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PubMed1993

Interleukin-8 (IL-8) in synovial fluid of rheumatoid and nonrheumatoid joint effusions.

IL-8 was measured in knee joint synovial fluid of 60 patients with rheumatoid arthritis, 8 with gout, 6 with osteoarthritis and 4 with meniscus lesions. IL-8 could be demonstrated in most SF samples. The highest levels were observed in rheumatoid joint effusions, yet mean levels were not significantly different between the different subgroups (mean +/- SE; RA 1537 +/- 3049 pg/ml, gout 570 +/- 952 pg/ml, OA/ML 178 +/- 188 pg/ml). In RA patients, IL-8 levels could not be related to various serological, clinical or radiological parameters. However, a correlation was observed between SF levels of IL-8 with those of lactate, LDH, beta 2-microglobulin and glucose. These observations suggest that next to the laboratory parameters IL-8 will be a parameter of the activity of the local inflammatory process. The results also demonstrate that IL-8 is not a disease-specific marker of joint inflammation.

Arthritis, Rheumatoid↗
PubMed1988

Multiple cytokine activities and loss of interleukin 2 inhibitor in synovial fluids of patients with rheumatoid arthritis.

Attempts to detect immune mediators in rheumatoid arthritis synovial fluids (RA-SF) by bioassays have yielded conflicting results, and so we analyzed the immune reactions occurring within rheumatoid joints using monospecific immunoassays for cytokines such as interleukin 1 beta (IL-1 beta), interleukin 2 (IL-2) and gamma interferon (gamma-IFN). Furthermore, we examined the IL-2 inhibitors to clarify the immunoregulatory mechanism in the lesion. SF from active RA contained a significant amount of IL-1 beta and IL-2 but not gamma-IFN. In contrast IL-2 inhibitor activity was depressed in RA-SF regardless of clinical disease activity. Our results suggest that cytokine overproduction and deficiency of inhibitory signals may result in the overactivity of cytokines and the overactivity may participate in the joint lesions of RA.

Antibodies, Monoclonal↗
PubMed1995

Development of a novel, rapid processing protocol for polymerase chain reaction-based detection of bacterial infections in synovial fluids.

We describe the development of a molecular detection system designed for use with synovial fluid (SF)-based infections. The methodology employs a lysis/extraction procedure that effectively disrupts microorganisms allowing for release of the microbial DNA and its amplification by polymerase chain reaction (PCR). We tested the effectiveness of adding a mixed-bed, ion-exchange resin to the extract to remove PCR inhibitory components present in the SF. After centrifugation to separate the resin, DNA contained in the supernatant is subjected to PCR using oligonucleotide primers designed for broad-spectrum microorganism detection. Amplification products are analyzed by agarose gel electrophoresis and/or DNA hybridization methodology. We report here the detection sensitivity and specificity of the protocol using SF inoculated with Escherichia coli and Staphyloccocus aureus. We have applied this new methodology to clinical SF specimens with results superior to standard laboratory culturing assays.

Bacterial Infections↗
PubMed1986

Immunocytology of synovial fluid cells may be of diagnostic and prognostic value in arthritis.

Cells of the synovial fluid (SF) have been examined by immunocytochemical methods. Samples were aspirated from four groups of patients with knee effusions: (a) seropositive inflammatory arthritis (n = 9); (b) seronegative inflammatory arthritis (n = 9); (c) osteoarthritic patients (n = 5); and (d) patients with traumatised knees (n = 4). The proportions of lymphocyte and macrophage subsets within the SF were determined with a panel of monoclonal antibodies. Patients with inflammatory arthritis had significantly larger proportions of activated T cells (RFT2+) and macrophages with the phenotype of interdigitating cells (RFD1+). No significant difference between groups could be found on differential count or when T4+/T8+ subset ratios were calculated. No significant difference in proportions of lymphocyte or macrophage subsets was found between the groups with seropositive and seronegative inflammatory arthritis. In two of three patients, where immunocytochemical analysis was performed before and after intra-articular steroids, reductions in the proportions of RFT2+ T cells and RFD1+ macrophage like cells were seen. It is suggested that such analysis may be of diagnostic or prognostic value.

Antibodies, Monoclonal↗
PubMedDate not supplied

Superoxide anion production by monocytes and synovial fluid macrophages of patients with chronic inflammatory joint disorders.

