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Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro

Heiner Ruschulte1, Dirk Scheinichen, Martijn van Griensven

  • 1Dept, of Anaesthesiology & Intensive Care Medicine, Hannover Medical School Hannover, Germany. ruschulte.heiner@mh-hannover.de.

BMC Research Notes
|March 1, 2011
PubMed

Insights

Bacterial stimulation increases endothelial adhesion molecules. However, beta-agonists like norepinephrine and terbutaline did not significantly alter ICAM-1 or VCAM-1 expression in sepsis models.

Area of Science:

  • Cellular Biology
  • Immunology
  • Pharmacology

Background:

  • Endothelial adhesion molecules, intercellular adhesion molecule-1 (ICAM-1/CD54) and vascular cell adhesion molecule-1 (VCAM-1/CD106), are crucial for cell adhesion and migration.
  • Cell adhesion and diapedesis play significant roles in the pathophysiology of shock and sepsis.
  • Elevated adrenoceptor agonist levels are observed in severe sepsis, yet their impact on endothelial adhesion molecule expression remains unclear.

Purpose of the Study:

  • To investigate the effect of beta-1 and beta-2 adrenoceptor agonists on the expression of ICAM-1 and VCAM-1 in endothelial cells during sepsis.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were stimulated with E. coli to mimic sepsis conditions.
  • Following bacterial stimulation, cells were treated with either the beta-2 agonist terbutaline or the beta-1 agonist norepinephrine.
  • Expression levels of ICAM-1 (CD54) and VCAM-1 (CD106) were quantified using flow cytometry.

Main Results:

  • Bacterial stimulation significantly increased the expression of adhesion molecules compared to unstimulated controls.
  • Norepinephrine administration did not induce further increases in CD54 or CD106 expression in stimulated HUVECs.
  • Terbutaline treatment did not result in a significant elevation of CD54 expression on activated endothelial cells.

Conclusions:

  • Bacterial challenge effectively upregulates endothelial adhesion molecule expression.
  • Adrenoceptor stimulation with beta-1 (norepinephrine) or beta-2 (terbutaline) agonists does not significantly enhance the expression of cellular adhesion molecules on activated endothelial cells in this model.
Abstract

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