Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Auranofin, an oral chrysotherapeutic agent effective in the treatment of rheumatoid arthritis (RA), was found to be a potent, noncytotoxic inhibitor of IgG-RF immune complex-induced lysosomal enzyme release (LER) from human leukocytes. At a concentration of 1 microg Au/ml (5 microM), auranofin produced a marked reduction in beta-glucuronidase (100%), acid phosphatase (88%), and lysozyme (72%) release. In contrast, gold sodium thiosulfate (GST, an injectable gold compound) had no inhibitory activity on LER at equivalent gold concentrations (i.e., 1 microg Au/ml) and only modest activity (less than 36% inhibition) at concentrations as high as 40 microg Au/ml. The 50% inhibitory dose (LD50) of auranofin on LER was calculated to be 3-4 microM (0.6-0.8 microg Au/ml). Blood gold levels in auranofin-treated RA patients were found to be within the range required for in vitro inhibition of LER, and correlated with decreases in IgG, RF titers, and IgG-RF immune-complex formation in vitro. These results suggest that the therapeutic action of auranofin may be caused, at least in part, by inhibition of LER and/or decreases in immune-complex formation.
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PMID:Effect of auranofin, a new antiarthritic agent, on immune complex-induced release of lysosomal enzymes from human leukocytes. 10 28

In the first part of this work patients with rheumatoid arthritis (RA), 36 cases and normal subjects, 49 cases have been studied by lymphocyte cultures stimulated by phytohaemagglutinin (PHA), Concanavalin A (Con A), pokeweed mitogen (PWM) and Con A convalently bound to sepharose 4 B (Con A-S). The comparisons between the two groups have shown a significant difference between the RA lymphocytes and the control lymphocytes stimulated by PHA and Con A. However no statistical difference has been found between the two lymphocytes populations stimulated by PWM and Con A-S. In view to determining the lymphocyte population stimulated by each mitogen, separations of B- and T-cells from peripheral blood have been performed according to the ability for the T-cells population to bind the sheep red blood-cells (rosette forming cells). The T-cell rich population was only stimulated by PHA, Con A and PWM. Although the T-cell depleted one has shown no response to these mitogens, a response to Con A-S was elicited. In the second part of this work, patients with RA, patients with positive tuberculin (PPD) skin-tests and controls were studied. The lymphocytes from these groups were cultured in serum-free medium to obtain cell-free supernatants. These lymphocyte cultures were preincubated with the appropriate antigen or reconstituted after removal of the cells. Supernants from RA lymphocytes stimulated in vitro by undenaturated IgG induced an inhibition of the leucocyte migration, as well as the supernatants from tuberculin-sensitized lymphocytes. However, supernatants from non-RA lymphocytes or tuberculin-unsensitized lymphocytes did not show such an inhibition. These MIF like supernatants have been studied by Sephadex G-100 gel filtration. A MIF like activity has been found for PPD and IgG supernatants between the chymotrypsinogen (MW 23,000) and the lysozyme (MW 17,000). This MIF like activity could be due to RA lymphocytes stimulated by undenatured IgG.
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PMID:Stimulation of lymphocytes from rheumatoid arthritis patients by mitogens and IgG. 13 82

1. The permeability of the synovial membrane for proteins is larger in rheumatoid arthritis than in osteoarthrosis, in rheumatoid arthritis with high CRP activity larger than in rheumatoid arthritis with low CRP activity. 2. The diffusion by the synovial membrane in most plasma proteins takes place depending on their molecular weight. Of the 14 proteins tested only haptoglobin and fibrinogen did not follow this regularity. 3. While the non-immune proteins proved in the synovial fluid only come from the blood plasma, the immune globulins IgG, IgA, and IgM as well as lysozyme are partly also locally synthetized and enriched in rheumatoid arthritis. In rheumatoid arthritis lysozyme is present in the synovia not only in free, but in most cases also in cell-bound form.
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PMID:[Synovial membrane permeability for plasma proteins and protein syntheses in rheumatic diseases]. 31 2

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

It appears that in rheumatoid arthritis and, to a lesser extent, in the other forms of inflammatory rheumatism, the level of zinc in the blood serum is lowered, whereas synovial zinc is increased. In the synovial fluid, there is a very significant correlation between enzyme activity and the concentration of zinc. Practical experiments aimed at demonstrating in vitro the action of zinc on lacticodeshydrogenase, acid phosphatase, lysozyme and beta-glucuronidase did not produce the anticipated results and do not explain the metabolic disorders of zinc seen during inflammatory rheumatisms.
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PMID:[Zinc and enzymes in the synovial fluid and blood in various types of rheumatism]. 74 83

