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PubMed1989

Antikeratin antibodies in synovial fluid in rheumatoid arthritis.

Serum and synovial fluid of 20 patients with classical or definite rheumatoid arthritis (RA) were tested for antikeratin antibodies (AKA) by indirect immunofluorescence using rat esophagus as antigen. AKA were found in 80% of the RA patients, in serum as well as in synovial fluid. None of the 54 serum control patients were AKA positive in serum. None of the 17 synovial fluid control patients were AKA positive in synovial fluid. F(ab)'2 fragments prepared from AKA positive RA serum retained antibody activity. AKA belonged to the IgG class of immunoglobulins. Corrected for the lower IgG content in synovial fluid, AKA constituted a higher percentage of the IgG in synovial fluid than in serum. This could imply a possibility of local production of AKA in the joint.

Adult↗
PubMed1980

[Technic for isolation and culture of macrophages from human synovial fluid].

Macrophages from synovial fluid were obtained by joint puncture of patients with rheumatoid arthritis or non-rheumatoid exudative arthropathies. This fluid was subsequently centrifuged and the resulting cell pellet was recovered and distributed for in vitro culture (Falcon Petri dishes: 60 x 15 or 35 x 10). Cells were washed after 4 hours in culture to eliminate non-macrophagic cells. A second cell wash was effected 24 hours later to eliminate non-adherent cells. The culture medium employed was fetal calf serum MMP 119 (Gibco). The macrophagic nature of the cultured cells was ascertained by non specific esterase determinations (Burstone method) and estimation of the phagocytic index (using zymosan). This technique permits the conservation of viable monocytes in culture thus facilitating investigation of their metabolic activity (for example: prostaglandins, prostanoids or fatty acids) and the effects of anti-inflammatory agents.

Arthritis, Rheumatoid↗
PubMed1991

The kinetics of flurbiprofen in synovial fluid.

Steady state plasma and synovial fluid flurbiprofen concentrations obtained from 26 rheumatoid arthritis patients receiving 100 mg of flurbiprofen b.i.d. were analyzed using the NONMEM program. Only one synovial fluid sample per patient was available. Population estimates for the plasma parameters, clearance, volume of distribution, and elimination half-life were 1.75 L hr-1, 11.9 L, and 4.8 hr, respectively, and the corresponding interindividual variances in these parameters were 29, 19 and 23%, respectively. The apparent elimination half-life from synovial fluid was 7.1 hr. After accounting for interindividual variability there was a residual variability of approximately 40% in both the plasma and synovial fluid concentrations.

Adolescent↗
PubMed1992

Antibodies in rheumatoid synovial fluids bind to a restricted series of protein antigens in rheumatoid synovial tissue.

OBJECTIVE: By searching the synovial fluid of patients with rheumatoid arthritis (RA) for antibodies that react to protein antigens in synovial tissue, we sought to identify putative antigens present in RA synovial tissue that might drive the pathologic immune response believed to be responsible for the joint inflammation. METHODS: Synovial tissue was homogenized in sodium dodecyl sulfate polyacrylamide gel buffer, electrophoresed, and analyzed by immunoblotting. RESULTS: Antibodies from synovial fluids of patients with RA bound to several proteins in rheumatoid synovial tissues, including a series of low (27.5-, 29-, and 30-kd), middle (43- and 53-kd), and high (140-, 164-, and 182-kd) molecular weight proteins. Most of these antigens were also detected in normal synovial tissue, and the high molecular weight proteins were also present in normal dermal, muscle, and liver tissues. The low and middle molecular weight proteins were detected in some, but not all, of the other normal tissues and in Jurkat cell lysates. Antibodies to the low and high series of proteins were present in all rheumatoid synovial fluids tested, but were generally absent from synovial fluids from patients with other arthritic diseases. CONCLUSION: These results show that antibodies in synovial fluids consistently react to several proteins in RA and normal synovial tissues. These antigens are possibly the same antigens provoking the T cell response in RA; therefore, understanding the mechanism of the immune response against these proteins will likely lead to important insight into the etiology of RA.

Antibodies↗
PubMed1993

Determination of lead in paired samples of blood and synovial fluid of bovines.

