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:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neutrophils respond to a variety of stimuli by generating superoxide anion, degranulating, and aggregating. Because it has been suggested that fusion of granules with the plasmalemma (degranulation) is necessary for aggregation and superoxide anion generation, we have tested whether these responses can be demonstrated in "neutrophilic cytoplasts" (granule-free vesicles of cytoplasm enclosed by plasmalemma). When examined by electron microscopy, cytoplasts were found to be approximately 4 microns in diameter and essentially granule free. Cytoplasts exposed to fMet-Leu-Phe (0.1 microM) generated superoxide anion after a lag of 16 sec but released no detectable beta-glucuronidase, lysozyme, or elastase. Aggregation of cytoplasts, as measured by changes in light transmission, was also activated by fMet-Leu-Phe; no lag period was observed. Electron microscopy of the aggregates demonstrated clusters of cytoplasts with a scalloped appearance. Superoxide anion generation and aggregation of cytoplasts were also activated by phorbol 12-myristate 13-acetate, concanavalin A, and leukotriene B4. Exposure of cytoplasts to the dye 3,3'-dihexyloxacarbocyanine iodide (DiOC6(3)] led to dye uptake and enhancement of fluorescence, implying that the vesicles were sealed and maintained a membrane potential across the plasmalemma. Exposure of DiOC6(3)-loaded cytoplasts to fMet-Leu-Phe and PMA caused a rapid loss of dye fluorescence that was not inhibited by CN-, compatible with their lack of mitochondria. Exposure of dye-loaded cytoplasts to concanavalin A or leukotriene B4 caused an increase in fluorescence--i.e., a hyperpolarization. These results demonstrate that degranulation is not a prerequisite for aggregation or superoxide anion generation. The retention of ionic gradients and changes in membrane potential, as measured by DiOC6(3) fluorescence changes, suggest a fundamental role for ionic movements in activating superoxide anion generation and aggregation.
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PMID:Granulocytes without degranulation: neutrophil function in granule-depleted cytoplasts. 630 64

The effects of adenosine were studied on human neutrophils with respect to their generation of superoxide anion, degranulation, and aggregation in response to soluble stimuli. Adenosine markedly inhibited superoxide anion generation by neutrophils stimulated with N-formyl methionyl leucyl phenylalanine (FMLP), concanavalin A (Con A), calcium ionophore A23187, and zymosan-treated serum; it inhibited this response to PMA to a far lesser extent. The effects of adenosine were evident at concentrations ranging from 1 to 1,000 microM with maximal inhibition at 100 microM. Cellular uptake of adenosine was not required for adenosine-induced inhibition since inhibition was maintained despite the addition of dipyridamole, which blocks nucleoside uptake. Nor was metabolism of adenosine required, since both deoxycoformycin (DCF) and erythro-9-(2-hydroxy-3-nonyl) adenine did not interfere with adenosine inhibition of superoxide anion generation. The finding that 2-chloroadenosine, which is not metabolized, resembled adenosine in its ability to inhibit superoxide anion generation added further evidence that adenosine metabolism was not required for inhibition of superoxide anion generation by neutrophils. Unexpectedly, endogenously generated adenosine was present in supernatants of neutrophil suspensions at 0.14-0.28 microM. Removal of endogenous adenosine by incubation of neutrophils with exogenous adenosine deaminase (ADA) led to marked enhancement of superoxide anion generation in response to FMLP. Inactivation of ADA with DCF abrogated the enhancement of superoxide anion generation. Thus, the enhancement was not due to a nonspecific effect of added protein. Nor was the enhancement due to the generation of hypoxanthine or inosine by deamination of adenosine, since addition of these compounds did not affect neutrophil function. Adenosine did not significantly affect either aggregation or lysozyme release and only modestly affected beta-glucuronidase release by neutrophils stimulated with FMLP. These data indicate that adenosine (at concentrations that are present in plasma) acting via cell surface receptors is a specific modulator of superoxide anion generation by neutrophils.
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PMID:Adenosine: a physiological modulator of superoxide anion generation by human neutrophils. 631 34

