Difference between revisions of "PMID:18694955"

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'''Bailey, AM , Paulsen, IT  and Piddock, LJ '''  (2008) RamA confers multidrug resistance in Salmonella enterica via increased expression of acrB, which is inhibited by chlorpromazine. ''Antimicrob. Agents Chemother.'' '''52''':3604-11
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Salmonella enterica serovar Typhimurium SL1344, in which efflux pump genes (acrB, acrD, acrF, tolC) or regulatory genes thereof (marA, soxS, ramA) were inactivated, was grown in the presence of 240 antimicrobial and nonantimicrobial agents in the Biolog Phenotype MicroArray. Mutants lacking tolC, acrB, and ramA grew significantly worse than other mutants in the presence of 48 agents (some of which have not previously been identified as substrates of AcrAB-TolC) and particularly poorly in the presence of phenothiazines, which are human antipsychotics. MIC testing revealed that the phenothiazine chlorpromazine had antimicrobial activity and synergized with common antibiotics against different Salmonella serovars and SL1344. Chlorpromazine increased the intracellular accumulation of ethidium bromide, which was ablated in mutants lacking acrB, suggesting an interaction with AcrB. High-level but not low-level overexpression of ramA increased the expression of acrB; conferred resistance to chloramphenicol, tetracycline, nalidixic acid, and triclosan and organic solvent tolerance; and increased the amount of ethidium bromide accumulated. Chlorpromazine induced the modest overproduction of ramA but repressed acrB. These data suggest that phenothiazines are not efflux pump inhibitors but influence gene expression, including that of acrB, which confers the synergy with antimicrobials observed.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=18694955 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2565896 PMC2565896]
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Online version:[http://dx.doi.org/10.1128/AAC.00661-08 10.1128/AAC.00661-08]
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Anti-Bacterial Agents/administration & dosage; Antipsychotic Agents/administration & dosage; Antipsychotic Agents/pharmacology; Bacterial Proteins/genetics; Base Sequence; Chlorpromazine/administration & dosage; Chlorpromazine/pharmacology; DNA Primers/genetics; DNA, Bacterial/genetics; Drug Resistance, Multiple, Bacterial/genetics; Drug Synergism; Ethidium/metabolism; Gene Expression/drug effects; Genes, Bacterial; Humans; Membrane Transport Proteins/genetics; Multidrug Resistance-Associated Proteins/genetics; Mutation; Oligonucleotide Array Sequence Analysis; Phenothiazines/administration & dosage; Phenothiazines/pharmacology; Salmonella typhimurium/drug effects; Salmonella typhimurium/genetics; Salmonella typhimurium/metabolism; Trans-Activators/genetics
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==Main Points of the Paper ==
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== Materials and Methods Used ==
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==Phenotype Annotations==
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==Notes==
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==References==
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[[Category:Publication]]

Revision as of 11:36, 17 September 2012

Citation

Bailey, AM , Paulsen, IT and Piddock, LJ (2008) RamA confers multidrug resistance in Salmonella enterica via increased expression of acrB, which is inhibited by chlorpromazine. Antimicrob. Agents Chemother. 52:3604-11

Abstract

Salmonella enterica serovar Typhimurium SL1344, in which efflux pump genes (acrB, acrD, acrF, tolC) or regulatory genes thereof (marA, soxS, ramA) were inactivated, was grown in the presence of 240 antimicrobial and nonantimicrobial agents in the Biolog Phenotype MicroArray. Mutants lacking tolC, acrB, and ramA grew significantly worse than other mutants in the presence of 48 agents (some of which have not previously been identified as substrates of AcrAB-TolC) and particularly poorly in the presence of phenothiazines, which are human antipsychotics. MIC testing revealed that the phenothiazine chlorpromazine had antimicrobial activity and synergized with common antibiotics against different Salmonella serovars and SL1344. Chlorpromazine increased the intracellular accumulation of ethidium bromide, which was ablated in mutants lacking acrB, suggesting an interaction with AcrB. High-level but not low-level overexpression of ramA increased the expression of acrB; conferred resistance to chloramphenicol, tetracycline, nalidixic acid, and triclosan and organic solvent tolerance; and increased the amount of ethidium bromide accumulated. Chlorpromazine induced the modest overproduction of ramA but repressed acrB. These data suggest that phenothiazines are not efflux pump inhibitors but influence gene expression, including that of acrB, which confers the synergy with antimicrobials observed.

Links

PubMed PMC2565896 Online version:10.1128/AAC.00661-08

Keywords

Anti-Bacterial Agents/administration & dosage; Antipsychotic Agents/administration & dosage; Antipsychotic Agents/pharmacology; Bacterial Proteins/genetics; Base Sequence; Chlorpromazine/administration & dosage; Chlorpromazine/pharmacology; DNA Primers/genetics; DNA, Bacterial/genetics; Drug Resistance, Multiple, Bacterial/genetics; Drug Synergism; Ethidium/metabolism; Gene Expression/drug effects; Genes, Bacterial; Humans; Membrane Transport Proteins/genetics; Multidrug Resistance-Associated Proteins/genetics; Mutation; Oligonucleotide Array Sequence Analysis; Phenothiazines/administration & dosage; Phenothiazines/pharmacology; Salmonella typhimurium/drug effects; Salmonella typhimurium/genetics; Salmonella typhimurium/metabolism; Trans-Activators/genetics

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Main Points of the Paper

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Materials and Methods Used

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Phenotype Annotations

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Phenotype of Taxon Information Genotype Information (if known) Condition Information OMP ID OMP Term Name ECO ID ECO Term Name Notes Status
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Notes

References

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