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:3.1.4.3 (phospholipase C)
18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Available information suggests that some instances of preterm birth or premature rupture of membranes are associated with clinically unrecognized infection and inflammation of the lower uterine segment, decidua, and fetal membranes. Various cervicovaginal microorganisms have been recovered from these sites. Many of these microorganisms produce factors that may lead to weakening of the fetal membranes, release of prostaglandins, or both. This study evaluated the presence of various lower genital tract microflora and bacterial conditions in 229 women enrolled in a double-blind, placebo-controlled trial of short-course erythromycin treatment at 26 to 30 weeks' gestation to prevent preterm birth. Demographic, obstetric, and microbiologic parameters were prospectively evaluated. Premature rupture of membranes occurred less frequently (p less than 0.01) among women who received erythromycin (6%) versus placebo (16%). Preterm premature rupture of membranes also occurred less frequently, although not significantly (p = 0.3) in patients who received erythromycin (2%) versus placebo (5%). Erythromycin treatment significantly decreased the occurrence of premature rupture of membranes among women who were initially positive for Chlamydia trachomatis infection. Logistic regression analysis demonstrated that C. trachomatis (p = 0.05; odds ratio, 9), vaginal wash phospholipase C (p = 0.08; odds ratio, 6) and prior preterm birth (p = 0.007; odds ratio 17) were associated with increased risk of preterm birth. Bacterial vaginosis, Mycoplasma hominis, Ureaplasma urealyticum were not significantly associated with increased risk of preterm birth or preterm rupture of membranes. These findings support a role for selected lower genital tract microflora in preterm birth and premature rupture. Large controlled treatment trials of specific infections or conditions associated with preterm birth and premature rupture of membranes are required to confirm the value of antimicrobial treatments in prevention of microbial-associated preterm birth.
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PMID:Cervicovaginal microflora and pregnancy outcome: results of a double-blind, placebo-controlled trial of erythromycin treatment. 224 Jan 10

A screening assay for phospholipase C using a chromogenic substrate incorporated into agar medium is described. The assay directly visualizes phospholipase C activity of mycoplasma lysates and membranes on agar plates, or the activity may be measured by spectrophotometry. The results from the assay confirm the presence in Ureaplasma urealyticum of phospholipase C, which is predominantly localized in the membrane fraction. The procedure has the potential to screen phospholipase C activity in other mycoplasmas and microorganisms in general.
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PMID:Rapid screening assay for phospholipase C activity in mycoplasmas. 357 80

Intact Haemophilus pleuropneumoniae cells (strain Shope 1, serotype 1), highly purified lipopolysaccharide (LPS) obtained from this strain of H pleuropneumoniae, as well as from Escherichia coli O111:B4, filter-sterilized H pleuropneumoniae cell-free culture supernatant fluid, and heat-inactivated supernatant fluid were given intranasally to CF1 mice and intratracheally to pigs. Pulmonary lesions induced by H pleuropneumoniae in mice were similar to those induced by H pleuropneumoniae in pigs. Histologically, lungs of mice and pigs killed 1 or 2 days after inoculation with 200 micrograms of highly purified H pleuropneumoniae LPS had lesions similar to one another and were similar to those in mice and pigs given intact H pleuropneumoniae, except that little or no necrosis or hemorrhage was observed. In mice killed 1 or 2 days after inoculation of 200 micrograms of E coli O111:B4 LPS, pulmonary lesions were similar to those in mice given H pleuropneumoniae LPS. Pulmonary lesions in mice given cell-free culture supernatant fluid obtained from a midlog-phase growth culture of H pleuropneumoniae cultivated in a chemically defined medium were severe and consisted of neutrophil infiltration and extensive necrosis. In mice, the heat-inactivated supernatant fluid produced mild lesions that consisted of foci of neutrophil aggregation and no necrosis. Extensive necrosis observed in lesions caused by cell-free culture supernatant fluid could be attributed to the action of a heat-labile component, perhaps by the extracellular heat-labile hemolysin produced by H pleuropneumoniae cultivated in chemically defined medium. A LPS endotoxin and a heat-labile factor may be involved in the pulmonary lesion development in the acute phase of porcine Haemophilus pleuropneumonia.
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PMID:Role of haemophilus pleuropneumoniae lipopolysaccharide endotoxin in the pathogenesis of porcine Haemophilus pleuropneumonia. 359 76

A Mycoplasma gallisepticum subcellular fraction (P2), which contains the deoxyribonucleic acid replication complex, can be isolated by differential centrifugation of freeze-thaw-lysed cells. The nascent deoxyribonucleic acid is released from P2 by Lubrol-WX, sodium dodecyl sulfate, Pronase, and deoxyribonuclease, but not by saponin, ribonuclease, phospholipase C, or high-frequency sonic treatment. Sonic treatment further fractionates the cell ghost and allows partial purification, on sucrose density gradients, of a deoxyribonucleic acid replication complex attached to the cells' polar membrane-bleb-infrableb structures.
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PMID:Partial purification of a membrane-associated deoxyribonucleic acid complex from Mycoplasma gallisepticum. 442 Sep 60