The reaction of FMLP with granulocytes causes aggregation and degranulation and enhances adherence to endothelium. To evaluate whether prevention of granule extrusion could impair these granulocyte activities, granulocytes were treated with either dexamethasone or hydrocortisone prior to treatment with FMLP. Dexamethasone was added to suspensions of cytochalasin B-treated granulocytes; it markedly impaired the aggregation response of the granulocytes of FMLP. When cytochalasin-B was not used, granulocyte aggregation in response to FMLP or PMA was inhibited by dexamethasone. Although dexamethasone prevented aggregation of cells following stimulation with FMLP or PMA, it failed to prevent the aggregation of granulocytes induced by rabbit lactoferrin. Adherence of granulocytes to human endothelial monolayers was enhanced by FMLP; dexamethasone inhibited the enhancement. However, with the addition of human lactoferrin to the granulocytes exposed to dexamethasone, the cells were able to adhere as well to endothelium as the cells exposed to FMLP but free of dexamethasone. When cytochalasin-B-treated granulocytes were incubated with dexamethasone or hydrocortisone prior to the addition of FMLP, the subsequent release of lactoferrin was substantially blocked, whereas the release of the primary granule products, lysozyme and beta-glucuronidase, was attenuated but not completely blocked. Thus, corticosteroids might block chemotactic-factor-induced granulocyte aggregation by selectively preventing release of specific granule products that contribute to and sustain aggregation.
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PMID:Mechanism of dexamethasone inhibition of chemotactic factor induced granulocyte aggregation. 705 39

The effect of the organochlorine insecticide lindane (gamma-hexachlorocyclohexane) administered intraperitoneally at 10 or 50 mg/kg body wt on some major immune functions of rainbow trout (Oncorhynchus mykiss) was examined. Fish were fed vitamin C as ascorbate-2-polyphosphate at a basal level (60 mg ascorbic acid-(AA)-equivalent/kg of feed) or a high level (2000 mg AA-equivalent/kg) 1 month before lindane exposure and during the whole experiment. The aim of the experiment was to determine whether dietary vitamin C is able to prevent immunosuppression due to lindane. The concentration of ascorbic acid in organs and the circulation was controlled, and the number of lindane residues in whole body was measured by gas chromatography. Nonspecific immune response was investigated through the determination of sera lysozyme and ceruloplasmin; both were significantly modified by lindane exposure while the immediate stimulating effects of vitamin C were observed. Cellular immunity was investigated by determining the number of B lymphocytes (analyzed by cytofluorometry) and their ability to proliferate with mitogens. One month after exposure to lindane (10 mg/kg) the proportion of Ig+ lymphocytes in head kidney was significantly decreased by the insecticide. Higher levels of vitamin C (2000 mg/kg) led to a significant increase in this parameter. Thus, vitamin C had a compensating effect on the number of Ig+ lymphocytes in exposed fish. Lindane at 10 mg/kg decreased the proliferation of B lymphocytes, but this was not confirmed at 50 mg/kg. Vitamin C stimulated the proliferation for the latter concentration after 2 months of intake. In lindane-exposed fish, the PMA-induced chemiluminescent response of head kidney phagocytic cells was variable from one assay to another, while most of the time vitamin C acted as a stimulant. The humoral response to Yersinia ruckeri was not modified by lindane but was significantly increased by vitamin C for 1 month after the antigen injection and thus 2 months after vitamin intake.
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PMID:Effect of lindane exposure on rainbow trout (Oncorhynchus mykiss) immunity. IV. Prevention of nonspecific and specific immunosuppression by dietary vitamin C (ascorbate-2-polyphosphate). 754 39

