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)

This review demonstrates that basophils reflect skin and lung mast cell reactivity and show characteristic changes in mediator release associated with clinical disease. Although the numbers of IgE molecules and IgE receptors on basophils have been enumerated, these have, in most instances, little influence on the release of histamine after challenge. There is, rather, a parameter of "releasability" that may be a major variable in allergic disease states. Basophils contain and release histamine, the eosinophil chemotactic factor of anaphylaxis (ECFA), a slow reacting substance of anaphylaxis (SRS-A), and a kallikrein. The release process is controlled by hormone-basophil receptor interactions that determine the cyclic AMP level; plasma and tissue adenosine levels appear prominent in this control. Histamine feeds back to negatively modulate basophil and mast cell release through a specific histamine 2-receptor; it also inhibits lymphocyte and neutrophil function. Like neutrophils, basophils contain beta-glucuronidase while neutrophils contain SRS-A and a low-molecular-weight ECF. The stimuli for primary basophil and neutrophil release are, however, quite different, although phagocytic stimuli, which fail to cause basophil mediator release, potentiate the IgE response. It is concluded that basophols play a significant in vivo role in inflammation by acting as an interface between foreign antigens, the serum cascade systems, and other inflammatory cells.
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PMID:The role of basophils in inflammatory reactions. 7 20

Phagocytosis was found to stimulate ECF release from neutrophils (PMN). Human PMN (less than 98%) were exposed to zymosan (Z), zymosan-coated with complement (Z(x)), or zymosan in the presence of serum (Z(s)). The release of ECF was shown to be time- and dose-dependent. Like ionophore-induced ECF, phagocytosis-derived ECF preferentially attracted and deactivated eosinophils. Chromatography on Sephadex G-25 revealed an elution pattern similar to the antigen-induced, basophil-derived and to the ionophore-induced PMN-derived ECF. The addition of complement either as Z(x) or Z(s) accelerated the release of ECF. With both stimuli, the initial kinetics of ECF paralleled the release of beta-glucuronidase and NBT reduction. With Z alone, beta-glucuronidase release and NBT reduction were negligible, whereas the amount of ECF released was similar to that induced by Z(x). In the presence of serum Z(s), decreased activity was noted. Supernatants of phagocytosis at late time periods showed less activity than early supernatants, suggesting that ECF might be inactivated. These data indicate that phagocytosis causes the release of an ECF, which appears to be similar to the IgE-induced ECF-A.
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PMID:Eosinophil chemotactic factor (ECF). II. Release from human polymorphonuclear leukocytes during phagocytosis. 93 26

As a basis for studies of the influence of lipids on the immune response and health, adult C57Bl mice were fed for 10 weeks or longer on one of the following diets: high (200 g/kg) polyunsaturated fatty acid, high (200 g/kg) saturated fatty acid and low (50 g/kg) polyunsaturated fatty acid purified diets and a standard commercial diet. The three test-fat diets were compounded to have approximately the same energy content and the mice of each group maintained similar body-weights. High-fat diets significantly reduced their subsequent delayed hypersensitivity response to challenge after sensitization with tuberculin. Immunoglobulin IgM antibody formation against Escherichia coli lipopolysaccharide was transiently decreased, but IgG antibody against sheep erythrocytes and killed salmonella vaccine, IgG and IgE antibodies against ovalbumin remained unaffected. Total and differential blood counts revealed no differences between mice on high-fat and control diets in either the absolute numbers or the proportions of the types of leukocytes. Studies on peritoneal macrophages from mice of each group showed no difference in morphology and they ingested non-toxic and toxic particles releasing similar amounts of lactate dehydrogenase (EC 1.1.1.27) and beta-glucuronidase (EC 3.2.1.31) for each substance, indicating that there were no differences in viability or phagocytic function. The present study shows that the C57 Bl mouse can provide a model for the investigation of some consequence of the reduced immunocompetence induced by high-fat diets.
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PMID:High-fat diets and the immune response of C57Bl mice. 154 99

Tioxamast (F 1865) is an antiallergic drug that, administered systemically, reduces anaphylaxis in various models in rats. This action is due mainly to the inhibition of the synthesis and release of certain mediators. Orally or intraduodenally administered tioxamast inhibits IgE-dependent passive cutaneous anaphylaxis (ED50 = 0.8 mg/kg), IgE-dependent passive pulmonary anaphylaxis (ED50 = 0.5 mg/kg), and IgG-dependent passive cutaneous anaphylaxis (ED50 = 0.6 mg/kg). It has little or not effect on the increase of cutaneous capillary permeability induced by various mediators. In IgE-dependent passive peritoneal anaphylaxis in rats, tioxamast reduces the release of histamine (IC50 = 0.024 micrograms/ml) and of beta-glucuronidase (IC50 = 0.102 micrograms/ml). Also, histamine release is inhibited in IgG-dependent peritoneal anaphylaxis (IC50 = 0.103 micrograms/ml). The antiallergic compound has less effect on the release of histamine induced by the compound 48/80 in the peritoneal cavity of rats (IC50 = 1.67 micrograms/ml). Tioxamast inhibits the synthesis in vitro of leukotriene B4 (LTB4) by peritoneal neutrophils from rats stimulated by A23187 (IC50 = 8.88 micrograms/ml). At higher tioxamast concentrations, metabolites of the cyclo-oxygenase pathway are inhibited at concentrations of the same order of magnitude as those that inhibit Naja naja phospholipase A2 (IC50 = 144 micrograms/ml). Tioxamast also reduces the production of free radicals by leukocytes from the pleural cavity of rats which had phagocytosed opsonized zymosan (IC50 = 5.21 micrograms/ml).
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PMID:Antiallergic and anti-inflammatory action of tioxamast in rats. I. Antiallergic activity in vivo and in vitro. 170 Sep 67

