Enterohaemorrhagic Escherichia coli O157: H7 Shiga-like toxin 1 is required for full pathogenicity and activation of the p38 mitogen-activated protein kinase pathway in Caenorhabditis elegans

T. C. Chou, H. C. Chiu, C. J. Kuo, C. M. Wu, W. J. Syu, W. T. Chiu, C. S. Chen

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Abstract

Enterohaemorrhagic Escherichia coli (EHEC) causes life-threatening infections in humans as a consequence of the production of Shiga-like toxins. Lack of a good animal model system currently hinders in vivo study of EHEC virulence by systematic genetic methods. Here we applied the genetically tractable animal, Caenorhabditis elegans, as a surrogate host to study the virulence of EHEC as well as the host immunity to this human pathogen. Our results show that E.coli O157:H7, a serotype of EHEC, infects and kills C.elegans. Bacterial colonization and induction of the characteristic attaching and effacing (A/E) lesions in the intact intestinal epithelium of C.elegans by E.coli O157:H7 were concomitantly demonstrated in vivo. Genetic analysis indicated that the Shiga-like toxin 1 (Stx1) of E.coli O157:H7 is a virulence factor in C.elegans and is required for full toxicity. Moreover, the C.elegans p38 mitogen-activated protein kinase (MAPK) pathway, anevolutionarily conserved innate immune and stress response signalling pathway, is activated in the regulation of host susceptibility to EHEC infection in a Stx1-dependent manner. Our results validate the EHEC-C.elegans interaction as suitable for future comprehensive genetic screens for both novel bacterial and host factors involved in the pathogenesis of EHEC infection.

Original languageEnglish
Pages (from-to)82-97
Number of pages16
JournalCellular Microbiology
Volume15
Issue number1
DOIs
Publication statusPublished - 2013 Jan 1

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Shiga Toxin 1
Shiga Toxins
Enterohemorrhagic Escherichia coli
Escherichia coli O157
Caenorhabditis elegans
p38 Mitogen-Activated Protein Kinases
Virulence
Escherichia coli Infections
Virulence Factors
Intestinal Mucosa
Innate Immunity
Immunity
Animal Models

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Virology

Cite this

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title = "Enterohaemorrhagic Escherichia coli O157: H7 Shiga-like toxin 1 is required for full pathogenicity and activation of the p38 mitogen-activated protein kinase pathway in Caenorhabditis elegans",
abstract = "Enterohaemorrhagic Escherichia coli (EHEC) causes life-threatening infections in humans as a consequence of the production of Shiga-like toxins. Lack of a good animal model system currently hinders in vivo study of EHEC virulence by systematic genetic methods. Here we applied the genetically tractable animal, Caenorhabditis elegans, as a surrogate host to study the virulence of EHEC as well as the host immunity to this human pathogen. Our results show that E.coli O157:H7, a serotype of EHEC, infects and kills C.elegans. Bacterial colonization and induction of the characteristic attaching and effacing (A/E) lesions in the intact intestinal epithelium of C.elegans by E.coli O157:H7 were concomitantly demonstrated in vivo. Genetic analysis indicated that the Shiga-like toxin 1 (Stx1) of E.coli O157:H7 is a virulence factor in C.elegans and is required for full toxicity. Moreover, the C.elegans p38 mitogen-activated protein kinase (MAPK) pathway, anevolutionarily conserved innate immune and stress response signalling pathway, is activated in the regulation of host susceptibility to EHEC infection in a Stx1-dependent manner. Our results validate the EHEC-C.elegans interaction as suitable for future comprehensive genetic screens for both novel bacterial and host factors involved in the pathogenesis of EHEC infection.",
author = "Chou, {T. C.} and Chiu, {H. C.} and Kuo, {C. J.} and Wu, {C. M.} and Syu, {W. J.} and Chiu, {W. T.} and Chen, {C. S.}",
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T2 - H7 Shiga-like toxin 1 is required for full pathogenicity and activation of the p38 mitogen-activated protein kinase pathway in Caenorhabditis elegans

AU - Chou, T. C.

AU - Chiu, H. C.

AU - Kuo, C. J.

AU - Wu, C. M.

AU - Syu, W. J.

AU - Chiu, W. T.

AU - Chen, C. S.

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N2 - Enterohaemorrhagic Escherichia coli (EHEC) causes life-threatening infections in humans as a consequence of the production of Shiga-like toxins. Lack of a good animal model system currently hinders in vivo study of EHEC virulence by systematic genetic methods. Here we applied the genetically tractable animal, Caenorhabditis elegans, as a surrogate host to study the virulence of EHEC as well as the host immunity to this human pathogen. Our results show that E.coli O157:H7, a serotype of EHEC, infects and kills C.elegans. Bacterial colonization and induction of the characteristic attaching and effacing (A/E) lesions in the intact intestinal epithelium of C.elegans by E.coli O157:H7 were concomitantly demonstrated in vivo. Genetic analysis indicated that the Shiga-like toxin 1 (Stx1) of E.coli O157:H7 is a virulence factor in C.elegans and is required for full toxicity. Moreover, the C.elegans p38 mitogen-activated protein kinase (MAPK) pathway, anevolutionarily conserved innate immune and stress response signalling pathway, is activated in the regulation of host susceptibility to EHEC infection in a Stx1-dependent manner. Our results validate the EHEC-C.elegans interaction as suitable for future comprehensive genetic screens for both novel bacterial and host factors involved in the pathogenesis of EHEC infection.

AB - Enterohaemorrhagic Escherichia coli (EHEC) causes life-threatening infections in humans as a consequence of the production of Shiga-like toxins. Lack of a good animal model system currently hinders in vivo study of EHEC virulence by systematic genetic methods. Here we applied the genetically tractable animal, Caenorhabditis elegans, as a surrogate host to study the virulence of EHEC as well as the host immunity to this human pathogen. Our results show that E.coli O157:H7, a serotype of EHEC, infects and kills C.elegans. Bacterial colonization and induction of the characteristic attaching and effacing (A/E) lesions in the intact intestinal epithelium of C.elegans by E.coli O157:H7 were concomitantly demonstrated in vivo. Genetic analysis indicated that the Shiga-like toxin 1 (Stx1) of E.coli O157:H7 is a virulence factor in C.elegans and is required for full toxicity. Moreover, the C.elegans p38 mitogen-activated protein kinase (MAPK) pathway, anevolutionarily conserved innate immune and stress response signalling pathway, is activated in the regulation of host susceptibility to EHEC infection in a Stx1-dependent manner. Our results validate the EHEC-C.elegans interaction as suitable for future comprehensive genetic screens for both novel bacterial and host factors involved in the pathogenesis of EHEC infection.

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