Exposure of synovial fluid to lead allows the entrance of this metal into the systemic circulation. In this study we report lead concentrations measured in bovine paired samples of synovial fluid and whole blood withdrawn from the coxo-femoral joints and jugular vein, respectively. Lead was determined by atomic absorption spectrophotometry. This study provides the "normal" values for lead in synovial fluid 12.15 +/- 5.41 and blood 3.54 +/- 1.31 micrograms% (mean +/- SD). The data distribution fits the GAUSSIAN curve (p < 0.02). The difference of concentration between synovial fluid and blood can not be explained only in terms of the solubility of lead in both fluids; other factors must be considered.

Animals↗
PubMed1987

Carbohydrate heterogeneity of fibronectins. Synovial fluid fibronectin resembles the form secreted by cultured synoviocytes but differs from the plasma form.

Large quantities of fibronectin (Fn) are present in inflammatory synovial fluid. Inflammatory synovial fluid Fn, while indistinguishable from plasma Fn on the basis of reactivity to polyclonal antibodies, displays alterations in molecular size and charge. Since biochemical differences between plasma and synovial fluid fibronectins might be in part due to differences in glycosylation we have compared the carbohydrate composition of plasma Fn, synovial fluid Fn, and Fn from synoviocyte conditioned medium by biochemical assay, glycopeptide analysis, and binding to a series of lectins. Synovial fluid Fn has a greater carbohydrate content but contains less sialic acid when compared with plasma Fn. Glycopeptides formed from synovial fluid Fn are smaller than plasma Fn glycopeptides. These data suggest the presence of an additional N-linked oligosaccharide chain on synovial fluid Fn. In addition, synovial fluid Fn contains N-acetyl galactosamine indicating the presence of O-linked oligosaccharides. Synovial fluid Fn and Fn isolated from rheumatoid synoviocyte-conditioned medium display strong reactivity with the lectins wheat germ agglutinin (WGA) and peanut agglutinin (PNA), whereas normal and rheumatoid plasma Fn react weakly. The PNA reactivity of synovial fluid Fn is mediated by terminal beta-galactose residues on the gelatin-binding domain, whereas the enhanced WGA reactivity of synovial Fn is mediated by a sialic acid containing oligosaccharide located on a 27-kD C-terminal fragment. These data demonstrate domain-specific biochemical differences between plasma and synovial fluid fibronectins. These differences suggest a local origin for synovial fluid Fn and may contribute to functional differences between these forms of the protein.

Acetylgalactosamine↗
PubMed2004

Differential induction and regulation of matrix metalloproteinases in osteoarthritic tissue and fluid synovial fibroblasts.

OBJECTIVES: To investigate the secretion profiles of matrix metalloproteinases (MMP) and their inhibitors (TIMP) in synovial fluid-derived fibroblasts and to compare them with those of tissue-derived fibroblasts. METHODS: Fibroblast cultures established from synovial tissues (TSC) and fluids (FSC) of the same OA patients were stimulated with tumor necrosis factor(TNF)-alpha, interleukin(IL)-1alpha, IL-1beta, IL-6 and a combination of TNFalpha and IL-1beta. Cocultures of fibroblasts and cartilage were stimulated either with the cytokine combination or with osteoarthritic synovial fluid. Secretion of MMP-1, MMP-3, MMP-8, MMP-13, TIMP-1, and TIMP-2 was measured by enzyme-linked immunosorbent assay. Gelatin zymography and immunoblotting were performed to demonstrate enzyme activity. RESULTS: TNFalpha, IL-1alpha, and IL-1beta led to marked increases in MMP-1 and MMP-3 release (up to 4.2-fold and 547-fold, respectively) by synovial fibroblasts, whereas secretion of MMP-13 was induced by concomitant administration of TNFalpha and IL-1beta. Expression of intracellular MMP-8 was stimulated by cytokines, but adhesion of synovial fibroblasts to cartilage was required for the release. Throughout the study, significantly higher levels of secreted MMPs were observed in stimulated FSC compared to TSC cultures. Furthermore, increases in MMP secretion were not accompanied by increases in secreted TIMP-1 and TIMP-2, resulting in marked imbalances between enzyme and inhibitor levels. CONCLUSIONS: The results provide strong evidence for a significant impact of synovial-derived MMPs on cartilage destruction in OA. In this context, fibroblasts present in the synovial fluid appeared to play an outstanding role.

