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Prepublished online as a Blood First Edition Paper on April 17, 2003; DOI 10.1182/blood-2002-10-3301.
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Blood, 15 August 2003, Vol. 102, No. 4, pp. 1323-1332
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Molecular and functional analysis of Shiga toxin–induced response patterns in human vascular endothelial cells
Andreas Matussek,
Joerg Lauber,
Anna Bergau,
Wiebke Hansen,
Manfred Rohde,
Kurt E. J. Dittmar,
Matthias Gunzer,
Michael Mengel,
Patricia Gatzlaff,
Maike Hartmann,
Jan Buer, and
Florian Gunzer
From the Mucosal Immunity Group, the Department of Microbiology, and the Department of Molecular Biotechnology, German Research Centre for Biotechnology (GBF), Braunschweig, Germany; the Institute of Medical Microbiology, Hannover Medical School, Hannover, Germany; the Department of Dermatology, University of Muenster, Muenster, Germany; and the Institute of Pathology, Hannover Medical School, Hannover, Germany.
Enterohemorrhagic Escherichia coli (EHEC) is the major cause of hemolyticuremic syndrome (HUS) characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. EHEC produces one or more Shiga toxins (Stx1 and Stx2), and it was assumed that Stx's only relevant biologic activity was cell destruction through inhibition of protein synthesis. However, recent data indicate that in vivo the cytokine milieu may determine whether endothelial cells survive or undergo apoptosis/necrosis when exposed to Stxs. In this study, we analyzed the genome-wide expression patterns of human endothelial cells stimulated with subinhibitory concentrations of Stxs in order to characterize the genomic expression program involved in the vascular pathology of HUS. We found that Stxs elicited few, but reproducible, changes in gene expression. The majority of genes reported in this study encodes for chemokines and cytokines, which might contribute to the multifaceted inflammatory response of host endothelial cells observed in patients suffering from EHEC disease. In addition, our data provide for the first time molecular insights into the epidemiologically well-established higher pathogenicity of Stx2 over Stx1.
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