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Study · In vitro (cells) · pseudomonas aeruginosa · 2019

2 results

Mutations in pmrB Confer Cross-Resistance between the LptD Inhibitor POL7080 and Colistin in Pseudomonas aeruginosa.

Romano KP, Warrier T, Poulsen BE, Nguyen PH, Loftis AR, Saebi A, Pentelute BL, Hung DT

Antimicrobial agents and chemotherapy23 Aug 2019Cited by 35 (Europe PMC)

PMID31235628 (opens in a new tab)PMCIDPMC6709506 (opens in a new tab)DOI10.1128/aac.00511-19 (opens in a new tab)PepBankPUB-31235628
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Summary

Pseudomonas aeruginosa is a major bacterial pathogen associated with a rising prevalence of antibiotic resistance. We evaluated the resistance mechanisms of P. aeruginosa against POL7080, a species-specific, first-in-class antibiotic in clinical trials that targets the lipopolysaccharide transport protein LptD. We isolated a series of POL7080-resistant strains with mutations in the two-component sensor gene pmrB Transcriptomic and confocal microscopy studies support a resistance mechanism shared with colistin, involving lipopolysaccharide modifications that mitigate antibiotic cell surface binding.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

2 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In Pseudomonas aeruginosa, POL7080-resistant strains carried pmrB mutations.

    In plain wordsIn lab tests, bacteria resistant to POL7080 carried pmrB mutations.

    Peptide
    Murepavadin
    Outcome
    Direction not reportedResistance associated with pmrB mutations
    Study

    Pseudomonas aeruginosan: not reported in source

    POL7080-resistant strains
    Outcome group
    Infection and antimicrobial activity · Infection
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We isolated a series of POL7080-resistant strains with mutations in the two-component sensor gene pmrB
  2. 02LabIn vitro (cells)Mechanism

    In resistant Pseudomonas aeruginosa, LPS modifications supported a mechanism shared with colistin that reduced antibiotic surface binding.

    In plain wordsIn lab tests, resistant bacteria showed evidence of LPS changes that reduced antibiotic surface binding.

    Peptide
    Murepavadin
    Outcome
    DecreaseResistance mechanism
    Study

    Pseudomonas aeruginosan: not reported in source

    POL7080-resistant strains
    Outcome group
    Infection and antimicrobial activity · Infection
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Transcriptomic and confocal microscopy studies support a resistance mechanism shared with colistin, involving lipopolysaccharide modifications that mitigate antibiotic cell surface binding.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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