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)

Because it has recently been hypothesized that human milk is antiinflammatory, the effects of aqueous human colostrum on human polymorphonuclear leukocyte (PMN) respiratory burst activity and selected enzymatic activities was examined. Aqueous colostrum was found to spontaneously reduce ferricytochrome C in a concentration-dependent manner, prohibiting use of the standard assay to measure superoxide production. It also caused a significant concentration-dependent prolongation of the lagtime from stimulation of PMN with phorbol myristate acetate to the appearance of hydrogen peroxide. Substitution of an enzymatic peroxide-generating system for PMN did not alter the effect of colostrum. Colostrum also suppressed myeloperoxidase activity and lysozyme activity, but not beta-glucuronidase activity in PMN lysates. Inclusion of colostrum in an in vitro assay of PMN-mediated cell detachment significantly suppressed this PMN-mediated effect. These data demonstrate that aqueous human colostrum significantly interferes with PMN oxygen metabolic and enzymatic activities that are important in the mediation of acute inflammation.
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PMID:Antioxidant properties of human colostrum. 284 22

Recombinant human interferon-alpha 2 (rIFN-alpha A) was evaluated as a modulator of neutrophil functions. Neutrophils treated with rIFN-alpha A for 1 h in vitro showed reduced chemiluminescence (CL) and aggregation in response to phagocytosis. In contrast, when certain soluble stimuli [f-met-leu-phe (fMLP) or leukotriene B4] were used, rIFN-alpha A treatment conferred a doubling of CL. This was paralleled by a similar increase in superoxide anion production and a 56% increase of release of beta-glucuronidase and lysozyme. The NBT test showed that IFN treatment did not increase the number of responding neutrophils. However, there was a significant increase in the displaceable binding of fML[3H]P. Enzyme release, aggregation, and CL in response to other soluble stimuli, the ionophore A23187 and phorbol myristate acetate were unaffected by IFN treatment. Likewise, chemotaxis was not affected. Thus, phagocytosis-associated events and aggregation were hampered by rIFN-alpha A whereas secretory responses to receptor-dependent soluble stimuli were augmented. The mechanism for the latter is most likely dependent on the observed modulation of binding of fMLP to its receptor.
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PMID:Recombinant human leukocyte interferon modulates neutrophil function in vitro. 284 26

Interrelationships of immunologic and enzymatic markers of histiocytes have been studied in malignant neoplasms of histiocytic/monocytic origin and in differential diagnostically relevant, large cell non-Hodgkin's lymphomas. Cryostat sections required for demonstrating cell surface antigens by monoclonal antibodies are inadequate for studying cellular detail, enzymatic maturation by alpha-naphthyl acetate esterase (ANAE), and demonstrating the classical cytoplasmic markers of histiocytes like lysozyme, alpha-1-antitrypsin (AT), and alpha-1-antichymotrypsin (ACT). These markers have been compared in gently fixed and vacuum paraffin-embedded material. The reactivity for monoclonal anti-human monocyte 1 (Mo 1) has also been preserved by this method. Malignant histiocytosis (MH) is characterized by a heterogeneous cell population. The mature, ANAE-positive cells with macrophage morphology usually show a diffuse cytoplasmic positivity for AT and ACT. Lysozyme is moderately positive to negative in these cells, but it is more efficient than these markers in revealing smaller cells resembling monocytes by focal positivity in the cytoplasm. The expression of Factor XIIIa (F-XIIIa) is connected with the phagocytic activation of histiocytic cells. F-XIIIa positive cells usually form a minority of the neoplastic population in MH, but the large cytophagocytic marcophages are invariably positive. Reactive macrophages in large cell non-Hodgkin's lymphomas are characterized by a coexpression of ANAE, AT, ACT, lysozyme, F-XIIIa and Mo 1. Typical cases of true histiocytic lymphoma (THL) are made up of a homogeneous population showing the above mature, phagocytizing phenotype. In MH, Mo 1 and ANAE recognize different subpopulations. The reciprocal relation of these markers is an abnormal phenotypic feature. The results presented in this article prove the diagnostic value of ANAE and lysozyme in confirming the histiocytic differentiation of malignant cells. Monoclonal anti-human monocyte 1 is useful for identifying the immature component in MH. Factor XIIIa can be considered a functional marker of mature phagocytic histiocytes and an aid in the diagnosis of THL.
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PMID:Diagnostic significance of histiocyte-related markers in malignant histiocytosis and true histiocytic lymphoma. 290 5

