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 experiment was performed on 3 groups of White Leghorn chickens kept under L : D = 6 : 18, 12 : 12 and 18 : 6 photoperiods, respectively. One half of each group was immunized twice with SRBC. Non-immunized birds served as controls. It was found that diurnal variations in lymphocyte and granulocyte number, serum lysozyme activity, agglutinins anti-sheep red blood cells (SRBC) and anti-rabbit red blood cells (RRBC) titer and plasma corticosterone concentration depended on light conditions. Immunization affected diurnal changes in different degree, depending also on the photoperiod applied. Various interrelationships between the diurnal changes in plasma corticosterone level and those in immune parameters were found. A distinct negative correlation between plasma corticosterone concentration and lymphocyte number was seen in L : D = 12 : 12 in the non-immunized group only.
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PMID:Diurnal changes in certain immunity indices and plasma corticosterone concentration in white Leghorn chickens. 668 41

In this study the antigenic profile of Hodgkin (H) and Sternberg-Reed (SR) cells from cases of Hodgkin's disease was analysed using a large panel of monoclonal and polyclonal antibodies reactive with cells of lymphoid and haemotopoietic origin. The aim of this investigation was, firstly, to throw light on the origin of H and SR cells and, secondly, to determine whether there is any evidence to support recent suggestions that H and SR cells differ antigenically between different histological categories of Hodgkin's disease. Frozen sections (from 24 cases) and paraffin sections (83 cases) were stained by immunoenzymatic methods and the results compared with those obtained from staining a wide variety of reactive and neoplastic tissue samples (including examples of tuberculosis, sarcoidosis, malignant histiocytosis, histiocytosis X, osteomyelosclerosis and non-Hodgkin's lymphoma). The results revealed that H and SR cells of all types of Hodgkin's disease consistently lack markers found on null cells, B cells, T cells, cells of monocyte/macrophage series, interdigitating reticulum cells, dendritic reticulum cells and erythropoietic and thrombopoietic cells. However, H and SR cells constantly expressed an antigen detectable with the recently produced monoclonal antibody Ki-I. The vast majority of typical and lacunar type H and SR cells contained the granulocyte-related antigens detected by monoclonal antibodies TU5, TU6, TU9 and 3C4, whereas other more or less specific granulopoietic cell markers (such as peroxidase, chloroacetate esterade, lysozyme, cationic leukocyte antigen and OKMI) were consistently absent. H and SR cells in cases of nodular paragranuloma (nodular type of Hodgkin's disease with lymphocyte predominance) were not monotypic in light chain type (as has been previously reported), but rather contained chi and lambda chains within the same cells, as do typical and lacunar type H and SR cells. Immunostaining of normal and hyperplastic lymphoid tissue with the Ki-I antibody led to the detection of a new, as yet unidentified, small-cell population of unknown origin and function, which is present between, around, and within cortical follicles. It is concluded from these findings that H and SR cells constitute a unique cell type that differs in many properties from all other known cell types. Furthermore, H and SR cells of the various histological types of Hodgkin's disease are more closely related than previously believed. It is suggested that the hitherto unknown cell population detected with the monoclonal antibody Ki-I in normal lymphoid tissue is the normal equivalent of H and SR cells.
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PMID:Identification of Hodgkin and Sternberg-reed cells as a unique cell type derived from a newly-detected small-cell population. 675 30

Captopril, competitive inhibitor of angiotensin converting enzyme, is clinically employed for its antihypertensive activity and drug-dependent granulocytopenia or agranulocytosis have been seldom observed during treatment. In previous unpublished studies an activating effect of the drug on the complement alternate pathway has been demonstrated. In this paper we demonstrate that captopril-treated serum is able to "in vitro" induce granulocyte activation and aggregation. Granulocyte aggregation was shown by the turbidimetric method and cellular activation was confirmed by the release of the granule associated enzyme lysozyme and beta-glucuronidase. On this basis complement-mediated leukoaggregation and leukosequestration in vivo could be proposed as the effector mechanism of peripheral leukopenia.
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PMID:Captopril-induced granulocyte aggregation. A possible complement mediated mechanism of peripheral leukopenia. 676 21

