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At least 1,495 records · Page 83Linked to original sources
PubMed1989

15-Hydroxy-eicosatetraenoic acid (15-HETE) inhibits carrageenan-induced experimental arthritis and reduces synovial fluid leukotriene B4 (LTB4).

15-Hydroxy-eicosatetraenoic acid (15-HETE), a product of arachidonic acid, has no proinflammatory capacity, but can inhibit the formation and the chemotactic response of neutrophils to leukotriene B4 (LTB4), a potent mediator of inflammation. The purpose of the present study was to determine whether intraarticular administration of 15-HETE in carrageenan-induced acute arthritis might decrease the levels of LTB4 in synovial fluid and modify the arthritis. A bilateral acute knee joint arthritis was established in 7 dogs by intraarticular injections of carrageenan every third day. To the right joints, 15-HETE was administered both concomitantly with the carrageenan injections and continuously via an osmotic pump. In samples of synovial fluid obtained on day 0, 3 and 10 PGE2 and LTB4 were determined using reversed phase high performance liquid chromatography combined with radioimmunoassays and neutrophil chemokinesis. In the presence of 15-HETE the clinical severity of arthritis was significantly reduced and the volume of synovial effusate was decreased on an average by 42%. Furthermore, the relative number of neutrophils in histological sections of synovial tissue was decreased by 58%. Intraarticular caragheenan injections induced LTB4 formation, and maximum levels were obtained on day 3 (279.2 +/- 148.2 pg/joint). PGE2 was also present on day 3, but maximum levels were detected on day 10 (9.5 +/- 4.8 ng/joint). In joints injected with both carragheenan and 15-HETE the levels of LTB4 on days 3 and 10 were inhibited by 90% and 83%, respectively. For PGE2 a small but insignificant decrease was found on both day 3 and on day 10. These results show that LTB4 may be an important mediator of acute arthritis induced by carragheenan in dogs, and that intraarticular administration of 15-HETE can modify this arthritis by inhibiting LTB4 formation.

Animals↗
PubMed2000

Alterations in cartilage type-II procollagen and aggrecan contents in synovial fluid in equine osteochondrosis.

The etiology and pathophysiology of osteochondrosis remain poorly understood because it is difficult to obtain material from lesions in the early stage of this disease and because there is no satisfactory experimental animal model. We wished to determine whether there are changes in articular cartilage turnover in equine osteochondrosis, which closely resembles the human disease, by assaying cartilage matrix molecules in synovial fluids. We used immunoassays that measure a keratan sulfate epitope and the epitope 846 on the cartilage proteoglycan aggrecan and the C-propeptide of cartilage type-II procollagen, which is released following the synthesis of this molecule, to analyse synovial fluids from equine tarsocrural joints with and without osteochondrosis. In young horses with osteochondrosis, there was a significant increase of C-propeptide of type-II procollagen accompanied by a decrease in the 846 and keratan sulfate epitopes. The results identify differential alterations in aggrecan and type-II collagen turnover in the cartilage matrix in young animals with osteochondrosis that may contribute to the pathological degeneration of articular cartilage in this disease.

Aggrecans↗
PubMed1998

Detection of a soluble form of B7-1 (CD80) in synovial fluid from patients with arthritis using monoclonal antibodies against distinct epitopes of human B7-1.

The costimulatory molecule B7-1 (CD80) has been shown to be an important component for T cell immune responses. We have generated several monoclonal antibodies (PSRM-1, -2, -3, -6, and -7) against B7-1 using a human glycosylphosphatidylinositol-anchored B7-1 (GPI-B7-1) as an antigen. These monoclonal antibodies are able to detect B7-1 by flow cytometry, ELISA, and Western blotting. One antibody in particular, PSRM-3, blocks the CD28/CTLA-4 interaction with B7-1 and consequently blocks costimulation of T cells. The other PSRM monoclonal antibodies did not compete with PSRM-3 for recognition of B7-1 and also failed to block B7-1 interaction with CTLA-4 and CD28, indicating that these antibodies bind to different epitopes. PSRM-3 and -7 detect phosphatidylinositol-specific phospholipase C-released soluble GPI-B7-1 in a sandwich ELISA. We used this sandwich ELISA to assay for the presence of a soluble form of B7-1 in synovial fluids of arthritis patients. By sandwich ELISA, B7-1 was detected in the synovial fluid of 5/11 patients with rheumatoid arthritis, 5/5 patients with osteoarthritis, and 2/6 patients with other forms, including crystalline-induced arthritis. The presence of soluble B7-1 was confirmed by immunoprecipitation using PSRM-3-coupled Sepharose beads. The source and function of soluble B7-1 are unknown at present; it is possible, however, that the soluble form of B7-1 molecule may play a local immunoregulatory role which may suppress or induce inflammation depending upon whether it interacts with the T cell costimulatory CD28 molecule or the negative signaling CTLA-4 molecule.