A comparative study of large cell lymphoma (LCL) (ten B and ten T), Hodgkin's disease (15 cases), and true histiocytic lymphoma (two cases) was undertaken, using formalin-fixed paraffin-embedded tissue sections, a panel of eight antibodies, and one lectin to determine if any particular antibody or immunologic profile could reliably distinguish between these entities. The antibodies used were against Leu-M1, alpha-1-anti-chymotrypsin (alpha-ACT), alpha-anti-trypsin (alpha-AT), lysozyme, kappa, lambda, leukocyte common antigen (LCA), and S-100 protein. The lectin used was peanut agglutinin (PNA). Although Leu-M1 staining was positive in 11 of 15 cases (73%) of Hodgkin's disease, it was also positive in 4 of 10 cases (40%) of T-cell lymphoma, 2 of 10 cases (20%) of B-cell lymphoma, and 1 of 2 cases (50%) of true histiocytic lymphoma. Peanut-agglutinin staining results were similar to Leu-M1. The only staining profile that emerged was the presence of Leu-M1, PNA-, alpha-ACT, and alpha-AT staining in Reed-Sternberg (RS) cells in 11 of 15 cases of Hodgkin's disease. Leu-M1 and its staining pattern is characteristic, but not entirely specific for RS cells, and it was not positive in at least 25% of the cases of Hodgkin's disease in formalin-fixed, paraffin-embedded tissues. The limitations of this antibody and others should be recognized.
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PMID:A comparative marker study of large cell lymphoma, Hodgkin's disease, and true histiocytic lymphoma in paraffin-embedded tissue. 294 20

Activated human polymorphonuclear leukocytes (PMN) isolated from peripheral blood specifically bind 125I-laminin after stimulation with phorbol 12-myristate 13-acetate (PMA) or f-Met-Leu-Phe (FMLP) at 37 degrees C. Changes in laminin receptor expression are stimulus dose dependent at both chemotactic (10(-10) M to 10(-6) M) concentrations of FMLP, and secretory (greater than 5 ng/ml) levels of PMA. In the presence of cytochalasin B (5 micrograms/ml), 10(-7) M FMLP activation stimulates specific laminin binding, with an apparent Kd = 3.9 X 10(-9) M and 6.47 X 10(5) binding sites/cell, reaching equilibrium within 10 min at 4 degrees C. This observed activation-dependent change in laminin receptor expression is not due to interference by endogenous laminin, because no fluorescein-visualized anti-laminin antibody bound to cells without added glycoprotein, regardless of the level of activation. Levels of neutrophil lysozyme release, which show a PMA dose dependence similar to that of receptor binding activity, suggest that granule-plasma membrane fusion may be significant during increases in receptor expression. A lack of receptor stimulation by PMA from a granule-deficient patient or in granule-depleted cytoplasts from normal donors additionally supports this hypothesis. Electroblot transfer and autoradiography of subcellular fractions from unstimulated PMN reveals the presence of a 68,000 dalton laminin-binding component in the secondary/tertiary granule (beta) fraction, which may represent an intracellular laminin receptor pool.
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PMID:Human neutrophil laminin receptors: activation-dependent receptor expression. 294 78

