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Infection and Immunity, March 2001, p. 1889-1894, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1889-1894.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

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

Patricia B. Eisenhauer,1 Prasoon Chaturvedi,2 Richard E. Fine,1 Andrew J. Ritchie,3 Jordan S. Pober,4 Thomas G. Cleary,5 and David S. Newburg2,*

Bedford VA Medical Center, Bedford, and Boston University, Boston,1 Shriver Center for Mental Retardation, Waltham, and Harvard Medical School, Boston,2 and Brigham and Women's Hospital, Boston,3 Massachusetts; Yale Medical School, New Haven, Connecticut4; and University of Texas Medical School, Houston, Texas5

Received 26 July 2000/Returned for modification 6 September 2000/Accepted 6 December 2000

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-alpha ) upregulates Gb3 in both human macrovascular umbilical vein endothelial cells and human microvascular brain endothelial cells. TNF-alpha 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.

* Corresponding author. Mailing address: Shriver Center, 200 Trapelo Rd., Waltham, MA 02452. Phone: (781) 642-0025. Fax: (781) 893-4018. E-mail: dnewburg{at}shriver.org.

Infection and Immunity, March 2001, p. 1889-1894, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1889-1894.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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