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)

A technique used for study of permeability and vasodilation in the middle ear has been adapted to study the response of nasal mucosa to common inflammatory mediators involved in the natural production of allergic or infectious rhinitis. All of the mediators tested (histamine, prostaglandin E1, bradykinin, the C3a fraction of complement, Escherichia coli endotoxin, and lysozyme) were found to increase nasal permeability to the isotopic tracer 99mTc as the pertechnetate ion. Histamine increased the permeability of nasal mucosa to technetium-labeled plasma protein. Results indicate that the nasal mucosa is approximately ten times as permeable to the pertechnetate ion as middle ear mucosa. Nasal mucosa was also noted to be permeable to protein, even in the absence of inflammatory mediator, in contrast to prior studies of middle ear mucosa that showed little or no permeability in the absence of inflammatory mediator. In almost all cases, a corresponding change in vasodilation accompanied permeability changes.
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PMID:Effect of inflammatory mediators on nasal mucosa. 32 89

Prostaglandin E1 (PGE1) has recently been used clinically as a purported modulator of activated neutrophils in certain forms of the adult respiratory distress syndrome (ARDS). We now report that PGE1 does not have a uniform inhibitory effect upon human neutrophil functions in vitro. Cells were first pretreated with PGE1 followed by incubation with either N-formyl-methionyl-leucyl-phenylalanine (FMLP), phorbol myristate acetate (PMA), or C5a. Lysosomal enzyme release (myeloperoxidase, lysozyme), superoxide anion generation, and chemotaxis were then quantitated. PGE1 alone lacked any appreciable effect on these neutrophil functions. However, neutrophils pretreated with PGE1 (50 to 100 microM) followed by stimulation with FMLP (50 nM) showed as much as 40% inhibition of lysosomal enzyme release compared with control values (p less than 0.0005). In contrast, 0.1 nM to 1 microM PGE1 enhanced FMLP-stimulated enzyme release as much as 50% above baseline control values (p less than 0.05). Preincubation with 0.1 nM PGE1 followed by stimulation with variable doses of FMLP also resulted in enhancement of lysosomal enzyme release by as much as 187 +/- 3% of control values. The enhancing but not inhibitory effects of PGE1 were reversible with serial washing of the neutrophil preparations. Enhancement of enzyme release was not observed when either PMA or C5a was used as a stimulus after PGE1 pretreatment. However, cells pretreated with PGE1 (50 to 100 microM) and subsequently stimulated with C5a showed as much as 40% inhibition of lysosomal enzyme release. Preincubation of neutrophils with PGE1 (1 microM) resulted in a slight (15%) enhancement of chemotaxis to FMLP, but it had no significant effect on C5a-induced chemotaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Concentration-dependent regulatory effects of prostaglandin E1 on human neutrophil function in vitro. 165 39

A group of 48 critically injured patients were entered into a prospective, double-blind, placebo-controlled trial to evaluate the efficacy of early infusion of PGE1 for reducing the incidence of severe respiratory failure and mortality. Secondary assessments examined the effects of the PGE1 infusion on plasma mediated suppression of PMN superoxide production and loss of PMN granule enzyme content. The incidence of severe respiratory failure was lower in the PGE1 group--13% versus 32%, but this did not reach significance. The overall morality was equivalent between the two groups--26% (PGE1) versus 28% (placebo). The suppressive activity of the patient plasma was assayed by measurement of normal PMN superoxide production relative to normal control plasma (ratio P:C). The baseline ratio P:C was 62 +/- 5% in the PGE1 group versus 60 +/- 5% in the placebo group. The day 1 plasma samples showed significant reversal of plasma suppressive activity in the PGE1 group--ratio P:C 88 +/- 5% versus 67 +/- 5% in the placebo group (P less than 0.02). In patients who received the full 7 days of infusion, the plasma suppressive activity remained significantly diminished in the PGE1 group--ratio P:C 77 +/- 4% versus 61 +/- 5% (P less than 0.04). The baseline lysozyme content of patient PMN's relative to that of normal control PMNs (ratio P:C) was 119 +/- 14% in the PGE1 group. A significant loss of lysozyme content was observed in the PGE1 group on day 1 of the infusion--ratio P:C 79 +/- 8% (P less than 0.03), and was associated with a reduction in the plasma suppressive activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of prostaglandin E1 for prevention of respiratory failure in high risk trauma patients: a prospective clinical trial and correlation with plasma suppressive factors for neutrophil activation. 166 93

