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Pseudomonas aeruginosa and epithelial permeability: role of virulence factors elastase and exotoxin A

A O Azghani1

  • 1Department of Biochemistry, University of Texas Health Science Center at Tyler 75710, USA.

American Journal of Respiratory Cell and Molecular Biology
|July 1, 1996
PubMed

Insights

Pseudomonas aeruginosa elastase damages lung epithelial barrier proteins, increasing permeability. Exotoxin A hinders protein repair, exacerbating lung injury during bacterial infection.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pulmonary Medicine

Background:

  • Bacterial infections, particularly with Pseudomonas aeruginosa, can cause lung injury.
  • Lung injury involves complex interactions between bacterial factors and host responses.
  • Epithelial barrier dysfunction is a key feature of lung injury.

Purpose of the Study:

  • To investigate the effects of Pseudomonas aeruginosa exoproducts, specifically elastase and exotoxin A, on epithelial barrier function.
  • To elucidate the mechanisms by which these toxins impact paracellular permeability in lung epithelial cells.

Main Methods:

  • Primary type II pneumocytes and Madin-Darby canine kidney (MDCK) cells were used.
  • Transepithelial electrical resistance (TER) and mannitol permeability coefficient (Pm) were measured.
  • Treated cells were analyzed for tight junction protein expression (ZO-1, ZO-2) and viability.

Main Results:

  • Pseudomonas elastase (PE) rapidly decreased TER and increased Pm, correlating with bacterial traversal.
  • Exotoxin A (Exo A) also decreased TER and increased Pm, but with a slower onset.
  • PE depleted ZO-1 and ZO-2 tight junction proteins, while Exo A reduced their levels without depletion.
  • Neither toxin affected cell viability.

Conclusions:

  • Pseudomonas elastase increases alveolar epithelial permeability by directly damaging tight junction-associated proteins.
  • Exotoxin A may impair the epithelial cells' ability to repair these junctions by affecting protein synthesis.
  • These distinct yet complementary actions of PE and Exo A contribute to diminished epithelial barrier function in bacterial lung infections.

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