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Updated: Jan 22, 2026

A Delayed Inoculation Model of Chronic Pseudomonas aeruginosa Wound Infection
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A Delayed Inoculation Model of Chronic Pseudomonas aeruginosa Wound Infection

Published on: February 20, 2020

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The Oxylipin Dependent Quorum Sensing System enhances Pseudomonas aeruginosa dissemination during burn-associated

Eriel Martínez1, Hansol Im1, Mohammed Mohasin1

  • 1Department of Microbiology, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, United States of America.

Plos Pathogens
|January 20, 2026
PubMed

Insights

Pseudomonas aeruginosa exploits host oleic acid via the Oxylipin Dependent Quorum Sensing (ODS) system to cause severe burn wound infections. Inhibiting the OdsA enzyme with AB012 reduces bacterial virulence and improves survival in mice.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Wound Healing

Background:

  • Pseudomonas aeruginosa is a major cause of severe burn wound infections.
  • The molecular mechanisms driving P. aeruginosa hypervirulence in burn patients are not fully understood.

Purpose of the Study:

  • To identify key regulators of P. aeruginosa pathogenicity in burn wounds.
  • To investigate the role of the Oxylipin Dependent Quorum Sensing (ODS) system in P. aeruginosa burn wound infections.
  • To evaluate OdsA as a potential therapeutic target.

Main Methods:

  • Utilized a murine burn model to assess P. aeruginosa virulence.
  • Analyzed bacterial conversion of host oleic acid into oxylipin autoinducers.
  • Generated and tested ODS-deficient mutants.
  • Administered OdsA inhibitors (including AB012) and recombinant OdsA in vivo.
  • Performed high-throughput screening to identify OdsA inhibitors.

Main Results:

  • Thermal injury increases skin oleic acid, activating P. aeruginosa's ODS system via OdsA and OdsB.
  • ODS activation promotes bacterial invasion, dissemination, and mortality in burned mice.
  • ODS-deficient mutants showed reduced virulence and improved survival.
  • OdsA inhibition (with AB012) and immunization with OdsA significantly reduced bacterial burden, systemic spread, and mortality.
  • AB012 suppressed oxylipin synthesis, ODS expression, and biofilm formation without impacting bacterial growth.

Conclusions:

  • P. aeruginosa utilizes host oleic acid to activate the ODS system, enhancing virulence in burn wounds.
  • The ODS system, particularly OdsA, is critical for P. aeruginosa hypervirulence.
  • Targeting OdsA with inhibitors like AB012 offers a promising therapeutic strategy to combat P. aeruginosa sepsis in burn patients.

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