Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of exogenous, purified phospholipase C (PLC) on neutrophil oxidative metabolism, lysosomal enzyme release and aggregation. We found that PLC inhibited O2- and H2O2 generation and oxygen consumption, but did not alter glucose oxidation via the hexose monophosphate shunt. In contrast, we found a striking stimulation of aggregation and release of the lysosomal enzymes lysozyme and beta-glucuronidase. In experiments designed to further characterize the mechanism of the PLC effect on membrane activation we studied the effect of PLC on intracellular calcium concentration [Ca2+]i and found that PLC did not interfere with the fMLP-mediated rise in [Ca2+]i, suggesting that its inhibitory effect on the respiratory burst does not involve inhibition of early signal transduction events. In addition, we found that PLC alone results in mobilization of intracellular Ca2+ stores, consistent with its stimulatory effect on aggregation and lysosomal enzyme release.
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PMID:Inhibition of polymorphonuclear leukocyte oxidative metabolism by exogenous phospholipase C. 216 37

Polymorphonuclear leukocytes (PMN) are predominant cells in the gingival crevice and saliva, and may play an important role in oral bacteria. Murine peritoneal PMN was used and stimulated with 9 genera, 17 species of oral bacteria, including cariogenic and periodontal pathogens. The PMN response to the bacteria was measured by the luminol mediated chemiluminescence (CL) response and phagocytic activities, and the activities of lysozyme in the reaction medium after the CL response were also measured. The bacteria which could induce a high level of CL response of PMN were Fusobacterium nucleatum, Treponema denticola and Bacteroides gingivalis; middle grade were Staphylococcus subsp. and Actinomyces subsp.; low levels were Lactobacillus subsp., all 5 species of Streptococci and Enterococcus faecalis. Phagocytic indexes of PMN to various kind of bacteria were distributed from 8 to 40% and the bacterial numbers in 100 PMN were 27 to 301. There was no correlation between CL values and phagocytic indexes or between CL values and the bacterial number in 100 PMN by limiting the data on Staphylococcus, Streptococcus subsp. and Lactobacillus subsp., the correlation efficiency which was obtained between their values was r = 0.91 or 0.86. There was only a little in the lysozyme activities released from PMN by stimulation of various kind of bacteria, and the maximum difference corresponded to only 2.8% of the whole lysozyme activity of PMN. Either catalase activities or SOD activities were measured by H2O2 decomposition or the inhibition of xanthine oxidase activity using the intact bacteria. Neither of the enzyme activities of bacteria were closely related to the level of CL response.
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PMID:[Chemiluminescence response and phagocytic activity of murine polymorphonuclear leukocytes to various species of oral bacteria]. 248 36

The data presented here demonstrate that recombinant human tumour necrosis factor beta (rHuTNF beta; lymphotoxin) is a neutrophil modulator. The lymphokine inhibited the locomotion of neutrophils and augmented the neutrophil oxygen-dependent respiratory burst in response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) and phorbol myristate acetate (PMA), as measured by their capacity to produce chemiluminescence, H2O2 and superoxide. The effects on the respiratory burst occurred at a tenth of the concentration of TNF beta required to inhibit locomotion. After incubation with TNF beta, the neutrophils could be washed without any reduction in their capacity to show augmented responses. The TNF beta enhanced granule enzyme (lysozyme and beta-glucuronidase) release of neutrophils stimulated with cytochalasin B-FMLP.
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PMID:Tumour necrosis factor beta (lymphotoxin) inhibits locomotion and stimulates the respiratory burst and degranulation of neutrophils. 283 16

