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Study · In vitro (cells) · pseudomonas aeruginosa · 2021

3 results

Colistin kills bacteria by targeting lipopolysaccharide in the cytoplasmic membrane.

Sabnis A, Hagart KL, Klöckner A, Becce M, Evans LE, Furniss RCD, Mavridou DA, Murphy R, Stevens MM, Davies JC, Larrouy-Maumus GJ, Clarke TB, Edwards AM

eLife6 Apr 2021Cited by 353 (Europe PMC)

PMID33821795 (opens in a new tab)PMCIDPMC8096433 (opens in a new tab)DOI10.7554/elife.65836 (opens in a new tab)PepBankPUB-33821795
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Summary

Colistin is an antibiotic of last resort, but has poor efficacy and resistance is a growing problem. Whilst it is well established that colistin disrupts the bacterial outer membrane (OM) by selectively targeting lipopolysaccharide (LPS), it was unclear how this led to bacterial killing. We discovered that MCR-1 mediated colistin resistance in Escherichia coli is due to modified LPS at the cytoplasmic rather than OM. In doing so, we also demonstrated that colistin exerts bactericidal activity by targeting LPS in the cytoplasmic membrane (CM). We then exploited this information to devise a new therapeutic approach. Using the LPS transport inhibitor murepavadin, we were able to cause LPS accumulation in the CM of Pseudomonas aeruginosa, which resulted in increased susceptibility to colistin in vitro and improved treatment efficacy in vivo. These findings reveal new insight into the mechanism by which colistin kills bacteria, providing the foundations for novel approaches to enhance therapeutic outcomes.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01LabIn vitro (cells)Mechanism

    In Pseudomonas aeruginosa, murepavadin caused LPS accumulation in the cytoplasmic membrane.

    In plain wordsIn lab tests, murepavadin increased LPS in the bacterial cytoplasmic membrane.

    Peptide
    Murepavadin
    Outcome
    IncreaseCytoplasmic membrane LPS accumulation
    Study

    Pseudomonas aeruginosan: not reported in source

    Pseudomonas aeruginosa
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using the LPS transport inhibitor murepavadin, we were able to cause LPS accumulation in the CM of Pseudomonas aeruginosa

Studies that did not test the peptide alone2

In this study, Murepavadin was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Murepavadin.

  1. 02AnimalNot a test of Murepavadin aloneAnimal study (in vivo)Efficacy outcome

    In vivo, the therapeutic approach using murepavadin and colistin improved treatment efficacy.

    In plain wordsIn animals, the approach using murepavadin and colistin improved treatment efficacy.

    Peptide
    Murepavadin
    Outcome
    IncreaseCombination treatment efficacy
    Study

    n: not reported in source

    Outcome group
    Infection and antimicrobial activity · Infection

    Source sentences

    Summary
    Using the LPS transport inhibitor murepavadin, we were able to cause LPS accumulation in the CM of Pseudomonas aeruginosa, which resulted in increased susceptibility to colistin in vitro and improved treatment efficacy in vivo.

    In this study, Murepavadin was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Murepavadin.

  2. 03LabNot a test of Murepavadin aloneIn vitro (cells)Mechanism

    In Pseudomonas aeruginosa in vitro, the approach using murepavadin and colistin increased susceptibility to colistin.

    In plain wordsIn lab tests, the approach using murepavadin and colistin increased bacterial susceptibility to colistin.

    Peptide
    Murepavadin
    Outcome
    IncreaseColistin susceptibility
    Study

    Pseudomonas aeruginosan: not reported in source

    Pseudomonas aeruginosa
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Using the LPS transport inhibitor murepavadin, we were able to cause LPS accumulation in the CM of Pseudomonas aeruginosa, which resulted in increased susceptibility to colistin in vitro and improved treatment efficacy in vivo.

    In this study, Murepavadin was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Murepavadin.

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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