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Invasion of respiratory epithelial cells by Burkholderia (Pseudomonas) cepacia

J L Burns1, M Jonas, E Y Chi

  • 1Division of Infectious Disease, Children's Hospital and Medical Center, Seattle, Washington 98105, USA. jburns@u.washington.edu.

Infection and Immunity
|October 1, 1996
PubMed

Insights

Burkholderia cepacia invades and replicates within lung epithelial cells in cystic fibrosis (CF) patients, contributing to persistent infections. This intracellular behavior is a potential virulence factor for CF lung disease.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pulmonary Medicine

Background:

  • Pulmonary infections by Burkholderia cepacia complex (Bcc) significantly increase morbidity and mortality in cystic fibrosis (CF) patients.
  • Bcc infections in CF are notoriously difficult to treat, often persisting despite antibiotic therapy.
  • Features like bacteremia suggest Bcc may possess mechanisms for evading host defenses, potentially involving intracellular survival.

Purpose of the Study:

  • To investigate the capacity of Burkholderia cepacia to invade and replicate within human lung epithelial cells.
  • To elucidate the cellular mechanisms underlying Bcc invasion and intracellular persistence.
  • To determine if bacterial invasion and intracellular replication represent a virulence factor in CF lung infections.

Main Methods:

  • Utilized a modified gentamicin protection assay to quantify Bcc invasion of A549 lung epithelial cells in vitro.
  • Employed transmission electron microscopy (TEM) to visualize intracellular bacteria and their relationship with host cell organelles.
  • Investigated the role of host cell cytoskeleton in invasion using cytochalasin D and colchicine.

Main Results:

  • Demonstrated significant in vitro invasion of A549 epithelial cells by Bcc, with saturable invasion kinetics.
  • TEM revealed intracellular Bcc within membrane-bound vacuoles, with no observed fusion with lysosomes.
  • Evidence of intraepithelial Bcc replication was confirmed through quantitative and visual assays.
  • Invasion was inhibited by cytochalasin D, implicating microfilaments in the process, but not by colchicine.

Conclusions:

  • Burkholderia cepacia invades and replicates intracellularly within lung epithelial cells, a novel mechanism of persistence in CF.
  • Intracellular replication and survival within vacuoles suggest a strategy for evading antibiotic treatment and host immune responses.
  • The invasion and intracellular replication phenotype is a potential key virulence factor contributing to chronic Bcc infections in cystic fibrosis.

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