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)

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

We investigated the ability of the lymphokine, interleukin-4 (IL-4), to function as a neutrophil (PMN) activator. IL-4 enhanced PMN-mediated killing of opsonized bacteria (by up to 91.6% at 3 units of IL-4; p less than 0.05). IL-4 was a weak secondary granule secretagogue and did not by itself generate a respiratory burst. However, IL-4 did increase in a dose-dependent fashion the respiratory burst mediated by the peptide formyl-methionyl-leucyl-phenylalanine (10(-7) mol/L). Maximal potentiation of PMN activity occurred at 100 units of IL-4 (6.3 nmol superoxide produced without IL-4 to 9.8 nmol at 100 units; p less than 0.01). Enhancement of the respiratory burst was not a generalized phenomenon, since IL-4 did not potentiate the respiratory burst mediated by either phorbol myristate acetate, calcium ionophore A23187, or zymosan-treated serum. Similarly, IL-4 potentiated the formyl-methionyl-leucyl-phenylalanine-stimulated secretion of both lysozyme (40.2%) and beta-glucuronidase (108.2%). Finally, IL-4 was demonstrated to enhance the ability of PMN to phagocytose sheep erythrocytes opsonized with rabbit IgG (by up to 94.2% at 30 units of IL-4). This increased phagocytosis correlated with the recruitment of a population of PMNs that did not phagocytose targets in the absence of IL-4. In conclusion, IL-4 enhanced neutrophil-mediated bactericidal activity. This increase may have occurred secondary to the stimulation of phagocytosis by IL-4 or by potentiation of degranulation and the respiratory burst.
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PMID:Interleukin-4 is a neutrophil activator. 254 Nov 92

This study examined the properties and responsiveness to cytokines of macrophages purified from normal and nephritic glomeruli to ascertain whether macrophages activated in vivo develop programmed unresponsiveness to cytokines as do bone marrow-derived macrophages in vitro when activated by interferon-gamma (IFN-gamma), tumor necrosis factor (TNF), interleukin-4 (IL-4), or transforming growth factor-beta (TGF-beta). Macrophages from normal glomeruli did not generate nitric oxide (NO) spontaneously but only after treatment with IFN-gamma and TNF-alpha. NO generation by these macrophages was abrogated by administering IL-4, TGF-beta, or TNF-alpha before but not after IFN-gamma treatment. Glomerular macrophages also expressed beta-glucuronidase, which was increased by TGF-beta and decreased by IFN-gamma and TNF. By contrast, glomerular macrophages from rats with nephrotoxic nephritis did not express beta-glucuronidase even after exposure to TGF-beta. Furthermore, they generated NO spontaneously, and this spontaneous generation of NO was not suppressed by IL-4, TGF-beta, or TNF-alpha. Systemic treatment of nephritic rats with IL-4 reduced NO generation by 40% but did not prevent activation, which is similar to the effect of IL-4 on bone marrow-derived macrophages in vitro when given simultaneously with IFN-gamma. We conclude that macrophages infiltrating inflamed glomeruli have developed programmed unresponsiveness to activating cytokines. This may enable them to function appropriately in the complex conditions within an inflammatory focus.
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PMID:Macrophages from inflamed but not normal glomeruli are unresponsive to anti-inflammatory cytokines. 1062 78

The purpose of this investigation was to determine the effects of bon narine treatment on macrophage and lymphocyte functions in mice. Twelve week-old female inbred BALB/c mice were given bon narine p.o. at 30 mg/kg per day and sacrificed after three months. Glucose consumption of peritoneal macrophages in the bon narine treated group during incubation up to 72 h was significantly higher than that in the control group. Activities of acid phosphatase (APH), beta-glucuronidase (GLU) and lactate dehydrogenase (LDH) in the peritoneal macrophages in the bon narine treated group significantly increased compared to that in the control group. Macrophage production of nitric oxide stimulated by lipopolysaccharide (LPS) in the bon narine treated group was significantly increased. Interleukin-1beta (IL-1beta) production of peritoneal macrophages stimulated by LPS was significantly higher in the bon narine treated group. Stimulation indices in splenic lymphocytes by concanavalin A (Con A) in the bon narine treated group were significantly higher than that in the control group. Interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) production stimulated by Con A were significantly increased in the bon narine treated mice. Interleukin-4 (IL-4) production of splenic lymphocytes stimulated by Con A was not different in the control group and the bon narine treated group. These findings might suggest that oral administration of bon narine effectively enhanced the macrophage function and lymphocyte responsiveness in mice.
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PMID:Enhanced macrophage functions and cytokine production of lymphocytes after ingestion of bon narine in female BALB/c mice. 1119 48