Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antibodies to type II collagen (Col II) in sera and synovial fluid (SF) were measured with an enzyme linked immunosorbent assay (ELISA) using a solid phase sandwich method. The subjects included: 42 patients with rheumatoid arthritis (RA); 31 cases of osteoarthritis (OA); 10 cases of gouty arthritis; 4 cases of ankylosing spondylitis (AS); 5 cases of systemic lupus erythematosus (SLE); and 44 normal controls. The antigens used to detect antibodies against Col II were in native and heat-treated denatured forms, both of which were purified from chicken sternal cartilage by limited enzyme digestion and differential precipitation with salt. The reactivity to native type II collagen was generally higher than the reaction to the denatured collagen. In sera, significant higher levels of Col II were detected in the different arthritis groups when compared with the normal control group, with the exception of AS. In SF, the Col II was significantly higher in RA than it was in OA (p less than 0.001), while no difference was present between gout and OA (p less than 0.05). When native Col II was simultaneously measured in sera and SF among arthritics, positive rates were both higher among RA (65% and 58%, respectively). Positive rates were only higher in sera among OA (59% in sera and 3% in SF) and were both lower among gouty arthritis. The above findings show that the measurement of Col II is more important in SF than in sera.
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PMID:[The occurrence and clinical significance of antibodies to type II collagen in sera and synovial fluid of Chinese patients with rheumatoid arthritis]. 197 52

Adherent synovial cells from both 13 patients without rheumatoid arthritis (RA) (gout, osteoarthritis and meniscal lesion) and 8 patients with RA consisted of dendritic cells, macrophage-like cells and fibroblast-like cells after cloning in a similar fashion as reported in our previous paper. All the adherent synovial cells from patients without RA did not release interleukin 1 (IL-1) beta and prostaglandin E2 (PGE2) spontaneously, while those cells released comparable amounts of IL-1 beta, but not PGE2 to RA cells after type II collagen stimulation. Only the synovial cells from RA, irrespective of morphology and cloning, released IL-1 beta and PGE2 without stimulation. Nonrheumatoid synovial cells may differ functionally from RA cells.
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PMID:Adherent synovial cells from nonrheumatoid arthritis do not release interleukin 1 beta and prostaglandin E2 spontaneously in longterm culture. 225 87

Serum IgG antibodies to native and denatured human type II collagen (Col II) were measured using an enzyme linked immunosorbent assay (ELISA). One hundred and thirty one patients with various forms of arthritis such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PSA). Reiter's Syndrome (RS), osteoarthritis (OA), and gout, 60 with autoimmune connective tissue disease, and 37 with the chronic inflammatory conditions--graft versus host disease and leprosy--were studied. With the exception of RS, PSA, OA, and gout, significant levels of Col II antibodies were detected in each disease group. Blocking studies with types I and II collagen on selected serum samples confirmed the specificity to native Col II, though some cross reactivity was apparent with denatured collagen. The patients with RA who were Col II antibody positive tended to fall into stage III of disease progression. There was, however, no correlation with rheumatoid factor, erythrocyte sedimentation rate, or disease duration and this, together with the finding that Col II antibodies are present in a wide array of diseases, makes their role in the pathogenesis of RA questionable. They may arise as a secondary disease perpetuating mechanism in some patients, or in turn may be an epiphenomenon secondary to generalised disturbed immunoregulation or B cell hyperreactivity, or both, that characterises these clinical conditions.
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PMID:Autoantibodies to type II collagen: occurrence in rheumatoid arthritis, other arthritides, autoimmune connective tissue diseases, and chronic inflammatory syndromes. 336 30

Synovial fluid (SF) mononuclear cells (MNC) from 13 patients with rheumatoid arthritis (RA) and 12 patients with other arthritic diseases (OD) including osteoarthritis (OA), gout and spondyloarthritis (SA) were cultured in the presence of collagen types I and II or lipopolysaccharide (LPS) for 24 h. Interleukin-1 (IL-1), IL-6 and tumor necrosis factor-alpha (TNF-alpha) in the SF and culture supernatants were assayed using ELISA. The results showed that one-half of the RA patients with high SF monocyte count had high SF IL-6 levels that coincided with the high spontaneous release of IL-6 by SF MNC. In the other RA patients with lower SF monocyte count, type II collagen induced significantly higher IL-1 beta than the medium control levels by SF MNC (P < 0.01) or that of the other diseases (P < 0.01). Similarly, type II collagen-induced IL-6 and TNF-alpha production rose significantly (P < 0.01) from SF MNC of RA but less from OD (P < 0.05). In addition, type I collagen could also induce IL-1, IL-6 and TNF-alpha in these samples from RA and OD patients but was less potent than type II collagen. Our results indicate that collagen-induced cytokines may be important in the pathogenesis of the disease.
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PMID:Collagen induces cytokine production by synovial fluid mononuclear cells in rheumatoid arthritis. 762 81