Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gonococci are capable of attaching to the surface of polymorphonuclear leukocytes (PMN). In this location they resist phagocytosis and are not killed by PMN. To delineate the factors involved in the survival of these gonococci, we investigated the interaction of virulent gonococci, which adhere to cells and resist phagocytosis, and avirulent gonococci, which are phagocytized and killed by PMN. In the presence of serum, both virulent and avirulent gonococci associate equally well with PMN and stimulate increases in oxidative metabolism. In the absence of serum virulent gonococci attached to PMN and stimulated PMN oxidative metabolism to a greater extent than avirulent gonococci which did not attach to PMN (P = 0.0009). Therefore, the survival of virulent gonococci attached to the PMN surface is not a result of failure to activate oxidative and bactericidal mechanisms. Both virulent and avirulent gonococci stimulated equivalent PMN specific granule release as measured by the appearance of lactoferrin in the media. Phagocytosis of avirulent gonococci stimulated significantly greater beta-glucuronidase release (P = 0.01) and myeloperoxidase-mediated iodination of protein (P = 0.001) by PMN than attachment of virulent gonococci. In the absence of serum neither type of gonococci stimulated beta-glocuronidase release or protein iodination by PMN. Thus, virulent gonococci fail to stimulate primary granule release by PMN. To further assess the role of attachment versus ingestion on the survival of gonococci, PMN were treated with cytochalasin B to block ingestion. Cytochalasin B-treated PMN were unable to kill either virulent or avirulent gonococci despite normal degranulation stimulated by the latter. The failure of PMN to kill surface-attached gonococci appears to be a consequence of the failure of PMN to enclose the virulent gonococci within a phagosome. The phagocytic vacuole thus plays a critical role in normal PMN bactericidal activity by providing a closed space in which the proper concentration of substances may be achieved to generate microbicidal activity.
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PMID:Gonococcal interactions with polymorphonuclear neutrophils: importance of the phagosome for bactericidal activity. 10 96

Rhesus monkey (Macaca mulatta) neutrophils were shown to contain the azurophilic granule maker enzymes myeloperoxidase and beta-glucuronidase but were deficient in the specific granule markers alkaline phosphatase (AKP) and lysozyme. Isopycnic centrifugation of leukocyte homogenates on linear sucrose gradients resulted in cosedimentation of myeloperoxidase and beta-glucuronidase with an equilibrium density of 1.18. After an intravenous inoculation of monkeys with Salmonella typhimurium AKP activity became marked, whereas that of beta-glucuronidase decreased and myeloperoxidase remained unchanged. Lysozyme was undetected throughout the course of the experiment, but was present in oil-induced peritoneal macrophages and peripheral mononuclear cells. The induced AKP exhibited partial latency and had an equilibrium density of 1.15. It is unclear, however, whether the induced AKP is associated with specific granules or cytoplasmic membranes. Hence, while these data are consistent with the presence of azurophilic granules in polymorphonuclear neutrophils from infected monkeys, the presence of specific granules in polymorphonuclear neutrophils of both uninfected and infected monkeys remains moot.
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PMID:Characterization of monkey peripheral neutrophil granules during infection. 17 Feb 8

The ability of epsilon-amino caproic acid (EACA)-treated normal serum and of cystic fibrosis (CF)-affected and carrier sera to promote the release of lysosomal enzymes from sensitized human polymorphonuclear leukocytes (PMN) was assessed through the measurement of beta-glucuronidase and myeloperoxidase activity after exposure of these cells to the various test sera. This study was initiated to extend the analogies between preciliary dyskinesia factor (pre-CDF), separated from the cell-free media of cultures derived from CF homozygous and heterozygous individuals, and C3a anaphylatoxin. The extent of lysosomal degranulation of human PMN exposed to fresh untreated sera of each of five controls, seven CF homozygotes, and eight heterozygotes, as expressed by the amount of beta-glucuronidase releases, was 7.84% (+/- 0.934) for countrol sera, 14.01% (+/- 1.79) for CF-affected sera, and 10.61% (+/- 1.43) for heterozygous sera. The difference between CF homozygotes and control subjects is significatn (P less than 0.0001), as is the difference between CF-affected and carrier individuals (0.001 less than P less than 0.005) and between control subjects and carriers (0.001 less than P less than 0.005), when beta-glucuronidase. However, the differences between control subjects and CF heterozygous individuals are not significant. Treatment of these sera with 1 M EACA gave values for beta-glucuronidase and myeloperoxidase release which are slightly reduced when compared with those obtained with fresh, untreated samples. EACA apparently reduces the activity of beta-glucuronidase released from PMN. Amicon filtration studies of these serum samples demonstrated that degranulating ability and the presence of cilicary dyskinesia, as assessed by rabbit tracheal bioassay, are not always associated. Therefore, the relationship between pre-CDF and the degranulator activity in native CF-affected and carrier sera is unclear, in part because of the limitations inherent in the test systems employed.
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PMID:Demonstration of human leukocyte degranulation induced by sera from homozygotes and heterozygotes for cystic fibrosis. 17 51