Lysozyme was purified from exocytosed granule material from PMA-stimulated human neutrophils by polyethyleneglycol precipitation, cation exchange chromatography and molecular sieve chromatography. Rabbit antibodies were biotinylated and affinity purified on a lysozyme column, for subsequent development of a novel ELISA. This ELISA for lysozyme is sensitive and accurate, and applicable to determination of lysozyme in neutrophils and plasma.
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PMID:Purification of lysozyme from human neutrophils, and development of an ELISA for quantification in cells and plasma. 784 19

Morphological and biochemical evidence indicates that in several cell types, lysozyme is found in both lysosomes and the medium. Here we report that in calcitriol-treated human promonocytes U937, in which approx. two-thirds of the synthesized lysozyme is secreted, most of the intracellular lysozyme co-localizes with cathepsin D in lysosomal organelles. In the presence of NH4Cl the lysosomal targeting of procathepsin D, but not that of lysozyme, is inhibited. In the presence of 4 beta-phorbol 12-myristate 13-acetate (4 beta-PMA; 'TPA'), the lysosomal packaging of lysozyme is almost completely inhibited, while that of procathepsin D is only partially so. However, the inhibition of the lysosomal targeting of procathepsin D by NH4Cl and 4 beta-PMA is additive. The targeting of lysozyme is partially inhibited in the presence of R-59022, an inhibitor of diacylglycerol kinase, whereas it is not affected by 4 alpha-phorbol 12-myristate 13-acetate, an isomer of 4 beta-PMA that does not activate protein kinase C. It is concluded that in U937 cells both carbohydrate-dependent and -independent recognition contributes to the lysosomal targeting of soluble proteins. We suggest that the carbohydrate-independent traffic of proteins to lysosomal compartments is controlled by a signalling pathway involving protein kinase C.
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PMID:Distinctive inhibition of the lysosomal targeting of lysozyme and cathepsin D by drugs affecting pH gradients and protein kinase C. 809 11

Cefdinir, a new oral 2-amino-5-thiazolyl cephalosporin, inhibited the luminol-amplified chemiluminescence (LACL) response of human neutrophils stimulated by PMA but not opsonized zymosan, in a concentration-dependent but not time-dependent manner. The LACL response to opsonized zymosan in cytochalasin B-treated neutrophils was, however, inhibited by cefdinir. Various cephalosporins, regardless of the presence of a 2-amino-5-thiazolyl moiety, did not significantly alter the neutrophil LACL response triggered by PMA and zymosan. The LACL response induced by the calcium ionophore A23187 and FMLP was also impaired by cefdinir, and this impairment was increased in cytochalasin B-treated neutrophils. Superoxide anion generation by neutrophils, measured in terms of lucigenin-amplified chemiluminescence and cytochrome c reduction, was not altered. Spontaneous and FMLP-induced neutrophil degranulation, assessed by lysozyme and beta-glucuronidase release, were not modified by cefdinir. Furthermore, cefdinir inhibited LACL generation in cell-free systems consisting of H2O2, NaI, and either horseradish peroxidase or a myeloperoxidase-containing neutrophil extract. Orthodianisidine oxidation in these two acellular systems was inhibited by cefdinir. Cefdinir did not alter neutrophil bacterial killing at concentrations that inhibited myeloperoxidase-containing neutrophil extract-dependent reactions induced by soluble stimuli. Taken together, these data strongly suggest that cefdinir directly inhibits the activity of myeloperoxidase-containing neutrophil extract released into the extracellular medium during neutrophil stimulation by soluble mediators, but has no effect on that released into the phagolysosome during phagocytosis. This unusual property of a member of the beta-lactam family could be of interest in modulating the exaggerated inflammatory process often associated with infectious diseases.
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PMID:Cefdinir (CI-983), a new oral amino-2-thiazolyl cephalosporin, inhibits human neutrophil myeloperoxidase in the extracellular medium but not the phagolysosome. 813 56