Human promyelocytic leukemia cells (HL-60) were induced to differentiate into macrophage-like cells in a dose-dependent manner by the tumor promoters phorbol-12-myristate-13-acetate and teleocidin, a non-phorbol ester promoter. An HL-60 cell variant, designated as R-59, which is resistant to differentiation induction by phorbol-12-myristate-13-acetate was also resistant to differentiation induction by teleocidin. Differentiation was determined by increases in the percent of morphologically mature cells and in lysozyme and nonspecific esterase activities. Both compounds inhibited the growth of HL-60 cells by blocking them from entering the synthesis phase of the cell cycle with an accumulation of cells after 48 h in G1 phase. No such effects were observed in the R-59 cells. They were, however, as susceptible as the parent HL-60 cells, to inducers which are not considered to be tumor promoters such as dimethylsulfoxide and retinoic acid. However, these inducers cause the HL-60 and R-59 cells to differentiate into granulocyte-like cells. These results indicate that teleocidin produces in both the HL-60 and R-59 cells effects which are similar to those cause by phorbol-12-myristate-13-acetate. The possibility that agents producing such effects in these two cell types may represent potential tumor promoters is discussed.
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PMID:Induction of differentiation of human promyelocytic leukemia (HL-60) cells by teleocidin and phorbol-12-myristate-13-acetate. 680 9

To determine the effect of transfusing granulocyte concentrates through microaggregate blood filters, granulocytes prepared with a cell processor were passed through screen and depth microaggregate filters. Pre- and postfiltration evaluations were made of total granulocyte count, levels of muramidase, granulocyte viability, motility, phagocytosis, bactericidal activity, and hydrogen peroxide-forming capacity. Compared to prefiltration levels, a significant (p less than 0.05) decrease in postfiltration granulocyte counts was seen for all the depth filters studied but not for the standard 170 microns (control) or the 40 microns screen filter. For the various tests of granulocyte function evaluated prefiltration, no significant postfiltration differences (p greater than 0.05) were seen for any of the filters studied. Screen microaggregate filters retained only 1 to 3 percent of granulocytes contained in the concentrates, and thus appear satisfactory for use in clinical transfusions. The large percentage of neutrophils retained by the depth filters (20-62%), however, precludes their use for transfusion of granulocyte concentrates.
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PMID:Effect of microaggregate blood filtration on granulocyte concentrates in vitro. 682 54

The effect of hematopoietic stem cell age on leukemogenesis in vitro was tested in nonrecharged, corticosterold-supplemented NIH Swiss [N:NIH(S)] mouse long-term bone marrow cultures infected with Friend murine leukemia virus of anemia-inducing strain (F-MuLV-A) or spleen focus-forming virus (SFFV) [Rauscher murine leukemia virus (R-MuLV)], a pseudotype virus derived by rescue of the SFFV genome from SFFV-Balb/3T3 clone A31 nonproducer cells with clonal helper R-MuLV. Cultures at 33 degrees C derived from 10-day-old or adult mouse marrow generated colony-forming unit culture granulocytic macrophage (CFUc) progenitor cells for over 20 weeks and colony-forming unit spleen cells for 14 weeks and generated permanent granulocytic leukemia cell lines after infection with F-MuLV-A at week 1, 2, or 4 but not at week 8. Leukemia lines were of granulocyte phenotype whether induced by F-MuLV-A or SFFV (R-MuLV) and synthesized myeloperoxidase and lysozyme but were restricted in ability to generate superoxide in response to phorbol myristate acetate stimulation. Cultures (31 degrees C) infected with temperature-sensitive (ts) helper virus mutant pseudotypes of SFFV as well as SFFV (R-MuLV) generated granulocytic leukemia lines, whereas only SFFV (R-MuLV) pseudotype virus-infected cultures became leukemic at 37 degrees C. R-MuLV wild type or ts mutant helper virus infection alone increased cell proliferation and numbers of CFUc but did not generate leukemia. These data indicated that gene(s) specific to F-MuLV-A or a virus rescued from SFFV-Balb/3T3 clone A31 nonproducer cells are required for transformation in vitro of a hematopoietic stem cell present in early but absent in late bone marrow cultures.
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PMID:Virus and cell requirements for Friend virus granulocytic leukemogenesis in long-term bone marrow cultures of NIH swiss [N:NIH(S)] mice. 692 98

