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)

Elevated activities of beta-D-glucuronidase, myeloperoxidase, and lysozyme were found in polymorphonuclear leukocytes (PMNs) of both hypopituitary dwarfs and normal subjects after the administration of growth hormone (GH), as compared to the activities in PMNs from blood drawn immediately before the administration of GH. During in vitro incubation, GH was able to inhibit the release of lysosomal enzymes from resting PMNs. This inhibition may be one of the reasons for the elevated lysosomal enzyme activities observed in PMNs after the administration of GH. GH can also affect hexose monophosphate shunt (HMPS) activity and superoxide production by PMNs. The activity of HMPS is stimulated by GH in resting PMNs, while in PMNs incubated with zymosan the GH inhibits both HMPS and superoxide production.
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PMID:Effect of growth hormone on the activity of some lysosomal enzymes in neutrophilic polymorphonuclear leukocytes of hypopituitary dwarfs. 299 87

The reducing equivalents used by the human neutrophil respiratory burst oxidase are derived from NADPH generated by the hexose monophosphate shunt. The CO2 generated by the HMP shunt is spontaneously hydrated and the protons (H+) are secreted upon the dissociation of carbonic acid. The mechanism and significance of H+ secretion by the resting and stimulated neutrophil was investigated. A basal rate of H+ secretion by resting neutrophils observed in a choline buffer was augmented with the addition of sodium (Na+) (Km for Na+ was 3.22 +/- 0.32 mM). Amiloride, a Na+/H+ antiporter inhibitor, reduced H+ secretion in Na+-containing buffers with a Ki = 1.02 microM. This Na+/H+ exchange mechanism was also operative in cells stimulated with a variety of agonists, and an increased H+ flux, relative to resting cells, was observed at higher Na+ concentrations. Cytoplasts incorporating acridine orange were also used to assess Na+-H+ flux. Cytoplasts were used to avoid alteration of the fluorescent pH probe by HOCl formed in intact neutrophils. Alkalinization of the cytoplasm was dependent on extracellular Na+ in concentrations similar to that found to augment H+ secretion in intact cells. Also, amiloride competitively inhibited H+ secretion by the cytoplasts. Both superoxide (O2-) production and lysozyme release in cells stimulated with opsonized zymosan or concanavalin A was significantly inhibited in the absence of Na+, restored to normal with the addition of Na+ in low concentrations, and inhibited again in the presence of amiloride. A Na+/H+ antiporter similar to that found in other cell types is present in the human neutrophil and appears linked to activation of the respiratory burst and degranulation.
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PMID:Proton secretion by the sodium/hydrogen ion antiporter in the human neutrophil. 300 66

The effects of clofazimine on phagocyte functions associated with antimicrobial activity have been investigated. Clofazimine at a variety of concentrations was capable of enhancing the spontaneous production of hydrogen peroxide and the intracellular killing ability of phagocytes; but had no effect on resting phagocyte lysozyme release, or hexose monophosphate shunt (HMPS) activity. However, when these latter functions were assessed in the presence of a phagocytic stimulus, clofazimine moderately increased both lysozyme release and HMPS activity. A 25 Kd glyco-lipoprotein derived from Mycobacterium tuberculosis has been shown to inhibit these antimicrobial functions. Clofazimine was capable of partially reversing the inhibitory effect of the mycobacterial component in all of the systems assessed. Partial restoration was observed at concentrations of 0.5 mg/l and was maximal at 2 mg/l. These studies indicate important mechanisms operative in the pathogenesis of tuberculosis and suggest that clofazimine may have clinical relevance in the treatment of mycobacterial diseases.
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PMID:Clofazimine reverses the inhibitory effect of Mycobacterium tuberculosis derived factors on phagocyte intracellular killing mechanisms. 312 22

The interaction between the pneumococcal toxin pneumolysin and human monocytes was examined. At non-cytotoxic concentrations (0.5-2.5 HU/10(6) cells) pneumolysin depressed the oxygen-dependent respiratory burst in monocytes, induced by opsonized zymosan or phorbol myristate acetate (PMA). This included depressed hexose-monophosphate shunt activity and hydrogen peroxide production. The toxin also depressed the ability of monocytes to degranulate (measured by release of lysozyme) in response to the above stimuli. Phospholipid transmethylation was also markedly decreased by pretreating monocytes with pneumolysin. These effects on monocyte functions were accompanied by a decreased ability of pneumolysin-treated monocytes to kill Streptococcus pneumoniae, the organism that produces the toxin. Cholesterol, which inhibits the haemolytic activity of the toxin, was shown to abrogate the effects of pneumolysin on monocytes.
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PMID:Inhibition of human monocyte respiratory burst, degranulation, phospholipid methylation and bactericidal activity by pneumolysin. 380 76

