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)

In conditions with increased neutrophil production, the serum total vitamin B(12)-binding capacity (TBBC) is considered to correlate with the blood pool size of neutrophil granulocytes. The serum lysozyme, on the other hand, is a measure of neutrophil (and monocyte) turnover. The mean serum TBBC was significantly raised in patients with ulcerative colitis (range 1.23-5.51 ng/ml; mean 2.64 ng/ml) and patients with Crohn's disease (range 1.58-9.29 ng/ml; mean 2.93 ng/ml). The elevated values were shown to be due to rises in the granulocyte-secreted binding proteins, transcobalamins I and III. The TBBC was shown to rise with increasing activity of disease and to correlate roughly with the blood neutrophil granulocyte count. Patients with inflammatory bowel disease also had a significantly raised mean level of serum lysozyme (range 3.1 to 10.4 mug/ml; mean 6.8 mug/ml), but there was no correlation in individual patients between serum lysozyme and total B(12)-binding capacity. These results are taken to indicate an enlarged granulocyte pool and increased granulocyte turnover in inflammatory bowel disease.
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PMID:Indices of granulocyte activity in inflammatory bowel disease. 444 10

In 10 psychiatric patients marrow granulocyte reserve, marginal granulocyte pool, granulocyte mobilization into skin chamber, serum lysozyme activity was estimated before and ten days after the lithium treatment. In all patients the peripheral neutrophil count rose significantly. The marrow granulocyte reserve did not change markedly. Moreover, the marginal granulocyte pool as expressed in percentages diminished. Serum lysozyme activity, total leukocyte mobilization, and blood granulocyte clearance remained unchanged. However, the serum lysozyme activity index fell significantly. The in vitro addition of lithium to the suspension of granulocytes obtained from healthy persons reduce the granulocyte adherence especially in concentrations similar to those induced in treated patients. Our findings suggest that lithium in vivo may diminish the granulocyte adherence resulting in the prolonged intravascular half-life time of the cells. Thus, the cell accumulation in the vascular bed seems to be the main reason for lithium induced granulocytosis rather than the intensification of marrow granulocyte system proliferation.
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PMID:Influence of lithium on neutrophil granulocyte distribution and turnover. 617 May 47

A number of cytochemical parameters of the hemocytes of larval Galleria mellonella, an insect frequently used as a model by comparative cellular immunologists, are described. Cytochemical methods were used to quantify hemocyte granule-associated components, the results are compared to those obtained for leukocytes from higher animals. Granulocytes contained a population of nonlysosomal granules rich in mucopolysaccharide not seen in plasmatocytes. The numbers and dimensions of these granules showed a positive correlation to cell size, probably reflecting a developmental sequence in granulocyte maturation. Both granulocytes and plasmatocytes had other granules containing the typical lysosomal enzymes, acid phosphatase, beta-glucuronidase, esterase, and lysozyme. The nonlysosomal enzyme alkaline phosphatase was not found in Galleria hemocytes; it is also absent from vertebrate monocytes, macrophages, and immature polymorphonuclear leukocytes. Insect hemocytes appear to lack certain components of antibacterial systems typical of mammalian blood cells, such as H2O2-generating systems, cationic proteins, and myeloperoxidase. The bactericidal mechanisms of hemocytes probably involve lysozyme, as well as other biologically active cellular and humoral factors unique to insects.
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PMID:Observations on the cytochemistry of the hemocytes of an insect, Galleria mellonella. 618 80

