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At least 1,315 records · Page 73Linked to original sources
PubMed1994

High frequency of specific T cell receptor rearrangements in rheumatoid arthritis: analysis of synovial fluid T lymphocytes.

1. We have searched for rearrangements in the beta chain T cell receptor genes to identify clonal T lymphocyte populations in the synovial fluid of 10 patients with well established rheumatoid arthritis, using a T cell population unbiased by preselection. 2. Analysis of the restriction fragments with the beta chain constant region probe C beta 2 disclosed a rearranged band in 50% of cases (5/10). No significant differences in age, duration of the disease, treatment employed and presence of articular deformities or erosion upon X-ray examination were observed when patients with or without rearrangements were compared. 3. The rearranged band observed after BamH I digestion was of the same size in the 5 patients (14 kb). In addition, two patients presented a 10-kb rearranged band upon restriction with Hind III. 3. These data indicate that a significant number of rheumatoid arthritis patients probably present oligoclonal T cell proliferation of their synovial fluid lymphocytes.

Adult↗
PubMed1992

Determination of tissue kallikrein and alpha 1-antitrypsin-tissue kallikrein complexes in synovial fluid of patients with rheumatoid, osteo and psoriatic arthritis.

An enzyme-linked immunosorbant assay was developed to determine tissue kallikrein and alpha 1-antitrypsin-tissue kallikrein complexes in pooled synovial fluid of patients with rheumatoid, osteo and psoriatic arthritis. Even though basal values could be determined, the addition of synovial fluid shifted the standard curves for both tissue kallikrein and alpha 1-antitrypsin-tissue kallikrein complex to the right, because of the presence of a novel inhibitor.

Arthritis, Psoriatic↗
PubMed1997

Induction of invasive and degradative phenotype in normal synovial fibroblasts exposed to synovial fluid from patients with juvenile rheumatoid arthritis: role of mononuclear cell population.

OBJECTIVE: To investigate the effect of synovial fluid (SF) from patients with juvenile rheumatoid arthritis (JRA) on proliferation and induction of degradative and invasive phenotype in normal synovial fibroblasts, and to elucidate the contribution of SF cells to this activity. METHODS: SF and/or conditioned medium (CM) from SF cells were evaluated for their ability to (1) stimulate a proliferative response, (2) induce the "activated phenotype" capable of invading cartilage matrix, and (3) promote the release of key matrix metalloproteinases (MMP) in normal synovial fibroblasts. RESULTS: Proliferation of normal synovial fibroblasts exposed to SF or CM from SF cells of patients with JRA was up to 3 times greater than untreated controls. Concomitant with induction of an activated phenotype in the treated synovial fibroblasts, the activated form exhibited up to 250% invasiveness of cartilage matrix compared to untreated synovial fibroblasts (100%), in addition to releasing increased MMP activity, not normally associated with these quiescent cells. This induction was not solely due to tumor necrosis factor-alpha, transforming growth factor-beta, interleukin 1beta (IL-1beta), and IL-6, as SF and/or CM depleted of these cytokines sustained about 40% of their invasive and inducing ability. We observed that the mononuclear cell (MNC) population that infiltrated into the joint cavity secretes this "inducing activity," which can be maintained in culture up to several weeks. CONCLUSION: Our data suggest that the cellular component of SF releases soluble factor(s) that directly or indirectly contribute to (a) proliferation of synovial fibroblasts, and (b) production and release of extracellular MMP by synovial fibroblasts, thereby inducing a degradative and invasive phenotype culminating in cartilage and bone destruction.

Antibodies↗
PubMed2000

Identification of Mycoplasma fermentans in synovial fluid samples from arthritis patients with inflammatory disease.

