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 levels of 13 proteins were measured in six tear samples collected atraumatically at progressively increasing flow rate from nonstimulated (less than 0.5 microliter/min) to highly stimulated (greater than 50 microliters/min) in ten subjects. Tears were fractionated initially by size-exclusion high-performance liquid chromatography (SE-HPLC). Enzyme-linked immunosorbent assays and kinetic assays were then applied to relevant SE-HPLC fractions to determine specific protein levels. Nine of the 13 proteins assayed showed significantly higher concentrations in nonstimulated tears than in any other tear sample. Immunoglobulin (Ig) M, secretory IgA, polymeric IgA1, and polymeric IgA2 all decreased progressively in concentration from nonstimulated tears to the higher flow-rate stimulated samples. The level of IgG, albumin, and transferrin showed a large drop in concentration between nonstimulated tears and the first (lowest flow-rate) stimulated sample, with relatively little decrease for any subsequent sample. Levels of lactoferrin, tear-specific prealbumin, lysozyme, and peroxidase were relatively constant throughout the series of tear samples. These results indicate that the mechanisms responsible for changes in concentration of constitutive, serum-derived, and regulated tear proteins with stimulus can be studied successfully using noninvasive methods to collect human tears. They also show that simply distinguishing between nonstimulated and stimulated tears is not sufficient to completely characterize the effect of stimulus conditions on tear protein composition.
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PMID:Changes in human tear protein levels with progressively increasing stimulus. 207 41

In the absence of serum, nonpiliated gonococci expressing PII outer membrane proteins (PIIs) adhere to human neutrophils whereas non-PII-expressing (PII-) gonococci do not. After an observation that neutrophils in monolayers bound more gonococci than neutrophils in suspension, we treated neutrophil suspensions with known stimulants of degranulation and measured subsequent gonococcal adherence to suspended neutrophils. The chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fmlp), the potent secretagogue phorbol myristate acetate, and the calcium ionophore A23187 all caused increased adherence of PII+ gonococci, but not PII- gonococci, to neutrophils in a dose-responsive manner. Increased adherence of gonococci to neutrophils was paralleled by increased degranulation of neutrophil myeloperoxidase, lysozyme, and lactoferrin. Inhibition of fmlp-induced neutrophil degranulation by pertussis toxin, the calmodulin inhibitors trifluoperazine and N-5-chloronaphthalene sulfonamide, or the intracellular calcium-binding agent trimethoxybenzoic acid also inhibited fmlp-induced gonococcal adherence to neutrophils. Neither undifferentiated nor myelocytically differentiated HL-60 cells, which possess primary but defective or nonexistent secondary granules, bound PII+ or PII- gonococci. Gonococci did not adhere to human monocytes, monocyte-derived macrophages, lymphocytes, platelets, or erythrocytes, indicating that several receptors, such as the complement receptors CR1, CR3 (CD11b/CD18), and CR4 (CD11c/CD18) or the adherence complex LFA-1 (CD11a/CD18), were probably not involved in gonococcal adherence to human neutrophils.
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PMID:Up-regulation of human neutrophil receptors for Neisseria gonorrhoeae expressing PII outer membrane proteins. 211 69

Erdosteine is a new thioderivative endowed with mucokinetic, mucolytic, and free-radical-scavenging properties. This study evaluated (in a double-blind design vs. placebo) its efficacy on biochemical and rheologic properties of sputum and on some indices of respiratory function in chronic patients with chronic bronchitis (10 per group), while receiving basic treatment with a controlled-release theophylline preparation. The pharmacokinetics of erdosteine and theophylline were also studied. We found that a 2 week treatment with erdosteine (300 mg 3 times daily) was able to reduce significantly (p less than 0.05) the sputum apparent viscosity, fucose content, and macromolecular dry weight (MDW) with no statistically significant influence on sputum elasticity, DNA, albumin, total proteins, total IgA, lactoferrin, and lysozyme content. The treatment caused a significant increase in the following ratios: total IgA/albumin, lactoferrin/albumin, and lysozyme/albumin. The pharmacokinetics of erdosteine, its metabolites, and theophylline were the same after 1 or 14 days of treatment, evidence both of absence of an enzymatic induction and of an accumulation process. Further confirmation that there was no interference between erdosteine and theophylline was obtained from the data available on the group of patients receiving only theophylline, since its plasma levels and related pharmacokinetic parameters were identical to those obtained in patients receiving both drugs. In conclusion, 2 weeks of therapy with erdosteine reduced the marker of mucus glycoproteins (fucose) in patients with chronic bronchitis but did not interfere with the pharmacokinetics of xanthine derivatives. We also suggest that the significant increment in the IgA/albumin ratio might be related to a sum of other local effects such as reduction of the inflammatory process and enhancement of the humoral defense mechanism.
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PMID:Effects of erdosteine on sputum biochemical and rheologic properties: pharmacokinetics in chronic obstructive lung disease. 212 36

