Pm. Schneeberger et al., LIPOPOLYSACCHARIDE INDUCES HYPERADHESION OF ENDOTHELIAL-CELLS FOR NEUTROPHILS LEADING TO DAMAGE, Shock, 2(4), 1994, pp. 296-300
Adhesion of polymorphonuclear leukocytes (PMN) to endothelial cells is
an early key event in the inflammatory response and plays an importan
t part in the pathogenesis of septic shock, contributing to vascular a
nd tissue injury. Lipopolysaccharides (LPS) activate endothelial cells
to enhanced expression of adhesion molecules. We investigated the int
eraction of human PMN with resting and LPS-activated human umbilical v
ein endothelial cells. The activation of endothelial cells by LPS alon
e did not lead to direct functional or morphological changes as measur
ed by detachment of the endothelial cells from a monolayer and transen
dothelial albumin flux. LPS induced an increased adhesion of unstimula
ted PMN to endothelial cells. This was accompanied by endothelial deta
chment and increased permeability across a monolayer. Endothelial cell
lysis as measured by Cr-51 release was unaffected. Stimulation of PMN
with phorbol ester did not further increase adherence, detachment, or
permeability. We conclude that LPS activates endothelial cells and re
nders cultured monolayers more susceptible to PMN-induced damage. This
may provide further insight into the relationship between PMN activat
ion and endothelial damage in Gram-negative sepsis.