Lysozyme and lactoferrin levels were measured in 71 synovial fluids (SF) of patients with traumatic effusions, osteoarthritis, rheumatoid arthritis, pseudogout, septic arthritis, and gout, as well as in 91 synovial fluids graded according to their neutrophil count. Elevated lysozyme levels were found in all the inflammatory arthritides and also in osteoarthritis. Lactoferrin levels were not increased in osteoarthritis but displayed a close correlation to the extent of the inflammatory response as judged by SF neutrophilia. The ratio of lysozyme to lactoferrin decreased progressively with increasing SF neutrophilia. In vitro experiments showed that lactoferrin is released from neutrophils isochronously with lysozyme and beta-glucuronidase. Lactoferrin was not found in hyaline cartilage, a tissue known to contain lysozyme. These results are consistent with belief that SF lysozyme has a major derivation from both cartilage and neutrophils, and that lactoferrin arises only from neutrophils. These findings indicate that the simultaneous measurement of lysozyme and lactoferrin provides a potentially useful index of both joint inflammation and cartilage degradation.
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PMID:Lactoferrin and lysozyme levels in synovial fluid: differential indices of articular inflammation and degradation. 83 40

Lactoferrin (LF) has been assayed by radioimmunoassay in plasma and arthritic exudates and compared with lysozyme (LZ) levels and leukocyte counts. The mean LF concentration in 38 rheumatoid arthritis (RA) exudates was 9.1 mg/l (range 0.02-39.2). In 30 non-RA exudates LF was 3.3 mg/l (range 0.01-14.6). The corresponding LZ levels were 7.4 mg/l (range 2.5-18.5) in RA and 4.7 (range 1.0-12.5) in non-RA fluids. Exudate/plasma ratios were much higher for LF than for LZ and higher in RA than in non-RA exudates, whereas leukocyte counts did not differ. The LF/leukocyte count ratio was significantly higher in RA than in the non-RA group. The data suggest a more prominent release of neutrophilic granulocyte components in RA than in non-RA arthritis.
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PMID:Lactoferrin and lysozyme in arthritic exudates. 92 Feb 51

Two cases of the development of acute myeloid leukemia (AML) after treatment with alkylating agents are reported. In Case 1, melphalan and then cyclophosphamide had been given for multiple myeloma. 46 months after onset of cytostatic treatment AML occurred, as confirmed cytochemically and by qualitative determination of urinary lysozyme. In Case 2, cyclophosphamide had been given for rheumatoid arthritis. After a latency of 34 months 'smouldering leukaemia' developed with an atypical monocytic leukaemic cell population. In a third case, multiple myeloma and monocytic leukaemia developed synchronously. The causative role of melphalan and cyclophosphamide in the development of AML seems securely established. Despite the risk of alkylating agents in the treatment of multiple myeloma or Hodgkin's disease causing AML, they should not be replaced, as other drugs have been shown to be less beneficial. On the other hand, alkylating agents should be used with great caution in the treatment of non-malignant diseases.
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PMID:[Plasmocytoma, alkylating agents, and acute myeloid leukemia (author's transl)]. 105 6

Patients with rheumatoid arthritis (RA), patients with positive tuberculin (PPD) skin-tests and controls were studied. The lymphocytes from these groups were cultured in serum-free medium to obtain cell-free supernatants. These lymphocyte cultures were pre-incubated with the appropriate antigen or reconstituted after removal of the cells. Supernatants from RA lymphocytes stimulated in vitro by IgG induced an inhibition of the leucocyte migration, as well as the supernatants from tuberculin-sensitized lymphocytes. However, supernatants from non-RA lymphocytes or tuberculin-unsensitized lymphocytes did not show such an inhibition. These MIF-like supernatants have been studied by Sephadex G-100 gel filtration. A MIF activity has been found for PPD and IgG supernatants between the chymotrypsinogen (MW 23,000) and the lysozyme (MW 17,000). This seems to agree with the classical region where MIF can be usually isolated.
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PMID:Production of MIF-like supernatants by rheumatoid arthritis lymphocytes stimulated by immunoglobulin G. 110 42

IL-1 and a specific receptor antagonist of IL-1, IL-1ra, may play important roles in the pathophysiology of rheumatoid arthritis and in other types of inflammatory synovitis. Measurement of IL-1ra in synovial fluids and in other body fluids may lead to a greater understanding of its possible activity as a modulator of the immune and inflammatory systems in vivo. Therefore, a modified sandwich ELISA was developed to measure IL-1ra protein concentration in synovial fluids. The antibodies used in this ELISA were polyclonal and derived from rabbits hyperimmunized with human recombinant IL-1ra. IgM rheumatoid factors within synovial fluid resulted in false elevation of determined IL-1ra by the sandwich ELISA through binding of the primary and secondary antibodies. Reduction and alkylation of synovial fluid samples before application to the ELISA plate eliminated the interference caused by greater than or equal to 2000 micrograms/ml IgM rheumatoid factor (latex agglutination titer of 1/5.120). This ELISA was specific for IL-1ra; there was no detection of IL-1 alpha, IL-1 beta, or lysozyme. The sensitivity of this ELISA was less than 200 pg/ml, making it a useful assay for the accurate measurement of synovial fluid IL-1ra protein concentration.
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PMID:IL-1ra ELISA: reduction and alkylation of synovial fluid eliminates interference by IgM rheumatoid factors. 182 49


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