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Journal of Clinical Microbiology, September 2008, p. 2987-2991, Vol. 46, No. 9
0095-1137/08/$08.00+0 doi:10.1128/JCM.00871-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Erik Riise,2
Søren Persson,1 and
Katharina E. P. Olsen1*
Department of Bacteriology, Mycology and Parasitology, Statens Serum Institut, Copenhagen, Denmark,1 Department of Pharmacology and Pharmacotherapy, Faculty of Pharmaceutical Sciences, University of Copenhagen, Copenhagen, Denmark2
Received 6 May 2008/ Returned for modification 22 June 2008/ Accepted 14 July 2008
Shiga toxins (Stx) are important virulence factors in the pathogenesis of severe disease including hemolytic-uremic syndrome, caused by Stx-producing Escherichia coli (STEC). STEC strains increase the release of Stx in vitro following the addition of fluoroquinolones, whereas protein synthesis inhibitors previously have been reported to suppress the release of Stx. The amount of Stx released from wild-type STEC strains incubated with protein synthesis inhibitors was examined by a Vero cell cytotoxicity assay. The amounts released were compared to the Stx type (Stx1 or Stx2) and additionally to the individual subtypes and toxin variants of Stx2. In general, Stx2 release was suppressed significantly upon exposure to protein synthesis inhibitors at MICs, which was not observed in the case of Stx1. Also, the average amount of different Stx2 toxin variants released was suppressed to various levels ranging from 14.0% (Stx2-O157-EDL933) to 94.7% (Stx2d-O8-C466-01B). Clinical studies exploring protein synthesis inhibitors as future candidates for treatment of intestinal infections caused by Stx2-producing STEC should therefore include knowledge of the toxin variant in addition to the subtype.
Published ahead of print on 23 July 2008.
Present address: Department of Pharmaceutics and Analytical Chemistry, Faculty of Pharmaceutical Sciences, University of Copenhagen, Copenhagen, Denmark.
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