot, though only HPLC provided more detailed quantitative information about this association. Because HPLC allows reproducible and rapid simultaneous analysis of the synovial fluid hyaluronate concentration and the degree of polymerisation in small volumes of unprocessed samples it can be used in well equipped rheumatological units to replace other methods used previously.

Chromatography, High Pressure Liquid↗
PubMed2006

Novel insights in the regulation of CCL18 secretion by monocytes and dendritic cells via cytokines, toll-like receptors and rheumatoid synovial fluid.

BACKGROUND: The T cell attracting chemokine CCL18 is produced by antigen presenting cells and a role for CCL18 has been suggested in the pathogenesis of a variety of diseases. Rheumatoid arthritis (RA) is one of these conditions, in which abundant CCL18 production is present. Although Th2 cytokines and IL-10 are known to have an effect on CCL18 production, there are several gaps in our knowledge regarding the exact regulation of CCL18 secretion, both in general and in RA. In this study we provide new insights in the regulation of CCL18 secretion by monocytes and dendritic cells. RESULTS: In contrast to a large panel of pro-inflammatory stimuli (IL-1beta, TNF-alpha, IL-10, IL-13, IL-15, IL-17, IL-18, IFN-gamma), T cell mimicking molecules (RANKL, CD40L) or TLR driven maturation, the anti-inflammatory IL-10 strongly stimulated DC to secrete CCL18. On freshly isolated monocytes, CCL18 secretion was induced by IL-4 and IL-13, in strong synergy with IL-10. This synergistic effect could already be observed after only 24 hours, indicating that not only macrophages and dendritic cells, but also monocytes secrete CCL18 under these stimulatory conditions. A high CCL18 expression was detected in RA synovial tissue and incubation of monocytes with synovial fluid from RA patients clearly enhanced the effects of IL-4, IL-13 and IL-10. Surprisingly, the effect of synovial fluid was not driven by IL-10 of IL-13, suggesting the presence of another CCL18 inducing factor in synovial fluid. CONCLUSION: In summary, IL-10 synergistically induces CCL18 secretion in combination with IL-4 of IL-13 on monocytes and monocyte derived cells. The effects of IL-14, IL-13 and IL-10 are strongly enhanced by synovial fluid. This synergy may contribute to the high CCL18 expression in RA.

Arthritis, Rheumatoid↗
PubMed1985

Inactivation of interferon by serum and synovial fluids.

The stability of interferons-alpha, -beta, and -gamma (IFN) in serum and synovial fluids were compared. Interferon-beta was the least stable interferon species, losing at least 75% of its activity during incubation in samples of both serum and synovial fluid. Interferon-alpha was the most stable IFN, but interferon-gamma under these conditions approached the stability of the alpha species. The inactivation of IFN-beta was found due to dialyzable factors and hence not classical antibodies.

Arthritis, Rheumatoid↗
PubMed1990

Synovial fluids from infected joints contain metalloproteinase--tissue inhibitor of metalloproteinase (TIMP) complexes.

Samples of synovial fluids aspirated from patients with septic arthritis prior to the commencement of any treatment contained active metalloproteinases but no proteinase inhibitory activity. We therefore assayed these samples for proteinase-inhibitor complexes. Although no biologically active alpha 2-macroglobulin or tissue inhibitor of metalloproteinase (TIMP) was present in the fluids, immunoassay of the samples clearly showed that high molecular weight proteinase-TIMP complexes were present. It is proposed that high levels of active metalloproteinases are released from neutrophils into septic synovial fluids and that these proteinases complex all the available TIMP, forming metalloproteinase-TIMP complexes.

Arthritis, Infectious↗
PubMed1991

Assay of synovial fluid hyaluronic acid using high-performance liquid chromatography of hyaluronidase digests.

A high-performance liquid chromatographic method for the determination of hyaluronic acid levels in synovial fluids has been developed. The hyaluronidase sample digests, containing an internal standard (benzoic acid), were separated on a reversed-phase octadecylsilyl column eluted with 0.01 M tetrabutylammonium phosphate-acetonitrile (83:17, v/v) at pH 7.35. The determination was made on 1:10 diluted samples, by using a calibration curve from 50 to 500 micrograms/ml of human umbilical cord hyaluronic acid. For validation, the synovial fluids were simultaneously analysed by this method and a radiometric method: a high correlation was found between the two (correlation coefficient 0.94). The proposed method can be used to determine specifically the high hyaluronic acid levels of synovial fluids without interferences from other glycosaminoglycans or non-steroidal anti-inflammatory drug treatment.

