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)

Superoxide anion (O-2-) generation by human peripheral blood polymorphonuclear leukocytes is enhanced when these cells encounter appropriate soluble or particulate stimuli. O-2- generation requires intact, viable cells and proceeds independently of phagocytosis. To investigate the possibility that the O-2--generating system is associated with the outer surface of the polymorphonuclear leukocyte plasma membrane, we have examined the effects upon O-2- production of p-diazobenzenesulfonic acid, a reagent which can react predominantly with proteins of the external cell membrane. When normal human polymorphonuclear leukocytes were preincubated with cytochalasin B (to minimize endocytosis) and then exposed to the surface-active lectin, concanavalin A, the cells were stimulated to generate O-2- in a concentration- and time-dependent fashion and selectively to discharge the granule-associated enzyme, lysozyme, into the surrounding medium. These responses, as well as cellular binding of [H] concanavalin A, could be blocked by alpha-methyl-D-mannoside. Brief treatment (less than 5 min at 4 degrees C) of the cells with p-diazobenzenesulfonic acid (1.0-5.0 mM) significantly interfered with concanavalin A-mediated O-2- generation but had no influence upon lysozyme release or upon binding of [3H] concanavalin A. The diazonium salt did not alter cell viability or the specific activity of the cytoplasmic enzyme, lactate dehydrogenase (inhibitable under conditions which allowed entry of this reagent into the cytosol). p-Diazobenzenesulfonic acid, therefore, very likely exerted its effects at the cell surface of the intact polymorphonuclear leukocyte, selectively inhibiting O-2- production (either directly or indirectly) without influencing another response to lectin-cell contact: release of lysozyme. These results support the possibility that a polymorphonuclear leukocyte ectoenzyme is responsible for O-2- production.
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PMID:Evidence that the superoxide-generating system of human leukocytes is associated with the cell surface. 18 67

Fourteen continuous tissue culture cell lines derived from mouse, rat, or human granulocyte-macrophage cancers were studied for expression of spontaneous and inducible markers of differentiated cells. Five cell lines (two mouse, two rat, and one human) synthesized myeloperoxidase spontaneously, and a fifth mouse line showed biochemically inducible enzyme. Twelve lines (6 mouse, 3 rat, and 3 human) produced lysozyme (muramidase), and all had detectable beta-glucuronidase. Superoxide generation was detected in one mouse, and three human cell lines following stimulation with phorbol myristate acetate. Maturation to differentiated polymorphonuclear leukocyte or macrophage morphology was induced in 3 cell lines (2 mouse and 1 human) following culture in diffusion chambers in total-body-irradiated rats. In vitro morphological differentiation was inducible in one (mouse) cell line exposed to casein, thioglycolate, or plasma from irradiated rats or mice. These findings indicate that mammalian cell lines derived from granulocyte-macrophage cancers stably express several combinations of differentiation markers. The patterns of expression of these markers did not always correlate with the morphological stage of differentiation.
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PMID:Constitutive and inducible granulocyte-macrophage functions in mouse, rat, and human myeloid leukemia-derived continuous tissue culture lines. 21 Sep 35

Polymorphonuclear leucocytes (PMN), monocytes and monocyte-derived macrophages were capable of interacting with opsonized C. albicans in both aerobic and anaerobic conditions. Superoxide anion release by these cells was inhibited in anaerobic conditions while lysozyme release and phagocytosis were equally efficient in both aerobic and anaerobic conditions. All cell types tested were capable of intracellular killing of C. albicans and this appeared to be maximum at 6 h for monocytes and macrophages and 24 h for PMN. Monocytes killed the lowest number of organisms, 1 x 10(6), and the killing was similar for aerobic and anaerobic conditions. In contrast, PMN and macrophages demonstrated greater killing of C. albicans in aerobic conditions compared with anaerobic conditions; PMN killed 1.9 x 10(6) organisms and macrophages 3 x 10(6) when incubated anaerobically. Inhibitors of oxygen metabolism decreased intracellular killing of C. albicans by macrophages and PMN in aerobic but not anaerobic conditions. The oxygen reaction products involved in the killing of C. albicans appeared to be different however: macrophage killing was decreased by superoxide anion and hydrogen peroxide inhibitors. PMN killing was decreased by superoxide anion, hydrogen peroxide, hypochlorous acid and hydroxyl radical inhibitors. The present study shows that although monocytes, macrophages and PMN function similarly in their interaction with C. albicans, they appear to use different oxygen reactive products for the intracellular killing of C. albicans.
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PMID:Interaction and intracellular killing of Candida albicans blastospores by human polymorphonuclear leucocytes, monocytes and monocyte-derived macrophages in aerobic and anaerobic conditions. 131 Apr 54

