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)

The outer coat fraction (OC-Fr) of Bacillus megaterium ATCC 12872 spore was isolated as a resistant residue after alkali extraction, sonic treatment, and pronase digestion of the spore coat preparation, and its backbone structure was determined by chemical analysis to be composed of galactosamine-6-phosphate (GalN-P) polymers with polypeptides and calcium. OC-Fr was not fully solubilized after ordinary acid hydrolysis. OC-Fr was insensitive to all hexosaminidases tested, and moreover, an isolated fragment, a pentamer of GalN-P, was also resistant to lysozyme and hexosaminidases even after N-acetylation, being sensitive to them to some extent after dephosphorylation. Molecular sieving experiments revealed that the outer coat limited the entry of compounds with a molecular weight of more than 2,000. Exchange of the metal on the spore surface also influenced the heat resistance. Spores of OC-Fr-deficient mutants were less resistant but were still much more resistant than the vegetative cells. These results suggest that the outer coat protects the contents of the spore against chemical, physical and enzymatic treatments owing to the chemical structure itself, composed mainly of GalN-P polymers, and the molecular sieving effect.
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PMID:Role of outer coat in resistance of Bacillus megaterium spore. 250 41

Calcium 2-keto-L-gulonate (Ca-2-KLG, a key intermediate in vitamin C synthesis) is produced from calcium 2,5-diketo D-gluconate (Ca-2,5-DKG) by a variety of bacteria. A few bacterial species which efficiently convert glucose to Ca-2,5-DKG have been isolated in our laboratory. Our bacterial collection included species that possess the genes for production of Ca-2-KLG from Ca-2,5-DKG; however, the yield of the former is poor. A procedure for the preparation of spheroplasts in Ca-2,5-DKG- and Ca-2-KLG-producing bacteria was developed for the construction of recombinants (fusants), combining the genes for conversion of glucose to Ca-2-KLG efficiently by protoplast fusion. The standard procedure for spheroplast formation in Gram negative bacteria by the Tris-sucrose-EDTA-lysozyme system did not work in the organisms under investigation. The need for an alternative method was necessary. Our results show that, while the Tris-NaCl-EDTA-lysozyme system (pH 8.3) worked very well with bacterial strains of Gluconobacter oxydans (ATCC9937) and Acetobacter melanogenus (NCIM2259), the Tris-sucrose-EDTA-lysozyme system worked well for Erwinia herbicola (ATCC21998), Pseudomonas chlororaphis (NCIM2041) and Corynebacterium species (ATCC31090). However, none of these systems produced spheroplasts in Brevibacterium ketosoreductum (ATCC21914), for which a separate system is under development.
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PMID:A fast spheroplast formation procedure in some 2,5-diketo-D-gluconate- and 2-keto-L-gulonate- producing bacteria. 251 94

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

In the absence of extracellular Ca2+, poly-L-arginine induces little lysozyme release from rabbit polymorphonuclear leukocytes (PMNs). The polycation causes plasma membrane damage, which is evident from the release of the cytoplasmic enzyme lactate dehydrogenase (LDH). In the presence of Ca2+ concentrations higher than 0.2 mM, poly-L-arginine induces a strong lysozyme release that is superimposed on the membrane-damaging effect. The results suggest that poly-L-arginine permeabilizes the plasma membrane, enabling Ca2+ to enter the cell, which results in the exocytotic release of granule constituents. The GTP analog GTP gamma S shifts the Ca2+ requirement of exocytosis to slightly higher concentrations, whereas it completely inhibits poly-L-arginine-induced LDH release. Pertussis toxin gives a moderate inhibition, and La3+ completely inhibits poly-L-arginine-induced enzyme release. Whereas poly-L-arginine alone induces little superoxide generation in rabbit PMNs, there is a synergistic enhancement of superoxide production when GTP gamma S and poly-L-arginine are present together. Guanine nucleotides apparently have a modulating effect on the actions of poly-L-arginine on the PMN, but the nature of this effect remains to be determined.
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PMID:Permeabilization and calcium-dependent activation of rabbit polymorphonuclear leukocytes by poly-L-arginine. 254 93