Adolescent↗
PubMed1978

Oral antibiotic therapy for skeletal infections of children. I. Antibiotic concentrations in suppurative synovial fluid.

To evaluate the feasibility of oral antibiotic treatment for pyogenic arthritis, one or more oral doses of antibiotics were substituted for the drugs being used for parenteral therapy. Synovial fluid and serum specimens obtained at randomized times after an oral dose of ampicillin, cephalexin, cloxacillin, dicloxacillin, or penicillin G were assayed for antibiotic content and antibacterial activity. Seventy specimens from 21 infants and children were studied. Peak synovial fluid concentrations were greater than 60% of peak serum concentrations with all drugs tested and there was adequate inhibitory activity against bacteria commonly causing arthritis. The degree of antibiotic binding to serum protein had no apparent effect on the degree of penetration into pyogenic synovial fluid.

Administration, Oral↗
PubMedDate not supplied

Simultaneous evaluation of membrane bound and soluble interleukin 2 receptor expression in the blood and synovial fluid of patients with rheumatoid arthritis.

We studied the levels of membrane-bound and soluble-form interleukin 2 (IL-2) receptors in forty patients with rheumatoid arthritis. Levels of IL-2 receptors in the sera and synovial fluid of patients with rheumatoid arthritis were elevated when compared to values observed in normal sera and synovial fluid derived from the osteoarthritic joint. Simultaneous elevation of IL-2 receptor expression in blood and synovial fluid lymphoid cells was also detected, but no correlation was found between the two parameters nor between serum IL-2 receptor levels and the hemosedimentation rate. We conclude that measurement of serum concentrations of soluble IL-2 receptors should be used with caution as an index of disease activity, but may be useful when used in conjunction with other parameters in the management of patients with rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1980

Plasma and synovial fluid pharmacokinetics and prostaglandin inhibitory effect of indoprofen in patients with rheumatoid arthritis.

Indoprofen was given intravenously (bolus followed by infusion) and orally to 7 patients suffering from active rheumatoid arthritis with knee joint effusion. Indoprofen readily penetrated into synovial fluid in amounts which were directly correlated with areas under curves of plasma drug levels. Synovial fluid acted as a compartment distinct from the central (plasma) compartment. Indoprofen caused a substantial decrease in E2 and F2 alpha prostaglandin concentration in synovial fluid.

Adult↗
PubMed1993

Synovial fluid macrophages and blood monocytes differ in their response to IL-4.

IL-4 has been described as a potential anti-inflammatory molecule because of its ability in vitro to down-regulate human monocyte production of proinflammatory mediators. In this study, the activity of IL-4 on mononuclear cells and CD14+ macrophages from a site of chronic inflammation, namely, the joints of patients with rheumatoid and psoriatic arthritis, was investigated and compared directly with its activity on PBMC and monocytes from the same patients. In contrast to the response by blood monocytes, the response to IL-4 by synovial fluid cells was selective; IL-4 did not significantly suppress LPS-induced TNF-alpha production, but decreased CD14 expression to a similar extent in the two cell populations. IL-4 induction of monocyte/macrophage CD23 expression was investigated as a stimulatory response to IL-4, and although significantly increased on synovial fluid CD14+ cells by IL-4, the induction was considerably reduced compared with that measured for blood cells. Activation and differentiation in vitro of blood monocytes reduced their response to IL-4 for decreased TNF-alpha production and induction of CD23 and suggested that these biologic phenomena may contribute to the decreased responsiveness to IL-4 by synovial fluid monocytes/macrophages. Thus, IL-4 does not have the same anti-inflammatory properties in vitro on synovial fluid cells as on blood monocytes.

Antigens, CD↗
PubMed2001

Decline after immobilisation and recovery after remobilisation of synovial fluid IL1, TIMP, and chondroitin sulphate levels in young beagle dogs.