The role of free radical generation and its scavenging enzymes in circulating mice polymorphonuclear leukocytes (PMNLs) has been studied following pulmonary thromboembolism. Levels of malonaldehyde (MDA), 02- radical generation, activity of superoxide dismutase (SOD), catalase (CAT), lactate dehydrogenase (LDH), myeloperoxidase (MPO) and lysozyme were estimated in lysed neutrophil preparations. Activities of SOD and CAT were increased in neutrophils, while animals showed 60 +/- 4% thrombocytopenia. Levels of MDA in PMNLs were also elevated significantly following thrombosis. However, there was no significant change in superoxide radical generation, after thrombotic challenge, in mice neutrophils. The present study provides evidence for the involvement of free radicals in mice pulmonary thromboembolism.
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PMID:Effect of pulmonary thromboembolism on circulating neutrophils in mice. 132 50

This study describes effects of sulphasalazine, 5-amino-salicylic acid (5-ASA) and sulphapyridine on polymorphonuclear neutrophils. Chemotaxis by polymorphonuclear neutrophils incubated with 5-ASA was reduced in a concentration dependent fashion (10(-5)-10(-4) M). Degranulation and release of lysozyme and beta-glucuronidase by activated polymorphonuclear neutrophils was inhibited by sulphasalazine but inhibited by sulphasalazine (IC50: 2 x 10(-4) M) and to a lesser extent by 5-ASA (IC50: 10(-3) M). Using a cell-free system sulphasalazine was found to be a strong scavenger and 5-ASA and sulphapyridine had only weak effects. Superoxide anion production requires translocation of a cytochrome b-245 and this translocation was reduced by sulphasalazine (P less than 0.01) but not by 5-ASA or sulphapyridine. In conclusion, the intact sulphasalazine molecule has an action of its own and marked differences exist between the action of sulphasalazine and 5-ASA, which may be important for the clinical activity.
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PMID:Effects of sulphasalazine and its metabolites on neutrophil chemotaxis, superoxide production, degranulation and translocation of cytochrome b-245. 168 23

A detoxified derivative of endotoxic lipopolysaccharides (LPS), monophosphoryl lipid A (MPL), which is capable of inducing nonspecific resistance against several infectious organisms, was tested for its capacity to activate peritoneal macrophages (M phi) from young and immunodeficient aging BALB/c and C3H/HeN mice. Superoxide generation and hydrogen peroxide release by M phi from aging mice were elevated following intraperitoneal injection with 25 micrograms of LPS or MPL, although they did not reach the peak levels achieved in LPS or MPL-treated young mice. Nitroblue tetrazolium reduction (NBT) by peritoneal M phi from aging C3H/HeN mice treated with MPL was higher than that in control aging mice, equalling that from MPL-treated young mice. LPS, its toxic counterpart, however, failed to increase NBT reduction in either group. MPL enhanced lysozyme activity in M phi from both aging and young C3H/HeN mice above initial control levels. On the other hand, LPS suppressed lysozyme activity in M phi from young, but not aging mice. Phagocytosis of Candida albicans by M phi from BALB/c mice was increased in both groups when stimulated by MPL, but not LPS. Similarly, MPL enhanced the ability to kill Candida in both aging and young BALB/c mice. This effect was not seen with LPS. Thus, a detoxified derivative of LPS was found capable of activating the respiratory burst, NBT reduction, elevating lysozyme activity, as well as phagocytosis and killing of Candida in murine peritoneal M phi from both young and aging mice.
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PMID:Activation of macrophages from aging mice by detoxified lipid A. 184 73

Neutrophil activation and infiltration into the ischemic myocardium after reperfusion may limit the amount of salvageable myocardium (reperfusion injury). The effects of intravenous perfluorochemicals (Fluosol-DA) on infarct size, ventricular contractility, and neutrophil function were assessed in an occlusion-reperfusion canine model. Closed-chest dogs were subjected to 90 minutes of left anterior descending artery occlusion followed by 24 hours of reperfusion. Animals were randomized to receive either Fluosol-DA (FDA, n = 8) or Ringer's lactate (CONT, n = 10) intravenously over 30 minutes just before left anterior descending artery reperfusion. Neutrophil demargination and infiltration into the myocardium were assessed in vivo with In111. Neutrophil chemotaxis, superoxide radical production, and lysozyme degranulation were evaluated ex vivo at baseline, 1 hour after occlusion, and 1 hour after reperfusion. Perfluorochemicals significantly reduced infarct size expressed as percent of area at risk (FDA, 7 +/- 4%; CONT, 24 +/- 6%; p less than 0.01). This was associated with positive wall motion in the jeopardized zone of Fluosol-DA animals compared with dyskinesis in control animals (FDA, +4.4 +/- 2.1%; CONT, -1.1 +/- 1.5%; p less than 0.05). Electron microscopy showed reduced neutrophil and erythrocyte plugging of capillaries with relative preservation of endothelial cells in the Fluosol-DA animals. Myocardial blood flow was greater in the ischemic endocardium of Fluosol-DA animals 1 hour after reperfusion (FDA, 1.23 +/- 0.21; CONT, 0.62 +/- 0.08 ml/g/min; p less than 0.01). Neutrophil demargination and infiltration into the ischemic myocardium was reduced in the animals treated with Fluosol-DA. (FDA, 2.5 +/- 0.7 x 10(3); CONT, 14.1 +/- 2.7 x 10(3) neutrophils/g; p less than 0.01). Neutrophil chemotaxis and lysozyme release were also markedly suppressed in the Fluosol-DA groups ex vivo. These results show that intravenous Fluosol-DA significantly reduces reperfusion injury with greater salvage of myocardium and improved left ventricular function. The chief mechanism of action of Fluosol-DA appears to be the suppression of neutrophil function.
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PMID:Limitation of myocardial reperfusion injury by intravenous perfluorochemicals. Role of neutrophil activation. 253 60