Mouse myeloid leukemia cells (M1) could be induced to differentiate into mature macrophages and granulocytes with dexamethasone or proteinaceous inducer. Retinoic acid inhibited functional and morphological differentiation of M1 cells, but the pyridyl analog of retinoic acid had no effect. M1 cells could be induced to produce a factor(s) inhibiting their own differentiation to macrophage- and granulocyte-like cells by retinoic acid but not by its pyridyl analog. This factor(s) inhibited induction by inducers of phagocytic activity, locomotive activity, lysozyme activity, and morphological changes in M1 cells. The production of the inhibitory factor(s) by M1 cells incubated with retinoic acid was inhibited by a low concentrations (5--10 ng/ml) of actinomycin D. The inhibitory factor seemed to be a protein(s), since it was susceptible to heat treatment and proteases. The effect of retinoic acid in inducing production of the inhibitory factor(s) by M1 cells seemed to be reversible, since it was low on washing the cells with fresh medium. Therefore, induction of this inhibitory factor may be involved in the mechanism of inhibition of functional and morphological differentiation of M1 cells by retinoic acid.
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PMID:Production of differentiation-inhibiting factor in cultured mouse myeloid leukemia cells treated with retinoic acid. 693 4

Neutrophil granulocyte chemotaxis and intraneutrophilic and plasma levels of lysozyme as well as the number of T and B lymphocytes and lymphocyte transformation in vitro on stimulation with mitogens and microbial antigens were studied in four groups of patients with diabetes mellitus (DM). Twelve patients with insulin-dependent diabetes mellitus (IDDM) and ketoacidosis and 4 patients with non-insulin-dependent diabetes mellitus were studied at the time of diagnosis and before and after start of treatment. Ten patients with IDDM of less than 10 years' duration which had been difficult to regulate well and 10 patients with IDDM well regulated for more than 20 years were studied at their regular outpatient visits. Apart from a slight increase in plasma lysozyme in group 1 from the first to the second examination, we found no differences between diabetics and healthy control persons. It is concluded that if patients with DM are more susceptible to infections, it is probably caused by elements of neutrophil or lymphocyte function not examined in this study or by factors unrelated to immunity.
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PMID:Neutrophil and lymphocyte function in patients with diabetes mellitus. 698 Dec 86

The behaviour of peripheral blood granulocyte pools, nitroblue tetrazolium reduction by granulocytes, migration of granulocytes out of skin windows, serum muramidase activity and bone marrow reserve of granulocytes during uncomplicated bronchopneumonia were studied. The time course of changes in these parameters during infection was established, and suggests maximal changes on day 2 of infection with gradual regression until 30 days after the disease onset, when they disappear.
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PMID:Reaction of the human granulocyte system in successfully treated bacterial bronchopneumonia. 703 62

The reaction of FMLP with granulocytes causes aggregation and degranulation and enhances adherence to endothelium. To evaluate whether prevention of granule extrusion could impair these granulocyte activities, granulocytes were treated with either dexamethasone or hydrocortisone prior to treatment with FMLP. Dexamethasone was added to suspensions of cytochalasin B-treated granulocytes; it markedly impaired the aggregation response of the granulocytes of FMLP. When cytochalasin-B was not used, granulocyte aggregation in response to FMLP or PMA was inhibited by dexamethasone. Although dexamethasone prevented aggregation of cells following stimulation with FMLP or PMA, it failed to prevent the aggregation of granulocytes induced by rabbit lactoferrin. Adherence of granulocytes to human endothelial monolayers was enhanced by FMLP; dexamethasone inhibited the enhancement. However, with the addition of human lactoferrin to the granulocytes exposed to dexamethasone, the cells were able to adhere as well to endothelium as the cells exposed to FMLP but free of dexamethasone. When cytochalasin-B-treated granulocytes were incubated with dexamethasone or hydrocortisone prior to the addition of FMLP, the subsequent release of lactoferrin was substantially blocked, whereas the release of the primary granule products, lysozyme and beta-glucuronidase, was attenuated but not completely blocked. Thus, corticosteroids might block chemotactic-factor-induced granulocyte aggregation by selectively preventing release of specific granule products that contribute to and sustain aggregation.
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PMID:Mechanism of dexamethasone inhibition of chemotactic factor induced granulocyte aggregation. 705 39


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