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PubMed1986

Neopterin production in inflamed knee joints: high levels in synovial fluids.

Neopterin levels of serum and fluid were determined in 30 patients with inflammatory synovial fluids and in 30 controls with joint effusions induced by trauma or osteoarthritis. Neopterin was significantly elevated in inflammatory fluids. There was no correlation with the acute phase reactants. Neopterin levels were significantly higher in inflammatory fluids than in serum, and vice versa in non-inflammatory conditions. Our results indicate that in arthritis neopterin is produced locally in the joint by monocytes induced by T-cell activation.

Adult↗
PubMed1993

Corticotropin-releasing hormone in synovial fluids and tissues of patients with rheumatoid arthritis and osteoarthritis.

Inflammation normally results in enhanced synthesis and secretion of hypothalamic corticotropin-releasing hormone (CRH) which, in turn, exerts antiinflammatory effects by virtue of increased adrenal glucocorticoid production. CRH and CRH binding sites are also expressed in the peripheral nervous and immune systems. Our groups have recently shown that CRH is secreted locally in acute carrageenin-induced inflammation in rats and has predominantly proinflammatory effects. We have also shown that CRH is expressed in the joints of Lewis rats with experimental arthritis. To determine if CRH is present in human inflammatory arthritis, we examined synovial fluids and tissues from patients with rheumatoid arthritis (RA) or osteoarthritis (OA) and normal individuals. We found markedly enhanced expression of immunoreactive CRH in situ in synovium from patients, which was significantly greater in RA than in OA (p < 0.01). CRH concentrations were also significantly higher in RA (140 +/- 33 pg/ml, mean +/- SEM; n = 10) than OA (25 +/- 4 pg/ml; n = 6) synovial fluids (p < 0.005). HPLC showed immunoreactive CRH extracted from RA and OA synovial tissues and fluids coeluted with CRH 1-41. CRH mRNA was present in low levels in synovial tissue from patients with RA and, to a lesser extent, OA. In summary, immunoreactive CRH is locally secreted in the synovium of patients with RA and, at lower levels, OA. These data support the view that CRH functions as an autocrine and/or paracrine mediator of inflammation in humans.

Arthritis, Rheumatoid↗
PubMed1988

Establishment of human Ig producing heterohybridomas by fusion of mouse myeloma cells with human lymphocytes derived from peripheral blood, bone marrow, spleen, lymph node, and synovial fluid. Effect of polyclonal prestimulation and cryopreservation.

50 fusion experiments were carried out to analyse heterohybridization efficiencies on mouse myeloma cells of the P3 X63 Ag8/653 line with human lymphocytes derived from peripheral blood, bone marrow, lymph node, spleen or synovial fluid. We found higher yields of growing and human Ig-producing hybridoma lines when lymphocytes from spleen or lymph node were fused. Although primary hybridomas could be established from fusions with bone marrow-derived cells, only in nine out of 1616 initially seeded wells was Ig production registered. Four fusions using immune cells from synovial fluid were made without success. Independently of the source of lymphocytes pokeweed mitogen (PWM) prestimulation had no enhancing effect on the percentage of wells with cell growth and this did not alter the IgM:IgG ratio in primary hybridomas (9:1), although cells from all compartments used here (with the exception of bone marrow cells) could be stimulated with PWM to produce both IgG and IgM in cultures. Cryopreserved lymphocytes from different sources could be used for fusions with comparable results registered for the fresh material.

Animals↗
PubMedDate not supplied

Collagenolytic protease expression in cranial cruciate ligament and stifle synovial fluid in dogs with cranial cruciate ligament rupture.

