Internalization of Clostridium difficile cytotoxin into cultured human lung fibroblasts
Identifieur interne : 003634 ( Main/Exploration ); précédent : 003633; suivant : 003635Internalization of Clostridium difficile cytotoxin into cultured human lung fibroblasts
Auteurs : Inger Florin [Suède] ; Monica Thelestam [Suède]Source :
- BBA - Molecular Cell Research [ 0167-4889 ] ; 1983.
Descripteurs français
- KwdFr :
- Cinétique, Clostridium (pathogénicité), Concentration en ions d'hydrogène, Fibroblastes (métabolisme), Humains, Lignée cellulaire, Masse moléculaire, Membrane cellulaire (), Potassium (métabolisme), Poumon (métabolisme), Protéines bactériennes, Toxines bactériennes (isolement et purification), Toxines bactériennes (métabolisme), Électrophorèse sur gel de polyacrylamide.
- MESH :
- isolement et purification : Toxines bactériennes.
- métabolisme : Fibroblastes, Potassium, Poumon, Toxines bactériennes.
- pathogénicité : Clostridium.
- Cinétique, Concentration en ions d'hydrogène, Humains, Lignée cellulaire, Masse moléculaire, Membrane cellulaire, Protéines bactériennes, Électrophorèse sur gel de polyacrylamide.
English descriptors
- KwdEn :
- Bacterial Proteins, Bacterial Toxins (isolation & purification), Bacterial Toxins (metabolism), Cell Line, Cell Membrane (drug effects), Clostridium (pathogenicity), Electrophoresis, Polyacrylamide Gel, Fibroblasts (metabolism), Humans, Hydrogen-Ion Concentration, Kinetics, Lung (metabolism), Molecular Weight, Potassium (metabolism).
- MESH :
- chemical , isolation & purification : Bacterial Toxins.
- chemical , metabolism : Bacterial Toxins, Potassium.
- drug effects : Cell Membrane.
- metabolism : Fibroblasts, Lung.
- pathogenicity : Clostridium.
- Teeft :
- Ammonium, Ammonium chloride, Antitoxin, Bacterial Proteins, Balanced salt solution, Biol, Cell Line, Cell biol, Cell surface, Chloroquine, Cytopathogenic, Cytopathogenic effect, Cytotoxic activity, Cytotoxin, Electrophoresis, Polyacrylamide Gel, Endocytotic vesicles, Energy metabolism, Fibroblast, Final concentration, Growth medium, Human lung fibroblasts, Humans, Hydrogen-Ion Concentration, Hydrophobic domain, Immun, Inhibitor, Kinetics, Latency, Latency period, Lectin, Lipid vesicles, Lung fibroblasts, Lysosomotropic, Lysosomotropic agents, Macromolecular synthesis, Microfilament system, Molecular Weight, Percent cytopathogenic effect, Potassium cyanide, Protective effect, Regular intervals, Sodium arsenate, Sodium azide, Sodium fluoride, Tcdso, Time periods, Time point, Toxin, Toxin exposure, Toxin solutions, Trypsin, Vesicle.
Abstract
Abstract: In cultured human lung fibroblasts treated with Clostridium difficile cytotoxin, the latency before appearance of the cytopathogenic effect was dose-related with a minimum of 45 min. At 37°C, the toxin was accessible on all cells to inactivation with trypsin or neutralization with antitoxin during the first tenth of the latency. At 0°C, the toxin was accessible considerably longer. The cytopathogenic effect was reversibly prevented by the lysosomotropic agents chloroquine and ammonium chloride, which had to be added within one-fifth of the latency to protect all cells. In the presence of chloroquine, but not of ammonium chloride, the time period during which the toxin remained amenable to neutralization with antitoxin was prolonged. The protective effect of ammonium chloride was not influenced by dropping the extracellular pH to 4.5, but that of chloroquine was abolished. The expression of the intoxication was not affected by inhibitors of the DNA, RNA or protein synthesis. Inhibitors of the energy metabolism prevented the cytopathogenic effect when added before the last phase of the latency. The results suggest that expression of the cytopathogenic effect requires internalization of the toxin, and that metabolic energy but no macromolecular synthesis is needed for the action of the toxin after this internalization.
Url:
DOI: 10.1016/0167-4889(83)90100-3
Affiliations:
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At 37°C, the toxin was accessible on all cells to inactivation with trypsin or neutralization with antitoxin during the first tenth of the latency. At 0°C, the toxin was accessible considerably longer. The cytopathogenic effect was reversibly prevented by the lysosomotropic agents chloroquine and ammonium chloride, which had to be added within one-fifth of the latency to protect all cells. In the presence of chloroquine, but not of ammonium chloride, the time period during which the toxin remained amenable to neutralization with antitoxin was prolonged. The protective effect of ammonium chloride was not influenced by dropping the extracellular pH to 4.5, but that of chloroquine was abolished. The expression of the intoxication was not affected by inhibitors of the DNA, RNA or protein synthesis. Inhibitors of the energy metabolism prevented the cytopathogenic effect when added before the last phase of the latency. The results suggest that expression of the cytopathogenic effect requires internalization of the toxin, and that metabolic energy but no macromolecular synthesis is needed for the action of the toxin after this internalization.</div></front></TEI><affiliations><list><country><li>Suède</li></country></list><tree><country name="Suède"><noRegion><name sortKey="Florin, Inger" sort="Florin, Inger" uniqKey="Florin I" first="Inger" last="Florin">Inger Florin</name></noRegion><name sortKey="Thelestam, Monica" sort="Thelestam, Monica" uniqKey="Thelestam M" first="Monica" last="Thelestam">Monica Thelestam</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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