Oxidative response of polymorphonuclear leucocytes to synovial fluids from patients with rheumatoid arthritis
Only a minority (7/35, 20%) of synovial fluids from patients with rheumatoid arthritis (RA) and none from patients with other arthritides stimulated the oxidative response of polymorphonuclear leucocytes (PMNs). Superoxide anion generation was measured by superoxide dismutase inhibitable reduction o...
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Published in | Annals of the rheumatic diseases Vol. 49; no. 9; pp. 661 - 664 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group Ltd and European League Against Rheumatism
01.09.1990
BMJ Elsevier Limited |
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Abstract | Only a minority (7/35, 20%) of synovial fluids from patients with rheumatoid arthritis (RA) and none from patients with other arthritides stimulated the oxidative response of polymorphonuclear leucocytes (PMNs). Superoxide anion generation was measured by superoxide dismutase inhibitable reduction of cytochrome c. The same synovial fluids stimulated superoxide release by PMNs regardless of their source, though they elicited a greater response from RA synovial fluid PMNs than from either RA blood PMNs or blood PMNs from normal subjects. The remaining synovial fluids failed to stimulate any of the PMNs, though some (2/10) stimulated PMNs pretreated with cytochalasin B. The stimulatory activity was removed from RA synovial fluids by protein A-Sepharose and eluted with the void volume on gel chromatography. It is considered that immunoglobulin aggregates in some RA synovial fluids may stimulate the oxidative response of PMNs in the joint space but that most do not because these fluids contain either a specific inhibitor or immunoglobulin aggregates of an inappropriate type, or both. |
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AbstractList | Only a minority (7/35, 20%) of synovial fluids from patients with rheumatoid arthritis (RA) and none from patients with other arthritides stimulated the oxidative response of polymorphonuclear leucocytes (PMNs). Superoxide anion generation was measured by superoxide dismutase inhibitable reduction of cytochrome c. The same synovial fluids stimulated superoxide release by PMNs regardless of their source, though they elicited a greater response from RA synovial fluid PMNs than from either RA blood PMNs or blood PMNs from normal subjects. The remaining synovial fluids failed to stimulate any of the PMNs, though some (2/10) stimulated PMNs pretreated with cytochalasin B. The stimulatory activity was removed from RA synovial fluids by protein A-Sepharose and eluted with the void volume on gel chromatography. It is considered that immunoglobulin aggregates in some RA synovial fluids may stimulate the oxidative response of PMNs in the joint space but that most do not because these fluids contain either a specific inhibitor or immunoglobulin aggregates of an inappropriate type, or both. Only a minority (7/35, 20%) of synovial fluids from patients with rheumatoid arthritis (RA) and none from patients with other arthritides stimulated the oxidative response of polymorphonuclear leucocytes (PMNs). Superoxide anion generation was measured by superoxide dismutase inhibitable reduction of cytochrome c. The same synovial fluids stimulated superoxide release by PMNs regardless of their source, though they elicited a greater response from RA synovial fluid PMNs than from either RA blood PMNs or blood PMNs from normal subjects. The remaining synovial fluids failed to stimulate any of the PMNs, though some (2/10) stimulated PMNs pretreated with cytochalasin B. The stimulatory activity was removed from RA synovial fluids by protein A-Sepharose and eluted with the void volume on gel chromatography. It is considered that immunoglobulin aggregates in some RA synovial fluids may stimulate the oxidative response of PMNs in the joint space but that most do not because these fluids contain either a specific inhibitor or immunoglobulin aggregates of an inappropriate type, or both.Only a minority (7/35, 20%) of synovial fluids from patients with rheumatoid arthritis (RA) and none from patients with other arthritides stimulated the oxidative response of polymorphonuclear leucocytes (PMNs). Superoxide anion generation was measured by superoxide dismutase inhibitable reduction of cytochrome c. The same synovial fluids stimulated superoxide release by PMNs regardless of their source, though they elicited a greater response from RA synovial fluid PMNs than from either RA blood PMNs or blood PMNs from normal subjects. The remaining synovial fluids failed to stimulate any of the PMNs, though some (2/10) stimulated PMNs pretreated with cytochalasin B. The stimulatory activity was removed from RA synovial fluids by protein A-Sepharose and eluted with the void volume on gel chromatography. It is considered that immunoglobulin aggregates in some RA synovial fluids may stimulate the oxidative response of PMNs in the joint space but that most do not because these fluids contain either a specific inhibitor or immunoglobulin aggregates of an inappropriate type, or both. Only a minority (7/35, 20%) of synovial fluids from patients with rheumatoid arthritis (RA) and none from patients with other arthritides stimulated the oxidative response of polymorphonuclear leucocytes (PMNs). Superoxide anion generation was measured by superoxide dismutase inhibitable reduction of cytochrome c. It is considered that immunoglobulin aggregates in some RA synovial fluids may stimulate the oxidative response of PMNs in the joint space but that most do not because these fluids contain either a specific inhibitor or immunoglobulin aggregates of an inappropriate type, or both. |
Author | Badesha, J S Dularay, B Dieppe, P A Elson, C J |
AuthorAffiliation | Department of Pathology, Bristol University |
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Cites_doi | 10.1172/JCI109947 10.1172/JCI108152 10.1016/0006-291X(85)91678-X 10.3109/08916938808997161 10.1172/JCI108191 |