Glucocorticoids exert their actions through a time-dependent, receptor-mediated, protein synthesis- and RNA synthesis-dependent mechanism. We have assessed the effects of 24-h culture of human neutrophils with dexamethasone on degranulation, chemotaxis, binding to vascular endothelium and formation of leukotriene B4. Purified neutrophils contained an average of 2896 [3H]dexamethasone binding sites per cell with a Kd of 4.1 X 10(-9) M for [3H]dexamethasone binding. Cells exposed to dexamethasone (10(-6) M) released equal or greater quantities of the lysosomal enzymes, lysozyme and beta-glucuronidase in response to formylmethionyl-leucyl-phenylalanine, serum activated zymosan, and the tumor promoting phorbol diester 12-O-tetradecanoylphorbol-13-acetate compared to controls. Culture with dexamethasone also did not inhibit neutrophil chemotaxis in response to a range of concentrations of formylmethionyl-leucyl-phenylalanine, or did it inhibit binding of neutrophils to cultured endothelial cells stimulated by either leukocyte activators (formylmethionyl-leucyl-phenylalanine and platelet-activating factor) or endothelial activators (interleukin-1, lipopolysaccharide or 12-O-tetradecanoylphorbol-13-acetate). Spontaneous adherence of neutrophils to endothelial cells was inhibited (82.9 +/- 6.8% of control, P less than .025, n = 18). Neither in vitro or in vivo glucocorticoids inhibited neutrophil leukotriene B4 formation induced by either the calcium ionophore A23187 or serum activated zymosan. We conclude that human neutrophils are not functionally inactivated by glucocorticoids and suggest that the mechanism by which glucocorticoids inhibit neutrophil accumulation at inflammatory sites may be by inhibition of the production of chemoattractants and endothelial activators rather than inhibition of their actions.
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PMID:An assessment of the effects of glucocorticoids on degranulation, chemotaxis, binding to vascular endothelium and formation of leukotriene B4 by purified human neutrophils. 254 40

Fusobacterium nucleatum expresses lectinlike adherence factors which mediate binding to a variety of human tissue cells. Adherence is selectively inhibited by galactose, lactose, and N-acetyl-D-galactosamine. In this study, adherence of F. nucleatum to human peripheral blood polymorphonuclear neutrophils (PMNs) was investigated. The results indicated that the fusobacteria adhered to live and metabolically inactivated or fixed PMNs. Adherence of F. nucleatum resulted in activation of PMNs as determined by PMN aggregation, membrane depolarization, increased intracellular free Ca2+, superoxide anion production, and lysozyme release. Transmission electron micrographs showed that F. nucleatum was phagocytized by the PMNs. Microbicidal assays indicated that greater than 98% of F. nucleatum organisms were killed by PMNs within 60 min. Adherence to and activation of PMNs by F. nucleatum were inhibited by N-acetyl-D-galactosamine or lactose greater than galactose, whereas equal concentrations of glucose, N-acetyl-D-glucosamine, mannose, and fucose had little or no effect on F. nucleatum-PMN interactions. Pretreatment of the fusobacteria with heat (80 degrees C, 20 min) or proteases inhibited adherence to and activation of PMNs, but superoxide production was also stimulated by heated bacteria. The results indicate that interaction of F. nucleatum with PMNs is lectinlike and is probably mediated by fusobacterial proteins which bind to other human tissue cells. Adherence of F. nucleatum to PMNs in the absence of serum opsonins, such as antibodies and complement, may play an important role in PMN recognition and killing of F. nucleatum in the gingival sulcus and in the subsequent release of PMN factors associated with tissue destruction.
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PMID:Lectinlike interactions of Fusobacterium nucleatum with human neutrophils. 255 9