Immunological, hematological, and biochemical studies were done at the time of referral in 135 homosexual subjects, 28 of whom were symptom free (SF), 74 of whom had the acquired immune deficiency syndrome (AIDS)-related symptom complex (ARC), and 33 of whom had AIDS with Kaposi's sarcoma, opportunistic infection, or both. Of 38 laboratory parameters, 11 were significantly different than controls in the SF patients, 19 in the ARC patients, and 20 in the AIDS patients. In SF patients, delayed hypersensitivity was significantly suppressed for 6 of 12 recall antigens. In addition, the percentage of circulating lymphocytes, the percentage of T3+ cells, the percentage and absolute number of T4+ cells, the T4/T8 ratio, the blastogenic responses to phytohemagglutinin, pokeweed mitogen, and concanavalin A were depressed significantly in this group. In contrast, the percentage and absolute granulocyte count, the serum lysozyme, and the serum thymosin alpha 1 were significantly elevated in these patients. In patients with more advanced disease (ARC and AIDS), immunological and hematological parameters tended to worsen. Thus, in the AIDS patients the white blood cell count, percentage, and absolute T11+ cells, absolute T3+ cells, percentage of T4+ cells and absolute level of B-cells, as well as the monocyte adherence and delayed hypersensitivity responses to 12 of 12 recall antigens were depressed. Serum levels of thymosin alpha 1 were equally elevated in all three groups. Serum interferon was found in 15 of 18 opportunistic infection patients with or without Kaposi's sarcoma, in 3 of 9 Kaposi's sarcoma patients without opportunistic infection, but in none of the ARC or SF patients. This study has demonstrated that SF sexually active homosexuals have a characteristic pattern of immune deficiency and that immunodeficiency worsens as one compares SF to ARC to AIDS patients. The study has provided a data base for the development of prognostic criteria and for characterization and evaluation of immunorestorative and immunomodulatory therapy.
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PMID:Immunological characterizations of patients with acquired immune deficiency syndrome, acquired immune deficiency syndrome-related symptom complex, and a related life-style. 620 6

Human polymorphonuclear leukocytes (PMN) exposed to particulate and soluble stimuli secrete lysosomal enzymes. These stimuli cause prompt (less than 10 sec) changes in membrane potential followed 30--45 sec later by superoxide anion (O-2.) production. We describe a new technique utilizing flow dialysis apparatus which monitors the first stages of lysosomal enzyme release with a resolution of approximately 6 sec. Secretion of beta-glucuronidase from cytochalasin B-treated PMN could be detected 19+/-5 sec after exposure to the chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP). The "lag" times for release of this enzyme were different for other stimuli: 35+/-8 sec (BSA/anti-BSA immune complex); 48+/-8 sec (serum-treated zymosan, "STZ"); 60+/-25 sec (calcium ionophore A23187). The lag times for lysozyme release were less dependent upon the stimulus presented (28+/-16 sec for FMLP, 28+/-8 sec fo BSA/anti-BSA, 32+/-10 sec for STZ, and 38+/-8 seconds for Con A); only A23187 had a long lag period: 74+/-27 sec. Lag periods for the onset of O-2. production (measured by the same mathematical criteria) were comparable to those for beta-glucuronidase release: 21+/-4 sec for FMLP, 43+/-14 sec for BSA/anti-BSA, 62+/-7 sec for Con A, and 50+/-13 sec for A23187. Changes in FMLP dose up to 100-fold affected the magnitudes of O-2. generation and beta-glucuronidase release, but did not alter the time required for the onset of these processes. A variety of agents, such as corticosteroids, colchicine, 2-deoxyglucose, and N-ethyl maleimide, also affected the magnitudes of the responses, but not the lag periods when FMLP was used as the stimulus. When BSA/anti-BSA immune complex was used as the stimulus, 2-deoxyglucose and N-ethyl maleimide increased the lag period for superoxide anion generation, but not for lysosomal enzyme release. This new flow dialysis technique has permitted us to demonstrate the O-2. production and lysosomal enzyme secretion are concurrent but dissociable processes which are subsequent to earlier responses of the granulocyte-to-ligand-receptor interactions as reflected by changes in membrane potential.
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PMID:Initial kinetics of lysosomal enzyme secretion and superoxide anion generation by human polymorphonuclear leukocytes. 624 64