Peripheral blood monocytes (PBMo) and synovial fluid macrophages (SFMO) of patients with rheumatoid arthritis (RA), HLA B27-positive reactive oligoarthritis and controls were investigated for their capacity to generate superoxide anions (O2-) upon stimulation with phorbolmyristoacetate (PMA) in a cytochrome c (cyt c) microassay. PBMo of RA patients, patients with reactive arthritis and controls did not reveal any significant differences and also treatment of RA patients with gold salts or immunosuppressive therapy had no effect on the oxidative burst in PBMo. In contrast, in SFMO of RA patients treated only with nonsteroidal anti-inflammatory drugs (NSAID) we found significantly enhanced O2- release, compared with PBMo of the same group. Treatment with gold salts had no effect on this enhanced oxidative response, whereas immunosuppressive therapy with azathioprin or corticosteroids significantly reduced the O2- release of SFMO. In patients suffering from reactive arthritis we did not find significant differences between SFMO and PBMo. The O2- release of SFMO of this group was significantly reduced, when compared to that of SFMO of RA patients, treated with NSAID. These results indicated that SFMO but not PBMo in RA in cyt c microassay produce increased levels of activated oxygen species. In comparison to PBMo, SFMO of patients suffering from reactive arthritis do not show such an increased oxidative burst. These findings suggest that in RA, activated oxygen species have a local destructive effect in inflamed joints. This seems to be caused by activation of catalytic enzymes and complement components, as well as induction of release of interleukins or prostaglandins, contributing to the augmentation of the chronic inflammatory process.

Adult↗
PubMed2005

Inhibition of integrative cartilage repair by proteoglycan 4 in synovial fluid.

OBJECTIVE: To determine the effects of the articular cartilage surface, as well as synovial fluid (SF) and its components, specifically proteoglycan 4 (PRG4) and hyaluronic acid (HA), on integrative cartilage repair in vitro. METHODS: Blocks of calf articular cartilage were harvested, some with the articular surface intact and others without. Some of the latter types of blocks were pretreated with trypsin, and then with bovine serum albumin, SF, PRG4, or HA. Immunolocalization of PRG4 on cartilage surfaces was performed after treatment. Pairs of similarly treated cartilage blocks were incubated in partial apposition for 2 weeks in medium supplemented with serum and (3)H-proline. Following culture, mechanical integration between apposed cartilage blocks was assessed by measuring adhesive strength, and protein biosynthesis and deposition were determined by incorporated (3)H-proline. RESULTS: Samples with articular surfaces in apposition exhibited little integrative repair compared with samples with cut surfaces in apposition. PRG4 was immunolocalized at the articular cartilage surface, but not in deeper, cut surfaces (without treatment). Cartilage samples treated with trypsin and then with SF or PRG4 exhibited an inhibition of integrative repair and positive immunostaining for PRG4 at treated surfaces compared with normal cut cartilage samples, while samples treated with HA exhibited neither inhibited integrative repair nor PRG4 at the tissue surfaces. Deposition of newly synthesized protein was relatively similar under conditions in which integration differed significantly. CONCLUSION: These results support the concept that PRG4 in SF, which normally contributes to cartilage lubrication, can inhibit integrative cartilage repair. This has the desirable effect of preventing fusion of apposing surfaces of articulating cartilage, but has the undesirable effect of inhibiting integrative repair.

Animals↗
PubMed1995

Analysis of junctional sequences of T cell receptor gamma chain transcripts in gamma delta T cells from rheumatoid synovial fluid.

OBJECTIVE: We previously reported the predominance of the V gamma 3 gene in synovial fluid mononuclear cells (SFMC) from patients with rheumatoid arthritis (RA); the V gamma 3 gene is rare in normal peripheral blood mononuclear cells (PBMC). Our objective was to sequence the nucleotide composition of the junctional region of gamma chain transcripts expressed in gamma delta T cells from RA SFMC and normal PBMC. METHODS: cDNA from RA SFMC and normal PBMC were amplified by polymerase chain reaction, and the nucleotide sequences of amplified clones were determined. We compared the frequencies of V gamma-J gamma rearrangements in inframe (functional) and out of frame (nonfunctional) V gamma transcripts to determine the effect of intrinsic gene rearrangement on the expressed repertoire. RESULTS: Most V gamma genes, including V gamma 9, both inframe and out of frame, were rearranged to the J1/J2 genes, indicating that the intrinsic rearrangement may be influential in molding the mature functional gamma delta T cell repertoire. V gamma 9 transcripts in RA SFMC predominantly used J1/J2, as opposed to JP in normal PBMC. Most N regions displayed extensive diversity in both RA SFMC and normal PBMC, but some functional V gamma 9 transcripts of RA SFMC from one patient showed an identical junctional sequence, and 2 functional clones from different RA SFMC showed an identical junctional sequence, implying that the V gamma 9-J1/J2 transcripts could be controlled by antigenic selection. CONCLUSION: These results demonstrate that the prominent occurrence of the J1/J2 genes in all V gamma genes and the oligoclonality of functional V gamma 9 transcripts, in addition to the predominance of the V gamma 3 gene, are striking features of gamma chain transcripts in RA SFMC:

Aged↗
PubMed1995

Interleukin-6 in synovial fluid and HLA-DR expression in synovium from patients with temporomandibular disorders.