OBJECTIVE: To determine expression of collagenolytic genes and collagen degradation in stifle tissues of dogs with ruptured cranial cruciate ligament (CCL). ANIMALS: Six dogs with CCL rupture and 11 dogs with intact CCL. PROCEDURES: Gene expression in CCL tissue and synovial fluid cells was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Collagen degradation was studied using CCL explant cultures and a synovial fluid bioassay. RESULTS: Expression of matrix metalloproteases (MMP) was not found in young Beagles with intact CCL; however, increased expression of MMP-3 was found in CCL tissue from older hounds with intact CCL, when compared with young Beagles. In dogs with ruptured CCL, expression of MMP-2 and -9 was increased in stifle tissues, when compared with dogs with intact CCL. Similar to MMP-9, expression of tartrate-resistant acid phosphatase (TRAP) and cathepsin S was only found in stifle tissues from dogs with ruptured CCL; in contrast, expression of cathepsin K was found in all ruptured and intact CCL. Collagen degradation was increased in ruptured CCL, when compared with intact CCL. CONCLUSION: Rupture of the CCL is associated with up-regulation of expression of MMP-2 and -9 (gelatinase A and B), TRAP, and cathepsin S, and increased degradation of collagen. CLINICAL RELEVANCE: These findings suggest that MMP-2, -9, cathepsin S, and TRAP may be important mediators of progressive joint destruction in dogs with CCL rupture. These genes are markers for macrophages and dendritic cells. MMP and cathepsin S pathways may offer novel targets for anti-inflammatory medical therapy aimed at ameliorating joint degradation associated with inflammatory arthritis.

Animals↗
PubMed1975

Tarsal degenerative joint disease in cattle: blood and synovial fluid changes.

Tarsal degenerative joint disease (DJD) in 27 cattle was classified as primary or secondary based on age, joint conformation defects, faulty hindlimb alignment, or history of trauma to the affected joint(s). Results of blood and synovial fluid analysis for cattle affected with primary or secondary tarsal DJD were grouped in compilation of data. Cattle with tarsal DJD had significantly (P smaller than 0.01) reduced hemoglobin (Hb) content in comparison to that in control cattle. There was highly significant (P smaller than 0.001) reduction in packed cell volume (PCV). A significant difference was not determined for mean corpuscular hemoglobin concentration (MCHC) values of the 2 groups of cattle. Total white blood cell (WBC) counts closely paralleled each other, although mean proportion of neutrophils was significantly (P smaller than 0.05) greater in cattle affected with tarsal DJD, as were mean proportion of lymphocytes (P smaller than 0.02). Synovial fluid samples were analyzed for physical, biochemical, and cytologic properties. Statistical comparisons were made between values determined for arthritic cattle and control cattle. All samples from cattle with tarsal DJD were transudative. Opacity and flocculation were attributed to the presence of cartilaginous fragments and fibrils. There was significant correlation between increased relative viscosity (RV) and higher grades of mucinous precipitate quality (MPQ; r = +0.294, P smaller than 0.05) for all cattle. Mean alkaline phosphatase (ALP) activity for arthritic cattle was significantly (P smaller than 0.001) reduced, as was the mean activity for lactic dehydrogenase (LDH; P smaller than 0.05). The mean aldolase (ALD) activity for arthritic cattle was increased, whereas mean activity values for glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) were reduced. Samples from arthritic cattle had reduced total leukocyte counts and significantly (P smaller than 0.05) increased proportion of macrophages in comparison to the values in control cattle.

Alanine Transaminase↗
PubMed2003

Fibrin generated in the synovial fluid activates intimal cells from their apical surface: a sequential morphological study in antigen-induced arthritis.

OBJECTIVE: Fibrin deposits adhered to the synovial surface are typical of rheumatoid joints. Since fibrin appears to have a role in arthritis perpetuation our aim was to investigate how these deposits are formed and the consequences of their adhesion to the tissue. METHODS: The appearance of fibrin aggregates either free in the synovial fluid or attached to the membrane was studied in rabbits with antigen-induced arthritis by histological techniques at different time points from challenge. In the fixed synovial membranes areas of fibrin-bound synovium were evaluated by qualitative variables to obtain a sequential profile of morphological changes. RESULTS: Fibrin aggregates appeared from the initial stages of the disease in the synovial effusion. Later on, they were localized on the synovial surface and progressive changes were noted at the fibrin-tissue interface, ending with the invasion of the aggregates by synovial cells and their incorporation into the tissue. CONCLUSION: Fibrin aggregates generated inside the joint cavity may constitute a source of activation and acquisition of invasiveness of the synovial fibroblasts, a process to explore within the perpetuating mechanisms of rheumatoid arthritis.

