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Related Experiment Videos

Bacterial adherence to human endothelial cells.

P D Thomas1, F W Hampson, G W Hunninghake

  • 1Department of Internal Medicine, Veterans Administration, Iowa City, Iowa.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|September 1, 1988
PubMed
Summary
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Endotoxin (lipopolysaccharide, LPS) exposure increases Staphylococcus aureus adherence to lung endothelial cells, potentially worsening adult respiratory distress syndrome (ARDS) and increasing infection risk.

Area of Science:

  • Immunology
  • Cell Biology
  • Pulmonary Medicine

Background:

  • Adult respiratory distress syndrome (ARDS) is often linked to lung endothelial exposure to endotoxin (lipopolysaccharide, LPS).
  • Pulmonary infections are common complications during ARDS.
  • Endothelial cells play a crucial role in the inflammatory response and host defense.

Purpose of the Study:

  • To investigate the effect of lipopolysaccharide (LPS) and inflammatory mediators on Staphylococcus aureus adherence to human umbilical vein endothelial cells (HUVECs).
  • To determine the role of interleukin-1 (IL-1) and gamma-interferon in LPS-induced bacterial adherence.
  • To elucidate the mechanisms by which LPS enhances bacterial adhesion to the endothelium.

Main Methods:

  • Exposure of HUVECs to LPS and various mediators.

Related Experiment Videos

  • Incubation of HUVECs with Staphylococcus aureus.
  • Quantification of bacterial adherence to endothelial cells.
  • Assessment of the role of serum opsonization and inhibitors like dactinomycin.

    • Main Results:

    • LPS and IL-1 significantly enhanced Staphylococcus aureus adherence to HUVECs.
    • Gamma-interferon had no effect on bacterial adherence.
    • LPS-induced adherence was time-dependent, peaking at 6 hours.
    • Adherence was dependent on complement-mediated opsonization and could be blocked by reduced temperature or dactinomycin.

    Conclusions:

    • Circulating LPS can promote ARDS development.
    • LPS enhances bacterial adherence to the lung endothelium, potentially predisposing to pulmonary infections.
    • Targeting LPS-mediated endothelial activation may offer therapeutic strategies for ARDS and associated infections.