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

Adolescent↗
PubMed1990

The effect of synovial fluid and serum on the growth of calcium hydroxyapatite crystals.

The presence or absence of natural crystal growth inhibitors in joint tissues and fluids may be important in the pathogenesis of several arthropathies. Synovial fluid (SF) has therefore been examined for inhibitors of seeded hydroxyapatite growth rate (Vo) using a pH stat system. Pretreatment of seed crystals with SF reduced growth (Vo = 56 +/- 5, control 117 +/- 141 mol/base/min/g hydroxyapatite, p less than 0.001). Addition of small amounts of serum or SF to the growth medium caused a dose dependent growth inhibition (0.04% SF reduced Vo by 16%). Pretreatment with protease, but not hyaluronidase, abolished this activity and gel filtration localized it to the 55-80 kDa fraction. A macromolecular factor(s) with potent inhibitory activity has therefore been detected.

Arthritis, Rheumatoid↗
PubMed1991

Structure of recombinant human rheumatoid arthritic synovial fluid phospholipase A2 at 2.2 A resolution.

Phospholipases A2 (PLA2s) may be grouped into distinct families of proteins that catalyse the hydrolysis of the 2-acyl bond of phospholipids and perform a variety of biological functions. The best characterized are the small (relative molecular mass approximately 14,000) calcium-dependent, secretory enzymes of diverse origin, such as pancreatic and venom PLA2s. The structures and functions of several PLA2s are known. Recently, high-resolution crystal structures of complexes of secretory PLA2s with phosphonate phospholipid analogues have provided information about the detailed stereochemistry of transition-state binding, confirming the proposed catalytic mechanism of esterolysis. By contrast, studies on mammalian nonpancreatic secretory PLA2s (s-PLA2s) have only recently begun; s-PLA2s are scarce in normal cells and tissues but large amounts are found in association with local and systemic inflammatory processes and tissue injury in animals and man. Such s-PLAs have been purified from rabbit and rat inflammatory exudate, from synovial fluid from patients with rheumatoid arthritis and from human platelets. Cloning and sequencing shows that the primary structure of the human s-PLA2 has about 37% homology with that of bovine pancreatic PLA2 and 44% homology with that of Crotalus atrox PLA2. The human s-PLA2 is an unusually basic protein, yet contains most of the highly conserved amino-acid residues and sequences characteristic of the PLA2s sequenced so far. Here we report the refined, three-dimensional crystal structure at 2.2 A resolution of recombinant human rheumatoid arthritic synovial fluid PLA2. This may aid the development of potent and specific inhibitors of this enzyme using structure-based design.

Arthritis, Rheumatoid↗
PubMed1992

VLA family in rheumatoid arthritis: evidence for in vivo regulated adhesion of synovial fluid T cells to fibronectin through VLA-5 integrin.

Adhesion of T cells to extracellular matrix (ECM) proteins through VLA integrin receptors is crucial for lymphocyte trafficking, tissue localization and inflammatory function. We have investigated the expression of different VLA integrins (VLA-1-5) on peripheral blood (PB) and synovial fluid (SF) T lymphocytes from patients with rheumatoid arthritis (RA). Their expression on different cell types from synovial membrane (SM) is also reported. The role of VLA-4 fibronectin (FN) receptors in the interaction of activated SF T cells from RA patients with a 38-kD fragment of FN has been previously demonstrated. Here we have focused functional studies on VLA-5 as an alternative FN receptor for RA T cells. A significant higher proportion of SF T cells were able to bind to an 80-kD fragment of FN, containing the Arg-Gly-Asp (RGD) cell binding site, compared with PB T cells. This attachment was almost completely inhibited by anti-VLA-5 MoAbs as well as by RGD peptides. This enhanced capability by SF T cells appears to be independent of the level of the surface expression of the receptor and correlates better with their activation state as determined by the expression of the activation molecule AIM (CD69). The evidence for the expression of VLA heterodimers on both SF and SM cells from RA patients suggests the possible implication of ECM proteins in mediating and perpetuating inflammation in vivo.

Adult↗
PubMed1996

The presence of interleukin-13 in rheumatoid synovium and its antiinflammatory effects on synovial fluid macrophages from patients with rheumatoid arthritis.