Animals↗
PubMed1989

Very late activation antigen on synovial fluid T cells from patients with rheumatoid arthritis and other rheumatic diseases.

We used flow cytometry and immunoprecipitation techniques to study the expression of the activation molecules transferrin receptor, interleukin-2 receptor, HLA-DR, and very late activation antigen 1 (VLA-1) on purified T lymphocytes from peripheral blood and synovial fluid of 9 patients with rheumatoid arthritis and 7 patients with other rheumatic diseases. We found a T cell subset bearing VLA-1 in synovial fluid from 8 rheumatoid arthritis patients and 4 patients with other rheumatic diseases. VLA-1 was not found in peripheral blood T lymphocytes from either group.

Antigens, Differentiation↗
PubMed1991

Collagenase reserves in polymorphonuclear neutrophil leukocytes from synovial fluid and peripheral blood of patients with rheumatoid arthritis.

Degradation of cartilage in rheumatoid arthritis (RA) may be in part due to release of collagenase from specific granules of polymorphonuclear neutrophil leukocytes (PMNs) during degranulation. We decided to study, not synovial fluid (SF) collagenase, but PMN collagenase reserves. PMN were isolated from parallel SF and peripheral blood (PB) samples obtained from 7-arthritis patients. PMNs were stimulated in vitro by tetradecanoyl-phorbol-13-acetate (TPA). Collagenase activity in the supernatant without and with phenylmercuric chloride activation was studied. Compared to PB PMNs, there was no consistent decrease in the total collagenase reserves in the inflammatory SF PMNs. This suggests that the release of collagenase in the inflammatory synovial fluid does not deplete SF PMNs of the collagenase synthesized at the myelocyte stage. The role of PMN collagenase in pathogenesis of cartilage destruction would then seem to be more dependent on local release and autoactivation at cartilage surface by adherent PMNs and not excessive collagenase release from free floating SF PMNs at single cell level. Furthermore, under the experimental conditions used the proportion of collagenase released in active form was higher in SF PMN specimens than in PB PMN specimens (p less than 0.01). The predominant collagenous component of adult cartilage, native type II collagen, was degraded by PMN collagenase as fast as native type I collagen. These findings suggest an important role for this enzyme in destruction of the free cartilage surface in RA.

Arthritis, Rheumatoid↗
PubMed1981

Ia+ T cells in synovial fluid and tissues of patients with rheumatoid arthritis.

Markedly elevated levels of T cells expressing Ia antigens were found in the synovial membranes and synovial fluids of patients with rheumatoid arthritis. The primary increase in expression of the Ia antigens was on the OKT 8+ (suppressor/cytotoxic) T cell subset. In addition, the total percentage of OKT 8+ T cells in intraarticular sites was usually greater than levels in peripheral blood. Small numbers of OKT 4+ (helper/inducer) cells bearing Ia antigens were also identified. The characteristic increase in the Ia+ T cells in peripheral blood was not encountered in most patients treated with D-penicillamine.

Arthritis, Rheumatoid↗
PubMed1999

Cytokine levels in synovial fluid from hips with well-functioning or loose prostheses.

We analysed synovial fluid from 88 hips, 38 with osteoarthritis and 12 with well-functioning and 38 with loose hip prostheses. The levels of TNF-alpha, IL-1beta (71 hips) and IL-6 (45 hips) were measured using the ELISA technique. Joints with well-functioning or loose prostheses had significantly increased levels of TNF-alpha compared with those with osteoarthritis. Hips with aseptic loosening also had higher levels of IL-1beta but not of IL-6 compared with those without an implant. The levels of TNF-alpha and IL-1beta did not differ between hips with stable and loose prostheses. Higher levels of TNF-alpha were found in hips with bone resorption of type II and type III (Gustilo-Pasternak) compared with those with type-I loosening. The level of cytokines in joint fluid was not influenced by the time in situ of the implants or the age, gender or area of the osteolysis as measured on conventional radiographs. Our findings support the theory that macrophages in the joint capsule increase the production of TNF-alpha at an early phase probably because of particle load and in the absence of clinical loosening. Since TNF-alpha has an important role in the osteolytic process, the interfaces should be protected from penetration of joint fluid.

