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Bacterial induction of pleural mesothelial monolayer barrier dysfunction

K A Mohammed1, N Nasreen, J Hardwick

  • 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, Veterans Affairs Medical Center, and Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|June 19, 2001
PubMed

Insights

Bacterial pneumonia can cause empyema by increasing vascular endothelial growth factor (VEGF) production. This VEGF alters pleural mesothelial cell permeability, leading to fluid buildup and infection in the pleural space.

Area of Science:

  • Pulmonary Medicine
  • Infectious Diseases
  • Cell Biology

Background:

  • Pneumonia is a leading cause of death globally.
  • Parapneumonic effusions, characterized by high neutrophils and protein, are common in pneumonia patients.
  • The role of pleural mesothelial barrier function in empyema development is not fully understood.

Purpose of the Study:

  • To investigate the hypothesis that bacterial pneumonia induces pleural mesothelial permeability changes via vascular endothelial growth factor (VEGF).
  • To quantify VEGF levels in complicated parapneumonic effusions (empyema) compared to other pleural effusions.
  • To elucidate the mechanism by which Staphylococcus aureus affects mesothelial barrier function.

Main Methods:

  • Analysis of VEGF levels in pleural fluids from patients with empyema, uncomplicated parapneumonic effusions, and congestive heart failure.
  • In vitro study using confluent mesothelial monolayers exposed to live Staphylococcus aureus.
  • Measurement of electrical resistance and protein leak across mesothelial monolayers.
  • Assessment of the effect of recombinant VEGF and anti-VEGF antibodies on mesothelial barrier function.

Main Results:

  • Empyema pleural fluids exhibited significantly higher VEGF levels compared to other pleural effusions.
  • Staphylococcus aureus infection caused a significant decrease in electrical resistance across mesothelial monolayers.
  • Recombinant VEGF mimicked the effect of S. aureus by reducing mesothelial electrical resistance.
  • Neutralizing antibodies against VEGF attenuated the S. aureus-induced drop in electrical resistance.
  • S. aureus infection led to increased protein leakage across mesothelial monolayers.

Conclusions:

  • Bacterial pathogens, such as Staphylococcus aureus, induce VEGF production in mesothelial cells.
  • VEGF plays a critical role in altering mesothelial permeability during bacterial pneumonia.
  • These VEGF-mediated changes contribute to protein exudation and the development of empyema.

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