Xenon prevents tumor necrosis factor alpha induced ICAM-1 expression in human umbilical vein endothelial cells

2006 ◽  
Vol 23 (Supplement 37) ◽  
pp. 154
Author(s):  
N. C. Weber ◽  
J. Kandler ◽  
J. Frädorf ◽  
W. Schlack ◽  
B. Preckel
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Umbilical Vein ◽  
Necrosis Factor Alpha ◽  
Human Umbilical Vein ◽  
Factor Alpha ◽  
Umbilical Vein Endothelial Cells ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor Alpha Increases Human Cerebral Endothelial Cell Gb3 and Sensitivity to Shiga Toxin

2001 ◽  
Vol 69 (3) ◽  
pp. 1889-1894 ◽  
Author(s):  
Patricia B. Eisenhauer ◽  
Prasoon Chaturvedi ◽  
Richard E. Fine ◽  
Andrew J. Ritchie ◽  
Jordan S. Pober ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Shiga Toxin ◽  
Tumor Necrosis ◽  
Umbilical Vein ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Hemolytic uremic syndrome (HUS) is associated with intestinal infection by enterohemorrhagic Escherichia coli strains that produce Shiga toxins. Globotriaosylceramide (Gb3) is the functional receptor for Shiga toxin, and tumor necrosis factor alpha (TNF-α) upregulates Gb3 in both human macrovascular umbilical vein endothelial cells and human microvascular brain endothelial cells. TNF-α treatment enhanced Shiga toxin binding and sensitivity to toxin. This upregulation was specific for Gb3 species containing normal fatty acids (NFA). Central nervous system (CNS) pathology in HUS could involve cytokine-stimulated elevation of endothelial NFA-Gb3 levels. Differential expression of Gb3 species may be a critical determinant of Shiga toxin toxicity and of CNS involvement in HUS.

Sign in / Sign up

Export Citation Format

Share Document