Aged↗
PubMed1990

Penetration of the active metabolite of nabumetone into synovial fluid and adherent tissue of patients undergoing knee joint surgery.

The concentration of 6-methoxy-2-naphthylacetic acid (6-MNA) in plasma, synovial fluid, synovial tissue and fibrous capsule tissue was determined in an open study with 20 patients scheduled for knee joint surgery after oral treatment with nabumetone under steady-state conditions. 6-MNA is the principle metabolite of the prodrug nabumetone arising from an extensive first-pass metabolism in the liver. Patients suffering from rheumatoid arthritis (n = 12) or osteoarthritis stage III or IV (n = 8) received a daily dose of nabumetone 1 g in the evening starting 4 days prior to surgery. On day 1 an additional loading dose of nabumetone 1 g was given in the morning. At the time of surgery (day 5), blood, synovial tissue and fibrous capsule tissue were taken simultaneously. The samples were analysed by high performance liquid chromatography. After 4 days of treatment mean 6-MNA concentration in plasma was 40.76 mg/L, in synovial fluid 34.79 mg/L, in synovial tissue 19.33 mg/g and in fibrous capsule tissue 11.43 mg/g. Under steady-state conditions mean synovial fluid levels of 6-MNA were higher than after administration of a single dose and, in common with levels in synovial tissue, persist in a range sufficient for in vitro cyclo-oxygenase inhibition.

Administration, Oral↗
PubMedDate not supplied

[Isoelectric focusing studies of synovial fluid in rheumatoid arthritis].

Synovial fluids obtained at operation in several different diseases were studied by means of isoelectrical focussing. All the punctates of patients with rheumatoid arthritis showed bands which migrated towards the cathode and which were not found in synovial fluid from other diseases, except in 2 meniscus lesions. In the range of pH 6.81-7.30, typical synovial proteins were demonostrated.

Adult↗
PubMed1978

Properties of fibrinogen-antigenic material on the rheumatoid synovial membrane and in the rheumatoid synovial fluid.

Fibrin deposits on rheumatoid synovial membranes and fibrinogen-antigenic material in rheumatoid synovial fluid were found to be identical by crossed immunoelectrophoresis into immunoglobulin against fibrinogen, by SDS-polyacrylamide gel electrophoresis, and by gel filtration on Sepharose CL 6B. The material was found to be neither fibrinogen nor fibrin, but degradation products. One of the fragments was purified by preparative agarose electrophoresis, and the physicochemical properties of this fragment were found to be different from those obtained by plasmin digestion of fibrinogen or fibrin. This indicates that other proteases than plasmin are responsible for the degradation products. The material was easily degraded by plasmin to D- and E-antigenic end products, identical to those obtained by plasmin digest of fibrinogen. The solubility of the material was poor in synovial fluid compared to serum and buffer. On the basis of these results, it is suggested that the fibrinlike material on the synovial membrane represents fibrinogen degradation products from the inflamed tissue. These products are likely released into the synovial fluid, and when their concentration here exceeds their solubility, they precipitate on the synovial membrane.

Arthritis, Rheumatoid↗
PubMed1992

Determination of cytokines in synovial fluids: correlation with diagnosis and histomorphological characteristics of synovial tissue.

In a study aimed at correlating cytokine levels in synovial fluid with the pathology of rheumatoid arthritis (RA), tumour necrosis factor alpha, interleukin 1 beta and interferon gamma were immunoassayed in 27 patients with RA, 16 patients with other arthritides, 23 with osteoarthritis, 13 patients with trauma, and 18 patients at necropsy without inflammatory disease and not known to have had joint disease (median 27 hours after death). The results for interleukin 1 beta clearly show higher cytokine levels in patients with RA and other arthritides than in patients with osteoarthritis, trauma, or the patients at necropsy. Interferon gamma levels in patients with osteoarthritis and the patients at necropsy, however, were significantly greater than in patients with RA, and tumour necrosis factor alpha levels were also greater in the patients at necropsy compared with patients with RA. This study also correlated histomorphological patterns of synovitis and indicators of local inflammatory activity with synovial fluid cytokine levels, showing, for example, a positive association of interleukin 1 beta titre and a negative association of interferon gamma titre with ulcerogranulomatous synovitis (itself associated with RA). Taken together, these results extend and strengthen data suggesting a possible part played by increased synovial fluid levels of interleukin 1 beta in joint destruction in RA, but provide no evidence for increases in levels of tumour necrosis factor alpha or interferon gamma affecting the disease pathology.