Superoxide formation and lysosomal enzyme liberation circulating neutrophils has been assessed in healthy subjects. Blood samples were obtained at 8:00, 14:00, and 20:00 o'clock. The formation of superoxide followed a circadian rythm. Lowest concentration was found a 14:00 hours (4.59 +/- 2.09 nM reduced cytochrome/10(6) neutrophils). No 24 hour variation of betaglucuronidase and lysozyme liberation was proven. The number of neutrophil receptors for formyl-methyonil-leucyl-phenyl-alamine (FMLP) at the same hours did not show any circadian variation. The circadian changes of the functional capacity of the neutrophils might be one of the mechanisms that could justify the 24 hour variation of symptomatology characteristic of some diseases.
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PMID:[Circadian variations in the production of superoxide and liberation of lysosomal enzymes of neutrophils in peripheral blood]. 253 12

Human neutrophils (PMNs) which have been incubated with lipoteichoic acid (LTA) from group A streptococci generated large amounts of superoxide (O2- chemiluminescence and hydrogen peroxide when challenged with anti-LTA antibodies. Cytochalasin B further enhanced O2- generation. The onset of O2- generation by the LTA-anti-LTA complexes was much faster than that induced by BSA-anti-BSA complexes. LTA-treated PMNs generated much less O2- when challenged with BSA complexes, suggesting that LTA might have blocked, nonspecifically, some of the Fc receptors on PMNs. PMNs treated with LTA-anti-LTA complexes further interacted with bystander nonsensitized PMNs resulting in enhanced O2- generation, suggesting that small numbers of LTA-sensitized PMNs might recruit additional PMNs to participate in the generation of toxic oxygen species. Protelolytic enzyme treatment of PMNs further enhanced the generation of O2- by PMNs treated with LTA-anti-LTA. Superoxide generation could also be induced when PMNs and anti-LTA antibodies interacted with target cells (fibroblasts, epithelial cells) pretreated with LTA. This effect was also further enhanced by pretreatment of the target cells with proteases. PMNs incubated with LTA released lysosomal enzymes following treatment with anti-LTA antibodies. The amounts of phosphatase, beta-glucoronidase, N-acetylglucosaminidase, mannosidase, and lysozyme release by LTA-anti-LTA complexes were much smaller than those released by antibody or histone-opsonized streptococci, suggesting that opsonized particles are more efficient lysosomal enzyme releasers. However, since the amounts of O2- generated by the LTA complexes equaled those generated by the opsonized particles, it is assumed that the signals for triggering a respiratory burst and lysosomal enzyme secretion might be different. Generation of O2- by LTA complexes was strongly inhibited by lipoxygenase inhibitors but not by cyclooxigenase inhibitors. Also phenylbutazone, trifluorperazine, and DASA markedly inhibited O2- generation induced by LTA complexes. These data suggest that bacterial products in the presence of antibody might have important biological effects on phagocytic cells and that these effects may be inimical to the host.
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PMID:Lipoteichoic acid-antilipoteichoic acid complexes induce superoxide generation by human neutrophils. 285 50

Neutrophil superoxide production has been recognized as an important pathway for microbicidal activity and regulation of the local inflammatory environment. To investigate neutrophil superoxide production in sepsis, we studied 22 patients with intra-abdominal infections, and correlated superoxide production with chemotactic response and granular enzyme content. Our results showed that neutrophils from infected patients had specific loss of chemotactic response to C5a, and were deficient in the granular enzymes, lysozyme, and beta-glucuronidase. Superoxide production in response to opsonized zymosan was intact, but response to the chemoattractant N-formyl-methionyl-leucyl-phenylalanine was markedly depressed. This could be reversed in vitro by the addition of cytochalasin B. These results suggest that down regulation of exocytosis of superoxide to nonphagocytic stimuli occurs during sepsis, possibly protecting the host from tissue injury due to oxide radical release. Superoxide response to phagocytic stimulation was intact.
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PMID:Regulation of neutrophil superoxide production in sepsis. 298 24


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