OBJECTIVE: To monitor the concentration of markers of cartilage and synovium metabolism in the knee (stifle) joint synovial fluid of young beagles subjected to immobilisation and subsequent remobilisation. METHODS: The right hind limb of 17 dogs was immobilised in flexion for 11 weeks. Simultaneously, the contralateral left knee was exposed to increased weight bearing. The remobilisation period lasted 50 weeks. Litter mates served as controls. The concentration in joint lavage fluid of interleukin 1alpha (IL1alpha) was measured by immunoassay, the activity of phospholipase A(2) (PLA(2)) was determined by an extraction method, chondroitin sulphate (CS) concentration by precipitation with Alcian blue, hyaluronan (HA) by an ELISA-like assay using biotinylated HA-binding complexes, matrix metalloproteinase 3 (MMP-3), and tissue inhibitor of metalloproteinases 1 (TIMP-1) by sandwich ELISA, and synovitis was scored by light microscopy. RESULTS: Synovitis or effusion was absent in all experimental and control groups. Immobilisation decreased the joint lavage fluid levels of IL1alpha (p<0.05), TIMP (p< 0.05), and the concentration of CS down to 38% (p<0.05) in comparison with untreated litter mates with normal weight bearing. Immobilisation did not affect the activity of PLA(2), or the concentration of MMP-3 or HA in synovial fluid. Joint remobilisation restored the decreased concentrations of markers to control levels. Increased weight bearing did not change the concentrations of markers in comparison with the control joints with normal weight bearing. CONCLUSIONS: 11 weeks' joint immobilisation decreased the concentration of markers of cartilage and synovium metabolism in the synovial fluid, and remobilisation restored the concentrations to control levels. The changes in joint metabolism induced by immobilisation, as reflected by the markers, are thus different from those found in osteoarthritis, where increased levels of these markers are associated with enhanced degradation and synthesis. These findings suggest that the change induced in joint metabolism by immobilisation is reversible in its early stages.

Animals↗
PubMed1994

Levels of circulating intercellular adhesion molecule 1 and E-selectin in serum and synovial fluid of juvenile chronic arthritis patients.

OBJECTIVE: To measure the levels of two adhesion molecules (AM), soluble intercellular adhesion molecule 1 (sICAM-1) and soluble E-selectin (sE-selectin), in serum and synovial fluid (SF) of patients with juvenile chronic arthritis (JCA). METHODS: Both soluble AM levels were tested, in serum and synovial fluid (SF) samples, with an enzyme-linked immunosorbent assay (ELISA) method. RESULTS: Serum levels of sICAM-1 and sE-selectin in JCA patients were not significantly different from those of a control group. Synovial fluid levels of sICAM-1, but not of sE-selectin, assayed significantly higher (p < 0.05) in JCA patients than in controls. Moreover SF levels of both molecules correlated negatively with disease duration, being higher in the earliest phases. No significant correlations were found between JCA sICAM-1 and sE-selectin levels and leukocyte count or ESR. CONCLUSIONS: These observations may signify a more important role of ICAM-1 than E-selectin in the migration of inflammatory cells into JCA SF. The negative correlation of both AMSF levels in JCA patients with disease duration could reflect a higher expression of ICAM-1 and E-selectin during the earliest phases of the disease.

Adolescent↗
PubMed1988

Cytokines in synovial fluid: II. The presence of tumour necrosis factor and interferon.

Cytokine-specific monoclonal antibodies were used in enzyme-linked immunoadsorbant assays (ELISA) to examine a variety of synovial fluids for the presence of cytokines which might be expected to play some part in the pathology of arthritis. Low, but significant, levels of tumour necrosis factor alpha (TNF-alpha) were present in the majority of synovial fluids obtained from rheumatoid arthritis patients with a sero-positive history. Low levels of interferon (IFN)-alpha and IFN-gamma were also detected, but only IFN-alpha was significantly increased in the sero-positive group. Tumour necrosis factor beta (TNF-beta) was present only in trace amounts. These results suggest that the presence of cytokines, such as TNF-alpha and IFN-alpha in synovial fluid may be associated with tissue changes observed in rheumatoid joint disease and thus contribute to the pathology of the arthritis, but support evidence for the minimal role likely to be played by IFN-gamma in the joint pathology of rheumatoid arthritis.

Arthritis↗
PubMed1990

Cytidine deaminase activity in synovial fluid of patients with rheumatoid arthritis: relation to lactoferrin, acidosis, and cartilage proteoglycan release.

It is claimed that cytidine deaminase activity reflects local granulocyte turnover or activity in the synovial fluid of patients with rheumatoid arthritis, but cytidine deaminase is not a granulocyte specific enzyme. Lactoferrin is a granulocyte specific protein that is released from the secondary granulae during activation. We measured cytidine deaminase activity and lactoferrin concentrations in 33 rheumatic synovial fluid samples. Cytidine deaminase activity and lactoferrin concentrations correlated closely, indicating that both analyses reflect similar events in the joint-that is, result in their release from granulocytes. Cytidine deaminase activity and granulocyte concentrations correlated less closely, suggesting that there are additional factors besides the cell number which contribute to this release. Joint acidosis may be one such factor, as pH and cytidine deaminase activity correlated inversely. There was no association with synovial fluid proteoglycan concentrations, a marker of cartilage degradation.