Fibronectin secreted by macrophages may contribute to the development of pulmonary fibrosis. Prostaglandins are important regulators of macrophage metabolism whose role in the regulation of fibronectin production is not known. In this study, we examined the effects of PGE1 and indomethacin on human monocyte-derived macrophages exposed to these agents in culture for 10 to 14 days. Indomethacin (10 micrograms/ml) reduced the ratio of supernatant fibronectin to adherent cell DNA by 32%, p < 0.01, and reduced lysozyme/DNA by 29%, p < 0.0001. Exogenous PGE1 (1 ng/ml) did not affect fibronectin, but increased lysozyme/DNA by 27%, p < 0.01. In additional experiments, supernatant fibronectin and total protein synthesized in the presence of 3H-leucine were measured. Indomethacin (10 micrograms/ml) had no effect on total supernatant protein radioactivity, but reduced fibronectin/DNA by 33%, p < 0.001, and reduced fibronectin/total protein by 19%, p < 0.01. Since indomethacin increases macrophage secretion of plasminogen activator and interleukin-1, these experiments add to the evidence that specific secretory products of macrophages are regulated independently. We conclude that indomethacin at 10 micrograms/ml decreases the production of fibronectin and lysozyme by monocyte-derived macrophages. The modest size of the effect, and its absence at lower doses of indomethacin, indicate that prostaglandins are unlikely to have a major role in the regulation of macrophage production of fibronectin.
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PMID:Effects of indomethacin and prostaglandin E1 on the production of fibronectin and lysozyme by monocyte-derived macrophages in vitro. 166 50

The ferret trachea was mounted in an organ bath containing Krebs-Henseleit solution with additional bovine serum albumin (BSA). Tracheal secretions were collected and analyzed for albumin, and lysozyme, a specific marker of serous cell secretion. The total secretion volume and output and concentrations of albumin and lysozyme were calculated. Secretion was stimulated with methacholine (20 microM) (Mch), and the effects of the prostaglandins PGD2, PGE1, and PGF2 alpha on methacholine-induced secretion were studied. All responses were dose dependent. PGF2 alpha at 10(-5) M increased the volume of Mch-stimulated secretion twofold, the lysozyme output sixfold, and concentration over threefold, while decreasing the albumin transport by one-half. PGD2 at 10(-5) M reduced Mch-induced secretion volume to 75% control, increased albumin transport to 135%, without affecting lysozyme secretion. PGE1 at 10(-5) M increased Mch-stimulated albumin transport and concentration over twofold, decreased lysozyme release to less than one-third of control, and had no effect on secretion volume. PGE1 caused the albumin concentration to exceed that of the outer bath, indicating active transport. We conclude that prostaglandins selectively alter tracheal secretion induced by cholinergic stimuli.
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PMID:Prostaglandins alter methacholine-induced secretion in ferret in vitro trachea. 240 40

The secretory response of cytochalasin B-treated human polymorphonuclear neutrophils to the peptide chemoattractant f-Met-Leu-Phe (FMLP), the calcium ionophore A23187 and other secretagogues was measured by assaying neutrophil supernatants for the granular enzymes beta-glucuronidase and lysozyme. The dose-dependent enzyme secretion in response to 10(-8)-10(-4) M FMLP and A23187 was unaffected by pretreatment with 10-75 microM forskolin (an activator of adenylate cyclase), but inhibited by high concentrations of prostaglandins E1 and E2. The phosphodiesterase inhibitors isobutyl-methyl-xanthine (IBMX), papaverine and Ro 20-1724 dose dependently inhibited enzyme secretion from FMLP- or A23187-treated cells, and this effect was augmented in the presence of 50-75 microM forskolin. Similar results for PGE1, forskolin and forskolin/IBMX combinations were also obtained using leukotriene B4, platelet activating factor and C5a des-Arg as secretagogues. We conclude that the adenylate cyclase system of human neutrophils is activatable by forskolin, but that the regulatory effects of adenylate cyclase stimulants in these cells are greatly attenuated unless cyclic AMP-phosphodiesterases are inhibited. Thus the phosphodiesterase activity of neutrophils may be of functional importance and is relevant to the modulation of neutrophil activity in inflammation.
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PMID:Inhibition of human neutrophil degranulation by forskolin in the presence of phosphodiesterase inhibitors. 301 41

Tissue macrophages produce several proteins of the complement system. The mechanisms that regulate this process are poorly understood. The established ability of certain prostaglandins to influence macrophage secretory activity suggests that these lipid mediators may also modulate complement production (CP). Using the guinea pig peritoneal macrophages, we determined the effects of selected prostaglandins on in vitro CP and found that PGE2 inhibited production of complement proteins but not lysozyme; the response of elicited and resident peritoneal cells to PGE2 was identical; and PGE1, PGF2 alpha, and PGI2 had no detectable effect. PGE2 may contribute to regulation of CP in vivo.
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PMID:Effect of prostaglandins on complement production by tissue macrophages. 392 Mar 40