The assignment of cytochrome b-558 as a component of the O2- (H2O2) -generating enzyme in guinea-pig alveolar macrophages was investigated. Guinea pig alveolar macrophages contained 76 pmol cytochrome b-558/mg protein, a value very similar to that of neutrophils. The rate of myristic acid-stimulated O2- generation by alveolar macrophages, calculated per cytochrome b-558, was only one-fourth that of neutrophils. An analysis of Percoll density gradient centrifugation profiles showed that the H2O2-generating activity of myristic acid-activated alveolar macrophages was concentrated in a single peak which was consistently associated with 5'-nucleotidase activity, a plasma membrane marker enzyme. A little H2O2-generating activity was seen with unactivated alveolar macrophages. Furthermore, the cytochrome b-558 of both myristic acid-activated and unactivated alveolar macrophages was also predominantly associated with 5'-nucleotidase activity and was found in trace amounts in a peak containing lysozyme activity, a marker of lysosome granules. Only about 6% of the cytochrome b-558 in plasma membranes from myristic acid-activated guinea-pig alveolar macrophages was anaerobically reduced by 0.5 mM NADPH, while under the same conditions about 30% of the heme protein of myristic acid-activated neutrophils was reduced. These results suggest two conclusions: firstly, that in both activated and unactivated alveolar macrophages, cytochrome b-558 is located in the plasma membrane, and the translocation of cytochrome b-558 does not occur during the activation of NADPH oxidase; and secondly, that a smaller part of cytochrome b-558 is associated with the activated NADPH oxidase of guinea pig alveolar macrophages compared with neutrophils.
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PMID:Presence of cytochrome b-558 in guinea-pig alveolar macrophages-subcellular localization and relationship with NADPH oxidase. 283 23

Addition of thiourea (TU) or dimethylthiourea (DMTU) decreased killing of Staphylococcus aureus, 502A, and decreased concentrations of hydrogen peroxide (H2O2), and hydroxyl radical (.OH), but not superoxide anion (O2-.) or lysozyme concentrations, in mixtures containing human neutrophils in vitro. Addition of TU or DMTU also decreased concentrations of H2O2, .OH, or hypochlorous acid (HOCl) in neutrophil-free mixtures exposed to beta-D-glucose and glucose oxidase, gamma irradiation, or HOCl, respectively. Our results suggest that TU or DMTU can decrease neutrophil-mediated killing of bacteria by inhibiting O2 metabolite-dependent bactericidal mechanisms.
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PMID:Thiourea and dimethylthiourea decrease human neutrophil bactericidal function in vitro. 284 72

The enzyme system composed of human neutrophilic myeloperoxidase (H2O2-oxidoreductase, EC 1.11.1.7), H2O2 and Cl-, at pH 4.5 interacts with egg white lysozyme (EC 3.2.1.17) in several stages. In the first stage, occurring at lysozyme to H2O2 molar ratio of 1:1.4-1.8, the lysozyme loses its enzyme activity but does not yield any derivative distinguishable from the native protein on polyacrylamide gel electrophoresis (PAGE). The second stage of oxidation begins at lysozyme to H2O2 molar ratio above 1:5, producing a change in the lysozyme spectrum at 260-290 nm, and yielding protein derivatives with molecular masses equal to multiples of 14.3 kDa, i.e. the lysozyme molecular mass. This implies that an excessive oxidation of lysozyme by the myeloperoxidase-H2O2-Cl- system produces cross-linking of lysozyme molecules to di-, tri-, tetra-, and pentameric structures. At lysozyme to H2O2 molar ratio exceeding 1:12 a water insoluble white product, which consists of a set of lysozyme cross-linked derivatives, is obtained.
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PMID:Action of myeloperoxidase-hydrogen peroxide-chloride system on the egg white lysozyme. 285 92

Hydrogen peroxide levels were measured in the breath condensate of 43 patients receiving mechanical ventilation. In 16 patients the mean breath condensate peroxide level was 1.68 +/- 0.35 mumol/l on the day they met diagnostic criteria for adult respiratory distress syndrome (ARDS). The peak breath condensate peroxide level in the 27 patients in whom ARDS did not develop was significantly lower (0.34 +/- 0.08 mumol/l). Plasma lysozyme, a measure of in-vivo neutrophil turnover, was significantly higher in ARDS than in non-ARDS patients (9.2 +/- 2.2 U/ml v 3.4 +/- 1.1 U/ml). These findings support the hypothesis that neutrophil activation and oxidant production are involved in the pathogenesis of ARDS.
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PMID:Oxidant activity in expired breath of patients with adult respiratory distress syndrome. 286 61