Adult↗
PubMed1979

Fluorescent lipid-peroxidation products in synovial fluid.

1. Samples and extracts from synovial effusions were examined for the presence of fluorescent degradation products of free-radical oxidation (peroxidation). 2. Two classes of fluorescent compounds were identified and their fluorescence and physical properties are described. The fluorescence in the aqueous methanol phase of the extracts had the characteristics of conjugated Schiff bases. 3. Changes in synovial fluid and synovial fluid extracts in vitro induced by u.v. irradiation, prolonged incubation and the enzymic generation of oxidizing free radicals, with or without admixed peroxidizing arachidonic acid, and in the absence and presence of antioxidants, suggest that the fluorescent material is derived from peroxidized polyunsaturated lipids in damaged synovial tissue.

Arachidonic Acids↗
PubMed1984

Generation of interleukin-2-dependent T cell lines from synovial fluids in rheumatoid arthritis.

Synovial fluids from rheumatoid arthritis (RA) patients were found to contain activated T lymphocytes that could be maintained as continuous T cell lines (CTCL) in the presence of the T cell growth factor, interleukin (IL)-2. The CTCL predominantly expressed the OKT8 phenotype and were Ia antigen positive. IL-2-dependent RA CTCL could be maintained in an active dividing state by the presence of RA synovial fluids, whereas IL-2-dependent CTCL from mitogen stimulated PBL failed to respond to the fluids, which were shown to contain IL-2. This suggested that RA CTCL exhibit unique properties not possessed by normal PBL CTCL. The CTCL generated from activated synovial T lymphocyte populations in RA may be used to assess the functions of these cells and their responses to regulatory factors.

Antigens, Surface↗
PubMed1991

Interleukin-1-like activity in synovial fluids and sera of horses with arthritis.

Synovial fluid samples of horses with osteoarthritis were investigated to detect interleukin-1 (IL-1) activity which could contribute to the disease pathogenesis. Of the 32 samples tested, 12 (37.5 per cent) showed an augmented phytohaemagglutinin induced proliferation of C3H/HeJ mouse thymocytes. Positive results were also seen in horses with infected arthritis, osteochondritis, traumatic arthritis and undefined synovial effusions. Normal synovial fluid and sera from all groups failed to show any detectable IL-1 activity. Fractionation of synovial fluid showed that the IL-1 activity was in the 15 to 20 Kd fractions. In the absence of mitogen, synovial fluid failed to stimulate thymocytes and did not stimulate the growth of an interleukin-2 (IL-2) dependent CTLL cell line, but synovial fluid stimulated IL-2 release by mouse spleen cells incubated with suboptimal doses of lectin. Evidence of an IL-1 inhibitor in synovial fluid from osteoarthritic horses was provided by ultrafiltration experiments and by the inhibitory activity of synovial fluid at particular dilutions in the thymocyte assay. The presence of IL-1-like activity could be relevant in the pathogenesis of arthritis in horses.

Animals↗
PubMed1990

Transforming growth factor-beta and cellular immune responses in synovial fluids.

