PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients

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Standard

PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients. / Miller, Amanda K; Brannon, Mark K; Stevens, Laurel; Johansen, Helle Krogh; Selgrade, Sara E; Miller, Samuel I; Høiby, Niels; Moskowitz, Samuel M.

In: Antimicrobial Agents and Chemotherapy, Vol. 55, No. 12, 03.10.2011, p. 5761-5769.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Miller, AK, Brannon, MK, Stevens, L, Johansen, HK, Selgrade, SE, Miller, SI, Høiby, N & Moskowitz, SM 2011, 'PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients', Antimicrobial Agents and Chemotherapy, vol. 55, no. 12, pp. 5761-5769. https://doi.org/10.1128/AAC.05391-11, https://doi.org/10.1128/AAC.05391-11

APA

Miller, A. K., Brannon, M. K., Stevens, L., Johansen, H. K., Selgrade, S. E., Miller, S. I., Høiby, N., & Moskowitz, S. M. (2011). PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients. Antimicrobial Agents and Chemotherapy, 55(12), 5761-5769. https://doi.org/10.1128/AAC.05391-11, https://doi.org/10.1128/AAC.05391-11

Vancouver

Miller AK, Brannon MK, Stevens L, Johansen HK, Selgrade SE, Miller SI et al. PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients. Antimicrobial Agents and Chemotherapy. 2011 Oct 3;55(12):5761-5769. https://doi.org/10.1128/AAC.05391-11, https://doi.org/10.1128/AAC.05391-11

Author

Miller, Amanda K ; Brannon, Mark K ; Stevens, Laurel ; Johansen, Helle Krogh ; Selgrade, Sara E ; Miller, Samuel I ; Høiby, Niels ; Moskowitz, Samuel M. / PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients. In: Antimicrobial Agents and Chemotherapy. 2011 ; Vol. 55, No. 12. pp. 5761-5769.

Bibtex

@article{bcb4979d7e27423baf744487c91e9591,
title = "PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients",
abstract = "Pseudomonas aeruginosa can develop resistance to polymyxin and other cationic antimicrobial peptides. Previous work has shown that mutations in the PmrAB and PhoPQ regulatory systems can confer low to moderate levels of polymyxin resistance (MICs of 8 - 64 mg/L) in laboratory and clinical strains of this organism. To explore the role of PhoPQ in high-level clinical polymyxin resistance, P. aeruginosa strains with colistin MICs > 512 mg/L that had been isolated from cystic fibrosis patients treated with inhaled colistin (polymyxin E) were analyzed. Probable loss-of-function phoQ alleles found in these cystic fibrosis strains conferred resistance to polymyxin. Partial and complete suppressor mutations in phoP were identified in some cystic fibrosis strains with resistance-conferring phoQ mutations, suggesting that additional loci can be involved in polymyxin resistance in P. aeruginosa. Disruption of chromosomal phoQ in the presence of an intact phoP allele stimulated 4-amino-L-arabinose addition to lipid A and induced transcription from the promoter of the pmrH (arnB) operon, consistent with the known role of this lipid A modification in polymyxin resistance. These results indicate that phoQ loss-of-function mutations can contribute to high-level polymyxin resistance in clinical strains of P. aeruginosa.",
author = "Miller, {Amanda K} and Brannon, {Mark K} and Laurel Stevens and Johansen, {Helle Krogh} and Selgrade, {Sara E} and Miller, {Samuel I} and Niels H{\o}iby and Moskowitz, {Samuel M}",
year = "2011",
month = oct,
day = "3",
doi = "10.1128/AAC.05391-11",
language = "English",
volume = "55",
pages = "5761--5769",
journal = "Antimicrobial Agents and Chemotherapy",
issn = "0066-4804",
publisher = "American Society for Microbiology",
number = "12",

}

RIS

TY - JOUR

T1 - PhoQ mutations promote lipid A modification and polymyxin resistance of Pseudomonas aeruginosa found in colistin-treated cystic fibrosis patients

AU - Miller, Amanda K

AU - Brannon, Mark K

AU - Stevens, Laurel

AU - Johansen, Helle Krogh

AU - Selgrade, Sara E

AU - Miller, Samuel I

AU - Høiby, Niels

AU - Moskowitz, Samuel M

PY - 2011/10/3

Y1 - 2011/10/3

N2 - Pseudomonas aeruginosa can develop resistance to polymyxin and other cationic antimicrobial peptides. Previous work has shown that mutations in the PmrAB and PhoPQ regulatory systems can confer low to moderate levels of polymyxin resistance (MICs of 8 - 64 mg/L) in laboratory and clinical strains of this organism. To explore the role of PhoPQ in high-level clinical polymyxin resistance, P. aeruginosa strains with colistin MICs > 512 mg/L that had been isolated from cystic fibrosis patients treated with inhaled colistin (polymyxin E) were analyzed. Probable loss-of-function phoQ alleles found in these cystic fibrosis strains conferred resistance to polymyxin. Partial and complete suppressor mutations in phoP were identified in some cystic fibrosis strains with resistance-conferring phoQ mutations, suggesting that additional loci can be involved in polymyxin resistance in P. aeruginosa. Disruption of chromosomal phoQ in the presence of an intact phoP allele stimulated 4-amino-L-arabinose addition to lipid A and induced transcription from the promoter of the pmrH (arnB) operon, consistent with the known role of this lipid A modification in polymyxin resistance. These results indicate that phoQ loss-of-function mutations can contribute to high-level polymyxin resistance in clinical strains of P. aeruginosa.

AB - Pseudomonas aeruginosa can develop resistance to polymyxin and other cationic antimicrobial peptides. Previous work has shown that mutations in the PmrAB and PhoPQ regulatory systems can confer low to moderate levels of polymyxin resistance (MICs of 8 - 64 mg/L) in laboratory and clinical strains of this organism. To explore the role of PhoPQ in high-level clinical polymyxin resistance, P. aeruginosa strains with colistin MICs > 512 mg/L that had been isolated from cystic fibrosis patients treated with inhaled colistin (polymyxin E) were analyzed. Probable loss-of-function phoQ alleles found in these cystic fibrosis strains conferred resistance to polymyxin. Partial and complete suppressor mutations in phoP were identified in some cystic fibrosis strains with resistance-conferring phoQ mutations, suggesting that additional loci can be involved in polymyxin resistance in P. aeruginosa. Disruption of chromosomal phoQ in the presence of an intact phoP allele stimulated 4-amino-L-arabinose addition to lipid A and induced transcription from the promoter of the pmrH (arnB) operon, consistent with the known role of this lipid A modification in polymyxin resistance. These results indicate that phoQ loss-of-function mutations can contribute to high-level polymyxin resistance in clinical strains of P. aeruginosa.

U2 - 10.1128/AAC.05391-11

DO - 10.1128/AAC.05391-11

M3 - Journal article

VL - 55

SP - 5761

EP - 5769

JO - Antimicrobial Agents and Chemotherapy

JF - Antimicrobial Agents and Chemotherapy

SN - 0066-4804

IS - 12

ER -

ID: 40216453