Since 1970 Mycoplasma fermentans has been suspected of being associated with rheumatoid arthritis. However, this association has been difficult to prove, and this has been our goal. The distribution of M. fermentans was studied in the synovial fluid of patients suffering from different arthritides. Samples of synovial fluid were taken from patients with well-defined disease and a clear diagnosis. After removal of the inflammatory cells and hyaluran, they were treated with proteinase K and tested by a single or fully nested PCR with primers directed against part of the two 16S rRNA genes of M. fermentans. The product was sequenced automatically, by using an ALF Express automatic sequencer, to confirm the mycoplasma species and to identify the strain since the two genes were usually found to be polymorphic. This was also true of the type strain, strain PG18. M. fermentans was detected in 23 of 26 (88%) rheumatoid arthritis patients, and four different strains were found. It was also found in 7 of 8 (88%) of the nonrheumatoid inflammatory arthritis patient group, which consisted of one patient with reactive arthritis, one patient with pauciarticular juvenile chronic arthritis, two patients with gout, two patients with ankylosing spondylitis, and two patients with psoriatic arthritis, only one of whom was infected with M. fermentans. It was not detected in any of the 10 osteoarthritis patients. M. fermentans was therefore found to be a variable and very common organism in arthritic patients with inflammatory joint exudates and may well prove to be important in the etiology of the diseases.

Adult↗
PubMed2004

Synovial fluid from an African spur-thighed tortoise (Geochelone sulcata).

A 4.5-year old, male African spur-thighed tortoise (Geochelone sulcata) was presented to the University of Florida Veterinary Teaching Hospital with a 2-week history of lethargy, anorexia, constipation, dyspnea, and coughing up fluid or vomiting. Laboratory results included an inflammatory leukogram and a marked increase in plasma uric acid concentration. Synovial fluid from multiple joints was thick, chalky white, and opaque, with a grainy consistency. Microscopically, the fluid contained numerous brown, needle-like crystals consistent with urates (gout). Gross necropsy findings and histopathology confirmed a diagnosis of systemic gout, with urate deposition, gout tophi, and underlying necrosis in multiple organs, including kidneys, lung, and liver. Dehydration with concurrent renal insufficiency may have impaired urate excretion and led to a build-up of urates in the blood and tissues of this tortoise. A high protein diet also may have contributed to the development of gout. Cytologic evaluation of synovial fluid can be used as a quick and definitive tool to diagnose gout in tortoises.

Animals↗
PubMed1992

Stimulation of synovial fluid mononuclear cells with the human 65-kD heat shock protein or with live enterobacteria leads to preferential expansion of TCR-gamma delta+ lymphocytes.

T lymphocyte responses to heterologous or self 65-kD heat shock protein (hsp) have been implicated in the pathogenesis of various forms of arthritis. To delineate the relationship of 65-kD hsp to different synovial fluid (SF) T cell subsets, we stimulated synovial fluid (SFMC) and peripheral blood mononuclear cells (PBMC) from patients with different inflammatory rheumatic diseases and from healthy controls with human or mycobacterial 65-kD hsp, tetanus toxoid (TT), heat-killed or live Yersinia enterocolitica. Phenotyping of the resulting T cell lines revealed an increase of up to 97% TCR-gamma delta+ lymphocytes in the 65-kD hsp-stimulated SF-derived lines. This expansion of TCR-gamma delta+ cells was less pronounced with cultures of PBMC. A preferential expansion of TCR-gamma delta+ cells was also shown after SFMC stimulation with live, but not with heat-killed Yersinia or with TT. We conclude that a common mechanism is involved in the selective expansion of TCR-gamma delta+ lymphocytes upon SFMC infection with live Yersinia or upon contact with 65-kD hsp. Out of a panel of TCR-gamma delta+ T lymphocyte clones (TLC) derived from a human 65-kD hsp-stimulated line, only a minority of TLC proliferated weakly upon restimulation with this antigen in the presence of autologous monocytes, whereas TCR-alpha beta+ TLC responded vigorously to the human 65-kD hsp and in some cases also cross-recognized the mycobacterial hsp homologue and/or heat-killed Yersinia. This implies that additional factors or cells may be present in the milieu of SFMC cultures that propagate the expansion of TCR-gamma delta+ cells in response to 65-kD hsp or live bacteria.

Cell Line↗
PubMedDate not supplied

Human monocyte elastolytic activity, the propeptides of types I and III procollagen, proteoglycans, and interleukin-6 in synovial fluid from patients with arthritis.

Elastolytic activity by live human monocytes (M phi) is mainly caused by cell surface related leucocyte elastase, capable of degrading matrix components. In order to examine the possible correlation between enzyme activity and tissue turnover in the joint, we examined 24 synovial fluids for M phi elastolytic activity, using the levels of synovial fluid interleukin-6 and serum C reactive protein as additional markers of cell activation. Proteoglycan levels were measured as an indication of cartilage degradation and the types I and III procollagen propeptides as markers of synovial membrane turnover. We found that elastolysis by live M phi and the levels of interleukin-6 and C reactive protein correlated significantly with proteoglycan concentrations but not with the procollagen propeptides. These findings suggest that human M phi elastolytic activation is a biologically relevant factor in cartilage degradation, but is unrelated to the collagen metabolism of the synovial membrane.