Abatacept↗
PubMedDate not supplied

The levels of collagenase, tissue inhibitor of metalloproteinases-1 (TIMP-1), collagenase approximately TIMP-1 complexes and glycosaminoglycan (GAG) in sequential samples of synovial fluid aspirated from patients with osteoarthritis.

OBJECTIVE: Collagen turnover in connective tissues is thought to be controlled by the balance between the levels of interstitial collagenase and tissue inhibitor of metalloproteinases (TIMP-1). The aim of this study was to measure the level of total collagenase (MMP-1), TIMP-1, collagenase approximately TIMP-1 complex and glycosaminoglycan (GAG) in sequential samples of osteoarthritic knee synovial fluid from well documented patients to determine if these parameters changed with time and correlated with clinical indices. METHODS: Twenty-one patients were recruited and randomly allocated to receive tiaprofenic acid, indomethacin or naproxen. Total collagenase, TIMP-1, collagenase approximately TIMP-1 complex and GAG were measured in 80 osteoarthritic synovial fluids taken over a period of six months. RESULTS: The majority of fluids contained a molar excess of TIMP-1 over collagenase, although in seven fluids collagenase was present in excess; six of these samples were from a single patient. GAG levels were relatively unchanged over the six months studied. CONCLUSION: The levels of collagenase and TIMP-1 varied between patients and over time in individual patients. No collagenase approximately TIMP-1 complex was found in any fluid. There was no significant difference in the median levels of collagenase, TIMP-1 or GAG in the different treatment groups. High levels of collagenase were found in one patient with a crystal related disease. These immunoassays give valuable information on the levels of collagenase and TIMP-1 in individual patients with time and may help to determine the mechanisms controlling the turnover of cartilage collagen in different arthritides.

Adult↗
PubMed1991

Synovial fluid ATP: a potential substrate for the production of inorganic pyrophosphate.

The enzyme nucleoside triphosphate pyrophosphohydrolase (NTPPPH) is present in all joint fluids and on intraarticular cells. It generates inorganic pyrophosphate (PPi) from nucleoside triphosphate substrate, thus serving as a potential source of the PPi which forms in the cartilages of patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition. NTPPPH is also important in matrix vesicle induced calcification with basic calcium phosphate (BCP) crystals. An articular substrate for this enzyme was sought. ATP was measured in the joint fluids from 107 patients with various forms of arthritis. Synovial fluid ATP levels were higher in patients with CPPD deposits than in osteoarthritis (p less than 0.02) or rheumatoid arthritis (p less than 0.002). ATP also correlated with PPi concentration (p less than 0.05) and with the presence of BCP crystals (p less than 0.05), but not with cellularity of the fluid, NTPPPH activity, or age of the donor. This substrate for NTPPPH may contribute to CPPD crystal deposition by generating PPi and may stimulate matrix vesicle induced formation of BCP crystals in several forms of arthritis.

Adenosine Triphosphate↗
PubMed1996

Regulation of surface and soluble TNF receptor expression on human monocytes and synovial fluid macrophages by IL-4 and IL-10.

