Cellular pharmacokinetics of telavancin, a novel lipoglycopeptide antibiotic, and analysis of lysosomal changes in cultured eukaryotic cells (J774 mouse macrophages and rat embryonic fibroblasts)
Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resis...
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| Published in | Journal of antimicrobial chemotherapy Vol. 61; no. 6; pp. 1288 - 1294 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Oxford University Press
01.06.2008
Oxford Publishing Limited (England) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0305-7453 1460-2091 1460-2091 |
| DOI | 10.1093/jac/dkn120 |
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| Abstract | Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin). Methods J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5–90 mg/L). The following studies were performed: measurement of 14C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content. Results The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of ∼10 mL/g of protein/h). Efflux (macrophages) was ∼5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-β-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis). Conclusions Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus. |
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| AbstractList | Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin).BACKGROUNDTelavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin).J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5-90 mg/L). The following studies were performed: measurement of (14)C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content.METHODSJ774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5-90 mg/L). The following studies were performed: measurement of (14)C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content.The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of approximately 10 mL/g of protein/h). Efflux (macrophages) was approximately 5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-beta-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis).RESULTSThe uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of approximately 10 mL/g of protein/h). Efflux (macrophages) was approximately 5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-beta-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis).Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus.CONCLUSIONSTelavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus. Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin). J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5-90 mg/L). The following studies were performed: measurement of (14)C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content. The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of approximately 10 mL/g of protein/h). Efflux (macrophages) was approximately 5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-beta-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis). Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus. Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin). Methods J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5-90 mg/L). The following studies were performed: measurement of 14C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content. Results The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of ∼10 mL/g of protein/h). Efflux (macrophages) was ∼5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-β-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis). Conclusions Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus. BACKGROUND: Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin). METHODS: J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5-90 mg/L). The following studies were performed: measurement of super(14)C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content. RESULTS: The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of similar to 10 mL/g of protein/h). Efflux (macrophages) was similar to 5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl- beta -hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis). CONCLUSIONS: Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus. Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin). Methods J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5–90 mg/L). The following studies were performed: measurement of 14C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content. Results The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of ∼10 mL/g of protein/h). Efflux (macrophages) was ∼5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-β-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis). Conclusions Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus. Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin). Methods J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5-90 mg/L). The following studies were performed: measurement of 14 C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content. Results The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of ~10 mL/g of protein/h). Efflux (macrophages) was ~5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-[beta]-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis). Conclusions Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus. [PUBLICATION ABSTRACT] |