By using IgG-sensitized erythrocytes as target cells, we found the antibody-dependent cytotoxicity mediated by monocytes and neutrophils to be depressed in atopic dermatitis. This change was accompanied by a reduction of phagocytosis of target cells by the effector cells, and also by a decreased lysozyme liberation from, and hexose monophosphate shunt activation in, the effector cells during the cytotoxic reaction. However, the binding of target cells to effector cells remained normal. In individual patients, cytotoxicity and phagocytosis were equally depressed. No relation was found between cytotoxicity and lysozyme liberation in atopic dermatitis, but a relation between cytotoxicity and hexose monophosphate shunt activity was highly significant. These results suggest that the decreased cytotoxicity mediated by monocytes and neutrophils in atopic dermatitis is caused by a diminished production of oxygen radicals during the respiratory burst. This reduced respiratory burst was not due to any defect in the enzymes responsible for this process, since the superoxide production of monocytes and neutrophils stimulated with phorbol myristate acetate was found normal in atopic dermatitis. It therefore seems that although binding of target cells to effector cells was normal, the signals created by the binding process were defective in activating monocytes and neutrophils in atopic dermatitis.
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PMID:Mechanisms of decreased antibody-dependent cytotoxicity mediated by monocytes and neutrophils in atopic dermatitis. 616 8

The effects of theophylline, isobutylmethylxanthine (IBMX), prostaglandin E1 (PGE1), and isoproterenol on monocyte antibody-dependent cytotoxicity (ADCC) were compared with their effects on monocyte cyclic adenosine 3':5'-monophosphate (cAMP) levels. Theophylline (2 mmol/l) halved ADCC and gave a 2-fold increase in cAMP levels. At concentrations not elevating cAMP theophylline inhibited ADCC significantly. In comparison, incubation of monocytes with IBMX, PGE1 and isoproterenol ADCC was only modestly inhibited while these agents gave larger increments (3- to 8-fold) in cAMP levels than theophylline did. Low concentrations of IBMX (50 mumol/l) elevated cAMP without affecting monocyte ADCC whereas PGE1 and isoproterenol inhibited ADCC dose-dependently comparable to increases in cAMP. However, in doses giving similar inhibition of ADCC addition of PGE1 resulted in larger cAMP increments than isoproterenol. The effects of IBMX, PGE1 and isoproterenol was dependent on target cell to effector cell ratio and increased during preincubation with the agents. The inhibition of ADCC by the agents was accompanied by a depressed monocyte lysozyme release and depressed activation of hexose monophosphate shunt. However, only theophylline affected monocyte attachment to sensitized target cells. These results argue against the general inverse relationship between cAMP content and inhibition of monocyte ADCC and demonstrate that theophylline independent on increases in cAMP inhibits ADCC probably by abrogation of monocyte binding activity.
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PMID:Divergent effects of methylxanthines and adenylate cyclase agonists on monocyte cytotoxicity and cyclic AMP levels. 618 23

The anti-inflammatory effects of gold compounds include suppression of PMN lysosomal enzyme release. Since lysosomal products can provoke PMN aggregation, we assessed the effect of two gold compounds, auranofin and GST, on suppressing aggregation, degranulation, and metabolic functions of the cells. Aggregation of 1 x 10(7) cytochalasin B-treated PMNs in response to 2 x 10(-7)M FMLP, as assessed by light scattering, was inhibited in a dose-dependent fashion by both drugs. Concentrations of auranofin ranging from 5 to 20 microM caused 30.8% to 89% inhibition, whereas 200 microM GST reduced aggregation by only 32%. FCS or BSA added to suspensions of normal PMNs considerably reduced the gold compound inhibitory effect on PMN aggregation. Cell viability assessed by dye exclusion and lactate dehydrogenase release was unaffected by the drugs. The suppressive activities of the drugs could not be removed by washing the PMNs. Correspondingly, the drugs suppressed lysosomal enzyme release induced by FMLP of PMNs rendered secretory with cytochalasin B. Concentrations of 20 microM auranofin and 200 microM GST resulted, respectively, in a 61.5% and 19.3% reduction of release of lysozyme, 61.7% and 27.1% reduction of beta-glucuronidase, 84.8% and 33.7%s reduction of myeloperoxidase, and 50.0% and 25.0% reduction of lactoferrin. Furthermore, auranofin inhibited 14C-1-glucose oxidation through the hexose monophosphate shunt in response to stimulation by either PMA or methylene blue. The in vivo studies suggested that auranofin could prevent neither neutropenia induced by zymosan-activated serum nor a corresponding rise in plasma lactoferrin levels. These findings suggest that the beneficial effect of gold compounds in rheumatoid arthritis are unlikely to be related to their ability to dampen PMN activation in vivo.
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PMID:Correlation of in vitro and in vivo effects of gold compounds on leukocyte function: possible mechanisms of action. 628 1

