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)

The effects of pertussis toxin (PT) on human neutrophil responses mediated by the 42-kDa IgG Fc R (Fc gamma R42) were compared with its effects on responses mediated by the FMLP receptor. Pre-treatment of neutrophils with PT completely inhibited FMLP stimulation of superoxide production and blocked over 95% of FMLP-stimulated degranulation. PT inhibited superoxide production stimulated by Fc gamma R42 cross-linking by 92%. In contrast, degranulation stimulated by Fc gamma R42 was only partially inhibited, with beta-glucuronidase release inhibited by 54%, lysozyme by 33%, and lactoferrin by 78%. With either stimulus, PT inhibition was maximal in the range from 1.8 to 2 micrograms/ml. Responses to both stimuli declined in a parallel fashion with increasing time of exposure to PT with maximal inhibition occurring after 2 h of exposure. Inhibition of FMLP responses and Fc gamma R42-mediated superoxide production, but not degranulation, correlated with ADP-ribosylation of a 45-kDa membrane protein. Inhibition by PT of Fc gamma R42-mediated responses was not due to a change in receptor number. These data suggest that activation of polymorphonuclear neutrophils via Fc gamma R42 proceeds through two pathways, only one of which is regulated by a PT-sensitive G protein.
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PMID:Pertussis toxin inhibits human neutrophil responses mediated by the 42-kilodalton IgG Fc receptor. 296 66

Chediak-Higashi Syndrome (CHS) has been associated with recurrent bacterial infections and defective polymorphonuclear (PMN) leukocyte function. Confirmation of the diagnosis of CHS and defective PMN function was established in a 2-month-old with accelerated phase CHS. The diagnosis was confirmed by demonstrating reduced PMN degranulation (beta-glucuronidase release 34.1 +/- 0.9% versus 5.1 +/- 4% and lysozyme release 17.6 +/- 1.2% versus 11.1 +/- 7% (control versus CHS) and staphylococcal bacterial killing at 15' 51.4 +/- 3.6% versus 24.9 +/- .4% (control versus CHS). Additional studies using fluorescent cytometric analysis were made to investigate other etiologies of PMN dysfunction in CHS. Total cell density and PMN granularity, as measured by fluorescent-activated cell sorter side scatter analysis, was no different from CHS and age-matched controls. Although CHS is characterized by large PMN granular inclusions, right angle light scatter analysis in this study suggests that the total cell density within the PMN of patients with CHS is normal (D less than .01). PMN granular release of surface receptors was also studied using antibody binding and fluorescent analysis. OKM1 antibody-binding demonstrated significantly reduced C3bi (MO-1) receptor expression (13% of control) p less than 0.001. Decreased surface reception expression of C3bi receptors may play an additional role in defective PMN mobility, chemotaxis, and bactericidal activity in patients with CHS.
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PMID:Fluorescent cytometric analysis of polymorphonuclear leukocytes in Chediak-Higashi syndrome: diminished C3bi receptor expression (OKM1) with normal granular cell density. 297 32

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

Myeloperoxidase (MPO)-deficient neutrophils (PMN) released considerably more beta-glucuronidase, lysozyme and vitamin B12-binding activities, when exposed to opsonized zymosan (STZ), than the normal counterpart. Release of the soluble enzyme lactate dehydrogenase was not appreciably changed over the incubation time with particles in either cell type. MPO-deficient PMN and normal PMN ingested STZ particles at a similar rate at early times, but thereafter phagocytosis by MPO-deficient PMN was significantly higher than that by normal PMN. The difference in degranulation between the two cell types greatly exceeded the difference in ingestion and was evident already at early phagocytosis times when no difference in phagocytosis was observed; this suggested that the higher degranulation in MPO-deficient PMN was at least in part independent of the increased ingestion. This was confirmed by experiments with the soluble stimulant N-formyl-L-norleucyl-L-leucyl-phenylalanine (FNLLP). MPO-deficient PMN and normal PMN exhibited a comparable respiratory burst when exposed to FNLLP plus cytochalasin B, but the defective cells released more azurophilic and specific granule markers than normal PMN. These results indicate that MPO-deficient PMN degranulate more than normal PMN and suggest a role for MPO in the regulation of degranulation.
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PMID:Increased degranulation of human myeloperoxidase-deficient polymorphonuclear leucocytes. 298 89

The ability of pepstatin A, a protease inhibitor produced by Streptomyces testaceus, to elicit a number of responses by the human PMN has been studied. In lysozyme and beta-glucuronidase release, pepstatin A 10(-5)M is equivalent to the synthetic oligopeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) 10(-7)M. In superoxide release, pepstatin A 10(-5)M produces 80% of that originated by FMLP 10(-7). After two minutes of incubation the superoxide release is important, there being no further increase after 10 minutes. Preincubation of the cells with cytochalasin B before stimulation with pepstatin A elicits a noticeable increase in O2- release. In chemotaxis, pepstatin A 10(-6) originates the same cell motility as FMLP 10(-9). Pepstatin A produces a cross deactivation with FMLP which adds further evidence to the hypothesis that both stimuli compete for the same receptor in the PMN.
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PMID:[Effects of pepstatin A on neutrophils; cross-deactivation with FMLP]. 298 85