In this report, we present data on the activation of different neutrophil effector functions by two distinct Fc-gamma receptors, FcRII and FcRIII. We and others have shown previously that IgG-dependent activation of phagocytosis and superoxide generation is mediated via FcRII. IgG-dependent exocytosis of granule proteins was assessed with Staphylococcus aureus Oxford opsonized with human IgG or with IgG-coated latex. Both anti-FcRII mAb and anti-FcRIII-F(ab')2 mAb inhibited this release, whereas the combination of these mAb inhibited this process more strongly than either mAb alone. This indicates that both FcRII and FcRIII are involved in IgG-dependent release of granule proteins. Cross-linking of the receptors by anti-FcR mAb and F(ab')2 fragments of goat-anti-mouse-Ig showed again that both FcRII and FcRIII mediate lysozyme release, whereas cross-linking of a control antigen (CD67) did not. By measuring the release of elastase and lactoferrin, we found that cross-linking of either FcRII or FcRIII induced release of both azurophilic and specific granules. Under these conditions, we did not measure any activation of the respiratory burst. When FcRIII was removed by treatment of neutrophils with glycosylphosphatidylinositol-specific phospholipase C, the lysozyme release induced by cross-linking of FcRIII was lower than the release from control neutrophils, whereas the release induced by cross-linking of FcRII was similar. Therefore, we conclude that IgG-dependent activation of neutrophils follows two distinct pathways: one via transmembrane FcRII, activating both the NADPH oxidase and the release of granule proteins (as was demonstrated previously by us and by others), and the other via phosphatidylinositol-linked FcRIII, activating exocytosis of granule proteins.
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PMID:Phosphatidylinositol-linked FcRIII mediates exocytosis of neutrophil granule proteins, but does not mediate initiation of the respiratory burst. 213 91

This study investigated the interaction between neutrophil myeloperoxidase (MPO) and the C1q component of the complement system. Using a dot-spot assay, MPO was found to bind to C1q in a dose-dependent manner. The specificity of this reaction was proved by the inhibitory effect of F(ab')2 antibodies to C1q and by the inability of MPO to bind to C1r, C1s and IgG. The interaction between MPO and C1q did not influence the enzymatic activity of the peroxidase but resulted in a more stable C1q as assessed by hemolytic assay for C1q. The protective effect of MPO on C1q did not require the presence of H2O2 in the reaction mixture nor was it inhibited by sodium azide, whereas it was abolished by heating the peroxidase. Lactoferrin and lysozyme, unlike MPO, were ineffective in protecting C1q from functional decay. Addition of H2O2 and chloride to MPO and C1q led to a complete inactivation of C1q, which could not be induced by H2O2 alone. The hypochlorite, which is known to be generated during the reaction of MPO with H2O2 and chloride, exhibited a similar inactivating effect on C1q, which was prevented by an external source of methionine.
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PMID:Protective and inactivating effects of neutrophil myeloperoxidase on C1q activity. 215 59

Two cell lines (ACCS and ACCY) were isolated from two individuals with adenoid cystic carcinoma (AdCC) using tissue culture techniques. Both cell lines have similar morphology, i.e., elongated and flattened cells with slender cytoplasmic processes. The two cell lines tend to form pseudocysts, which are a specific architectural feature of AdCC. Coexpression of cytokeratin and vimentin was found in the two cell lines, which occasionally also contained S-100 protein and lactoferrin or lysozyme immunoreactivity. Moreover, ACCS and ACCY displayed potential for the production of a large amount of extracellular matrix including basal lamina components such as fibronectin, laminin, and type IV collagen and glycosaminoglycans which are also part of the basal lamina. These findings suggest that the tumor cells, probably basal or myoepithelial like cells, are responsible for the formation of the peculiar stroma of AdCC consisting of a large amount of collagen-like fibers, basal lamina components, and mucopolysaccharides.
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PMID:Biological characterization of pseudocyst-forming cell lines from human adenoid cystic carcinomas of minor salivary gland origin. 216 54

