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)

65 children with the severe course of bronchial asthma (BA) were examined. The character of respiratory tract microflora, humoral immunity characteristics, mediators, of inflammation and pathomorphological features of the bronchial tree during the severe course of BA in children at the period of remission were studied. The specific features of the colonization of the bronchial tree by microflora in the severe form of BA were established. The severe course of BA in children at the period of remission was characterized by a higher content of tumor necrosis factor and an increase in the lysozyme activity of bronchoalveolar fluid. Disturbances in the proportion of cAMP and cGMP in smooth muscles and an increase in the number of apudocytes containing adrenalin and serotonin may probably be one of the mechanisms of bronchial hyperreactivity.
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PMID:[The nature of the respiratory tract microflora and the immunity indices in a severe form of bronchial asthma in children]. 1085 93

We have recently reported the lateral and rotational diffusion parameters for I-A(k) molecules expressing various cytoplasmic truncations (Int. Immunol. 12 (2000) 1319). We now describe the membrane dynamics of I-A(k) with various mutations in the presumed contact region between alphabeta-heterodimers in an (alphabeta)2 dimer of dimers structure. Such mutations are known to strongly affect the antigen presentation ability of these molecules (Int. Immunol. 10 (1998) 1237-1249) but cause relatively small changes in the molecular dynamics of I-A(k). Lateral diffusion coefficients of I-A(k) wild-type molecules and mutants obtained via fringe fluorescence photobleaching recovery (FPR) ranged from 1.1 to 2.3x10(-10)cm2/s at room temperature while fractional mobilities averaged 75+/-6%. For all cell types examined, treatment with either hen egg lysozyme 46-61 peptide or db-cAMP reduced the I-A(k) mobile fraction by about 10% relative to untreated cells, suggesting that these treatments may increase lateral confinement of class II in lipid rafts or cytoskeletal interactions of the molecules. Wild-type I-A(k) and mutants capable of normal or partial antigen presentation exhibited, as a group, slightly longer rotational correlation times (RCT) at 4 degrees C than did mutants inactive in antigen presentation, 14+/-4 versus 10+/-1 micros, respectively. Moreover, peptide, cAMP and anti-CD40 mAb treatment all increased rotational correlation times for fully- and partially-functional I-A(k) but not for non-functional molecules. For example, 16 h peptide treatment yielded average RCTs of 28+/-12 and 10+/-1 micros for the groups of functional and non-functional molecules, respectively. Such modulation of the dynamics of functional class II molecules is consistent with these treatments' stabilization of class II or induction of new gene expression. Measurements of fluorescence resonant energy transfer between I-A(k), though complicated by cellular autofluorescence, averaged 6+/-7% over 15 cells or treatments, a result consistent with the presence of a small fraction of I-A(k) as a dimer of dimers species. In summary, our results suggest subtle changes in the molecular motions of class II molecules correlate with a significant impact on class II function. Molecules active in antigen presentation exhibit more restricted motion in the membrane, and thus presumably more extensive intermolecular interactions, than non-functional molecules. Further, treatments, such as db-cAMP and anti-CD40, which rescue antigen presentation by partially defective mutants, appear to increase such interactions, several types of which have already been reported for class II. A more detailed understanding of these phenomena will require both more sensitive biophysical tools and a more refined model of the role of class II intermolecular interactions in antigen presentation.
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PMID:Molecular dynamics of point mutated I-A(k) molecules expressed on lymphocytes. 1141 Feb 53

Lysozyme is secreted in large quantities in human airways (10-20 mg/day), where it helps to defend against bacterial and fungal infection. Lysozyme expression is restricted to the serous cells of the submucosal glands, which also express high levels of cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels. It is often assumed that mucus secretion in human airways is coupled to anion secretion through CFTR Cl(-) channels located in the apical membrane. Therefore, a defect in CFTR function could cause abnormal mucus secretion leading to persistent bacterial infection and inflammation of the airways. In this study we measured simultaneous secretion of lysozyme and Cl(-) from human airway epithelial serous cells. Secretion of lysozyme was measured by a turbidimetric assay that relies on the ability of lysozyme to disrupt the wall of the bacterium Micrococcus lysodeikticus, thus causing a fall in the optical density of the sample. Secretion of Cl(-) was measured as short-circuit current in a modified Ussing chamber. Activation of Cl(-) secretion by stimulation of cAMP- or Ca(2+)-dependent pathways caused comparable increases in lysozyme secretion. Similarly, blockers of Cl(-) secretion, such as diphenylamine-2-carboxylate (DPC), also reduced lysozyme secretion. However, while treatment of airway submucosal gland cells with antisense oligonucleotides directed against CFTR reduced Cl(-) secretion, it had no significant effect on the total amount of lysozyme secretion. These results suggest a role for functional CFTR in regulation of lysozyme secretion in human airways.
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PMID:CFTR and lysozyme secretion in human airway epithelial cells. 1184 2