By regulating monocyte and macrophage production of IL-1, its receptor, and its receptor antagonist, IL-4 and IL-10 may exert significant anti-inflammatory activity. We determined whether a similar multicomponent process controlling TNF activity was regulated by IL-4 and IL-10 in nonadherent monocytes and synovial fluid macrophages. Previous studies differed in their conclusions. For both the p75 and p55 TNF receptors, mRNA levels, surface receptor expression, and soluble receptor levels were measured for blood monocytes incubated in vitro for 17, 40, or 64 h with IL-4 or IL-10. The predominant TNF receptor on monocytes, the p75 receptor, was down-regulated by IL-4 at the mRNA level. In turn, both surface and soluble receptor levels on LPS-stimulated cells were reduced and the inhibitory effects were maintained for at least 64 h. In contrast, IL-10 increased surface and soluble p75 TNF receptor levels on monocytes for approximately 40 h, which reflected an increase in receptor mRNA. These studies suggest that IL-4 and IL-10 do not directly regulate the cleavage of TNF receptors from monocytes and macrophages. Addition of an Ab to IL-10 suggested that the stimulatory effects of LPS on p75 TNF receptor expression were due, at least in part, to LPS stimulation of IL-10 production and that IL-4 acted, in part, by decreasing IL-10 production. IL-4 was down-regulatory and IL-10 stimulatory for TNF receptor expression by synovial fluid macrophages. By increasing surface receptor levels, IL-10 enhanced the activities of TNF on monocytes for IL-1beta production. By increasing soluble TNF receptor levels, IL-10 may limit only temporarily the activity of other TNF-responsive cells. This study questions the benefit of IL-10 to resolving TNF-associated inflammation.

Arthritis, Rheumatoid↗
PubMed2004

Cefotaxime kinetics in plasma and synovial fluid following intravenous administration in horses.

Cefotaxime powder was diluted with sterile water to a concentration of 100 mg/mL. The volume of solution was adjusted for each experimental horse to provide a total dose of 15, 20, and 25 mg/kg and was administered by infusion through a jugular vein catheter over a 10-min period. All three doses were administered to each of the six experimental horses at three different times. Cefotaxime concentrations in plasma and synovial fluid samples were measured by high-performance liquid chromatography (HPLC). Standard compartmental analysis techniques and the WinSAAM modeling program were used to determine standard pharmacokinetic parameters for cefotaxime. The plasma and synovial fluid data from the five horses administered the 25 mg/kg dose was analyzed. Plasma cefotaxime concentrations appeared to be linearly related to dose infused and declined in parallel, suggesting linear drug kinetics. Moreover, cefotaxime concentrations declined monotonically suggesting that its disposition kinetics could essentially be described by a one-compartment model rather than the fact that sampling occurred after the infusion was discontinued. Maximum concentration of cefotaxime in plasma occurred immediately after cessation of the infusion. Minimum inhibitory concentrations were determined for Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, and Klebsiella pneumoniae, common isolates from septic arthritis in horses. Based on our pharmacokinetic data, a regimen of 25 mg/kg administered i.v. every 6 h appears appropriate for susceptible joint infections in adult horses.

Animals↗
PubMed1977

Acute pseudogout in the absence of synovial fluid Leukocytes.

A case of acute pseudogout that occurred in the absence of synovial fluid leukocytes is described. This finding implies that there may be an alternative inflammatory mechanism for acute pseudogout that does not depend on polymorphonuclear leukocytes.

Acute Disease↗
PubMed2006

Cytokine profile in synovial fluid from patients with internal derangement of the temporomandibular joint: a preliminary study.

OBJECTIVES: Temporomandibular joint disorders (TMD) comprise a group of chronic painful conditions of mastication in the temporomandibular joint (TMJ). Although the association between TMD and internal derangement of the TMJ is well documented, the functional relevance is still unclear. Increased concentrations of inflammatory mediators have been identified in the synovial fluid of affected patients with TMD, suggesting an underlying degenerative or inflammatory process. The aim of this study was to generate a comprehensive cytokine expression profile in TMD. METHODS: 15 samples from patients with internal derangement of TMJ were analysed using a novel cytokine array that enables the analysis of 79 different cytokines simultaneously. RESULTS: Cytokine levels were correlated with the presence of joint effusion (JE) determined by MRI. In the majority of synovial fluid samples, angiogenin (Ang), fibroblast growth factor (FGF)-9, insulin-like growth factor-binding protein (IGFBP)-3, interleukin (IL)-1alpha, IL-1beta, IL-8, inducible protein (IP)-10, macrophage inflammatory protein (MIP)-1beta, osteoprotegerin (OPG), transforming growth factor (TGF)-beta2, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, tumour necrosis factor (TNF)-beta and vascular endothelial growth factor (VEGF) were detectable. Furthermore, the expression levels of Ang, brain-derived neurotrophic factor (BDNF), FGF-4, FGF-9, IGFBP-2, IL-8, MIP-1beta, OPG, pulmonary and activation-regulated protein (PARC), TGF-beta2, TIMP-2 and VEGF were significantly associated with the presence of JE; among these, nine cytokines (Ang, BDNF, FGF-4, FGF-9, IGFBP-2, MIP-1beta, PARC, TGF-beta2 and TIMP-2) were hitherto not described in TMD. CONCLUSIONS: This study confirmed previous reports of elevated cytokine levels in TMD. Additionally, we identified previously undescribed cytokines that were upregulated and correlated significantly with the presence of JE. We were able to identify novel cytokines that have hitherto not been described in TMD. Strategies targeting the identified cytokines may represent a novel therapy option in TMD.