Bernheimer, Alan W. (New York University School of Medicine, New York, N.Y.). Disruption of wall-less bacteria by streptococcal and staphylococcal toxins. J. Bacteriol. 91:1677-1680. 1966.-Earlier studies demonstrating that staphylococcal alpha-toxin and streptolysin S have the capacity to lyse protoplasts and spheroplasts of certain species of bacteria and Mycoplasma have been extended to encompass additional kinds of wall-less bacteria including L forms. It is suggested that sensitivity to staphylococcal alpha-toxin and streptolysin S may be explicable in terms of specific phospholipid composition of cell membranes, whereas sensitivity to streptolysin O is dependent upon the presence in cell membranes of cholesterol. The results suggest that streptolysin O might prove to be a useful reagent for differentiating L forms from parasitic pleuropneumonia-like organisms.
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PMID:Disruption of wall-less bacteria by streptococcal and staphylococcal toxins. 532 3

Total lipid extracts were obtained from SH-SY5Y human neuroblastoma cells grown to confluency in mycoplasma-free 10% fetal calf serum. The major glycerophospholipid classes and free diacylglycerols (DAG) were isolated and quantitated by silicic acid and DEAE-cellulose column and thin-layer chromatography. The choline (CGPL), ethanolamine (EGPL), serine (SGPL), and inositol (IGPL) glycerophospholipids were converted to the corresponding diradylglycerols by phospholipase C. The molecular species of the diradylglycerols were determined by capillary gas-liquid chromatography of the trimethylsilyl or t-butyldimethylsilyl ethers. The CGPL was rich in the oligoenoic species and IGPL was rich in the polyenoic species, especially the 18:0-20:4(n-6). The EGPL contained 30-40% diacyl, 60-64% alkenylacyl, and 1-3% alkylacyl species, which were also rich in polyenoic derivatives. Small amounts of alkenylacyl species were detected also in CGPL. The cellular DAG possessed a molecular species composition halfway between those of the DAG moieties of CGPL and IGPL. The cells grown in the presence of 10% calf serum exhibited great variability in the content of 20:3(n-9) fatty acid, which was found to substitute for the 20:4(n-6) acid in the molecular species with 18:0 in both IGPL and DAG. The 20:3(n-9) was largely absent from the CGPL, but occurred also in EGPL, where it was preferentially associated with 18:0 in the diacyl but with 18:1 in the alkylacyl and alkenylacyl species. The detailed documentation of molecular species of glycerophospholipids of the neuroblastoma cells offers new opportunities for identification of the source of free DAG released in transmembrane signalling.
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PMID:Molecular species of glycerophospholipids and diacylglycerols of cultured SH-SY5Y human neuroblastoma cells. 839 72

Mycoplasma fermentans-derived membrane lipoproteins (LAMPf) have been demonstrated to stimulate monocytic cells and to induce the secretion of proinflammatory cytokines by a mechanism involving the triggering of protein tyrosine kinase and mitogen-activated protein kinase cascades. Herein, we have examined the effects of LAMPf on the activation of a series of transcription factors potentially involved in cytokine gene expression. LAMPf was capable of inducing NF-kappa B, activated protein 1 (AP-1), and c-fos activation in macrophages and of stimulating NF-kappa B and AP-1 transactivation. Furthermore, we have delineated the contribution of each mitogen-activated protein kinase pathway to the LAMPf-mediated activation of AP-1, c-fos, and NF-kappa B. Whereas the selective extracellular signal-regulated kinase pathway inhibitor PD-98059 did not affect the LAMPf-mediated transactivation of AP-1, c-fos, or NF-kappa B, the specific p38 inhibitor SB203580 abrogated this activity. A c-Jun N-terminal kinase-dominant negative was shown to block the activation of AP-1 without altering NF-kappa B or c-fos activation by LAMPf. In addition, D609, a selective inhibitor of phosphatidylcholine-specific phospholipase C, was shown to block both translocation and transactivation of either NF-kappa B or AP-1 in response to LAMPf. Although LAMPf-mediated macrophage activation is CD14 independent, we could not distinguish between the intracellular mechanisms leading to the macrophage activation triggered by either LPS or LAMPf. This suggests that macrophages display a common signaling machinery leading to the secretion of proinflammatory cytokines in response to different bacterial products. The comprehension of these mechanisms may help to better understanding the bacterial pathogenesis and to elucidate general mechanisms of macrophage activation leading to cytokine secretion.
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PMID:Signal transduction pathways involved in the activation of NF-kappa B, AP-1, and c-fos by Mycoplasma fermentans membrane lipoproteins in macrophages. 997 95