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Keywords | Human Synovial fluid Chronic Hyperoxia Rheumatoid arthritis Granulocyte Diseases of the osteoarticular system Exploration Inflammatory joint disease Technique Gel permeation chromatography |
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Immunoglobulin aggregates are found in – volume: 66 start-page: 1166 year: 1980 ident: ref_21 article-title: Lipoxygenation of arachidonic acid as a source of polymorphonuclear leukocyte chemotactic factors in synovial fluid and tissue in rheumatoid arthritis and spondyloarthritis publication-title: J Clin Invest doi: 10.1172/JCI109947 – volume: 79 start-page: 195 year: 1990 ident: ref_14 article-title: Depressed degranulation response of synovial fluid polymorphonuclear leukocytes known, however, that PMNs pretreated with cytochalasin B, unlike untreated PMNs, will from patients with rheumatoid arthritis to IgG aggregates. ClGn Exp Immunol – volume: 29 start-page: 379 year: 1986 ident: ref_3 article-title: loss of activity is due to the removal of IgG aggregates. Additionally, both stimulatory and Tschesche H. Superoxide radicals as effectors of cartilage destruction publication-title: Arthritis Rheum – volume: 56 start-page: 1053 year: 1975 ident: ref_2 article-title: Stimulation of human neutrophils by soluble and insoluble immunoglobulin aggregates. of superoxide anion generating activity and as monomeric IgG was shown, by this and other Secretion of granule constituents and increased oxidation of glucose publication-title: J Clin Invest doi: 10.1172/JCI108152 – year: 1973 ident: ref_11 article-title: Cytochalasin B: effect on lysosomal enzyme release from human polymorphonuclear leukocytes publication-title: Proc Nail Acad Sci USA; 70: superoxide radicals with cellular and synovial fluid components have been detected in synovial 844-8 – volume: i: start-page: 69 year: 1987 ident: ref_20 article-title: Mechanism of exacerbation of rheumatoid synovitis by total dose iron dextran infusion: in vivo demonstration ofiron promoted oxidant stress publication-title: Lancet – volume: 110 start-page: 297 year: 1983 ident: ref_16 article-title: In vitro and in vivo stimulation of rat neutrophils and alveolar globulin aggregates, able to stimulate PMNs to release superoxide, may not be continuously macrophages by immune complexes publication-title: Am J7 Pathol – volume: 39 start-page: 297 year: 1980 ident: ref_19 article-title: Analysis of immune complexes in synovial effusions ofpatients with rheumatoid arthritis. Clin Exp Immwnol – volume: 109 start-page: 1182 year: 1972 ident: ref_15 article-title: The release of granule enzymes from human neutrophils stimulated by aggregated immunoglobulins of different classes and subtissue surfaces, but not those in synovial fluid, stimulate PMNs publication-title: Alternatively, immunoclasses. J Immnol – volume: 8 start-page: 21 year: 1978 ident: ref_10 article-title: Protein A reactivity of various mammalian immunoglobulins – volume: 48 start-page: 311 year: 1982 ident: ref_9 article-title: A convenient replacement for cyanogen bromide activated solid phases by immunoradiometric assays publication-title: J Immwuol Methods; aggregated IgG stimulated superoxide production.26 The activity was found in most synovial – volume: 128 start-page: 297 year: 1985 ident: ref_12 article-title: Activation of NADPH oxidase in human neutrophils. Synergism between FMLP and the fluids.9 27-29 Thus it is perhaps surprising that only a small number of synovial fluids stimulate neutrophil products PAF and LTB4 publication-title: Biochem Biophys Res Comman doi: 10.1016/0006-291X(85)91678-X – volume: 1 start-page: 159 year: 1988 ident: ref_17 article-title: Enhanced oxidative present in synovial fluids. Finally, superoxide anions may be generated by cells other than response of polymorphonuclear leukocytes from synovial fluids of patients with rheumatoid arthritis publication-title: Autoimmunity doi: 10.3109/08916938808997161 – volume: 129 start-page: 1589 year: 1982 ident: ref_13 article-title: Mechanism of luminol dependent chemiluminescence of human neutrophils. fluids that failed to elicit a response from untreated PMNs (either normal or RA) publication-title: It is J Immunol – volume: 23 start-page: 455 year: 1980 ident: ref_4 article-title: Effect of oxygen-derived free non-stimulatory synovial fluids were fractionated according to size, but only stimulatory synovial radicals on hyaluronic acid publication-title: Arthritis Rheum – volume: 52 start-page: 741 year: 1973 ident: ref_8 article-title: Biological defence mechanisms. 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Firstly, the size and concentration of immunonumbers of fully viable human neutrophils: a preparative technique using Percoll density gradient centrifugation. Exp Hematol year: 1979 ident: ref_6 article-title: Phagocyte produced free radicals: roles of cytotoxicity and inflammation. In: Oxygen free radicals and tissue damage. Amsterdam: Elsevier/Excerpta most synovial fluids,24 yet only a fraction of the fluids stimulate superoxide release. There are at Medica/North – volume: 31 start-page: 960 year: 1983 ident: ref_7 article-title: Rapid method for identification of macrophages in suspension by acid alpha-naphthyl acetate esterase activity publication-title: J Histochem; response elicited, with large insoluble immunoglobulin aggregates being potent stimulators of |
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SubjectTerms | Arthritis, Rheumatoid - metabolism Biological and medical sciences Cytochalasin B - pharmacology Cytochrome c Group - metabolism Diseases of the osteoarticular system Female Humans Immunoglobulin G - immunology Inflammatory joint diseases Lymphocyte Activation Male Medical sciences Middle Aged Neutrophils - drug effects Neutrophils - metabolism Stimulation, Chemical Superoxides - metabolism Synovial Fluid - immunology Synovial Fluid - metabolism |
Title | Oxidative response of polymorphonuclear leucocytes to synovial fluids from patients with rheumatoid arthritis |
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