The effects of theophylline, isobutylmethylxanthine (IBMX), prostaglandin E1 (PGE1), and isoproterenol on monocyte antibody-dependent cytotoxicity (ADCC) were compared with their effects on monocyte cyclic adenosine 3':5'-monophosphate (cAMP) levels. Theophylline (2 mmol/l) halved ADCC and gave a 2-fold increase in cAMP levels. At concentrations not elevating cAMP theophylline inhibited ADCC significantly. In comparison, incubation of monocytes with IBMX, PGE1 and isoproterenol ADCC was only modestly inhibited while these agents gave larger increments (3- to 8-fold) in cAMP levels than theophylline did. Low concentrations of IBMX (50 mumol/l) elevated cAMP without affecting monocyte ADCC whereas PGE1 and isoproterenol inhibited ADCC dose-dependently comparable to increases in cAMP. However, in doses giving similar inhibition of ADCC addition of PGE1 resulted in larger cAMP increments than isoproterenol. The effects of IBMX, PGE1 and isoproterenol was dependent on target cell to effector cell ratio and increased during preincubation with the agents. The inhibition of ADCC by the agents was accompanied by a depressed monocyte lysozyme release and depressed activation of hexose monophosphate shunt. However, only theophylline affected monocyte attachment to sensitized target cells. These results argue against the general inverse relationship between cAMP content and inhibition of monocyte ADCC and demonstrate that theophylline independent on increases in cAMP inhibits ADCC probably by abrogation of monocyte binding activity.
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PMID:Divergent effects of methylxanthines and adenylate cyclase agonists on monocyte cytotoxicity and cyclic AMP levels. 618 23

1. Antinociceptive activity of hen egg white lysozyme (Fleming's lysozyme) was determined against abdominal contractions provoked by irritants injected intraperitoneally into mice. Carrageenan (2 mg) (CA) injected with arachidonic acid (15 micrograms) (AA) or prostaglandins PGE1 or PGF2 alpha (0.04 ng), brewer's yeast (10 mg), caolin (10 mg), mepartricin (80 U) and phenylquinone (50 micrograms) were used as irritants. 2. Lysozyme was active at 400-800 mg/kg i.v. against CA + AA, CA + PG, brewer's yeast and caolin nociceptive stimulation. The compound was more effective against CA + AA than against CA + PG. Acetylsalicylic acid at 50-100-200 mg/kg p.o. was equally active against CA + AA and CA + PG. 3. Lysozyme was inactive in the tail pinch and hot plate tests that mainly detect central analgesics. 4. The results are discussed in relation to the claim advanced years ago that lysozyme is an effective analgesic agent in humans. The compound was found active against herpes zoster or cancer pain but did not find use despite the favourable reports presented. 5. The experimental results obtained on laboratory animals do not contradict the conclusions drawn after the clinical use of the compound.
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PMID:Is Fleming's lysozyme an analgesic agent? Experiments on mice. 622 Aug 50

Mouse myeloid leukemia M1 cells were induced to differentiate in vitro into macrophages and granulocytes by various inducers including ascitic fluid. Differentiated M1 cells induced with ascitic fluid expressed a differentiation-associated cell surface glycoprotein with a molecular weight of 180,000 (p180), which can be labeled by lactoperoxidase-catalyzed radioiodination or metabolic labeling with L-[14C]fucose. p180 was also induced by treatment with conditioned medium of hamster embryo cells, dexamethasone, dibutyryl cyclic adenosine 3':5'-monophosphate, and prostaglandin E1. Ascitic fluid, conditioned medium of hamster embryo cells, and dexamethasone induced all the differentiation-associated properties tested, whereas dibutyryl cyclic adenosine 3':5'-monophosphate and prostaglandin E1 induced lysozyme activity and adhesiveness to the substratum but not phagocytosis, locomotive activity, Fc receptors, or morphological changes. The adherent cells induced by dibutyryl cyclic adenosine 3':5'-monophosphate produced a large amount of p180, while the floating cells produced very little, but no difference was detected in the lysozyme activities of the two cell types. These results suggest that p180 is associated with cell-substratum adhesion of differentiated M1 cells.
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PMID:Expression of a cell surface glycoprotein (p180) related to cell-substratum adhesion during differentiation of mouse myeloid leukemia cells. 625 64


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