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:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inhibitory potency of the antiallergic compounds picumast (PIC; Boehringer Mannheim) and ketotifen (K; Sandoz) on the release of 3 preformed and 3 newly generated inflammatory mediators was estimated as an indicator for their antiallergic activity. Peripheral human leukocytes (HL) or rat alveolar macrophages (RAM) were stimulated by opsonized zymosan (C3-Z) and/or anti-IgE antibody, following preincubation times with PIC and K. SRS-A was measured with the help of a guinea pig ileum bioassay, PGE2 and TxB2 by RIA (NEN), histamine (H) by an automated fluorimetric procedure, tryptic proteinase (P) by a colorimetric test employing Tos-Gly-Pro-Arg-pNA (Chromozym TH; Boehringer Mannheim) as chromogenic substrate and beta-glucuronidase (beta-G) by a colorimetric test (Sigma). PIC (IC30: 2 X 10(-5) mol/l) was 100 times more potent than K as inhibitor of the anti-IgE-induced release of H and P and also 5 times more potent as inhibitor of SRS-A-formation/release in/from HL. In contrast, on RAM, K (IC30: 7 X 10(-6) mol/l) had a 3 times greater potency as inhibitor of the C3-Z-induced SRS-A formation and suppressed PGE2 release (4 X 10(-5)-2 X 10(-4) mol/l), whereas PIC (2 X 10(-5) mol/l) potentiated PGE2 release remarkably. TxB2 release from RAM was inhibited nearly equipotently by PIC and K. beta-G release was strongly potentiated by K (greater than or equal to 8 X 10(-6) mol/l), but weakly inhibited by PIC (2 X 10(-5) mol/l). PIC (greater than or equal to 4 X 10(-5) mol/l) also increased the beta-G release and in the same manner the anti-IgE- or C3-Z-induced release of other 'preformed' mediators like H and P from HL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition profiles of picumast and ketotifen on the in vitro release of prostanoids, slow-reacting substance of anaphylaxis, histamine and enzyme from human leukocytes and rat alveolar macrophages. 243 54

The demonstration of a specific receptor for IgE on non-mast cell or basophil leucocytes, such as mononuclear phagocytes, eosinophils and platelets, suggests that these cells may participate directly in immunological disorders of allergy. In this study, inhibition by nedocromil sodium of IgE-dependent activation of human alveolar macrophages, blood monocytes and platelets was investigated. Nedocromil sodium produced an inhibition of IgE-mediated generation of cytotoxic molecules from monocytes and platelets together with a concomitant inhibition of their oxidative metabolism, measured by chemiluminescence. In addition, nedocromil sodium reduced the ability of alveolar macrophages to synthesise and release mediators, estimated by beta-glucuronidase activity. Furthermore, nedocromil sodium inhibited the abnormal response to aspirin of platelets from aspirin-sensitive asthmatics at therapeutic concentrations. These studies confirm that nedocromil sodium acts on a cell compartment other than the classical mast cell population in IgE-dependent allergy and asthma.
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PMID:Nedocromil sodium inhibition of IgE-mediated activation of human mononuclear phagocytes and platelets from asthmatics. 254 66

The demonstration of a specific receptor for IgE on nonmast cell or basophil leukocytes, such as mononuclear phagocytes, eosinophils, and platelets, suggests that these cells may participate directly in immunological disorders of allergy. Thus, a full understanding of the mode of action of antiallergic or antiasthma drugs must take into account their activity on these nonmast cell leukocytes. Consequently, inhibition by nedocromil sodium of IgE-dependent activation of human alveolar macrophages, blood monocytes and platelets, was investigated. This compound induced an inhibition of the IgE-mediated generation of cytotoxic molecules from monocytes and platelets, together with a concomitant inhibition of their oxidative metabolism, measured by chemiluminescence, and a reduction of the potential ability of alveolar macrophages to synthesize and release mediators, estimated by lysosomal beta-glucuronidase activity. These observations confirm the hypothesis that nedocromil sodium acts on a cell compartment other than the classical mast cell population, in IgE-dependent allergy and, more particularly, in asthma.
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PMID:Inhibition by nedocromil sodium of IgE-mediated activation of human mononuclear phagocytes and platelets in allergy. 282 42