The in vitro effect of unfractionated heparin and dermatan sulfate, as well as oligo-heparin and oligo-dermatan sulfate, on human PMN function was investigated. Superoxide anion generation in fMLP-stimulated PMN was dose-dependently reduced by heparin and oligo-heparin, while DS and oligo-DS lacked inhibitory activity. FMLP-stimulated PMN adhesion to endothelial cells was reduced to a similar extent by both heparin and oligo-heparin, but not by DS and oligo-DS. On the other hand, none of the compounds affected the adhesion of unstimulated PMN to either IL-1- or PMA-activated endothelial cells. Heparin and oligo-heparin also inhibited the homotypic aggregation of fMLP-stimulated PMN. As reported, coincubation of platelets with fMLP-stimulated PMN resulted in platelet activation, a process mainly mediated by the PMN-derived serine protease cathepsin G. Both heparin and DS, as well as their oligo-derivatives, reduced platelet activation induced by either fMLP-stimulated PMN or purified leukocytic cathepsin G. Finally, besides cathepsin G, also the activity of beta-glucuronidase and lysozyme released by stimulated PMN were reduced by heparin, oligo-heparin and DS. These data support the hypothesis that heparin and other GAGs may exert an antiinflammatory role.
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PMID:Effect of heparin, dermatan sulfate, and related oligo-derivatives on human polymorphonuclear leukocyte functions. 843 35

Respiratory epithelial and gland cells cultured in vitro demonstrate changes from differentiated serous and mucous cells toward intermediate "seromucous" cells. This spontaneous process was examined by culturing human nasal mucosal explants in CMRL 1066 medium without growth factors for 6 days and measuring the concentrations of spontaneously released serous cell products [lactoferrin, lysozyme, 7F10-immunoreactive mucoglycoconjugates (7F10-irm)] and Alcian blue-staining mucous cell products. 7F10-irm was progressively and significantly increased on each day of culture. In contrast, lysozyme, lactoferrin, and Alcian blue-staining material decreased significantly. Each had its own pattern of decreasing release. Dexamethasone (1 microM) had no effect on these trends. Phorbol myristate ester (PMA; 100 nM) reduced 7F10-irm release on days 4-6 and delayed the drop in lactoferrin release. Dexamethasone blunted these effects of PMA. These data indicate that respiratory secretory cells alter their phenotypes when cultured in vitro and progressively change the relative amounts of mucoglycoconjugates and proteins spontaneously released. These changes should be anticipated when interpreting experiments involving cultured respiratory cells.
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PMID:Spontaneous release of submucosal gland serous and mucous cell macromolecules from human nasal explants in vitro. 892 19

It is generally accepted that the foam cells in atherosclerotic lesions are derived mainly from monocytes/macrophages. We investigated whether the macrophage-derived foam cells, isolated from the atherosclerotic lesions of cholesterol-fed rabbits, would exhibit properties similar to those of blood monocytes in vitro and whether the cholesterol concentration of the macrophage-derived foam cells would decrease in the presence of an appropriate cholesterol acceptor in culture. We found that most (> 98%) of the foam cells isolated from atherosclerotic lesions were positive for anti-monocyte-macrophage antibody and nonspecific esterase. While almost all (> 98%) of the foam cells exhibited NaF-resistant, nonspecific esterase activity, the blood monocytes exhibited no such activity. Macrophage-derived foam cells contained larger amounts of cholesterol, most of it esterified, than the blood monocytes. Although blood monocytes exhibited a substantial amount of lysozyme, the freshly isolated, macrophage-derived foam cells showed no detectable lysozyme activity. The production of superoxide by macrophage-derived foam cells stimulated by PMA or opsonized zymosan was lower than that of stimulated monocytes. The cholesterol concentration of macrophage-derived foam cells decreased during five days of culture in the presence of an appropriate acceptor, such as normal and hypercholesterolemic rabbit serum and high density lipoprotein, although the rate of decrease was slow. Results suggest that macrophage-derived foam cells may be involved in both the progression and the regression of early atherosclerotic lesions.
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PMID:Characteristics of macrophage-derived foam cells isolated from atherosclerotic lesions of rabbits. 943 Mar 74


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