Adult↗
PubMed2004

Simple and rapid determination of adenosine in human synovial fluid with high performance liquid chromatography-mass spectrometry.

A simple, fast, sensitive and selective reversed-phase high performance liquid chromatography-mass spectrometry coupling with an electrospray ionization (ESI) interface method is described for the determination of adenosine in human synovial fluid. This method involved the use of the [M + H](+)ions of adenosine and 2-chloroadenosine (internal standard for the assay) at m/z 268 and 302 in positive ion mode with selective ion monitoring (SIM). Separation was carried out on a 2.0 x 150 mm Shimadzu VP-ODS column by using an isocratic elution with a mobile phase consisting of water (94%),methanol (5%) and formic acid (1%). No interference with the components of the biological matrix was observed in the determination conditions. The calibration curve was linear in the range of 0.2-140 microgml(-1). The limits of quantification (LOQ) and detection (LOD) were 0.2 and 0.03 microgml(-1), respectively. The standard recoveries were between 93.3 and 104.0%. The method was successfully applied to determination of adenosine in some synovial fluids of patients affected by rheumatoid arthritis.

Adenosine↗
PubMed1992

Inhibition by prostaglandin E1 and E2 of 1,25-dihydroxyvitamin D3 synthesis by synovial fluid macrophages from arthritic joints.

Previous work has shown that renal metabolism of 25-dihydroxyvitamin D3 (25(OH)D3) to the active metabolite, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is stimulated by prostaglandin E2 and inhibited by acetylsalicylate (aspirin). As prostaglandins are primary inflammatory mediators and synovial fluid macrophages are known to synthesise 1,25(OH)2D3 in vitro, the effects of prostaglandin E1, prostaglandin E2, and aspirin on the metabolism of 25(OH)D3 by cells cultured from synovial fluid of patients with inflammatory arthritis were investigated. Most cultures contained non-proliferating macrophages which formed 1,25(OH)2D3; however, two of 13 cultures contained colonies of rapidly proliferating fibroblast-like cells which formed 24,25(OH)2D3 (24,25(OH)2D3). Prostaglandin E1 and prostaglandin E2 (0.01-10 mumol/l) induced marked inhibition of 1,25(OH)2D3 synthesis (up to 94%) in a dose dependent manner after preincubations of 24 hours but not over straightforward six hour incubations. Exposure of macrophages to aspirin (1 mumol/l-1 mmol/l) for 24 hours did not affect 1,25(OH)2D3 synthesis unless the cells had been pretreated with lipopolysaccharides, in which instance 1 mM aspirin increased 1,25(OH)2D3 synthesis. Lipopolysaccharide is a macrophage activating factor which stimulates macrophages to form 1,25(OH)2D3, and it also induces prostaglandin synthesis which would be inhibited by aspirin. Taken together these results suggest that prostaglandin E1 and prostaglandin E2 synthesised by macrophages may act in an autocrine manner to attenuate the ability of macrophage activating factors, such as lipopolysaccharide, to stimulate 1,25(OH)2D3 synthesis. Prostaglandins synthesised by other inflammatory cells may also inhibit 1,25(OH)2D3 synthesis in a paracrine manner. In contrast, prostaglandin E2 and aspirin had limited effects on fibroblast 24,25(OH)2D3 synthesis. This study shows that the effects of prostaglandin E1, prostaglandin E2, and aspirin in macrophages contrast with those previously reported for the renal 25(OH)D3-1alpha-hydroxylase, where prostaglandin E2 stimulated and aspirin inhibited enzyme activity. These results further emphasise that synthesis of 1,25(OH)2D3 in non-renal sites is independently regulated, which is consistent with it having an immunological role at a local level rather than playing a part in systemic calcium homeostasis.

Alprostadil↗
PubMed1993

Effects of intra-articularly administered endotoxin on clinical signs of disease and synovial fluid tumor necrosis factor, interleukin 6, and prostaglandin E2 values in horses.