Recent evidence confirms that cytokines such as IL-1, IL-4, IL-5, and GM-CSF may enhance or inhibit eosinophil function. Functions that are susceptible to modulation include eosinophil-mediated antibody-dependent damage of helminthic parasites, oxidative metabolism and degranulation. We have employed IgG and IgE-coated Sepharose beads to investigate selective modulation of IgG and IgE-mediated enzyme release by IL-1 beta. Both IgG and IgE-coated beads induced release of granular enzymes beta-glucuronidase and arylsulfatase. Enzyme release from IgG-stimulated eosinophils was inhibited by preincubation with IL-1 beta (100 pg/ml, P less than or equal to 0.05). In contrast, enzyme release by IgE-stimulated eosinophils was enhanced by IL-1 beta (100 pg/ml, P less than or equal to 0.05). These studies support the hypothesis that IL-1 beta has specific selective actions on eosinophil function. Furthermore, these actions on particle-stimulated enzyme release suggest that IgG and IgE mediated processes in eosinophils are differentially regulated.
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PMID:Selective regulation of eosinophil degranulation by interleukin 1 beta. 174 16

Triggering of eosinophil secretory and cytotoxic functions by stimulation of the IgG and IgE FcR is thought to have major importance in the pathophysiology of tissue eosinophilia. We studied the ability of human rIL-4 to regulate this triggering event in human eosinophils. At doses ranging from 0.1 to 10 pg/ml, IL-4 suppressed eosinophil secretion of beta-glucuronidase and arylsulfatase by up to 65% after stimulation with IgG-coated Sepharose beads. This effect required prolonged preincubation (16 h) of eosinophils with IL-4; no effect was detected after 1 h preincubation. Enzyme secretion stimulated by IgE-coated beads was not affected. Further, IL-4 (after 16 h preincubation), suppressed eosinophil antibody-dependent killing of schistosomula (Schistosoma mansoni) targets by 24 to 39% in four experiments (p less than 0.05). Flow microfluorimetry analysis showed that IL-4 reduced the expression of IgG FcR, but not IgE FcR, suggesting that this mechanism underlies the suppression of IgG-mediated secretion. Taken collectively, these results demonstrate a mechanism for T lymphocyte suppression of IgG-stimulated eosinophil functions via IL-4.
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PMID:Inhibition of IgG-triggered human eosinophil function by IL-4. 213 96

IgE binds to two types of Fc receptors, called Fc epsilon R1 (or high-affinity Fc epsilon R) and Fc epsilon R2 (or low-affinity Fc epsilon R). The Fc epsilon R1 is composed of four polypeptide chains, one alpha, one beta, and two gamma chains. The alpha chain contains the IgE binding site and is a member of the immunoglobulin supergene family. The Fc epsilon R2, also called CD23, consists of one polypeptide chain which shows homology to animal lectin receptors. Fc epsilon R1 are expressed on mast cells and basophils. Crosslinking of the Fc epsilon R1 induces immediate release of mediators of inflammation such as histamine and leukotrienes and delayed secretion of interleukins 4, 5, and 6. Fc epsilon R2 are expressed on resting mu delta + B cells, monocytes/macrophages (M phi), eosinophils, and platelets but rarely on T cells. Interleukin-4 upregulates Fc epsilon R2 expression on B cells and M phi. The functions of Fc epsilon R2 on the different cell types are not fully established and are controversial. Fc epsilon R2 on M phi, eosinophils, and platelets mediate cytotoxicity to schistosomules, enhance phagocytosis, and induce the release of granule enzymes. However, M phi from patients with atopic dermatitis expressing significantly more Fc epsilon R2 than M phi from normals do not release more leukotriene C4, prostaglandin E2, or beta-glucuronidase after incubation with aggregated IgE than normal monocytes. Furthermore, aggregated IgG1 is much more efficient than IgE in inducing mediator release from M phi and IgG1 antibodies are not known to induce immediate-type hypersensitivity reactions. Therefore, definitive proof that Fc epsilon R2 are involved in the pathogenesis of allergic disorders is still lacking. IL-4 appears to play a central role in immediate-type hypersensitivity. It induces human B cells to secrete IgE and IgG4, Ig isotypes typical for antibodies to helminthic parasites and allergens. IL-4 stimulates mast cell growth and upregulates Fc epsilon R2 expression. Interferon-gamma and IL-2 inhibit the IL-4-induced IgG4 and IgE secretion. Whether the abnormally high IgE antibody production in atopic patients is the result of overproduction of IL-4 or deficient IFN-gamma/IL-2 production is presently unknown.
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PMID:Fc receptors for IgE and interleukin-4 induced IgE and IgG4 secretion. 219 Oct 55