The stimulation of granulocyte O2- production by concanavalin-A can be reversed with alpha-methylmannoside. Such cells can be reactivated to generate O2- by adding phorbol myristate acetate or N-formyl-methionyl-leucyl-phenylalanine. Opsonized zymosan, however, is not an effective stimulant to these cells. alpha-Methylmannoside prevents, but does not reverse, depolarization of granulocytes by concanavalin-A. Previously activated cells have a shorter lag time for reactivation by phorbol myristate acetate. Incubation in 2-deoxyglucose of cells previously treated with concanavalin-A and alpha-methylmannoside prevents reactivation. EGTA prevents concanavalin-A-stimulated O2- production only when added prior to the stimulant. EGTA has only a slight effect on reactivation. alpha-Methylmannoside prevents concanavalin-A-stimulated release of lysozyme only when added prior to the stimulant. Prior treatment of cells with concanavalin-A and alpha-methylmannoside inhibits subsequent ingestion of complement-coated particles. We conclude that although the O2--generating system can be reversibly activated with concanavalin-A followed by alpha-methylmannoside, these cells are different from untreated cells. Cells treated in such a way do not respond to all stimuli, remain depolarized, have shortened lag times, no longer require calcium for activation, continue to degranulate, and do not ingest well. Thus, although some changes that accompany the interaction of stimuli with granulocytes are reversible, some are not, and the previously activated cell does not return to a true resting state.
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PMID:Is activation of the granulocyte by concanavalin-A a reversible process? 631 85

When exposed to zymosan or latex particles or heat-inactivated staphylococci, freshly prepared human blood monocytes and granulocytes rapidly released a large fraction of their lysozyme content. Within 24 hours the total lysozyme activity in the monocyte suspensions tripled, while it doubled in the granulocyte suspensions, indicating synthesis of the enzyme following release. The monocytes in particular seemed to release and synthesize lysozyme without any other stimulus than contact with lymphocytes and the tube walls. Potassium caseinate in solution did not influence the lysozyme release. Myeloperoxidase and beta-glucuronidase, which in the granulocytes are kept in lysosomal fractions separate from most of the lysozyme, were neither released nor synthesized to a significant degree. Moreover, the minute amount of lactate dehydrogenase released indicated that the lysozyme release was not the result of cell lysis. Accordingly, the monocytes, which are not already stimulated by adherence to nonphagocytosable surfaces, are capable of selective enzyme release similar to that of the granulocytes.
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PMID:In vitro release of lysozyme from monocytes and granulocytes. 632 67

Surface marker analysis with rosette tests and a large panel of xenoantisera and monoclonal antibodies was done on the malignant cells of 55 patients with acute myeloid leukemia (AML). The diagnosis was made on morphological and cytochemical grounds, and the leukemias were classified according to the quantified FAB criteria. The marker tests included the E- and EA-rosette test, immunofluorescence with rabbit-polyclonal antisera against human Ig, kappa, and lambda light chains, thymocytes, granulocytes, erythrocytes, platelets, lysozyme, (leukemic) myeloblasts, the common ALL antigen, SB cell-line cells (anti-Ia), and a mouse anti-Ia serum. The monoclonal mouse antibodies applied were anti-T-cell antibody (3A1), two anti-granulocyte-monocyte antibodies (OKM1 and B2.12), four antigranulocyte antibodies (MI/N1, UJ 308, B4.3, and B13.9), an antiplatelet antibody (C17.28), anti-HLA heavy chains (w6/32.HLK), anti-Ia antigen (OKI1), and OKT10. AML cells from many patients lacked the expression of myeloid markers, and we found that a correlation existed between the relative maturity of the leukemia subtype and the extent of positivity for these markers. Surface marker analysis discriminated poorly between the "myeloid" and "monocytoid" subtypes; OKT10 and the "T-cell marker" 3A1 were often expressed on AML cells. In two cases of AML, there was an unexpected expression of platelet antigens with the monoclonal antiplatelet antibody. One of them, classified as M1, was ultrastructurally a megakaryoblastic proliferation with a positive reaction for platelet peroxidase. Only with the help of computerized analysis, was it possible to prove a clear correlation between the surface marker profile and the FAB classification.
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PMID:A comparison of surface marker analysis and FAB classification in acute myeloid leukemia. 657 76

