[Frontiers in Bioscience 2, d635-642, December 15, 1997]
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SHIGA TOXIN MODE OF ACTION IN E. COLI O157:H7 DISEASE

Tom G. Obrig

Department of Microbiology and Immunology, University of Rochester, Box 672, 601 Elmwood Avenue, Rochester, NY 14642

Received 12/2/97 Accepted 12/8/97

TABLE OF CONTENTS:

1. Abstract
2.. The Shiga toxins (Stx)-Overview.
2.1 Shiga toxin production by gram-negative pathogenic bacteria.
2.2 Evolution of Stxs and the "emerging pathogen", E. coli O157:H7
2.3 Stx is a vascular acting toxin.

3. Biochemical features of the Shiga toxins.
3.1 Subunit protein structure
3.2 Stx removal of a single base from 28S rRNA.
3.3 Stx is a member of the ribosome inactivating protein family.

4. Stx Isotypes produced by E. coli O157:H7.
5. Stx Receptors expressed on eukaryotic cells.
5.1 The Stx receptor is a glycosphingolipid, Gb3.
5.2 Specificity of Stx-receptor interaction.
5.3 Potential receptor-based therapeutics for EHEC disease.

6. Internalization and processing of Stx by eukaryotic cells.
6.1 Stx enters cells by receptor-mediated endocytosis.
6.2 Processing and activation of Stx in target cells.

7. A Role for Shiga toxins in vascular disease.
7.1 Evidence for Stxs' role in EHEC-associated vascular disease.
7.2 Additional bacterial factors in EHEC-associated vascular disease.

8. Sensitivity of human endothelial cells to Stxs.
8.1 Endothelial cells are the putative target of Stxs.
8.2 Host cytokine regulation of Stx-sensitivity in endothelial cells.

9. Acknowledgments
10. References
11. Entire manuscript

Key words: Shiga toxin, Verotoxin, E. coli O157:H7, Vascular disease, Endothelium, Kidney, Protein synthesis

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