Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study analyzed the neutrophils and sera of patients with rheumatoid arthritis and of normal controls. No significant differences were found in the activities of the granular enzymes beta-glucuronidase and lysozyme or the cytoplasmic enzyme lactic dehydrogenase (LDH). Normal neutrophils were found to release significant (P less than 0.05) amounts of the granular enzymes, but not of LDH in response to immunoglobulin G aggregates. There was no difference in the percent release exhibited by rheumatoid versus control neutrophils. Studies delineating the effects of rheumatoid factor sera and normal sera on aggregate-induced enzyme release revealed a significant negative correlation between the amount of rheumatoid factor in the sera and the percent release of beta-glucuronidase and lysozyme but not of LDH. These studies thus demonstrate no abnormalities in rheumatoid neutrophil or rheumatoid serum enzyme activities or in neutrophil response to immunoglobulin G aggregates. They suggest, however, that rheumatoid factor may partially inhibit the release of lysosomal enzymes, thus suppressing this important component of the rheumatoid inflammatory process.
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PMID:Neutrophil enzyme activities in rheumatoid inflammation. 47

The interactions of soluble and insoluble immunoglobulin G (IgG) complexes with macromolecular rheumatoid factor (RF) and platelets were examined in an in vitro system permitting observation of platelet activities which may contribute to rheumatoid inflammation. Studies of the aggregation phenomenon by the nephalometric technique and by selective sedimentation of 51Cr-labelled platelets revealed no aggregation by platelets exposed to heat aggregated IgG (HAIgG) complexes or their RF precipitates in a plasma test system. Release of serotonin was demonstrated by the increasing radioactivity of platelet supernates to 45 min by 14C-serotonin labelled platelets exposed to insoluble IgG heat aggregates. Significantly less release was shown with saline, native IgG, and soluble IgG complexes. When RF was added to soluble HAIgG complexes, the resulting precipitate caused significantly higher release than controls. No concomitant release of the lysosomal enzyme beta-glucuronidase was detected. Thus, although soluble complexes do not cause significant release of biologically active amines, conversion of soluble complexes to insoluble immune precipitates by RF is associated with this activity which is independent of platelet aggregation and/or lyosomal enzyme release in our test system. Release of biologically active amines from platelets exposed to insoluble complexes may be important in the initiation and propagation of inflammation in rheumatoid arthritis.
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PMID:SOluble and insoluble immune complex-platelet interactions in rheumatoid inflammation. 71 74

A neutrophil monolayer system was used to study the effects of uric acid on neutrophil-aggregate interactions important in rheumatoid inflammation. No effect on immunoglobulin G aggregate phagocytosis was seen, but hyperuricaemic levels of uric acid were associated with an enhancement of phagocytosis-induced release of the azurophilic granular enzyme beta-glucuronidase. A trinitrophenyl-coupled mononuclear leucocyte rheumatoid factor plaque-forming assay was utilised to study uric acid effects on polyclonal activation of immunocompetent cells. Low levels of uric acid enhanced and high levels suppressed this system. Hyperuricaemia may enhance some aspects of rheumatoid inflammation, while uric acid may modulate an important component of rheumatoid autoimmunity.
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PMID:Uric acid effects on in vitro models of rheumatoid inflammatory and autoimmune processes. 685 66

Spontaneous synovitis developed in the limb joints and rheumatoid factor-like component appeared in the sera of two rabbits from a pool 36 animals in the course of a long-term immunization with bovine nasal cartilage antigens. A single intra-articular injection of proteoglycan antigens regularly provoked a heavy synovitis and cartilage destruction irrespective of whether the booster injections were administered in physiological saline, or in Freund's complete adjuvant. The dose-dependent severity of arthritis suggested that the antibody titre against proteoglycan antigens played an important role in this mechanism. The synovial extract and synovial fluid of knee joints injected with proteoglycan antigens showed an increased enzyme activity concerning the four acid hydrolases (acid phosphatase, cathepsin D, hyaluronidase and beta-glucuronidase). The high activity of lysosomal acid hydrolases which persisted for several months can derange the molecular structure of proteoglycans of cartilage. The degraded proteoglycans may trigger autoimmune reactions, and the process eventually leads to chronic inflammation and joint destruction.
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PMID:Experimental arthritis produced by proteoglycan antigens in rabbits. 745 41