Adult↗
PubMed1976

Transformation of human lymphocytes in vitro by autologous and allogeneic rheumatoid synovial fluids.

To assess the possible participation of cellular immune mechanisms in the pathogenesis of rheumatoid arthritis (RA) in vitro studies of the blastogenicity of rheumatoid and non-rheumatoid synovial fluids for human peripheral blood lymphocytes were conducted. In autologous cultures it was found that 13 of 19 rheumatoid fluids induced significant lymphocyte blastogenesis, whereas only 1 of 13 nonrheumatoid fluids induced such a response. In allogeneic cultures rheumatoid fluids induce significant blastogenesis of RA lymphocytes in 18 of 23 experiments, and of non-RA lymphocytes in 8 of 18 experiments. By contrast, nonrheumatoid fluids induced significant blastogenesis of RA lymphocytes in 2 of 13 experiments, and of non-RA lymphocytes in 1 of 14 experiments. The blastogenicity of fluids was found to correlate significantly with the presence therein of immunofluorescent intracellular inclusions of immunoglobulin and complement. These studies support the concept that the presence of immune complexes in the majority of rheumatoid synovial fluids might render the latter blastogenic for human lymphocytes in vivo, thereby perpetuating rheumatoid synovitis.

Arthritis, Rheumatoid↗
PubMed1992

HLA-DP restricted Chlamydia trachomatis specific synovial fluid T cell clones in Chlamydia induced Reiter's disease.

Synovial fluid (SF) mononuclear cells from a patient with Chlamydia trachomatis induced acute Reiter's disease were directly by limiting dilution in a representative protocol using phytohemagglutinin in the cloning medium. Out of 76 alpha beta-TCR+ CD4+ T lymphocyte clones, 7 were shown to specifically recognize C. trachomatis in a proliferation assay. The antigen recognition of these clones was HLA-DP restricted. Unexpectedly, 2 HLA-DR restricted clones showed a proliferative response to Yersinia enterocolitica O3, though the patient had no history of yersinia infection. The high frequency of SF derived T cells with specificity for species-specific chlamydial antigens and the limited diversity of HLA class II restriction of these clones may indicate an oligoclonal synovial T cell response to persistent intraarticular chlamydia.

Adult↗
PubMed1997

The presence of secretoneurin in human synovium and synovial fluid.

Secretoneurin is a neuropeptide formed from the proprotein secretogranin II. It is found in afferent nerve fibres and has chemotactic activity for monocytes, neutrophils and fibroblasts. We investigated the presence of secretoneurin in synovial fluid and synovium from patients with osteoarthritis and rheumatoid arthritis. The secretoneurin immunoreactive material found in synovial fluid was identified by high performance liquid chromatography as the free peptide secretoneurin. Its level in hip joints was 15.6, in knee joints of osteoarthritis patients 17.3 and in rheumatoid patients significantly lower (8.6 fmol/ml). Immunocytochemistry provided evidence for the presence of sub-intimal secretoneurin-immunoreactive nerve fibres in knee synovium in osteoarthritic patients. In rheumatoid synovium, only very few immunoreactive fibres were found these being mostly localised in deep stroma. The results show that secretoneurin is present in osteoarthritic joint and suggest that secretoneurin levels are down-regulated in rheumatoid joint. Therefore, secretoneurin may participate in acute or mild phases of inflammation but is unlikely to have a major role when more severe inflammation is present such as that seen in rheumatoid joint.

Antibody Specificity↗
PubMed1977

Concentrations of flurbiprofen in serum and synovial fluid from patients with active rheumatoid disease: some preliminary observations.

In 3 patients with active rheumatoid disease, concentrations of flurbiprofen of approximately 2 microgram per ml were achieved in synovial fluid 3 hours after a single oral dose of flurbiprofen (100 mg). The highest concentrations were seen between 3 and 9 hours after administration of the dose. The concentration of flurbiprofen in synovial fluid seemed to fall more slowly than in the circulation, but more extensive data would be needed to confirm this. In all 3 patients the drug was absorbed rapidly into the circulation, the highest serum concentrations of 7 microgram to 9 microgram per ml being seen in the first blood sample withdrawn 1.5 hours after administration of the dose. Serum concentrations fell with a mean apparent half-life of approximately 3 hours.