As a result of a complex survey of 120 patients with erosive gastroduodenal affections, significant abnormalities of the aggressive-protective balance of the mucous coat of the stomach were discovered. In addition to affections of local protection factors, the change of the hormonal status characterized by hypercortisolemia, hyperinsulinemia, hypergastrinemia and increased level of such cyclic nucleotides as cAMP and cGMP was revealed. The dependence of the mucus-producing function, lysozyme activity and acid production on the level of blood hormones was discovered. Alternate dependencies of cortisol, insulin and gastrin levels on cAMP and cGMP levels as well as alternate impact of cAMP and cGMP on acid-producing gastric cells were established.
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PMID:[The role of the hormones-cyclases system in the pathogenesis of erosive gastric and duodenal affections]. 1577 Aug 54

Protein kinase A (PKA) activity was detected in the fat body of Galleria mellonella larvae by a non-radioactive method using a specific peptide substrate-kemptide. The enzyme activity was stimulated by cAMP and its analogues: BzcMP, 8-Chl-cAMP and 8-Br-cAMP in concentrations of 1-4muM. Cyclic GMP was not effective in PKA activation. A two-fold increase in PKA activity was detected in the fat body of G. mellonella LPS-challenged larvae. Selective, membrane-permeable PKA inhibitors, H89 and Rp-8-Br-cAMPS, inhibited protein kinase A activity in the fat body of G. mellonella larvae in vitro and in vivo. The inhibition of PKA activity in vivo was correlated with a considerable lowering of haemolymph antibacterial activity and a decrease in lysozyme content in the fat body of immune challenged larvae. The use of phospho-motif antibodies recognising PKA phosphorylation consensus site allowed identification of four potential PKA phosphorylation substrates of 79, 45, 40 and 36kDa in G. mellonella fat body.
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PMID:Studies on the role of protein kinase A in humoral immune response of Galleria mellonella larvae. 1673 Jul 43

The activity of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) can be mediated by surface G protein-coupled receptors such as the beta(2)-adrenergic receptor. In this study, we explored the effect of a long-acting beta(2)-adrenergic agonist, salmeterol, on the CFTR-dependent secretory capacity of a human CF tracheal gland serous cell line (CF-KM4), homozygous for the delF508 mutation. We showed that, compared with the untreated CF serous cells, a 24-hour pre-incubation period with 200 nM salmeterol induced an 83% increase in delF508-CFTR-mediated chloride efflux. The restoration of the bioelectric properties is associated with increased apical surface pool of delF508-CFTR. Salmeterol induced a decrease in ion concentration and an increase in the level of hydration of the mucus packaged inside the CF secretory granules. The effects of salmeterol are not associated with a persistent production of cAMP. Western blotting on isolated secretory granules demonstrated immunoreactivity for CFTR and lysozyme. In parallel, we measured by atomic force microscopy an increased size of secretory granules isolated from CF serous cells compared with non-CF serous cells (MM39 cell line) and showed that salmeterol was able to restore a CF cell granule size similar to that of non-CF cells. To demonstrate that the salmeterol effect was a CFTR-dependent mechanism, we showed that the incubation of salmeterol-treated CF serous cells with CFTR-inh172 suppressed the restoration of normal secretory functions. The capacity of salmeterol to restore the secretory capacity of glandular serous cells suggests that it could also improve the airway mucociliary clearance in patients with CF.
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PMID:Salmeterol restores secretory functions in cystic fibrosis airway submucosal gland serous cells. 1893 28

This study investigated the sweetness of the sweet-tasting protein thaumatin and lysozyme by both an in vitro cell-based assay and an in vivo sensory analysis to elucidate the differences between in vitro and in vivo response profiles. Hek293 cells were constructed that stably expressed the human T1R2+T1R3 sweet-taste receptor, and their responses to thaumatin and lysozyme were analyzed by monitoring the levels of intracellular cAMP. The results indicated that thaumatin and lysozyme as well as aspartame induced a decrease in the intracellular cAMP accumulation of the T1R2+T1R3-transfected cells and that EC(50) values of thaumatin and lysozyme determined by cell-based assay are well-consistent with the results of the sweetness threshold value determined by sensory analysis in the presence of 140 mM NaCl. The results of both in vitro and in vivo experiments confirmed that the sweetness inhibitor lactisole significantly suppressed the sweetness of thaumatin and lysozyme.
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PMID:Interactions of the sweet-tasting proteins thaumatin and lysozyme with the human sweet-taste receptor. 1948 7

Malfunction of airway submucosal glands contributes to the pathology of cystic fibrosis (CF), and cell cultures of CF human airway glands show defects in Cl(-) and water transport. Recently, a transgenic pig model of CF (the CF pig) has been developed. Accordingly, we have developed cell cultures of pig airway gland epithelium for use in investigating alterations in gland function in CF. Our cultures form tight junctions (as evidenced by high transepithelial electrical resistance) and show high levels of active anion secretion (measured as amiloride-insensitive short-circuit current). In agreement with recent results on human airway glands, neurohumoral agents that elevate intracellular Ca(2+) potently stimulated anion secretion, while elevation of cAMP was comparatively ineffective. Our cultures express lactoferrin and lysozyme (serous gland cell markers) and MUC5B (the main mucin of airway glands). They are, therefore, potentially useful in determining if CF-related alterations in anion transport result in altered secretion of serous cell antimicrobial agents or mucus.
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PMID:Chloride secretion by cultures of pig tracheal gland cells. 2236 83


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