In each of 4 horses, sterile synovitis was induced by intra-articular injection of 3 micrograms of Escherichia coli endotoxin (lipopolysaccharide, LPS) into one antebrachiocarpal joint; an equal volume (2 ml) of phosphate-buffered saline solution (PBSS) was injected into the opposite, control carpus. Blood and 1.5 ml of synovial fluid were obtained at postinjection hours (PIH) 0, 2, 4, 8, 12, 18, 42, 66, and 144. Synovial fluid sample collection was accomplished by use of an indwelling, intra-articular catheter through PIH 12, and by arthrocentesis subsequently. Joint fluid samples were analyzed for cell counts, protein concentration, cytologic variables, and tumor necrosis factor (TNF), interleukin 6 (IL-6), and prostaglandin E2 (PGE2) values. Tumor necrosis factor and IL-6 activities and WBC count were also measured in blood. To monitor local inflammation, skin temperature of each carpus was imaged, using a thermographic scanner prior to each sample collection time. Horses had minimal systemic effects. Mean (+/- SEM) rectal temperature increased significantly to 39.02 +/- 0.15 C only at PIH 18 after intra-articular injection of LPS. One horse had signs of mild depression from PIH 7 to 18, but its vital signs did not change appreciably. Each horse had mild signs of discomfort in the LPS-injected limb from PIH 1 to 3 until PIH 8 to 10. Mean peak surface temperature of the LPS-injected carpi was significantly higher than that of control carpi from PIH 8 to 144 (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1969

Breakdown products of C 3 in human synovial fluids.

Activation of the complement sequence results in conversion of the third component of complement (C'3) to an inactive product (C'3i) and the elaboration of additional fragments of smaller molecular weights and faster electrophoretic mobilities. Immunoelectrophoretic analysis of fresh synovial fluids with an anti-human C'3 antiserum disclosed in some a variable degree of conversion of C'3 to C'3i, but a more striking finding was an additional line in the alpha-globulin region. This faster migrating protein gave a reaction of partial identity with C'3/C'3i. With this antiserum a similar pattern developed when fresh human serum was incubated with immune complexes, or aggregated gamma-globulin. The same breakdown product of C'3 was obtained by treatment of fresh human serum with Zymosan, ammonium, hydrazine, agar, or dextran. Heating serum at 56 degrees C for 1 hr destroys the breakdown product; aging of serum produces it. Breakdown products of C'3 were looked for in 49 synovial fluids from patients with a variety of joint diseases. A significant correlation was found between the demonstration of the fast migrating breakdown product of C'3 and the diagnosis of rheumatoid arthritis and the presence of rheumatoid factor. A similar immunoelectrophoretic pattern was not found in the serum of any of the patients studied. When human gamma-globulin, which has been reduced and alkylated, is heat aggregated it loses the ability to fix human complement but still reacts with rheumatoid factor. Addition of reduced, aggregated gamma-globulin to fresh normal human serum produced no conversion of C'3, but when incubated with serum containing a high titer of rheumatoid factor, there was conversion of C'3 and the appearance of a breakdown product. Quantitative complement fixation studies with fresh serum from normal subjects and patients with rheumatoid arthritis disclosed complement fixation by reduced, aggregated gamma-globulin. The per cent of complement fixation was proportional to the titer of rheumatoid factor present in the test serum. These findings were interpreted as showing that rheumatoid factor can fix complement.The possibility is discussed that the presence of breakdown products of C'3 in the synovial effusions of most patients with seropositive rheumatoid arthritis and the ability of rheumatoid factor to fix complement are related phenomena.

Animals↗
PubMed1997

Low-level production of interleukin-13 in synovial fluid and tissue from patients with arthritis.

