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Updated: Jun 18, 2026

Pseudomonas aeruginosa Induced Lung Injury Model
07:24

Pseudomonas aeruginosa Induced Lung Injury Model

Published on: October 29, 2014

The two-component sensor response regulator RoxS/RoxR plays a role in Pseudomonas aeruginosa interactions with airway

Bryan P Hurley1, Andrew L Goodman, Karen L Mumy

  • 1Mucosal Immunology Laboratory, Massachusetts General Hospital, Charlestown MA 02129, USA. bphurley@partners.org

Microbes and Infection
|December 8, 2009
PubMed

Insights

Pseudomonas aeruginosa infection in cystic fibrosis lungs involves bacterial interactions with epithelial cells. A study found the roxR gene regulates bacterial factors crucial for this interaction and neutrophil migration.

Area of Science:

  • Microbiology
  • Immunology
  • Pulmonary Medicine

Background:

  • Pseudomonas aeruginosa is an opportunistic pathogen frequently infecting the lungs of cystic fibrosis patients.
  • Aberrant neutrophil (PMN)-dominated inflammation of airways is a hallmark of P. aeruginosa lung infections.
  • Trans-epithelial PMN migration across the lung epithelial barrier is a critical event in PMN recruitment.

Purpose of the Study:

  • To identify bacterial factors of P. aeruginosa involved in interactions with lung epithelial cells.
  • To investigate bacterial two-component system response regulators that modulate PMN trans-epithelial migration.

Main Methods:

  • A mutant library of forty-eight two-component system response regulators of P. aeruginosa was screened.
  • Mutants were evaluated for defects in inducing PMN trans-epithelial migration.
  • Interactions between bacterial mutants and lung epithelial cells were assessed.

Main Results:

  • Five mutants showed reproducibly reduced PMN trans-epithelial migration.
  • These five mutants also exhibited decreased interaction with lung epithelial cells.
  • A mutant lacking the roxR response regulator gene demonstrated impaired PMN migration and epithelial cell interaction.

Conclusions:

  • The roxR gene regulates factors facilitating P. aeruginosa interaction with lung epithelial cells.
  • RoxR likely plays a significant role in P. aeruginosa-mediated lung disease pathogenesis.
  • Targeting RoxR-regulated factors could be a therapeutic strategy for P. aeruginosa lung infections.

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