Monocyte and neutrophil function assessed as antibody-dependent cell-mediated cytotoxicity (ADCC) using IgG-sensitizing human erythrocytes as target cells was enhanced in patients with severe psoriasis when compared to healthy controls. We found significant correlation between increased monocyte ADCC and increased neutrophil ADCC, No differences in basal cAMP levels and cAMP responses during initiation of the ADCC reaction was observed between psoriatics and normals. Also degranulation determined as lysozyme release during ADCC was normal. In contrast, the increase in ADCC was significantly correlated to an enhanced hexose monophosphate shunt activation in the effector cells during the cytotoxic reaction. Activity of enzymes responsible for the respiratory burst was not altered in psoriasis since superoxide production after stimulation with phorbol myristate acetate was normal. Likewise, oxygen consumption and degranulation following phagocytosis of opsonized zymosan particles in neutrophils was found normal in psoriasis. Since monocytes showed increased binding of IgG-sensitized erythrocytes these data indicate that the enhanced monocyte and neutrophil ADCC is caused by an enhancement of the respiratory burst possibly induced by increased Fc receptor activity.
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PMID:On the mechanism of enhanced monocyte and neutrophil cytotoxicity in severe psoriasis. 628 40

Implanted foreign bodies are highly susceptible to pyogenic infections and represent a major problem in modern medicine. In an effort to understand the pathogenesis of these infections, we studied the phagocytic function in the vicinity of a foreign body by using a recently developed guinea pig model of Teflon tissue cages subcutaneously implanted (Zimmerli, W., F.A. Waldvogel, P. Vaudaux, and U.E. Nydegger, 1982, J. Infect. Dis., 146:487-497). Polymorphonuclear leukocytes (PMN) purified from tissue cage fluid had poor bactericidal activity against a catalase-positive microorganism. When compared with blood or exudate PMN, they exhibited a significant reduction in their ability to generate superoxide in response to a particulate or a soluble stimulus (72 and 57%, respectively, P less than 0.001). Not only their total contents in myeloperoxidase, beta-glucuronidase, lysozyme, and B12 binding protein were significantly reduced (by 62, 21, 47, and 63%, respectively, P less than 0.01), but also their capability for further secretion of residual B12 binding protein upon stimulation. Ingestion rates of endotoxin-coated opsonized oil particles were reduced by 25% (P less than 0.05). In an effort to reproduce these abnormalities in vitro, fresh peritoneal exudate PMN were incubated with Teflon fibers in the presence of plasma. Interaction of PMN with the fibers led to significant increases in hexose monophosphate shunt activity and exocytosis of secondary granules (P less than 0.01). PMN eluted after such interaction showed defective bactericidal activity, oxidative metabolism, and granular enzyme content similar to those observed in tissue cage PMN. The local injection of fresh blood PMN into tissue cages at the time of, or 3 h after, inoculation with 100 microorganisms (Staphylococcus aureus Wood 46) reduced the infection rate from 50 to 56 cages to 1 of 21 (P less than 0.001) and 3 of 8 cages (P less than 0.001), respectively. These results suggest that the in vivo as well as in vitro interaction of PMN with a nonphagocytosable foreign body induces a complex PMN defect, which may be partly responsible for the high susceptibility to infection of foreign bodies.
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PMID:Pathogenesis of foreign body infection. Evidence for a local granulocyte defect. 632 36

To evaluate the role of NK cell granules in the lytic activity of NK cells, cytoplasmic granules of rat NK tumors were purified by centrifugation of the cell homogenates in a Percoll gradient. Analysis of such gradients showed a band of light-scattering material near the bottom of the tube; assay of gradient fractions for lytic activity against SRBC showed a potent lytic activity giving a sharp peak in this region. Complete lysis of SRBC was achieved with less than 1 microgram/ml protein of the most active fractions. Examination in the electron microscope showed that a pool of fractions containing lytic activity consisted of pure cytoplasmic granules showing similar morphology to those found in the LGL tumors. The lytic band was associated with a peak in the activity of four different lysosomal enzymes. Analysis of Percoll gradient fractions showed that marker enzymes for mitochondria, plasma membrane, and cytosol were well separated from this activity peak. Analysis of the Percoll gradient fractions by SDS gel electrophoresis showed that this granule fraction was free of contamination of proteins from other parts of the gradient. The granules contained major protein bands of 62, 58, 30, 29, and 28 kilodaltons. In addition to protein, the purified granule fractions contain hexose and uronic acid, but no nucleic acids or phospholipids were detected in chemical assays. Major amounts of chymotryptic, tryptic, and elastase activities were not present, nor were peroxidase or lysozyme activities detectable in substantial amounts. These data show that NK tumor cell cytoplasmic granules contain a potent lytic activity and have biochemical properties that distinguish them from granules present in granulocytes and mast cells.
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PMID:Purification and properties of cytoplasmic granules from cytotoxic rat LGL tumors. 637 25


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