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Cell death of human polymorphonuclear neutrophils induced by a Pseudomonas aeruginosa cystic fibrosis isolate

D Dacheux1, I Attree, C Schneider

  • 1Département de Biologie Moléculaire et Structurale, BBSI, UMR-314 CNRS, CEA Grenoble, Grenoble, France.

Infection and Immunity
|October 26, 1999
PubMed

Insights

Pseudomonas aeruginosa isolates from cystic fibrosis patients resist human immune cells. A specific bacterial secretion system is required for this immune evasion and cell death induction.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Pseudomonas aeruginosa is an opportunistic pathogen frequently found in cystic fibrosis (CF) patients.
  • Human polymorphonuclear neutrophils (PMNs) are critical immune cells for combating bacterial infections.
  • Certain CF-associated P. aeruginosa strains exhibit resistance to PMN-mediated killing.

Purpose of the Study:

  • To investigate the role of the type III secretion system (T3SS) in P. aeruginosa-induced PMN death.
  • To understand the mechanisms by which CF P. aeruginosa isolates evade immune responses.

Main Methods:

  • Coincubation of a CF P. aeruginosa isolate with human PMNs.
  • Utilizing an isogenic mutant lacking a functional T3SS.
  • Assessing PMN viability and bactericidal activity.

Main Results:

  • The wild-type CF P. aeruginosa isolate resisted PMN bactericidal action and induced PMN cellular death.
  • The isogenic mutant with a nonfunctional T3SS was unable to induce PMN cellular death.
  • This suggests the T3SS is crucial for P. aeruginosa virulence in the context of PMN interaction.

Conclusions:

  • The type III secretion system of P. aeruginosa plays a key role in overcoming host immune defenses.
  • T3SS-mediated evasion of PMN activity contributes to P. aeruginosa pathogenesis in cystic fibrosis.
  • Targeting the T3SS may represent a therapeutic strategy against CF-associated P. aeruginosa infections.

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