Acidosis↗
PubMed1989

Changes in equine carpal joint synovial fluid in response to the injection of two local anesthetic agents.

The effects of repeated arthrocentesis and injection of local anesthetic agents, lidocaine HCl or mepivacaine HCl on the equine middle carpal joint were investigated. Synovial fluid samples were evaluated before, and 12, 24 and 48 hours following, treatment. The greatest changes from pretreatment values occurred in synovial fluid cellularity. Repeated arthrocentesis caused a moderate increase in cell counts, while injection of local anesthetics caused a greater increase. Alterations in mucin clot quality, hyaluronic acid content, fluid viscosity, total protein and immunoglobulin G were generally of no significance. The most sensitive sampling time to detect changes caused by a given treatment was 24 hours following treatment while the 12 hour sampling period appeared to be the best at detecting differences between treatments. Repeated arthrocentesis has a definite effect on synovial fluid composition but the effects appear to decrease with repeated centesis. Lidocaine HCl and mepivacaine HCl are irritating to the synovial environment. Clear differences between responses to the drugs could not be identified.

Animals↗
PubMed1990

Trimer and tetramer complexes containing C1 esterase inhibitor, C1r and C1s, in serum and synovial fluid of patients with rheumatic disease.

During activation, the first component of complement C1q (C1r-C1s)2 is dissociated in conjunction with the formation of complexes containing C1 esterase inhibitor (C1-INH). Trimer complexes, with zymogen C1s associated with a firm C1-INH-C1r complex (C1-INH-C1r-C1s) can be distinguished from tetramer complexes C1-INH-C1r-C1s-C1-INH) in which C1-INH is firmly bound to both proteases. In the present study a two-stage electroimmunoassay was developed for the specific measurement of C1-INH-C1r-C1s. In the first step, C1-INH and its complexes were immunoprecipitated with anti-C1-INH during electrophoresis in the presence of Ca2+. In the second step, C1s contained in C1-INH-C1r-C1s was dissociated in the presence of EDTA and was measured by immunoprecipitation with anti-C1s. C1-INH-C1r-C1s were consistently found in normal sera. Normal sera did not contain C1-INH-C1r-C1s-C1-INH as assessed with a previously described ELISA procedure. Sera and synovial fluids from two groups of patients with inflammatory arthritis were investigated. In rheumatoid arthritis patients (n = 15) C1-INH-C1r-C1s complexes were usually found at high concentration both in serum and synovial fluid. C1-INH-C1r-C1s-C1-INH complexes were also present with values that were higher in synovial fluid than in serum, in accord with previous findings of classical pathway activation in the inflamed joints of the patients. Patients with spondylarthritic syndromes (n = 7) had serum and synovial fluid C1-INH-C1r-C1s concentrations that were comparable to those of the rheumatoid arthritis patients. If at all present, C1-INH-C1r-C1s-C1-INH were detected in trace amounts. Thus, C1 activation in patients with spondylarthritic syndromes appeared to be efficiently controlled at the C1r level. Distinguishing between C1-INH-C1r-C1s and C1-INH-C1r-C1s-C1-INH may prove of value in further studies of the activation and control of C1 in disease.

Animals↗
PubMed1986

beta-Endorphin, immunological and biochemical changes in synovial fluid in rheumatic disorders.

In 120 patients with rheumatic disorders concomitant assays of serum and synovial fluid were done for acute phase reactants, immunoglobulins and the neuropeptide beta-endorphin. One-third of the patients with rheumatoid disease demonstrated synovial fluid levels of endorphin to be several-fold higher than serum levels, while in two-thirds the opposite results were found. These changes are discussed as adaptive or defense mechanisms. The synovial membrane is postulated to synthesize beta-endorphin.

Aged↗
PubMed1978

Collagenase in synovial fluid.

Free collagenase activity was demonstrated in all 13 normal, 5 osteoarthrotic and 54 rheumatoid synovial fluids studied. Osteoarthrotic, normal, and rheumatoid fluids showed a free collagenase content increasing in that order. However, the total activities after trypsin activation did not differ significantly. The concentrations of alpha1-at and alpha2-M in synovial fluids reflected those in sera. The complex interactions between serum inhibitors, and free or latent collagenase released from both synovial cells and leukocytes are discussed.

Arthritis, Rheumatoid↗