Purified peripheral blood monocytes isolated from patients with atopic dermatitis (AD) and from nonallergic normal donors were compared for their abilities to release leukotriene C4 (LTC4), leukotriene B4 (LTB4) and beta-glucuronidase in response to challenge with aggregated immunoglobulins or anti-immunoglobulins. The relationship between mediator release and the number of monocytes that formed rosettes with immunoglobulin-coated indicator cells was examined. Patients with AD had twice as many IgA- and three times as many IgE-rosetting monocytes as normal donors (48 +/- 12% versus 27 +/- 10% and 40 +/- 15% versus 14 +/- 3%, respectively), and yet the amounts of IgA- and IgE-induced LTC4 released were similar for both groups. This apparent discrepancy did not result from a decreased capacity for arachidonate metabolism via the C5-lipoxygenase pathway, since stimulation of monocytes from patients and normal donors with the calcium ionophore A23187 induced similar amounts of LTC4 and LTB4 release (LTC4, 3.0 +/- 1.7 versus 3.0 +/- 1.0 ng/10(6) cells; LTB4, 5.3 +/- 0.7 versus 5.2 +/- 0.5 ng/10(6) cells, respectively). In addition, aggregated IgG-induced LTC4 release by monocytes of both groups was similar, concomitant with an equivalent number of IgG-rosetting cells. Determination of cytophilically bound IgG and IgE by flow cytometry demonstrated that monocytes from atopic patients had more IgG bound than monocytes from normal donors. Similar amounts of IgE were detected on most monocytes from both groups, despite the higher serum IgE levels of patients. However, approximately 3% to 8% of monocytes from atopic but not normal donors stained brightly for IgE, suggesting that relatively large amounts of cytophilic IgE were bound to a small percentage of the patients' monocytes. Challenge of monocytes with anti-IgE or anti-IgG induced release of similar amounts of LTC4 for both groups, despite the presence of more cytophilic IgG on monocytes from atopic donors. These data indicate that monocytes from patients with AD release LTC4 and LTB4 in response to challenge with aggregated IgE or anti-IgE, as well as aggregated IgG, IgA, and anti-IgG. However, under our in vitro conditions, stimulation of patients' monocytes with aggregated IgA or IgE was not associated with increased mediator release, despite higher percentages of IgA- and IgE-rosetting cells compared to normal donors.
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PMID:IgG-, IgA-, and IgE-induced release of leukotriene C4 by monocytes isolated from patients with atopic dermatitis. 284 75

Basophilic granulocytes were purified from the blood of normal individuals by successive isopyknic centrifugation and elutriation centrifugation. Starting with the leukocyte-rich fraction of 500 ml of blood, we recovered 31 to 80% (mean 51%, n = 20) of the basophils in 45 to 87% purity (mean 69%, n = 23). The contaminating cells were mainly lymphocytes. The basophils were greater than 98% vital (exclusion of ethidium bromide and hydrolysis of fluorescein diacetate). The histamine content of the basophils was 1.1 to 2 pg/cell (mean 1.6 pg/cell, n = 22). With anti-IgE, 30 to 50% of the histamine was released; with phorbol myristic acetate (PMA) or the calcium ionophore A23187, 70 to 100% of the histamine was released. Serum-opsonized zymosan (STZ) did not induce histamine release. Reactions with monoclonal antibodies revealed that the basophils expressed the C3bi receptor (CR3) and the leukocyte function-associated antigen 1 (LFA1), but not the gp 150,95 antigen, the C3b receptor (CR1), or the low avidity Fc gamma receptor. Basophils carry class I but not class II HLA antigens. During incubation of the basophils with serum-opsonized Staphylococcus aureus or Escherichia coli, these bacteria were neither phagocytized nor killed. STZ, PMA, A23187, or anti-IgE did not initiate an "oxidative burst" in the basophils. This was tested with oxygen consumption, cytochrome c reduction, NBT reduction, chemiluminescence, and release of hydrogen peroxide. Moreover, we did not detect cytochrome b558, superoxide dismutase, catalase, or peroxidase in the basophils. Of the typical granule-associated enzymes lysozyme, Vitamin B12-binding protein, and beta-glucuronidase, only beta-glucuronidase was present in the basophils in detectable amounts. This enzyme was released, together with histamine, on incubation of the cells with PMA, A23187, or anti-IgE, but not with STZ. We conclude that basophils from normal human blood are not phagocytes and are probably not involved in the oxidative defense of the host against foreign antigens.
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PMID:Metabolic comparison between basophils and other leukocytes from human blood. 300 19

Disodium cromoglycate (DSCG) has well-established stabilizing properties on mast cells and basophils. However, the potential inhibitory effect of DSCG has been little demonstrated on the IgE stimulation of cell populations expressing epsilon receptors type II, (Fc epsilon RII), such as mononuclear phagocytes, eosinophils or platelets. Therefore, using various parameters of IgE-mediated triggering, we demonstrated the inhibitory role of DSCG on: (i) the release of neutrophil chemotactic factor by human alveolar macrophages, (ii) the oxygen metabolite-dependent chemiluminescence of human alveolar macrophages, rat peritonal macrophages, human eosinophils, human and rat platelets, and (iii) the beta-glucuronidase release and synthesis by human alveolar macrophages. The inhibition of IgE-dependent stimulation ranged from 60% to 80%, according to the cells and to the measured parameter. It could therefore be considered that the action of DSCG was not restricted to its effects on mast cells and basophils, but also on other cells expressing Fc epsilon R leading to a potential reduction of the physiopathological consequences of allergic asthma and, possibly, of the late phase reaction sometimes associated with the disease, insofar as these cells are involved.
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PMID:Effect of disodium cromoglycate on inflammatory cells bearing the Fc epsilon receptor type II (Fc epsilon RII). 314 3