Like in the polymorphonuclear leukocyte (PMN), the platelet-derived growth factor (PDGF) purified to homogeneity is capable of inducing monocyte activation responses as evaluated by generation of superoxide anion (O-.2) from membrane-associated oxidase system, release of granule enzymes, and enhanced cell adherence and cell aggregation. Superoxide anion release was maximized at 10 ng/mL PDGF and was comparable to that induced by 10(-7) mol/L formyl-methionyl-leucyl-phenylalanine. The potency of PDGF to induce this response in monocytes was of the same magnitude as that observed in PMNs. Similarly, lysozyme release and monocyte adherence were also increased in a dose-dependent manner and achieved maximal responses at 40 ng/mL concentration of PDGF. The PDGF concentration required to achieve maximal monocyte aggregation was two-fold (60 ng/mL) of that found for PMNs. In contrast to PMNs, a positive correlation (gamma = .93; P less than .01) was observed between the increases of PDGF concentration and beta-glucuronidase release. These findings indicate that PDGF can induce the full sequence of cell activation events in human monocytes similar to human PMNs.
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PMID:Platelet-derived growth factor promotes human peripheral monocyte activation. 298 67

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

A modified zymosan preparation was used to probe the interaction of particulate stimuli with human neutrophils (PMNs). After extraction with alkali and detergent, the zymosan particles retained their ability to be opsonized in serum and to stimulate PMNs. Serum-treated zymosan (STZ) induced dose-dependent superoxide (O2-) production and membrane potential depolarization in the range of 1 to 10 mg/mL of STZ. The rate and extent of secretion of lysozyme and beta-glucuronidase were also dose-dependent in the range of 1 to 10 mg/mL of STZ. Cytochemical studies using nitroblue tetrazolium, however, showed that 92% of PMNs were stimulated to produce O2- at 0.1 mg/mL of STZ. The dose response of O2- production induced by STZ is therefore due to increasing O2- production by individual PMNs and not to the stimulation of more PMNs to produce O2-. Evidence for O2- production was found only in the area of PMN-zymosan contact, suggesting a mechanism for the graded responses of PMNs treated with particulate stimuli. In order to determine the nature of the dose dependence of depolarization (a measure of PMN activation), PMNs equilibrated with the fluorescent probe 3,3'-dipentyloxacarbocyanine were analyzed by flow cytometry. The results demonstrate that STZ induces a dose-dependent depolarization of the membrane potential of individual PMNs. These results also demonstrate that increasing concentrations of STZ can induce increasing PMN responses even when all of the PMNs have been activated. These results are consistent with the hypothesis that receptor-mediated particulate stimulation of PMNs is a phenomenon that results in graded PMN responses.
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PMID:Graded responses of human neutrophils induced by serum-treated zymosan. 299 62

The degranulation reactions of human neutrophils induced by 1-oleoyl-2-acetylglycerol (OAG), phorbol 12-myristate 13-acetate (PMA), and calcium ionophore A23187 or their combinations, were studied. OAG in the absence of the Ca2+-ionophore A23187 stimulated the releases of both lysozyme and lactoferrin, constituents of the specific granules, but did not stimulate the release of beta-glucuronidase, an enzyme of the azurophil granules. Electron microscopy revealed a selective decrease in the numbers of the specific granules in this case. The combined effects of A23187 at a concentration higher than 0.1 microM and OAG were essentially additive. W-7, known to be an inhibitor of both Ca2+-activated phospholipid-dependent protein kinase (C-kinase) and calmodulin, inhibited the degranulation induced by OAG or PMA, while it inhibited the reaction induced by A23187 less markedly. The release of lysozyme reached a plateau at about 0.1 microM A23187 and increased again at higher concentrations of A23187. The observations suggest that degranulation can be induced by the activation of the C-kinase, and the degranulation by A23187 at low concentrations may be due to the activation of the C-kinase; the effects of A23187 at high concentrations, however, could not be explained only in terms of the activation of the C-kinase.
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PMID:The role of Ca2+ and Ca2+-activated phospholipid-dependent protein kinase in degranulation of human neutrophils. 300 50

Fibrin formation and turnover are intimately associated with inflammation and wound healing. To explore whether fibrin(ogen)-derived peptides exert direct effects upon cells involved in inflammation and tissue repair we examined the capacity of human fibrinopeptide B (hFpB), a thrombin-derived proteolytic cleavage product of the fibrinogen B beta-chain, to stimulate neutrophils (PMN), monocytes, and fibroblasts. hFpB caused directed cell migration of PMN and fibroblasts that was optimal at approximately 10(-8) M. This chemotactic activity was blocked by preincubating hFpB with antiserum to hFpB. hFpB was not chemotactic for monocytes. The chemotactic potency of hFpB for PMN was equivalent to that of anaphylatoxin from the fifth component of human complement (C5a), leukotriene B4 (LTB4), and formyl-methionyl-leucyl-phenylalanine (fMLP), and for fibroblasts its chemotactic activity was comparable to that of platelet-derived growth factor. hFpB did not interact with PMN receptors for C5a, LTB4, or fMLP as (a) desensitization with 10(-7) M hFpB abolished chemotaxis to hFpB but had no effect upon chemotaxis to C5a, LTB4, or fMLP and (b) induction of chemotactic responses to fMLP and LTB4 in neutrophilic leukemic cells (HL-60 cells) by incubation with dimethylsulfoxide did not extend to hFpB. Like fMLP, hFpB caused a rapid, dose-dependent increase in PMN cytoskeletal associated actin, but unlike fMLP, hFpB did not cause PMN aggregation, release of lysosomal enzymes (lysozyme and beta-glucuronidase), or the production of superoxide anion. These results suggest that hFpB may have a role in recruiting PMN and fibroblasts at sites of fibrin deposition and turnover. The capacity of hFpB to cause PMN chemotaxis without causing concurrent release of lysosomal enzymes or the production of superoxide anion is further evidence for the complexity of PMN responses to chemotactic agents.
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PMID:Effects of fibrinogen derivatives upon the inflammatory response. Studies with human fibrinopeptide B. 300 61


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