The functional significance of granule enzymes in polymorphonuclear leukocytes (PMN) is not fully understood because of the multiplicity of the enzymes and the rare occurrence of deficiencies in man. In order to select appropriate laboratory animals for functional studies, a phylogenetic comparison of enzyme levels in animal and human PMN was undertaken. Neutrophils were obtained from a variety of laboratory animals and man; the activities of alkaline phosphatase, lysozyme, myeloperoxidase, and beta-glucuronidase were determined by histochemical and analytical techniques. Marked interspecies differences in enzyme activity were found; many species were deficient in alkaline phosphatase or lysozyme. Differences in pH optima and metal requirements of alkaline phosphatase were not of sufficient magnitude to explain the variations of this enzyme.
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PMID:Granule enzymes of polymorphonuclear neutrophils: A phylogenetic comparison. 17 39

The granulocytes of a patient with generalized pustular psoriasis (GPP) were found to have impaired ability to fix iodine after ingestion of yeast particles. Since hexose monophosphate shunt (HMS) activity was increased and the contents of 3 other lysosomal enzymes, beta-glucuronidase, N-acetyl-beta-glucosaminidase and lysozyme, were within normal range, the impaired iodination appeared to be due to a selective defect of myeloperoxidase (MPO) activity within the phagocytic cells. The deficient iodination was accompanied by a decreased intracellular killing of E. coli and C. albicans. Since hexose monophosphate shunt activity was enhanced and azide and cyanide inhibited the intracellular killing of E. coli only moderately, the patient's granulocytes may possess azide- and cyanide-resistant, MPO-independant microbicidal systems coupled to the oxidative metabolism. Assessment of granulocyte iodination and enzyme contents of the relatives of the patient revealed no hereditary transmission. Since GPP is characterized by the development of subcorneal pustules containing granulocytes, the MPO-deficiency may be the cause of or enhance the development of the disease.
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PMID:Function of granulocytes with deficient myeloperoxidase-mediated iodination in a patient with generalized pustular psoriasis. 17 20

Human monocytes, lymphocytes, granulocytes, red cells, and platelets were completely separated from each other by zonal centrifugation on linear sucrose density gradient. The monocytes contained only one tenth the amount of myeloperoxidase, one half the amount of lysozyme, one half the amount of acid ,hosphatase, and one half the amount of beta-glucuronidase found in granulocytes; the monocytes contained no alkaline phosphatase or neutral protease. The lymphocyte fraction contained only acid phosphatase and beta-glucuronidase in amounts one half as much as in the monocytes. Fluctuations in enzyme levels of monocytes and granulocytes were noted following infection. In vitro, the isolated monocytes transformed into macrophages. The results suggest that lymphocytes, monocytes, and granulocytes may be linked biochemically in a differentiation sequence through sets of commonly shared enzymes as well as by groups of enzymes specific for each divergent cell line.
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PMID:Isolation of enzymatically homogeneous populations of human lymphocytes, monocytes, and granulocytes by zonal centrifugation. 20 68

Fourteen continuous tissue culture cell lines derived from mouse, rat, or human granulocyte-macrophage cancers were studied for expression of spontaneous and inducible markers of differentiated cells. Five cell lines (two mouse, two rat, and one human) synthesized myeloperoxidase spontaneously, and a fifth mouse line showed biochemically inducible enzyme. Twelve lines (6 mouse, 3 rat, and 3 human) produced lysozyme (muramidase), and all had detectable beta-glucuronidase. Superoxide generation was detected in one mouse, and three human cell lines following stimulation with phorbol myristate acetate. Maturation to differentiated polymorphonuclear leukocyte or macrophage morphology was induced in 3 cell lines (2 mouse and 1 human) following culture in diffusion chambers in total-body-irradiated rats. In vitro morphological differentiation was inducible in one (mouse) cell line exposed to casein, thioglycolate, or plasma from irradiated rats or mice. These findings indicate that mammalian cell lines derived from granulocyte-macrophage cancers stably express several combinations of differentiation markers. The patterns of expression of these markers did not always correlate with the morphological stage of differentiation.
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PMID:Constitutive and inducible granulocyte-macrophage functions in mouse, rat, and human myeloid leukemia-derived continuous tissue culture lines. 21 Sep 35