Propionibacterium acnes, the target of inflammation in acne, was tested for its sensitivity to the bactericidal and degradative functions of human polymorphonuclear leukocytes (PMN), monocytes, and their fractions. P. acnes strains were not killed by PMN under any conditions and were variably killed by monocytes in the presence of serum from acne patients. Control strains of Staphylococcus aureus and Micrococcus lysodeicticus were susceptible to both PMN and monocyte killing. P. acnes strains were also not killed by lysozyme, chymotrypsin, H2O2, human serum, PMN granule lysate, and PMN and monocyte cell lysates. The organism was sensitive to the bactericidal activity of myeloperoxidase in acid pH. In addition, P. acnes was shown to be relatively resistant to the degradative action of PMN and monocyte lysates, whereas M. lysodeicticus, S. aureus, and Staphylococcus epidermidis were all degraded to various degrees. The moieties that were liberated from P. acnes by PMN enzymes were predominantly low in molecular weight (1,000 to 25,000) and were consistent with cell wall fragments.
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PMID:Susceptibility of Propionibacterium acnes to killing and degradation by human neutrophils and monocytes in vitro. 298 78

The relationship between the generation of active species of oxygen (O-2, H2O2 and OH.), chemiluminescence, and the release of lysosomal enzymes (lysozyme, alpha-mannosidase and beta-glucuronidase) was examined in human neutrophils stimulated with opsonized zymosan in the presence or absence of active-oxygen scavengers. In the absence of scavengers, increasing zymosan concn stimulated a marked increase in active-oxygen production in a concn-dependent manner and a less rigorously dose-dependent increase in enzyme secretion. Addition of OH. and/or 1O2 scavengers (benzoate, 1,4-diazo-bicyclo-2,2,2-octane or xanthine) caused a marked increase in enzyme release and a decrease in the generation of active-oxygen species except O-2 and H2O2. These findings suggest that exocytosis of lysosomal enzymes by stimulated neutrophils might be attenuated by the active generation of OH. and chemiluminescence. Superoxide dismutase (SOD) at low concns inhibited lysosomal enzyme release while promoting OH formation; and SOD at high concns decreased OH. and O-2 formation and chemiluminescence, accompanied by higher levels of lysosomal enzyme release. Catalase showed an effect similar to that of SOD. Our data suggest that the reduction by scavengers of active-oxygen levels, particularly of the species detected in the OH. and chemiluminescence assays, results in an increase in lysosomal enzyme release.
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PMID:Reverse relationship between lysosomal-enzyme release and active-oxygen generation in stimulated human neutrophils. 299 96

Human recombinant tumor necrosis factor (TNF) was shown to be a weak direct stimulus of the neutrophil respiratory burst and degranulation. The stimulation, as measured by iodination, H2O2 production, and lysozyme release, was considerably increased by the presence of unopsonized zymosan in the reaction mixture, an effect which was associated with the increased ingestion of the zymosan. TNF does not act as an opsonin but, rather, reacts with the neutrophil to increase its phagocytic activity. TNF-dependent phagocytosis, as measured indirectly by iodination, is inhibited by monoclonal antibodies (Mab) 60.1 and 60.3, which recognize different epitopes on the C3bi receptor/adherence-promoting surface glycoprotein of neutrophils. Other neutrophil stimulants, namely N-formyl-methionyl-leucyl-phenylalanine, the Ca2+ ionophore A23187, and phorbol myristic acetate, also increase iodination in the presence of zymosan; as with TNF, the effect of these stimulants is inhibited by Mab 60.1 and 60.3, whereas, in contrast to that of TNF, their stimulation of iodination is unaffected by an Mab directed against TNF. TNF may be a natural stimulant of neutrophils which promotes adherence to endothelial cells and to particles, leading to increased phagocytosis, respiratory burst activity, and degranulation.
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PMID:Stimulation of neutrophils by tumor necrosis factor. 300 19


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