Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effect of 4-H-2-carboxamido-4-phenyl-thieno-[3,2c]-[1]-benzopyran (Zy 16039) was examined on the smooth muscle contraction, mucus secretion and albumin transudation in the ferret whole trachea in vitro. 2. Zy 16039 (0.1-20 microM) produced a concentration-dependent relaxation of the ferret trachea contracted by methacholine (1 microM) and phenylephrine (10 microM). The relaxations were about 20% of the full contractions. 3. Zy 16039 has no effect on the resting (zero) output of mucus in the ferret trachea. Methacholine-induced mucus secretion was significantly inhibited by Zy 16039, whereas phenylephrine-induced secretion was significantly increased. 4. Methacholine-induced secretion of lysozyme, a marker of serous cell secretion, was inhibited by Zy 16039 both with regard to output and concentration of lysozyme. In contrast, Zy 16039 significantly increased the output of lysozyme due to phenylephrine, with no effect on concentration. 5. Zy 16039 had no significant effect on the rate of output of fluorescent albumin through the tracheal wall. However the concentration of albumin in the mucus samples was changed because of the effect of Zy 16039 on mucus secretion induced by methacholine and phenylephrine. 6. We conclude that Zy 16039 relaxes airway smooth muscle, and either promotes or inhibits mucus secretion depending on its source. It has qualitatively similar actions to vasoactive intestinal peptide.
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PMID:Action of a novel drug (Zy 16039) on mucus secretion in the ferret isolated trachea in vitro. 304 31

The effect of vasoactive intestinal peptide (VIP) was examined on the smooth muscle contraction and mucus secretion produced by methacholine and phenylephrine in the ferret whole trachea in vitro. VIP (0.5 to 800 nM) produced a concentration-dependent relaxation of the ferret trachea contracted by methacholine (1 microM) and phenylephrine (10 microM). The concentration-response curves for methacholine- and phenylephrine-induced contractions were both shifted to the right by VIP (0.1 microM). Methacholine-induced secretion was inhibited in a concentration-dependent manner by VIP, whereas that due to phenylephrine was enhanced. The concentration-response curve for methacholine-induced secretion was shifted to the right by VIP, whereas the curve for phenylephrine was shifted to the left. Methacholine produced a concentration-dependent increase in the rate of output of lysozyme from the ferret trachea with no corresponding increase in the concentration of lysozyme in the mucus. Phenylephrine produced a concentration-dependent increase in the rate of output and in the concentration of lysozyme. VIP (0.1 microM) significantly increased the concentration of lysozyme in the mucus produced by methacholine with no increase in the rate of lysozyme output. However, the rate of lysozyme output due to phenylephrine was significantly increased by VIP (0.1 microM) with no increase in concentration. We suggest that VIP inhibits secretion from mucous cells stimulated by methacholine, and enhances the secretion produced by phenylephrine from serous cells.
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PMID:The effect of vasoactive intestinal peptide on smooth muscle tone and mucus secretion from the ferret trachea. 359 72

Human and canine airway mucosa in vitro synthesizes and secretes mucus glycoprotein, proteoglycans and lipids which can be separated by density gradient ultracentrifugation in caesium bromide. In secretions from unstimulated explants, the small amount of mucus glycoprotein present is found in association with proteoglycans. 'Free' mucus glycoprotein of typical buoyant density is present only after stimulation of submucosal gland secretion by methacholine. Lipids are synthesized, at least in part, by the airway mucosa and occur in explant secretions as a viscoelastic gel, suggesting that they significantly influence the rheological properties of airway mucus. In addition to cholinergic and adrenergic secretomotor neurons, the airway mucosa is innervated by peptidergic fibres containing immunoreactivity to vasoactive intestinal peptide (VIP) and substance P (SP). In explants of non-bronchitic human airway, VIP inhibits baseline glycoprotein and lysozyme secretion; in canine airway mucosa, by contrast, VIP is a weak partial secretory agonist. SP is the most potent agonist of canine airway glycoprotein release described to date and appears to evoke secretion by a direct action on a stereospecific SP receptor rather than by inducing release of other endogenous secretagogues. VIP and SP have little effect on glycoprotein discharge by mucous and serous cells of the submucosal gland; SP appears to induce secretion by causing contraction of submucosal gland ducts. This may represent the most rapid way for delivering mucus into the airway in response to injury or irritation of airway epithelium.
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PMID:Airway mucus: composition and regulation of its secretion by neuropeptides in vitro. 608 50

