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

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

The data presented here demonstrate that recombinant human tumour necrosis factor beta (rHuTNF beta; lymphotoxin) is a neutrophil modulator. The lymphokine inhibited the locomotion of neutrophils and augmented the neutrophil oxygen-dependent respiratory burst in response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) and phorbol myristate acetate (PMA), as measured by their capacity to produce chemiluminescence, H2O2 and superoxide. The effects on the respiratory burst occurred at a tenth of the concentration of TNF beta required to inhibit locomotion. After incubation with TNF beta, the neutrophils could be washed without any reduction in their capacity to show augmented responses. The TNF beta enhanced granule enzyme (lysozyme and beta-glucuronidase) release of neutrophils stimulated with cytochalasin B-FMLP.
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PMID:Tumour necrosis factor beta (lymphotoxin) inhibits locomotion and stimulates the respiratory burst and degranulation of neutrophils. 283 16

Cell-mediated cytotoxicity involves a localized secretory process in which lytic agents stored in specialized granules of the effector cells are released upon contact with the appropriate target cell membrane and cause membrane damage. The protonophore carbonylcyanide m-chlorophenylhydrazone (CCCP) inhibits cytotoxicity of natural killer cells, cytotoxic T-lymphocytes and lymphokine-activated killer cells. This inhibition is due to an effect of CCCP on the cytolytic cells, rather than on their targets, and is reversible. Treatment with CCCP does not inhibit the formation of effector-target conjugates, but seems to affect the programming of the effector cells for lysis. CCCP only inhibits lysis if added during a certain period of the lytic cycle: it has an effect only if added before, or within 5 minutes of the initiation of killing by a pulse of Ca++. Effector cells treated with CCCP retain their characteristic beta-glucuronidase-positive granules, but in the presence of the drug, these are no longer oriented to face the contact area with the target cell membrane.
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PMID:Cell-mediated cytotoxicity and the reorientation of effector cell granules towards the target cell are inhibited by the protonophore carbonylcyanide m-chlorophenylhydrazone. 326

The purpose of these studies was to establish whether extracellular calcium (Cao2+) plays a role in the process of activation of RAW-264 macrophages for tumor cell killing. We found that these cells were capable of developing a significant level of cytolytic activity under treatment with lymphokine (LK) and lipopolysaccharide (LPS), in the absence of Cao2+ and that responses developed in Ca2+-free media were only 6-18% lower in comparison with the responses developed in the presence of Cao2+. The determination of 45calcium uptake in RAW-264 cells treated with LK and LPS showed that the rate of 45calcium uptake has displayed no increase during either the course of activation or in activated, highly cytolytic cells. Finally, three calcium channel blockers examined here: verapamil, diltiazem and flunarizine, with concentrations ranging from 1 X 10(-7) M - 2.5 X 10(-5) M, showed no inhibitory effect on the process of activation. Nifedipine, another calcium channel blocker, inhibited the development of cytolytic activity with concentrations ranging from 1 X 10(-6) M - 2.5 X 10(-5) M. It could be argued, however, that this inhibition was nonspecific, since this agent was 13 times more potent with regard to the calcium ionophore A23187-induced release of beta-glucuronidase, the function which is entirely dependent on Cao2+. Taken together, these results suggest that Cao2+ is not an absolute requirement for the process of tumoricidal activation of RAW-264 macrophages but it may play some supportive role in this process.
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PMID:Extracellular calcium is not an absolute requirement for tumoricidal activation of RAW-264 macrophage-like cell line. 346 Oct 96