Abstract
BackgroundEndothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration. Cell adhesion and diapedesis have a key role in the course of shock and sepsis. During severe sepsis, adrenoceptor agonist levels may be increased due to endogenous production or due to intensive care treatment. As yet, the influence of β1 or β2 agonists on adhesion molecule formation on endothelial cells has remained unclear.MethodsCultured human umbilical vein endothelial cells were stimulated with E. coli. Following bacterial stimulation the cells were incubated with either β2 receptor agonist terbutaline or β1 agonist norepinephrine. ICAM-1 and VCAM-1 expression were examined using flow cytometry.ResultsAdministration of norepinephrine did not cause increases of both CD54 and CD106 in stimulated HUVEC. Compared to negative controls the bacterial stimulation itself led to an increase of adhesion molecules. Following administration of terbutaline no significant increase in CD54 expression was found.ConclusionsBacterial stimulation led to an increase of adhesion molecule expression. Adrenoceptor stimulation of activated endothelial cells did not cause significant increases of cellular adhesion molecules.
Highlights
Endothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration
CD106 Serotec, Düsseldorf, Germany) both marked with the green fluorescent fluorescein isothiocyanate (FITC) were added. 20 μl of the red fluorescent propidium iodide (PI; Sigma Aldrich, Taufkirchen, Germany) to stain DNA of dead cells, which should be excluded from our calculation, were added
HUVEC were investigated if there was a change in expression of the cellular adhesion molecules ICAM-1 and VCAM-1 caused by either the b1-stimulating agent norepinephrine or the b2-agonist terbutaline with and without bacterial stimulation with E. coli
Summary
Endothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration. Adrenoceptor agonist levels may be increased due to endogenous production or due to intensive care treatment. The influence of b1 or b2 agonists on adhesion molecule formation on endothelial cells has remained unclear. The main function of endothelial cells is to work as a communicative barrier between intravascular and extravascular spaces. Contact and communication among cells either from identical or different types and sites depend on receptors and adhesion molecules anchored in the membrane of the cell. ELAM-1 (E-selectin), intercellular adhesion molecule 1 (ICAM-1 (CD54)) and vascular adhesion molecule 1 (VCAM-1 (CD106)) are important for the interaction with peripheral blood cells. Hypodynamic or hyperdynamic circulatory dysregulation frequently require adrenoceptor agonist therapy. Besides treating the underlying condition, microvascular resuscitation is a crucial part of sepsis treatment [5]
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