Thromb Haemost 2005; 94(02): 312-318
DOI: 10.1160/TH05-04-0265
Theme Issue Article
Schattauer GmbH

Consequences of enterohaemorrhagic Escherichia coli infection for the vascular endothelium

Martina Bielaszewska
1   Institute for Hygiene, and the National Consulting Laboratory on Haemolytic Uraemic Syndrome, University Hospital Münster, Münster, Germany
,
Helge Karch
1   Institute for Hygiene, and the National Consulting Laboratory on Haemolytic Uraemic Syndrome, University Hospital Münster, Münster, Germany
› Author Affiliations

Financial support: Grant support: The research on the identification of non-Shiga toxin virulence factors of enterohaemorrhagic Escherichia coli in the laboratory of Prof. Dr. Helge Karch has been supported by the Deutsche Forschungsgemeinschaft (DFG) program “Infections of the endothelium” SPP 1130, grants KA 717/4–1 and 717/4–2.
Further Information

Publication History

Received: 18 April 2005

Accepted after major revision: 30 March 2005

Publication Date:
05 December 2017 (online)

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Summary

Microvascular endothelial damage underlies the pathological changes in haemorrhagic colitis and the haemolytic uraemic syndrome (HUS) caused by enterohaemorrhagic Escherichia coli (EHEC). Shiga toxins (Stxs) are presently the best characterised EHEC virulence factors that can cause the microvascular endothelium injury. Stxs are released by EHEC in the intestine, absorbed across the gut epithelium into the circulation, and transported to small vessel endothelial cells. Then, they presumably injure the host cell by inhibiting protein synthesis, stimulating prothrombotic messages,or inducing apoptosis. The net result is a multi-organ thrombotic process. Moreover, Stxs stimulate a variety of non-endothelial cells to produce and secrete inflammatory mediators (cytokines, chemokines, adhesion molecules) which could potentiate the effects of Stxs on endothelial cells. The association of HUS with Stx-negative E. coli strains stimulated intensive research on putative non-Stx virulence factors, which might also contribute to the pathogenesis of HUS and haemorrhagic colitis. Based on current data, cytolethal distending toxin, EHEC haemolysin, and subtilase cytotoxin might be such candidates.