Human milk is characterized not only by a complex host defense system that prevents the colonization and proliferation of common microbial pathogens that may pervade the alimentary tract and respiratory tract of the infant but also by a paucity of inflammatory agents and an array of anti-phlogistic factors. Clinical observations support the notion that the protection provided by human milk involves not only antimicrobial factors, but also anti-inflammatory agents. The major anti-inflammatory agents include enzymes that degrade mediators of inflammation, anti-proteases, lysozyme, lactoferrin, secretory IgA and a number of antioxidants including cysteine, ascorbate, alpha-tocopherol, and beta-carotene. It is pertinent that most of these factors are either absent or poorly represented in cow's milk or other artificial feedings that substitute for breast feeding and that the attainment of adult serum levels of some of these antioxidants in early infancy is dependent upon breast feeding. It may be that the provision of these antioxidants may help to protect the recipient's developing immunologic system which is quite susceptible to oxidant damage. The absence of breast feeding will thus deprive the infant of valuable protection against common enteric-respiratory disorders and their inflammatory consequences. It should be pointed out that the protective systems in human milk including the anti-inflammatory components may not be completely delineated, and that little is known of the in vivo fate of the factors and precisely how they protect the recipient. Those questions should form the basis of important research in the next decades.
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PMID:Anti-inflammatory systems in human milk. 218 25

Numerous studies have demonstrated that patients with dry eyes have a compromised ocular surface. Furthermore, these patients suffer deficiencies of various surface defense mechanisms, such as tear volume, tear components (lysozyme, lactoferrin, and beta-lysin), the mucin network, cellular exfoliation, and subsurface immune secretions. When such individuals wear contact lenses (CLs), a special set of circumstances arises that increases the risk of ocular infection. The risk is greatest if the lenses are soft and, therefore, provide for little tear exchange beneath their surface. Under such circumstances, limited tear flow allows for a greater buildup of lens deposits and metabolic wastes, while permitting increased tear evaporation from the lens surface. The pathogenesis of infection is attributed to various mechanisms, including decreased tear flow beneath the lens, decreased tear components, stagnation of the mucin network, changes in surface cell exfoliation, and putative changes in the subsurface immune secretory system. Dry eye patients who wear soft CLs also run a greater risk of bacterial conjunctivitis, blepharitis, and sterile corneal infiltrates.
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PMID:Is the dry eye contact lens wearer at risk? Yes. 218 82

We investigated and compared the initial composition, morphology, and time course of deposits on individual soft contact lenses of different water contents and surface charges in order to evaluate the potential for antigenic reactions and to predict the optimal frequency of lens replacement. Newly manufactured lenses were worn for graduated periods of time from 1 min to 8 h by subjects who were first adapted to daily wear soft lenses. The morphology and composition of the deposits were analyzed by histological staining, light microscopy, scanning electron microscopy (SEM), sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) with silver nitrate staining, and immunofluorescence microscopy. The protein bands of the acrylamide gels were divided according to their molecular weights into six groups which have been defined in the literature from tear analyses by electrophoretic techniques and include lysozyme, proteins migrating faster than albumin (PMFA), protein G, albumin, lactoferrin, and other proteins heavier than albumin such as Ig-G and secretory Ig-A. Specific proteins (lysozyme, PMFA, and protein G) were detected on individual lenses after as little as 1 min of wear. There was an increasing amount of protein deposited as the wearing time increased. Differences in the rates and amounts of deposition were more dependent on lens water content and ionic characteristics than on intersubject differences. Such early significant protein deposition may occur in wearers of disposable lenses as well as in those subject to complications due to accumulation of protein.
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PMID:Initial in vivo tear protein deposition on individual hydrogel contact lenses. 220 14

Granulocyte infiltration was studied in 88 biopsies of antrum mucosa from patients with B-gastritis. Evidence of IgA-, IgG- and IgM-antibodies as well as of lysozyme in the mucosa was demonstrated by immunohistochemical methods. Helicobacter pylori (Hp) is coated by antibodies and a significant correlation between extent of opsonisation and number of plasma cells in the connective tissue of the lamina propria could be stated. Thus, the infiltration of plasma cells is a specific immune response against Hp. In the depths of gastric pits the antibody-coating of bacteria is faint. Instead, lysozyme and lactoferrin are produced there. By means of a Cross-sectional study a model is developed which characterizes B-gastritis as a dynamic process. Lagging behind, the inflammation follows the motile bacteria resulting in a patchy distribution of inflamed areas in the mucosa. At the peak of these local inflammation-waves the production of antibodies and lysozyme is intensified. Coating the bacteria with IgG and IgM results in complement activation liberating chemotaxin C5a. Consequently, there is a massive granulocyte infiltration leading to local reduction or eradication of Hp.
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PMID:[Gastritis: immunohistochemical detection of specific and nonspecific immune response to Helicobacter pylori]. 223 61


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