Enzymatically homogeneous populations of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from 5 untreated patients with chronic lymphocytic leukemia (CLL) and 2 patients with CLL in full remission. The cells were then quantitatively analyzed for six leukocytic enzymes and compared with cells from normal subjects. CLL monocytes were deficient in beta-glucuronidase (0.06 units; normal, 0.16), myeloperoxidase (0.07 mg; normal, 0.5 mg), and lysozyme (0.7 mg; normal, 3.3 mg). In 2 cases, CLL neutrophils were severely deficient in lysozyme (1 to 2 mg; normal, 7 mg) and myeloperoxidase (2 to 3 mg; normal, 7 mg). Neutrophil alkaline phosphatase and neutral protease were unaffected. CLL lymphocytes shared with the monocytes the deficiency of beta-glucuronidase (0.03 units; normal, 0.09 units). The 2 CLL patients in full remission carried normal enzyme levels in leukocytes of all three cell lines. The CLL lymphocytes of untreated patients were unresponsive to mitogens but became responsive in remission. The CLL monocytes from both untreated and treated patients transformed into macrophages. The pattern of shared enzyme deficiency among lymphocytes, monocytes, and neutrophils of CLL patients and its normalization in all three cell types under remission suggest that the differentiation of the three leukocytic cell lines may be an enzymatically interlinked process and that the deficiency of these enzymes in leukemia may reflect an interrelated aberrant differentiation of the leukemic cells.
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PMID:Monocyte and granulocyte defect in chronic lymphocytic leukemia. 21 99

Enzymaticaly homogeneous fractions of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from peripheral blood of a patient with hairy cell leukemia, or leukemic reticuloendotheliosis, LRE,(with leukopenia, neutropenia, lymphocytosis, and massive splenomegaly). To detect enzymatic deficiencies, the cells were analyzed quantitatively for six leukocytic enzymes on three occasions: 1) before splenectomy, 2) 5 days after splenectomy, and 3) 6 weeks after splenectomy. Before splenectomy, the patient's cells showed moderate deficiency of beta-glucuronidase in lymphocytes and monocytes; server to modorate deficiency of lysozyme and myeloperoxidase in monocytes and granulocytes; and complete absence of neutral protease and alkaline phosphates in neutrophils. Full restoration of neutral protease and a three-fold rise in alkaline phosphatase activities occurred in the patient's neutrophils 5 days after splenectomy. Lysozyme and myeloperoxidase returned to normal in both monocytes and neutrophils of the patient. Six weeks following splenectomy, the alkaline phosphatase activity again disappeared from patient's neutrophils, although neutral protease remained normal. The patient's lymphocytes were unresponsive to PHA and PW mitogen before splenectomy but became responsive 6 weeks postoperatively. Monocytic transfomation into macrophges was supressed before and after splenectomy. The findings indicate that developmenally, in lymphocytic leukemia, a biochemical defect involves the patient's monocytes and neutrophils much more severely than it affects the leukemic lymphocytes. Functionally, the results partly explain the susceptibility of LRE patients to microbial infections.
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PMID:Absence of neutral protease and alkaline phosphatase in neutrophils of a case of hairy cell leukemia. 43 13

In 24 men aged 32 to 58 years with precancerous states of the larynx, i.e., leukoplakia, papillomas and pachydermia the peripheral blood lymphocytes were cytochemically stained for N-acetyl-beta-glucosaminidase, beta-glucuronidase, acid phosphatase and glycogen; and the neutrophils were stained for alkaline phosphatase, myeloperoxidase and lipids. The results were expressed in terms of the absolute counts of reaction-positive cells and of the activity index score. The serum immunoglobulins IgG, IgA and IgM were also determined by Mancini's method. The results obtained were compared with those in 20 healthy men aged 20 to 30 years. The patients exhibited elevated numbers of N-acetyl-beta-glucosaminidase and beta-glucuronidase-positive lymphocytes. A characteristic feature was an increase in the absolute counts of lymphocytes with diffuse and granular-diffuse types of cytochemical reaction for all enzymes studied. The number of cells with the granular type of enzymatic reaction (intact enzyme-positive lysosomes) was significantly diminished. These cytochemical alterations were accompanied by a significant increase in the serum IgA level. These results are discussed with reference to the lymphoid system response to tissues of precancerous lesions of the larynx. So far as the neutrophils are concerned the patients exhibited significant intracellular deficiency of beta-glucuronidase and decrease in the lipid content as well as an elevated alkaline phosphatase activity. The possible significance of the beta-glucuronidase deficiency in neutrophils for the diminished cytotoxic response of these cells against the tumor and precancerous lesion cells is discussed.
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PMID:Lymphocytes, neutrophils and serum immunoglobulins in patients with precancerous states of the larynx. 44 57


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