Adult↗
PubMed1983

Pronounced production of polyclonal immunoglobulin G1 in the synovial fluid of goats with caprine arthritis-encephalitis virus infection.

Infection of goats with caprine arthritis-encephalitis virus, a lentivirus, resulted in arthritis characterized by the production of intrasynovial immunoglobulin G1 concentrations that were 2 to 5.3 times the serum concentrations in the inoculated carpi at 6 months postinoculation. The intrasynovial immunoglobulin was polyclonal, and its presence was accompanied by increased albumin leakage into the joints. Synovial fluid immunoglobulin levels fluctuated temporally but remained elevated compared with medium-inoculated controls for 38 months after infection. Elevated immunoglobulin G1 concentrations correlated with focal sublumenal plasmacytic infiltrates in the synovia of inoculated carpi at 5 months postinoculation. Inflammation in the uninoculated joints of infected goats was also accompanied by increased intrasynovial immunoglobulin G1 levels. Antibody to systemically administered antigens was a greater proportion of the immunoglobulin population in sera than in synovial fluids of infected goats, suggesting that antibody production to local antigens was responsible for increased intrasynovial immunoglobulin G1 levels.

Animals↗
PubMed1998

Soluble VCAM-1 induces chemotaxis of Jurkat and synovial fluid T cells bearing high affinity very late antigen-4.

It has been shown that cells with high affinity very late Ag (VLA)-integrins have up-regulated expression of a beta1-subunit epitope, which is detected by 15/7 mAb. In this study, we demonstrate that soluble VCAM-1 (sVCAM-1) exhibits chemotactic activity of T cells with high affinity VLA-4 against VCAM-1, such as Jurkat T cells and IL-2-dependent T cells. Moreover, we found that T cells in the synovial fluid show high basal migration in the absence of sVCAM-1, compared with peripheral blood T cells in patients with rheumatoid arthritis. Among T cells in the synovial fluid, CD45RO+ memory T cells, in response to sVCAM-1, showed a much higher than basal migratory response when compared with CD45RA+ naive cells, while no significant difference was observed between CD4+ and CD8+ T cells. The chemotactic activity of sVCAM-1 is inhibited in the presence of anti-VCAM-1 and anti-VLA-4, which interfered with the binding between VCAM-1 and VLA-4. Inhibition studies using various kinase inhibitors (C3 exoenzyme, KN62, and H7) show that Rho, Ca2+/calmodulin-dependent kinase II, and protein kinase C are involved in signal transduction in sVCAM-1-induced chemotaxis, respectively, whereas tyrosine kinase seems to play a lesser role, since genistein showed only partial inhibition of T cell chemotaxis. Western blot analysis using an anti-phospho-serine mAb (MO82) reveals that Ser82 in the vimentin is phosphorylated specifically by Ca2+/calmodulin-dependent kinase II through sVCAM-1 activation in the IL-2 dependent T cells. Collectively, by inducing migration and recruitment of T cells through several kinase activations, sVCAM-1 contributes to the development of the inflammation of synovial lesion.

Adult↗
PubMed1990

Interleukin 1 beta in synovial fluid is related to local disease activity in rheumatoid arthritis.

Interleukin 1 beta (IL-1 beta) is a polypeptide with pro-inflammatory and immunopotentiating effects in vivo and in vitro. With relevance to rheumatoid arthritis (RA) IL-1 augments release of prostanoids, proteinases and oxygen metabolites and is a potent inducer of bone and cartilage resorption. Although high levels of IL-1 have been found in rheumatoid synovial fluids, intra-individual variation in IL-1 production has made it difficult to correlate these levels with disease activity. To overcome this problem we have studied patients with symmetrical and asymmetrical knee joint inflammation. Local disease activity was documented using Ritchie score and joint circumference; IL-1 beta levels were quantitated in synovial fluid by ELISA. In patients with symmetrical joint involvement almost identical levels of IL-1 beta were detected in the right and left knee joints. In contrast, in patients exhibiting asymmetrical knee joint involvement, IL-1 beta levels in the inflamed joints were significantly higher than in the contralateral joints. The study provides further evidence for the role of IL-1 in the pathogenesis of rheumatoid inflammation.