A summarizing survey of different studies in atopic eczema involving three types of cells (platelets, neutrophils, basophils) and their mediators is given. Platelets were found to release normal amounts of serotonin upon stimulation with epinephrine, thrombin and slightly reduced amounts after aggregated IgG stimulation. Serotonin uptake by washed platelets was found to be slower in atopics than in normals. Neutrophils showed a decreased release of beta-glucuronidase to stimuli like zymosan or aggregated IgG in atopics compared to controls. This might be regarded as a contributory factor to the well-known decreased resistance to infections observed in atopic eczema. Basophils in most studies released increased amounts of histamine in the atopic population compared to controls, especially after stimulation with anti-IgE. Concomitantly to the histamine release there was a slight increase in prostaglandin E2 production both in atopics and normals, which was increased by preincubation with reduced glutathion-a coenzyme of PGE2 isomerase. Histamine release tended to occur faster in atopics. Two possible factors influencing releasability characteristics were studied, namely the cyclic nucleotide system and arachidonic acid (AA) dependent mechanisms. Leucocytes of atopics showed a decreased response of cAMP to beta-adrenergic and an increased response of cGMP to cholinergic stimulation. Significant augmentation of anti-IgE-induced histamine release was observed after cholinergic stimulation. AA metabolites obviously play a regulating role in mediator release. PGE2 inhibited histamine release to various stimuli both in atopics and in normals. Indomethacin enhanced histamine release, especially after anti-IgE stimulation in atopics, while it inhibited complement-dependent release reactions both in atopics and in normals. The exogenous inhibitors of lipoxygenase eicosatetraynoic acid (ETYA) and nordihydroguaretic acid (NDGA) inhibited histamine release equally in atopics and normals. The endogenous lipoxygenase inhibitor 15-HETE showed no inhibitory but rather a slight enhancing effect upon histamine release. It is concluded that patients with atopic eczema often exhibit altered releasability patterns to a variety of stimuli. On the basis of our findings we describe "altered releasability" as one factor of a vicious cycle between increased IgE-production, mediator secretion and T cell regulatory disturbances in the pathogenesis of atopic eczema.
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PMID:Altered releasability of vasoactive mediator secreting cells in atopic eczema. 240 33

Platelets, basophils and neutrophils from a patient with the Wiskott-Aldrich syndrome (WAS) were exposed to stimuli that activate specific membrane receptor or directly initiate biochemical events (e.g. the Ca2+ ionophore A23187 and ionomycin or arachidonic acid). Platelets from this patient did not aggregate in response to ADP, collagen, thrombin or adrenaline, which activate specific membrane receptors. Platelet aggregation, however, was normal in response to compound A23187, ionomycin or exogenous arachidonic acid. Histamine release from basophils of the WAS patient was normal in response to anti-IgE, a formylated peptide (f-met peptide), and to A23187. Similarly, the release of the lysosomal enzymes, beta-glucuronidase and lysozyme, from neutrophils of the WAS patient in response to serum treated zymosan (Zx), f-met peptide, and A23187 was not significantly different from that of his parents and 13 normal donors. These results suggest that the primary defect in WAS is selectively present in platelets and is located in a biochemical step between receptor activation and Ca2+ influx and/or initiation of arachidonate metabolism.
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PMID:The Wiskott-Aldrich syndrome: studies of platelets, basophils and polymorphonuclear leucocytes. 242 57

We studied beta-glucuronidase release from human monocytes induced with aggregated immunoglobulins of the nine different human classes and subclasses. Release was induced in a time and dose-dependent manner by all aggregated IgG subclasses. Aggregated IgA1 caused a greater beta-glucuronidase release than aggregated IgM, IgD, and IgE, but the difference was not statistically significant. Release of beta-glucuronidase was not phagocytosis dependent since inhibition of phagocytosis by cytochalasin B or dihydrocytochalasin B did not diminish enzyme release. On the contrary, cells incubated with cytochalasin B prior to addition of aggregated IgG released approximately twice as much enzyme compared to untreated controls. Enzyme release induced by latex particles, a non-Fc receptor mechanism, was decreased by cytochalasin B. Monomeric IgG1, IgG2, IgG3, and IgG4 inhibited aggregated IgG1 enzyme release in a dose-dependent manner. The ability of monomeric IgG to inhibit beta-glucuronidase release correlated with previous reports describing the binding affinities of monomeric IgG to monocytes, i.e., IgG2 was relatively ineffective compared to the other subclasses. Monomeric IgA, IgE, and pentameric IgM were unable to diminish IgG-induced enzyme release. The data indicate that normal peripheral blood monocytes express predominantly Fc receptors for IgG and that all four IgG subclasses induce the release of the lysosomal enzyme beta-glucuronidase.
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PMID:beta-Glucuronidase release from human monocytes induced with aggregated immunoglobulins of different classes. 242 25


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