Adult↗
PubMed1991

Generalized dispersion in a synovial fluid of human joints.

An unsteady convective diffusion in a synovial fluid of human joints modeled as a power-law fluid is studied using the generalized dispersion model of Gill and Sankara-subramanian [12]. The contributions of convection and diffusion, and pure convection on the dispersion of nutrient are investigated in detail. It is shown that the effect of decrease in non-Newtonian parameter is to decrease the dispersion coefficient. The mean concentration distribution appears to increase as the non-Newtonian parameter decreases upto a certain value of the axial distance. Beyond this point, however, the reverse pattern is observed.

Biomechanical Phenomena↗
PubMed1992

HTLV-I associated arthritis: characteristics of an HTLV-I virus infected T cell line from synovial fluid.

A T cell line from mononuclear cells in the synovial fluid of a patient with polyarthritis was established. The T cell line reacted with serum samples positive for antibodies to human T cell lymphotropic virus type I (HTLV-I) and with monoclonal antibody to HTLV-I p19. In Southern blotting with an env-pX-LTR HTLV-I probe and digestion of T cell line DNA with the restriction enzymes ClaI, DraI, and PstI generated fragments that were identical to those found in two HTLV-I infected T cell lines established from adult T cell leukaemia or HTLV-I associated myelopathy. The T cell line expressed CD2, CD3, CD4, CD45RA, CD29, HLA-DR, CD25, and CD26 antigens, but not CD8 and CD20 antigens. Large amounts of interleukin 6, interferon gamma, and tumour necrosis factor alpha were secreted in the culture supernatants of this cell line. This line helped immunoglobulin production by B cells, but not K562, Raji, and synovial cell lysis.

Aged↗
PubMed1992

Regulation of IL-2 production by mononuclear cells from rheumatoid arthritis synovial fluids.

Products of polyamine oxidation down-regulate IL-2 production by peripheral blood T cells. We show here that the production of IL-2 by rheumatoid arthritis synovial fluid mononuclear cells is inversely correlated with the concentrations of polyamines in these cells. In addition, the inhibition of polyamine biosynthesis or oxidation in cultures of these cells enhances their ability to produce IL-2. Our findings suggest that polyamine oxidation plays an important role in the suppression of T cell function characteristic of rheumatoid arthritis synovial fluids.

Arthritis, Rheumatoid↗
PubMed1983

The penetration of trimethoprim and sulphamethoxazole into synovial fluid.

A group of six patients with non-infected synovial effusions requiring diagnostic or therapeutic aspiration, were given a short oral course of 'Septrin' (two tablets bd for two doses, each tablet containing 80 mg of trimethoprim plus 400 mg of sulphamethoxazole). Serum and synovial fluid (SF) were sampled frequently following antibiotic administration. It was found that concentrations of trimethoprim in SF approached serum levels after a short lag time (about 3 h) and thereafter approximated to the serum levels, whereas sulphamethoxazole did not as readily penetrate into SF. With the regimens used MIC levels for trimethoprim were achieved in SF, which suggests that this drug could be usefully prescribed in normal doses for the treatment of septic arthritis due to bacterial infection.

Adult↗
PubMed1978

[Correlations between inflammatory activity, immunoglobulins and complement components in the synovial fluid of patients with rheumatoid arthritis and arthrosis].

In 81 synovial fluids (39 from rheumatoid arthritis and 42 from osteoarthritis patients), levels of IgG, IgM, IgA, and complement components C3, C4, and C3-proactivator were estimated. Lactatedehydrogenase (LDH) was used as the parameter of inflammatory activity. With increased LDH activity, the concentrations of all immunoglobulins rose in both groups. In the complement components, this positive linear correlation was demonstrated only in the osteoarthritic group. In rheumatoid arthritis, the results were best demonstrated by means of a regression type curve of the 3rd degree (p less than 0.01). In low inflammatory activity there was a rise in the level of the complement components. With higher LDH activity (greater than 500 U/l), however, there was a drop in the curve and the positive correlation changed to negative.

Arthritis↗