OBJECTIVE: To study the production of interleukin-13 (IL-13) in rheumatoid synovium and the effects of recombinant IL-13 on the phenotype and function of synovial fluid (SF) macrophages and T cells derived from patients with rheumatoid arthritis (RA). METHODS: The presence of IL-13 in SF was studied using an IL-13-specific enzyme-linked immunosorbent assay (ELISA); the production of IL-13 was studied in SF mononuclear cells (SFMC) by reverse transcriptase-polymerase chain reaction. The effects of recombinant IL-13 on cytokine production by and phenotype of SFMC were evaluated using cytokine-specific ELISAs and flow cytometry, respectively. The effect of IL-13 on the proliferation of SFMC was determined by 3H-thymidine incorporation. The production and the effects of IL-13 were compared with those of IL-4. RESULTS: IL-13 was present in 27 of 28 SF samples, and IL-13 messenger RNA (mRNA) was detectable in SFMC. Importantly, IL-13 levels were significantly higher than those of IL-4, and IL-13 protein and mRNA were expressed in several samples, although IL-4 synthesis was undetectable. Recombinant IL-13 significantly reduced the production of IL-1 beta and tumor necrosis factor alpha and the expression of CD16 and CD64 by SF macrophages, whereas the expression of HLA-DR and CD23 was increased. These effects on SF macrophages were similar to those observed with IL-4, but in contrast to IL-4, IL-13 had no growth-promoting effect on SF T cells. CONCLUSION: IL-13 is consistently present in rheumatoid synovium. The ability of exogenous IL-13 to decrease the production of proinflammatory cytokines by SFMC suggests that it may have therapeutic potential in the treatment of patients with RA.

Adult↗
PubMed1985

Synovial fluid analysis--another look at the mucin clot test.

We analyzed the relationship between the mucin clot test and the synovial fluid (SF) leukocyte count in osteoarthritis, rheumatoid arthritis (RA), gout, and calcium pyrophosphate dihydrate crystal deposition disease. Except for RA there was no statistically significant relationship between white count and a tight mucin determination within the disease categories. For low (2 X 10(9) cells/l or less) leukocyte counts, the crystal induced arthropathies had a significantly greater proportion showing a tight reaction than found in the osteoarthritic and rheumatoid fluids. We propose that mucin clot determinations may reflect synovial membrane activity rather than SF leukocyte counts.

Adult↗
PubMedDate not supplied

Bactericidal/permeability increasing protein and proinflammatory cytokines in synovial fluid of psoriatic arthritis.

OBJECTIVE: Bactericidal/permeability increasing protein (BPI) is a leukocyte product exerting antibacterial activity. Its production may be stimulated by cytokines, mainly Tumor Necrosis Factor (TNF) alpha. We studied BPI in the synovial fluid (SF) of psoriatic arthritis (PsA), a disease suspected to be influenced by infectious agents. METHODS: The levels of BPI and various indices of SF inflammation, including cytokines and its receptors, were determined in the SF of 18 patients with PsA and compared with those of 12 patients with rheumatoid arthritis (RA) and 9 with osteoarthritis (OA). RESULTS: The lowest SF levels of BPI were found in PsA (145.3 +/- 97.3 ng/ml), significantly lower than in RA (307.7 +/- 42.8 ng/ml, p = 0.0001) and similar to those in OA (151.1 +/- 52.4 ng/ml). Furthermore, only in PsA, and not in the RA and OA subgroups, correlations were observed between BPI and the indices considered, including TNF alpha (r = 0.746, p = 0.0004). CONCLUSION: Due to its relationship with local inflammation, SF BPI may play a role in the pathogenesis of arthropathies, in particular PsA.

Antimicrobial Cationic Peptides↗
PubMed1987

Elastase and collagenase activities in synovial fluid of patients with arthritis.

The activity of elastase and collagenase was measured in the synovial fluid (SF) of 24 patients with inflammatory and 6 patients with traumatic joint effusions. The enzyme activity was compared with local and systemic variables of the disease. Elastase and collagenase activity could be detected in 79 and 83%, respectively, of the arthritic SF, whereas no enzyme activity was found in the traumatic joint effusions. The SF enzyme activity showed no correlation with clinical, laboratory or radiographic variables of arthritis in the joint from which the fluid was obtained. Our results show that proteolytic enzyme activity in SF may help to distinguish inflammatory from noninflammatory joint effusions but does not reflect the severity of the arthritic process.

Arthritis↗
PubMed1989

Response of synovial fluid T cell clones to Yersinia enterocolitica antigens in patients with reactive Yersinia arthritis.

From synovial fluids of two patients with reactive arthritis following Yersinia enterocolitica infection, T lymphocyte clones were obtained that showed proliferative responses to Y. enterocolitica. The responses required autologous T-cell-depleted peripheral blood mononuclear cells as antigen presenting cells. Three clones were studied in detail; two of them showed a marked and specific response to Yersinia antigens alone, the other one recognized both Yersinia and Salmonella typhimurium antigens. The antigen-specific proliferation of the clones could be completely blocked by monoclonal antibodies to HLA-DR. These experiments show that synovial T lymphocytes presumably involved in the in situ immune response to microbial antigens triggering reactive arthritis can be cloned directly from the site of inflammation.

Adult↗