We have previously shown that peptides released after the cleavage of IgG by parasite proteinases were strong inhibitors of the macrophage effector functions against schistosome larvae. The results presented here demonstrate that a single tripeptide set, Thr-Lys-Pro (TKP), inhibits various macrophage functions and can be considered as an immunologically active peptide. Indeed, not only IgE-dependent cytotoxicity but also beta-glucuronidase release, chemiluminescence and ILI production were reduced when rat macrophages were previously incubated with TKP or some analogues. Moreover, chemotaxis and IgE-specific receptor expression were inhibited in both rat and human macrophages after treatment with TKP, without affecting the cell viability. The substitution or acetylation of Thr diminished or suppressed the inhibitory effect of TKP.
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PMID:Regulatory role of a tripeptide (TKP) from the second constant domain of immunoglobulin G--I. Inhibition of rat and human macrophage activities. 315 17

Alveolar macrophages (AM) from control (n = 12) and atopic patients (n = 19, 12 without treatment, 4 treated with theophylline and 3 with theophylline and corticosteroid) were compared for their capacity to release mediators. AM were purified by 2 h adherence and challenged with either ubiquitous allergen, specific sensitizing allergens, anti-IgG or anti-IgE serum. The release of paf-acether, lyso paf-acether and beta-glucuronidase was measured. Paf-acether and its lyso derivative were assayed on washed rabbit platelets. Enzyme and mediator releases were obtained after specific allergenic or anti-IgE serum challenge of AM from untreated atopic patients. No release of paf-acether was detected from AM, from control or treated atopic patients after in vitro immunological challenge, whereas that of lyso paf-acether was greatly reduced in both treated groups. Release was obtained by immunological challenge of AM from control patients after passive sensitization with atopic serum. The release of mediators with bronchoconstriction activity by AM could represent an alternative causal pathway in human asthma.
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PMID:Antigenic release of paf-acether and beta-glucuronidase from alveolar macrophages of asthmatics. 360 26

Macrophages incubated with complexed or aggregated IgE released beta-glucuronidase (beta-G) within 30 min. In contrast in the presence of aggregated or complexed IgG, macrophages liberated equivalent amount of beta-G only after 6 h incubation. In addition the rapid macrophage stimulation induced by aggregated IgE was also followed by a faster 3H-glucosamine incorporation when compared to the delayed activation caused by aggregated IgG. However, macrophages stimulated either by IgG or by IgE oligomers produced the same percentage of plasminogen activator at 24 h. In contrast, while the interaction between macrophages and aggregated IgE was only followed by a peak of cyclic GMP and a beta-G release during the first 30 min of incubation, the interaction between macrophages and IgG oligomers was accompanied by a simultaneous increase of cyclic GMP and AMP nucleotides and by an absence of beta-G exocytosis. Moreover, the beta-G release induced by aggregated IgE was increased when macrophages were preincubated with aggregated IgG. This additive effect was not observed in the reverse situation. Finally macrophages activated by IgG oligomers were demonstrated to exert a cytotoxic effect on tumour cells and to kill schistosomula in the presence of a low level of complement. Taken together these results underline the peculiar ability of aggregated or complexed IgE to trigger rapidly the macrophage activation compared to aggregated IgG and can explain the important role of complexed IgE in some macrophage dependent cytotoxicity mechanisms (i.e. in parasitic diseases).
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PMID:Macrophage triggering by aggregated immunoglobulins. II. Comparison of IgE and IgG aggregates or immune complexes. 608 35

Alveolar macrophages from nonatopic donors were passively sensitized with allergen-specific IgE antibody from the serum of asthmatic patients. A selective release of 4-8% of the lysosomal beta-glucuronidase of these cells occurred within 30 min of contact with the related allergen or with anti-human IgE antibody, in the absence of any mast or basophil cells. The cell reactivity was dependent on the interaction of macrophages with IgE, as shown by the disappearance of the allergen-induced enzyme release after heating or IgE-immune adsorption of the sensitizing serum, but not after IgG-adsorption. Alveolar macrophages from asthmatic patients behaved similarly to passively sensitized normal macrophages. Contact with the related allergen or with anti-IgE antibody induced the same percentage of enzyme release, demonstrating that these cells possess allergen-specific IgE bound on their surface. 18% of them formed rosettes with anti-IgE-coated sheep erythrocytes, and 15-22% with allergen-coated erythrocytes, but lost this property after preincubation with the specific allergen. The presence of IgE-specific receptors on the macrophage surface was demonstrated both at the ultrastructural level with immunoperoxidase labeling, and at low magnification by the formation of 15-18% rosettes with human IgE-coated erythrocytes. The formation of such rosettes was inhibited after incubation of alveolar phagocytes with aggregated myeloma IgE. On the basis of these observations, the participation of the alveolar macrophages in IgE-mediated pulmonary hypersensitivity must be considered. Its precise involvement requires, however, further investigations.
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PMID:Involvement of immunoglobulin E in the secretory processes of alveolar macrophages from asthmatic patients. 618 40


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