| Author | Mouaden, Fatima Barcia-Macay, Maritza Van Bambeke, Françoise Mingeot-Leclercq, Marie-Paule Tulkens, Paul M. |
| AuthorAffiliation | Université catholique de Louvain , Faculté de Médecine, Unité de Pharmacologie cellulaire et moléculaire, B-1200 Brussels , Belgium |
| AuthorAffiliation_xml | – name: Université catholique de Louvain , Faculté de Médecine, Unité de Pharmacologie cellulaire et moléculaire, B-1200 Brussels , Belgium |
| Author_xml | – sequence: 1 givenname: Maritza surname: Barcia-Macay fullname: Barcia-Macay, Maritza organization: Université catholique de Louvain, Faculté de Médecine, Unité de Pharmacologie cellulaire et moléculaire, B-1200 Brussels, Belgium – sequence: 2 givenname: Fatima surname: Mouaden fullname: Mouaden, Fatima organization: Université catholique de Louvain, Faculté de Médecine, Unité de Pharmacologie cellulaire et moléculaire, B-1200 Brussels, Belgium – sequence: 3 givenname: Marie-Paule surname: Mingeot-Leclercq fullname: Mingeot-Leclercq, Marie-Paule organization: Université catholique de Louvain, Faculté de Médecine, Unité de Pharmacologie cellulaire et moléculaire, B-1200 Brussels, Belgium – sequence: 4 givenname: Paul M. surname: Tulkens fullname: Tulkens, Paul M. organization: Université catholique de Louvain, Faculté de Médecine, Unité de Pharmacologie cellulaire et moléculaire, B-1200 Brussels, Belgium – sequence: 5 givenname: Françoise surname: Van Bambeke fullname: Van Bambeke, Françoise email: vanbambeke@facm.ucl.ac.be, Corresponding author. Tel: +32-2-764-7378; Fax: +32-2-764-7373; vanbambeke@facm.ucl.ac.be organization: E-mail: vanbambeke@facm.ucl.ac.be |
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| Keywords | vancomycin glycopeptides lipids oritavancin membrane cellular pharmacokinetics Peptides Rat Rodentia Lysosome Lipids Vancomycin In vitro Telavancin Vertebrata Antibiotic Mammalia Mouse Polypeptide Glycopeptide Animal Antibacterial agent Oritavancin Pharmacokinetics Fibroblast Macrophage |
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| References_xml | – reference: 4606365 - Biochem Pharmacol. 1974 Sep 15;23(18):2495-531 – reference: 7558665 - Int J Tissue React. 1994;16(5-6):211-20 – reference: 15855483 - Antimicrob Agents Chemother. 2005 May;49(5):1695-700 – reference: 7210003 - Toxicology. 1980;17(2):195-9 – reference: 19866613 - J Cell Biol. 1962 Dec 1;15(3):481-7 – reference: 7159463 - Biochem Pharmacol. 1982 Dec 1;31(23):3861-70 – reference: 10198278 - Toxicol Appl Pharmacol. 1999 Apr 15;156(2):129-40 – reference: 17923490 - Antimicrob Agents Chemother. 2008 Jan;52(1):92-7 – reference: 24449 - Biochem Pharmacol. 1978 Feb 15;27(4):415-24 – reference: 16955686 - Curr Opin Investig Drugs. 2006 Aug;7(8):740-9 – reference: 17062609 - J Antimicrob Chemother. 2006 Dec;58(6):1177-84 – reference: 16495241 - Antimicrob Agents Chemother. 2006 Mar;50(3):841-51 – reference: 15728913 - Antimicrob Agents Chemother. 2005 Mar;49(3):1127-34 – reference: 332066 - Annu Rev Biochem. 1977;46:669-722 – reference: 14907713 - J Biol Chem. 1951 Nov;193(1):265-75 – reference: 15303493 - J Antibiot (Tokyo). 2004 May;57(5):326-36 – reference: 16436747 - Antimicrob Agents Chemother. 2006 Feb;50(2):788-90 – reference: 14576125 - Antimicrob Agents Chemother. 2003 Nov;47(11):3602-4 – reference: 431047 - Lab Invest. 1979 Apr;40(4):481-91 – reference: 15616296 - Antimicrob Agents Chemother. 2005 Jan;49(1):195-201 – reference: 10920387 - Trends Microbiol. 2000 Aug;8(8):341-3 – reference: 12821480 - Antimicrob Agents Chemother. 2003 Jul;47(7):2283-92 – reference: 15273091 - Antimicrob Agents Chemother. 2004 Aug;48(8):2853-60 – reference: 12441132 - Exp Cell Res. 2002 Nov 15;281(1):86-100 – reference: 3579258 - Antimicrob Agents Chemother. 1987 Mar;31(3):410-6 – reference: 11499789 - Eur J Cell Biol. 2001 Jul;80(7):466-78 |
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| Snippet | Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows... Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows... Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal... BACKGROUND: Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows... |
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| SubjectTerms | Aminoglycosides - metabolism Aminoglycosides - toxicity Animals Anti-Bacterial Agents - metabolism Anti-Bacterial Agents - toxicity Antibiotics Antibiotics. Antiinfectious agents. Antiparasitic agents Biological and medical sciences Carbon Radioisotopes - metabolism Cell Fractionation Cell Line Cells, Cultured Cellular biology cellular pharmacokinetics Cholesterol - analysis Drug resistance Fibroblasts - chemistry Fibroblasts - drug effects glycopeptides Kinetics lipids Lysosomes - chemistry Lysosomes - drug effects Lysosomes - ultrastructure Macrophages - drug effects Medical sciences membrane Mice Microbiology Microscopy, Electron, Transmission Original Research oritavancin Pharmacology Pharmacology. Drug treatments Phospholipids - analysis Rats Staphylococcus aureus Staphylococcus infections Time Factors vancomycin |
| Title | Cellular pharmacokinetics of telavancin, a novel lipoglycopeptide antibiotic, and analysis of lysosomal changes in cultured eukaryotic cells (J774 mouse macrophages and rat embryonic fibroblasts) |
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