Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors. / Pedersen, Malene Gantzhorn; Hansen, Claus; Riise, Erik; Persson, Søren; Olsen, Katharina E P.

In: Journal of Clinical Microbiology, Vol. 46, No. 9, 2008, p. 2987-91.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Pedersen, MG, Hansen, C, Riise, E, Persson, S & Olsen, KEP 2008, 'Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors', Journal of Clinical Microbiology, vol. 46, no. 9, pp. 2987-91. https://doi.org/10.1128/JCM.00871-08

APA

Pedersen, M. G., Hansen, C., Riise, E., Persson, S., & Olsen, K. E. P. (2008). Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors. Journal of Clinical Microbiology, 46(9), 2987-91. https://doi.org/10.1128/JCM.00871-08

Vancouver

Pedersen MG, Hansen C, Riise E, Persson S, Olsen KEP. Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors. Journal of Clinical Microbiology. 2008;46(9):2987-91. https://doi.org/10.1128/JCM.00871-08

Author

Pedersen, Malene Gantzhorn ; Hansen, Claus ; Riise, Erik ; Persson, Søren ; Olsen, Katharina E P. / Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors. In: Journal of Clinical Microbiology. 2008 ; Vol. 46, No. 9. pp. 2987-91.

Bibtex

@article{f5c0c250a03e11dd86a6000ea68e967b,
title = "Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors",
abstract = "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.",
keywords = "Former Faculty of Pharmaceutical Sciences",
author = "Pedersen, {Malene Gantzhorn} and Claus Hansen and Erik Riise and S{\o}ren Persson and Olsen, {Katharina E P}",
year = "2008",
doi = "10.1128/JCM.00871-08",
language = "English",
volume = "46",
pages = "2987--91",
journal = "Journal of Clinical Microbiology",
issn = "0095-1137",
publisher = "American Society for Microbiology",
number = "9",

}

RIS

TY - JOUR

T1 - Subtype-specific suppression of Shiga toxin 2 released from Escherichia coli upon exposure to protein synthesis inhibitors

AU - Pedersen, Malene Gantzhorn

AU - Hansen, Claus

AU - Riise, Erik

AU - Persson, Søren

AU - Olsen, Katharina E P

PY - 2008

Y1 - 2008

N2 - 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.

AB - 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.

KW - Former Faculty of Pharmaceutical Sciences

U2 - 10.1128/JCM.00871-08

DO - 10.1128/JCM.00871-08

M3 - Journal article

C2 - 18650349

VL - 46

SP - 2987

EP - 2991

JO - Journal of Clinical Microbiology

JF - Journal of Clinical Microbiology

SN - 0095-1137

IS - 9

ER -

ID: 6747552