Mononuclear cells in synovial fluids (SF) from patients with rheumatoid arthritis and other arthropathies are characterized by functional and phenotypic changes, including impaired mitogen responsiveness and inverted ratios of CD4+/CD8+ T lymphocytes. This is related to previously described activities in synovial fluids that inhibit proliferation of lymphocytes induced by mitogens and cytokines. The present study examines the relationship of these activities and transforming growth factor beta (TGF-beta), which is now known as the most potent endogenous inhibitor of lymphocyte function. It is shown that most of the activity in SF that inhibits IL-1-induced thymocyte or T cell proliferation is neutralized by a specific antibody to TGF-beta. Analysis of the SF in the CCL64 assay, a standard test for TGF-beta, showed a close correlation between the levels of immunosuppressive activity and TGF-beta. SF contain spontaneously active inhibitors of T cell function and this is caused by the presence of active TGF-beta. Higher titers are found after transient acidification, which is known to activate the latent form of TGF-beta. Characterization of the TGF-beta isoforms showed that most of the material in SF is TGF-beta 2. Analysis of TGF-beta effects on T cell subsets demonstrated that it completely inhibits proliferation of CD4+ cells whereas at the same concentrations of purified or rTGF-beta CD8+ cells are only inhibited by maximally 31.1%. SF also preferentially inhibit CD4+ Th cell proliferation and this effect is neutralized by antibody to TGF-beta. Collectively these results indicate that the presence of TGF-beta accounts for most of the immunosuppressive activities in SF and that this factor may be responsible for functional and phenotypic changes of SF lymphocytes.

Arthritis, Rheumatoid↗
PubMed1991

Relationship between leukotriene B4 and immunological parameters in rheumatoid synovial fluids.

Leukotriene B4 (LTB4) was measured in synovial fluid from 20 patients with rheumatoid arthritis and 15 patients with osteoarthritis. The level of LTB4 was significantly higher in synovial fluid from rheumatoid arthritis patients as compared with synovial fluid from osteoarthritis patients. LTB4 levels also significantly correlated with cell numbers, rheumatoid factor, and immune complexes in synovial fluid from rheumatoid arthritis patients. There was an inverse correlation between LTB4 levels and complement components. The high-pressure liquid chromatography peak of immunoreactivity extracted from the synovial fluid occurred at a retention volume identical to that of authentic LTB4. These results suggest that the increased level of this mediator in synovial fluid may contribute to perpetuation of inflammation and tissue destruction in rheumatoid arthritis.

Adult↗
PubMed1986

Plasma and synovial fluid kinetics of flurbiprofen in rheumatoid arthritis.

Clinical assessment, plasma and synovial fluid kinetics were studied in 29 rheumatoid patients receiving 100 mg flurbiprofen twice daily. Clinical assessment and pharmacokinetic measurements varied widely within the group of patients. The average values for plasma clearance, volume of distribution and elimination halflife of flurbiprofen were 0.65 +/- 0.24 ml min-1 kg-1, 0.160 +/- 0.093 l kg-1 and 3.1 +/- 1.7 h, respectively. Synovial fluid drug concentrations peaked later and were lower than corresponding plasma concentrations: 5.2 h and 4.4 mg l-1 as against 1.49 h and 12.5 mg l-1, respectively. At 48 h after an oral dose of flurbiprofen, all the drug had been cleared from the synovial fluid. Synovial fluid drug concentrations were not related to synovial fluid albumin concentration or pH. There was a weak relationship between synovial fluid drug concentration and the thermographic measurements of disease activity. The fractions of flurbiprofen not bound to protein in synovial fluid and plasma were not significantly different. A simple model is proposed to account for the plasma and synovial fluid pharmacokinetics.

Adolescent↗
PubMedDate not supplied

Modified spontaneous and mitogen-stimulated IgG synthesis in lymphocytes from rheumatoid synovial fluid.

Lymphocytes from rheumatoid synovial fluid (RASFL) synthesized lower levels of IgG than normal or rheumatoid peripheral blood lymphocytes (PBL) when cultured in vitro with a plant lectin, pokeweed mitogen (PWM). Conversely, RASFL produced higher levels of IgG than normal or rheumatoid PBL when the plant mitogen was omitted. B cell rich fractions from RASFL showed an enhancement in both spontaneous and PWM-induced IgG synthesis when they were combined with normal PBL T cells, suggesting that the RASFL B cells had already been partially activated in vivo. Presumably, RASFL T cells are defective in that they are not able to assist B cells effectively in the response to PWM stimulus. We also found that rheumatoid synovial fluid contains some humoral factors which render normal PBL T cells capable of helping normal PBL B cells synthesize IgG spontaneously. These findings may contribute to the inflammatory process of rheumatoid synovitis.

Arthritis, Rheumatoid↗