Adult↗
PubMed1984

Neutral protease, collagenase and elastase activities in synovial fluids from arthritic patients.

Neutral protease, collagenase and elastase activities were high in synovial fluids from inflammatory arthritic diseases such as gout, active rheumatoid arthritis and ankylosing spondylitis. The activities correlated well with biochemical parameters such as CRP, ESR and total protein. Values were much lower in a non-inflammatory fluid from a patient with osteoarthrosis. Treatment of fluids with trypsin released both collagenase and elastase. The fluids possessed reserve inhibitory action against these enzymes presumably due to plasma antiproteases being present. The collagenase present was found to possess a MW of 32,700 daltons.

Arthritis↗
PubMed2001

Etofenamate levels in human serum and synovial fluid following iontophoresis.

The absorption of etofenamate (CAS 30544-47-9, Rheumon gel) by iontophoresis in 11 patients with low back pain and in 13 patients with synovitis of the knee was evaluated. During the 5-day treatment period, the test gel in a quantity corresponding to 100 mg etofenamate was applied to affected body regions every day by 20-min iontophoresis sessions. Two hours after the fifth application, the concentration of etofenamate in serum and synovial fluid (in patients who had knee joint iontophoresis) were measured by HPLC. Iontophoresis of etofenamate into the lumbar region as well as to the knee joint resulted in consistent serum levels: 219 +/- 136.3 micrograms/l and 191 +/- 84.6 micrograms/l, respectively. In patients with synovitis of the knee, the synovial level of etofenamate (368 +/- 109.2 micrograms/l) was almost twice as high than the serum concentration. The authors conclude that with topical application of etofenamate by iontophoresis the drug appears not only in the serum but also--with higher levels--in the synovial fluid.

Administration, Topical↗
PubMed1983

Synovial fluid lactate and the diagnosis of septic arthritis.

To assess the value of synovial fluid lactate estimation in the diagnosis of septic arthritis, 238 specimens received for routine culture and 75 reference samples were examined using a rapid enzyme technique. Samples were collected without special treatment and the effect of delay in transport to the laboratory investigated. Raised levels were found in all cases of untreated septic arthritis, in six out of ten partially treated patients and in 19 out of 219 non-septic fluids. Special treatment of the sample was unnecessary if it was examined within six hours of aspiration. The predictive value of a negative result was 98 per cent and the value of the test appeared to be in the rapid exclusion of sepsis in untreated patients.

Arthritis, Infectious↗
PubMed1990

Elevated soluble CD8 in the synovial fluid from patients with rheumatoid arthritis.

Suppressor/cytotoxic T cells express the surface marker CD8, which can be measured in a soluble form in culture supernatants of activated human lymphocytes. Using a sandwich immunoassay, we assessed the levels of soluble CD8 (sCD8) in serum from patients with rheumatoid arthritis (RA; n = 82), patients with degenerative joint disease (DJD; n = 40), and healthy controls. There were no differences in serum sCD8 levels among these groups. In contrast, the levels of soluble CD8 in the synovial fluid (SF) from patients with RA (n = 53) were significantly increased compared with the levels in 23 samples from patients with DJD (821 +/- 110 U/ml versus 213 +/- 13 U/ml, p less than 0.001). Synovial fluid sCD8 levels in the RA group were strikingly elevated, to a maximum value of 5,026 U/ml. In the majority of RA SF specimens (39 of 53), the values were significantly higher in the SF than the serum. Although the RA group had higher values of sCD8, such values were not significantly correlated with measured laboratory or clinical parameters. Current clinical and laboratory methods of evaluating patients may not be adequate in dealing with the complexity and heterogeneity of RA. Soluble CD8 values may be useful in further grouping patients with this disease.

Antibodies, Monoclonal↗
PubMed1995

Cartilage matrix molecules in serum and synovial fluid.

The search continues for constituents of articular cartilage in the serum and synovial fluid of patients with arthritis. This work is driven by the hope that such "markers" will be useful in the diagnosis and management of rheumatic diseases. Absent information about the kinetics of these molecules continues to hinder interpretation of their concentration. Recent progress includes recognition of markers that appear to be specific for diseased cartilage and identification of factors that may distinguish between reversible and irreversible disease.

Cartilage↗