Human promyelocytic leukemia cells (HL-60) were induced to differentiate into macrophage-like cells in a dose (3 X 10(-10) to 10(-7) M) and time (1 to 6 days)-dependent manner by 1,25-dihydroxyvitamin D3 and the tumor promoter, phorbol-12-myristate-13-acetate. Differentiation was determined by an increase in the percentage of morphologically mature cells, in lysozyme and nonspecific esterase activities, and in reactivity with the murine OKM1 monoclonal antibody. Two HL-60 cell variants, designated as R-80 and B-II, were also examined. R-80 cells, which are resistant to induction of cell differentiation by phorbol-12-myristate-13-acetate, also exhibited resistance, although to a lesser degree, to induction of cell differentiation by 1,25-dihydroxyvitamin D3. The resistance to the action of the two compounds is presumably not due to similar binding sites for the two inducers, since 1,25-dihydroxyvitamin D3 was unable to compete for the phorbol diester binding sites as measured by [3H]phorbol-12,13-dibutyrate binding. B-II cells were resistant to induction of cell differentiation by 1,25-dihydroxyvitamin D3, phorbol-12-myristate-13-acetate, retinoic acid, and dimethyl sulfoxide. Two-dimensional electrophoretic analysis of HL-60 cell protein patterns indicated that treatment of the HL-60 cells with 1,25-dihydroxyvitamin D3, phorbol-12-myristate-13-acetate, retinoic acid, and dimethyl sulfoxide caused the cells to express various monocyte-macrophage and granulocyte marker proteins. None of the inducers caused a protein pattern identical to that of peripheral monocytes or granulocytes in the HL-60 cells, but the protein pattern of the HL-60 cells treated with 1,25-dihydroxyvitamin D3 was the closest to that of peripheral blood monocytes. These results indicate that 1,25-dihydroxyvitamin D3 induces in the HL-60 cells a phenotype that resembles, but is not identical to, that of peripheral monocytes-macrophages.
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PMID:Control of macrophage cell differentiation in human promyelocytic HL-60 leukemia cells by 1,25-dihydroxyvitamin D3 and phorbol-12-myristate-13-acetate. 657 56

A transplantable myelomonocytic leukemia was established from a leukemia of a WKA/Hok rat which had been inoculated with Rauscher virus at birth. The tumor grew in ascites form in normal syngeneic rats and, after the middle stage of i.p. transplantation, leukemia cells consisting of a mixed population of monocytic and granulocytic cells were observed in the peripheral blood. A complement-dependent cytotoxicity test failed to demonstrate Rauscher virus-related antigen on the tumor cell surface. Membrane marker analysis revealed that most of the tumor cells possessed receptors for both complement and neuraminidase-treated sheep RBC. More than 90% of ascitic tumor cells displayed phagocytic activity and a positive nonspecific esterase reaction. Serum from rats bearing this tumor contained high levels of muramidase. Ultrastructurally, the tumor cells resembled both immature and mature cells of the monocyte-macrophage series. On serial transplantation into the peritoneal cavity, the tumor displayed consistent differentiation from undifferentiated blast cells to monocytes and cells indistinguishable from granulocytes. The karyotype analysis revealed that the modal number of chromosomes of the tumor cells was 81, and no structural abnormalities of chromosomes were observed after quinacrine mustard staining. This transplantable leukemia will provide a useful experimental model for the study of granulocyte-monocyte differentiation and for human myelomonocytic leukemia.
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PMID:Establishment and characterization of a transplantable rat myelomonocytic leukemia. 657 49


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