Rheumatoid arthritis (RA) is a chronic, aggressive disease characterized by inflammatory cells in the synovial tissue (ST) and synovial fluid (SF). Interleukin (IL)-13 inhibits the production of proinflammatory cytokines, chemokines, and hematopoietic growth factors by activated human monocytes. The aim of this study was to determine the production of IL-13 in various forms of arthritis. The presence of IL-13 in RA was found to be low, in that 18 of 26 RA SF samples and 10 of 14 RA peripheral blood (PB) samples had nondetectable levels (</=12 pg/ml). Similar low levels were found in SF and PB from patients with osteoarthritis (OA) and other arthritides. In contrast, RANTES, IL-8, monocyte chemotactic protein-1, and soluble P-selectin were found at levels of 13-, 120-, 1200-, and 2000-fold excess of IL-13, respectively. Mononuclear cells isolated from RA SFs did not produce significant levels of IL-13 in culture (</=12 pg/ml) but were able to do so when stimulated with phytohemagglutinin. Likewise, tissue explants from RA synovium cultured for 24 or 48 hr with or without serum did not produce appreciable quantities of IL-13 (</=12 pg/ml). Immunohistochemical data were in accordance with this result in that antigenic IL-13 was not detected on the majority of RA, OA, and normal (NL) ST cells. These results demonstrate a paucity of IL-13 within the joints of RA, OA, NL, and other arthritic patients by comparison with levels of other cytokines.

Arthritis↗
PubMed1998

Autoantibody patterns in synovial fluids from patients with rheumatoid arthritis or other arthritic lesions.

Patients with rheumatoid arthritis (RA) produce a variety of autoantibodies, not only demonstrable in the circulation, but also locally in the inflamed joint. We investigated the local production of several autoantibodies in the synovial fluid (SF) of 24 patients with RA and of 26 patients with other arthritic lesions. RA patients had higher titres of immunoglobulin M (IgM) and immunoglobulin G (IgG) rheumatoid factors (RFs) and of collagen type II antibodies in SF, whereas there were no demonstrable differences between groups with regard to antibodies against double-stranded (ds) DNA, C1q or the hapten 2,4,6-trinitrobenzene sulfonic acid (TNP). No differences were observed for total synovial levels of IgM or IgG. There was no autoantibody pattern that was typical of RA patients, except for the local presence of RF, primarily in seropositive RA patients. Our findings therefore support the notion that RF and collagen type II antibodies are induced by immunogenic material present in the local inflamed environment. In the accompanying paper we studied various synovial fluid cytokines in the same patient groups. Here we correlated the level of these cytokines with autoantibody titres in SF, but no specific cytokine associated with the production of RF was found. Hence, we conclude that several different inflammatory mediators might contribute to the chronic inflammation and autoantibody production in the joint of RA patients. An inverse correlation was established between concentrations of tumour necrosis factor-alpha (TNF-alpha) and levels of total IgG.

Adult↗
PubMed1998

Analysis of type 1 and type 2 T cells in synovial fluid and peripheral blood of patients with rheumatoid arthritis.

OBJECTIVE: It has been reported that CD4+ helper T cells play an important role in the pathogenesis of rheumatoid arthritis (RA). We evaluated the presence of intracellular cytokines interleukin 4 (IL-4) and interferon-gamma (IFN-gamma) produced by CD4+ and CD8+ T cells in the synovial fluid and peripheral blood of patients with RA at the single cell level. METHODS: We used 3 color flow cytometric analysis. Synovial fluid mononuclear cells (SFMC) and peripheral blood mononuclear cells (PBMC) were stimulated with phorbol myristate acetate (PMA) and calcium ionophore. The stimulated SFMC and PBMC were triple stained with conjugated mononuclear antibodies (Mab) against cytokines and surface antigens after fixation and permeabilization with a saponine buffer solution. The cells were analyzed for intracellular cytokines (IFN-gamma, IL-4) and surface antigens (CD3, CD4, CD8) using a flow cytometer. RESULTS: The CD4/CD8 ratio was significantly lower in SFMC than in PBMC. The positive rates of IFN-gamma producing cells among CD4+ T cells were significantly higher than those of IL-4 producing cells in both the SFMC and the PBMC of patients with active RA. In the SF of these patients, we also found CD8+ T cells that produce IL-4 alone, or both IL-4 and IFN-gamma. CONCLUSION: In the SF of patients with RA, CD4+ type 1 T cells, which may infiltrate into the synovium and cause pathogenic immune responses in the tissue, are predominant. We believe this cell type also induces migration and activation of CD8+ type 2 T cells into the active site of inflammation, which appears to downregulate the activity of CD4+ type 1 T cells, modulating the excess immune response.

Aged↗