Two mouse monoclonal antibodies, L12.2 and S5.22, were developed that are specific for human neutrophilic granulocytes and produce a twofold to threefold stimulation of n-formyl-methionine-leucyl-phenylalanine (FMLP)-induced chemotaxis. Stimulation of chemotaxis by the antibodies is specific for FMLP and is concentration dependent. L12.2 appears to be more potent in stimulating chemotaxis and is isotypically distinct from S5.22. In addition, although L12.2 reacts only with mature peripheral blood granulocytes, S5.22 reacts with leukemic cells of both myeloid and monocytic origin and with immature granulocyte precursor cells. This suggests that L12.2 interacts with an antigen that appears late in the differentiation pathway, whereas S5.22 binds to an antigen that is present throughout the myeloid lineage. By means of the under-agarose and Boyden chamber techniques, L12.2, but not S5.22, by itself was also found to be a potent granulocyte chemoattractant. Cells in a gradient of L12.2 display polarized and oriented morphology. L12.2 alone, but not S5.22, also stimulates granulocyte phagocytosis and induces superoxide anion production. Neither L12.2 nor S5.22 affected the release of myeloperoxidase or lysozyme from granulocytes either alone or in combination with FMLP, C5a, or the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA). These results suggest that L12.2 interacts with a single antigenic determinant on granulocytes that is involved in chemotaxis, phagocytosis, and superoxide anion release.
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PMID:Stimulation of human neutrophilic granulocyte chemotaxis by monoclonal antibodies. 298 Dec 60

Preparation of chitin-coated Celite as an affinity adsorbent for high-performance liquid chromatography of lysozymes and its application to separation of N-bromosuccinimide-oxidized lysozymes are described. By pH gradient elution, two diastereomers of oxindolealanine-62-lysozyme, delta 1-acetoxytryptophan-62-lysozyme (intermediate product in the reaction in acetate buffer), and native lysozyme were all separated within 40 min.
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PMID:Chitin-coated Celite as an affinity adsorbent for high-performance liquid chromatography of lysozyme. 298 84

Pretreatment of human neutrophils with pertussis toxin inhibits platelet-activating factor-mediated chemotaxis, superoxide generation, aggregation, and release of lysozyme. By contrast, superoxide generation observed in the presence of phorbol-12-myristate-13 acetate is unaffected. Our results suggest that a target protein for pertussis toxin, probably a GTP binding protein termed "Ni", is involved in the actions of platelet-activating factor on human neutrophils.
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PMID:Platelet-activating factor mediated effects on human neutrophil function are inhibited by pertussis toxin. 299 Apr 62

Lidocaine is used extensively in coronary care units, yet the effect of lidocaine infusions on neutrophil function has not been known. Lidocaine and other local anesthetics impair leukocyte antibacterial functions when added in vitro. We found that lidocaine added to human neutrophils in vitro markedly impaired the release of superoxide anion (O2-) and the granule enzymes lysozyme and myeloperoxidase after stimulation by phorbol myristate acetate or opsonized zymosan. We then measured production of O2- during stimulation of neutrophils from eight normal subjects, five coronary artery disease patients not receiving lidocaine and 13 coronary artery disease patients receiving lidocaine infusions for at least 12 hr. Release of O2- by cells from lidocaine-treated patients (14.2 +/- 3.8 nmol/2.5 X 10(6) neutrophils per 15 min) was significantly lower than from cells of the normal subjects (78.4 +/- 7.2 nmol; P less than .001) and the coronary patients not receiving lidocaine (70.6 +/- 4.0 nmol; P less than .001). Bactericidal assays at a high concentration (2 mg/ml) of lidocaine demonstrated slight reductions in 2 hr killing rates for Escherichia coli (70% with lidocaine vs. 95% control). Inhibition by lidocaine of the release of toxic oxygen metabolites from neutrophils could potentially reduce infarct size in patients with acute myocardial infarction; but as there is only a slightly reduced ability to kill bacteria, increased susceptibility to infections is unlikely although it cannot be excluded.
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PMID:Reduced neutrophil superoxide anion release after prolonged infusions of lidocaine. 299 33

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


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