The effects of vasoactive intestinal peptide (VIP) were analyzed on the in vitro release of radioactively labeled mucus glycoconjugates and lysozyme by explants of human bronchial mucosa from normal subjects and from patients with chronic bronchitis. These effects were compared with the effects of VIP on the discharge of labeled macromolecules (analyzed by quantitative autoradiography) from mucous and serous cells of the airway submucosal glands. In explants of 9 mucosal specimens of normal airways, VIP (10 ng to 1 micrograms/ml) caused a dose-dependent inhibition of baseline and methacholine-stimulated release of both glycoconjugates and lysozyme. At a concentration (1 micrograms/ml) that caused maximal inhibition of glycoconjugate and lysozyme release, VIP also caused a small inhibition of baseline but not methacholine-induced discharge of labeled macromolecules from mucous and serous cells of the submucosal glands. In explants from 5 patients with chronic bronchitis, VIP did not inhibit baseline or methacholine-stimulated glycoconjugate release and mucous or serous cell discharge, even at doses greater than 1 micrograms/ml. By contrast, VIP did inhibit baseline and methacholine-stimulated release of lysozyme, but this was less marked than in explants of normal airways. In view of the proximity of neurons containing VIP to submucosal gland cells, this study supported the hypothesis that VIP may contribute to the neurohumoral regulation of mucus secretion by the human airway. It was evident, however, that the effects of VIP could not be accounted for in terms of inhibiting cell discharge alone. In chronic bronchitis, the reduction or absence of sensitivity to VIP inhibition suggests a functional difference in the regulation of mucus secretion, which may contribute to mucus hypersecretion.
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PMID:Inhibition by vasoactive intestinal peptide of glycoconjugate and lysozyme secretion by human airways in vitro. 730 6

Sudden Infant Death Syndrome (SIDS) victims have significantly thickened bronchiolar walls with increased mononuclear cells in the adventitia. An immunohistochemical study was performed on 25 SIDS and 18 aged-matched control infants to characterize these cells. The panel of antibodies included alpha-1-antitrypsin, lysozyme, actin, vimentin, Leu M1, NSE, S-100, Leu 6, bombesin, serotonin, anti-substance P, vasoactive intestinal peptide, MAC 387, and Factor XIIIa. The bronchiolar cells stained with S-100 antibody and demonstrated slender processes similar to dendritic cells, such as Langerhans' cells, and interdigitating reticulum cells, present in normal tissues as well as in certain tumors and inflammatory diseases. Manual counting of the S-100 positive cells and fibers revealed both of these to be significantly increased in SIDS infants as compared to age-matched control infants. Morphologically, the bronchiolar dendritic cells closely resembled Langerhans' cells and therefore may have similar immunologic functions, such as antigen presentation and viral and neoantigen immunosurveillance. We hypothesize that the proliferation of these dendritic cells in SIDS victims is a result of exposure to environmental antigens, resulting in a thickening of the bronchiolar walls, narrowing of the lumen, and reduction in airflow, thus causing a chronic or persistent hypoxia.
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PMID:Proliferation of dendritic cells in the bronchioles of sudden infant death syndrome victims. 834 85

Chemorepellents are compounds that cause ciliated protozoans to reorient their swimming direction. A number of chemorepellents have been studied in the ciliated protozoans, Paramecium and Tetrahymena. Chemorepellents, such as polycations, cause the organism to exhibit "avoidance behavior," a swimming behavior characterized by jerky movements and other deviations from normal forward swimming, which result from ciliary reversal. One well-characterized chemorepellent pathway in Tetrahymena is that of the proposed polycation receptor that is activated by lysozyme and pituitary adenylate cyclase activating polypeptide (PACAP). In this study, we compare the response of Paramecium to the chemorepellents lysozyme, vasoactive intestinal peptide (VIP), and PACAP to the previously studied polycation response in Tetrahymena. Our results indicate that lysozyme, VIP, and PACAP are all chemorepellents in Paramecium, just as they are in Tetrahymena. However, the signaling pathways involved appear to be different. While previous pharmacological characterization indicates that G-proteins are involved in polycation signaling in Tetrahymena, we present evidence that similar reception in Paramecium involves activation of a tyrosine kinase pathway in order for lysozyme avoidance to occur. Polycation responses of both organisms are inhibited by neomycin sulfate. While PACAP is the most effective of the three chemorepellents in Tetrahymena, lysozyme is the most effective chemorepellent in Paramecium.
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PMID:A comparison of the polycation receptors of Paramecium tetraurelia and Tetrahymena thermophila. 1831 60