Previous studies have shown that 'toxic malarial antigens' released by Plasmodium yoelii can induce hypoglycaemia in mice and act synergistically with insulin in stimulating lipogenesis in rat adipocytes in vitro. In this study, it was shown that similar bioactivity could be detected in Plasmodium falciparum culture supernatant, and the molecular basis of this activity was further investigated. Boiled spent culture medium from P. falciparum cultures ('BS-Pf') (exclusively released into the culture supernatant when schizonts rupture) acts in synergy with insulin to increase lipogenesis in a rat adipocyte assay by more than 250% (P < 0.001). Control preparations prepared from non-parasitized erythrocytes grown under similar conditions had no effect (P < 0.001). While contamination with mycoplasma has previously been shown to interfere with the interpretation of data obtained with other molecules thought to be released from P. falciparum in culture, including those inducing TNF-alpha and NO production by macrophages, such contamination was unequivocally ruled out here. BS-Pf alone did not stimulate the lipogenesis in short-term assays (less than 4 h), while long-term exposure of rat adipocytes to BS-Pf alone (12-24 h) caused a stimulation of lipogenesis at a level comparable to that observed with insulin. Furthermore, lipogenesis-inducing activity was also detected in the serum of squirrel monkeys infected with different species of malaria parasites (P. vivax, P. falciparum and P. brasilianum). Preliminary biochemical characterization showed that the biological activity was found in the solvent-extracted polar lipid fraction of boiled supernatant of P. falciparum cultures. All the different polar lipid fractions, collected from silica gel column chromatography, showed a comparable lipogenesis-inducing activity. Enzymatic treatment by phospholipase C of the lipid fraction, which co-migrated with the phosphatidylcholine standard, showed that the activity of the fraction was associated with the 1,2-diacylglycerol (1,2-DAG) moieties released from polar lipids. When this exogenous 1,2-DAG was added to the adipocyte cultures (short- and long-term cultures), it induced stimulation of lipogenesis in rat adipocytes, while no lipogenic activity was obtained from bacterial polar lipids and 1,2-DAG isolated from unparasitized erythrocytes. The importance of these findings is discussed with reference to other toxic malarial antigens and also to the potential role of these molecules in the induction of hypoglycaemia in the severe forms of malaria.
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PMID:Polar Plasmodium falciparum lipids induce lipogenesis in rat adipocytes in vitro. 1116 22

We investigated the effects of intact pathogenic Mycoplasma hyopneumoniae, nonpathogenic M. hyopneumoniae, and Mycoplasma flocculare on intracellular free Ca2+ concentrations ([Ca2+]i) in porcine ciliated tracheal epithelial cells. The ciliated epithelial cells had basal [Ca2+]i of 103 +/- 3 nM (n = 217 cells). The [Ca2+]i increased by 250 +/- 19 nM (n = 47 cells) from the basal level within 100 s of the addition of pathogenic M. hyopneumoniae strain 91-3 (300 microg/ml), and this increase lasted approximately 60 s. In contrast, nonpathogenic M. hyopneumoniae and M. flocculare at concentrations of 300 microg/ml failed to increase [Ca2+]i. In Ca2+-free medium, pathogenic M. hyopneumoniae still increased [Ca2+]i in tracheal cells. Pretreatment with thapsigargin (1 microM for 30 min), which depleted the Ca2+ store in the endoplasmic reticulum, abolished the effect of M. hyoneumoniae. Pretreatment with pertussis toxin (100 ng/ml for 3 h) or U-73122 (2 microM for 100 s), an inhibitor of phospholipase C, also abolished the effect of M. hyopneumoniae. The administration of mastoparan 7, an activator of pertussis toxin-sensitive proteins G(i) and G(o), increased [Ca2+]i in ciliated tracheal cells. These results suggest that pathogenic M. hyopneumoniae activates receptors that are coupled to G(i) or G(o), which in turn activates a phospholipase C pathway, thereby releasing Ca2+ from the endoplasmic reticulum. Thus, an increase in Ca2+ may serve as a signal for the pathogenesis of M. hyopneumoniae.
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PMID:Mycoplasma hyopneumoniae increases intracellular calcium release in porcine ciliated tracheal cells. 1195 88

Six strains representing three species of Mycoplasma were examined for susceptibility to lysis by staphylococcal and streptococcal toxins. All were sensitive to staphylococcal alpha-toxin, two to streptolysin S, and three to streptolysin O. The results support the concept that the limiting membrane of pleuropneumonia-like organisms is basically similar to those of many other cell types and provide additional evidence for the participation of cholesterol in cytolysis induced by streptolysin O.
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PMID:LYSIS OF PLEUROPNEUMONIA-LIKE ORGANISMS BY STAPHYLOCOCCAL AND STREPTOCOCCAL TOXINS. 1428 3


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