Chrysotile asbestos is cytotoxic for rabbit polymorphonuclear leukocytes (PMNs) which is evident from the release of the cytoplasmic enzyme LDH. In the presence of Ca2+, but not in its absence, a strong lysozyme release occurs. High concentrations of Ca2+ are required for exocytosis. In the presence of the stable guanine nucleotide GTP gamma S exocytosis occurs at lower Ca2+ concentrations. The results suggest that the plasma membrane is permeabilized by asbestos, allowing the influx of extracellular Ca2+ which causes exocytosis. At high Ca2+ concentrations asbestos-induced cytotoxicity is strongly reduced. The cytotoxic LDH release and, to a lesser degree, the exocytotic enzyme release are inhibited by Co2+, Mn2+ and La3+. Cytochalasin B and the glycolytic inhibitors 2-deoxyglucose and iodoacetate inhibit asbestos-induced cytotoxicity, indicating that microfilaments and glycolytic energy are required for the membrane-damaging actions of asbestos.
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PMID:Chrysotile asbestos-induced cytotoxicity and calcium-dependent exocytosis in polymorphonuclear leukocytes. 255 37

Blood neutrophils, when exposed to appropriate stimuli, aggregate, degranulate and generate superoxide anion. Curcumin, a non-steroidal antiinflammatory agent, modulated these functions, depending upon the kind of stimulus used. It inhibited monkey neutrophil aggregation induced by chemotactic peptide fmlp and zymosan activated plasma (ZAP) but did not affect that induced by serum treated zymosan (STZ) and arachidonic acid (AA). Generation of O2- radical was inhibited by curcumin, when cells were stimulated by AA, STZ and fmlp. Curcumin inhibited the release of myeloperoxidase, an azurophilic granule marker enzyme. Release of lysozyme was less susceptible to inhibition by curcumin. The results suggest that curcumin interferes with neutrophil responses to various physiological stimuli and a part of its antiinflammatory action is mediated via inhibition of neutrophil function. Inhibition of neutrophil function by curcumin appears to be mediated via calcium dependent mechanisms.
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PMID:Inhibition of neutrophil response by curcumin. 255 3

The enthalpy change of the binding of Ca2+ and Mn2+ to equine lysozyme was measured at 25 degrees C and pH 7.5 by batch microcalorimetry: delta H degrees Ca2+ = -76 +/- 5 kJ mol-1, delta H degrees Mn2+ = -21 +/- 10 kJ mol-1. Binding constants, log KCa2+ = 6.5 +/- 0.2 and log KMn2+ = 4.1 +/- 0.5, were calculated from the calorimetric data. Therefore, delta S degrees Ca2+ = -131 +/- 20 JK-1 mol-1 and delta S degrees Mn2+ = 8 +/- 44 JK-1 mol-1. Removal of Ca2+ induces small but significant changes in the circular dichroism spectrum, indicating the existence of a partially unfolded apo-conformation, comparable with, but different from, the apo-conformation of bovine alpha-lactalbumin.
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PMID:Comparison of the binding of Ca2+ and Mn2+ to bovine alpha-lactalbumin and equine lysozyme. 260 May 98

The influence of experimentally induced hyperlipidemia and aging on the development of pulmonary foam cells (PFCs) was examined in Fischer 344 rats. The male and female rats were administered orally with cholesterol at a dosage level of 1000 mg/kg/day for 30 days from 6 to 10 weeks or from 33 to 37 weeks of age. The control rats received the vehicle only in the same manner. Plasma levels of total cholesterol, phospholipid, triglyceride (TG), beta-lipoprotein (beta-LP) and calcium in both control and cholesterol-administered groups were higher at 37 weeks than at 10 weeks of age. Plasma beta-LP and TG levels in the treated groups were significantly higher or tended to be higher than those of the controls at 10 and 37 weeks of age. Males of the treated group showed the highest level of beta-LP at 37 weeks of age, positively correlated with the highest incidence of PFCs. PFCs developed singly or in a small cluster in peribronchial and subpleural regions. PFCs had an abundant cytoplasm filled with many fine vacuoles containing neutral lipid and cholesterol. PFCs stained with PAS and reacted immunohistochemically with both anti-rat monocytes/macrophages monoclonal antibody and anti-lysozyme antibody. Moderately swollen macrophages with a foamy appearance were detected in perivascular connective tissues of the lungs and they were considered to represent an initial stage of the development of PFCs. These observations suggest that hyperlipidemic conditions, particularly hyper beta-lipoproteinemia, resulting from cholesterol administration or aging may be involved in the development of PFCs in rats.
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PMID:Influence of cholesterol administration and aging on the development of pulmonary foam cells in F344 rats. 260 22


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