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EcoSal Plus

Domain 8:

Pathogenesis

Adhesins of Enterohemorrhagic

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  • Authors: Mark P. Stevens1, and Timothy S. Wallis2
  • Editor: Michael S. Donnenberg3
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire RG20 7NN, United Kingdom; 2: Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire RG20 7NN, United Kingdom; 3: University of Maryland, School of Medicine, Baltimore, MD
  • Received 20 January 2005 Accepted 05 May 2005 Published 26 August 2005
  • Address correspondence to Mark P. Stevens mark-p.stevens@bbsrc.ac.uk
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  • Abstract:

    Enterohemorrhagic (EHEC) was first recognized as a cause of human disease in 1983 and is associated with diarrhea and hemorrhagic colitis, which may be complicated by life-threatening renal and neurological sequelae. EHEC are defined by their ability to produce one or more Shiga-like toxins (Stx), which mediate the systemic complications of EHEC infections, and to induce characteristic attaching and effacing lesions on intestinal epithelia, a phenotype that depends on the locus of enterocyte effacement. Acquisition of Stx-encoding bacteriophages by enteropathogenic is believed to have contributed to the evolution of EHEC, and consequently some virulence factors are conserved in both pathotypes. A key requirement for to colonize the intestines and produce disease is the ability to adhere to epithelial cells lining the gastrointestinal tract. Here, we review knowledge of the adhesins produced by EHEC and other Stx-producing , with emphasis on genetic, structural, and mechanistic aspects and their contribution to pathogenesis.

  • Citation: Stevens M, Wallis T. 2005. Adhesins of Enterohemorrhagic , EcoSal Plus 2005; doi:10.1128/ecosalplus.8.3.2.3

Key Concept Ranking

Bacterial Proteins
0.5135708
Mobile Genetic Elements
0.483193
Type III Secretion System
0.47165948
Outer Membrane Proteins
0.4106694
0.5135708

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ecosalplus.8.3.2.3.citations
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/content/journal/ecosalplus/10.1128/ecosalplus.8.3.2.3
2005-08-26
2017-05-27

Abstract:

Enterohemorrhagic (EHEC) was first recognized as a cause of human disease in 1983 and is associated with diarrhea and hemorrhagic colitis, which may be complicated by life-threatening renal and neurological sequelae. EHEC are defined by their ability to produce one or more Shiga-like toxins (Stx), which mediate the systemic complications of EHEC infections, and to induce characteristic attaching and effacing lesions on intestinal epithelia, a phenotype that depends on the locus of enterocyte effacement. Acquisition of Stx-encoding bacteriophages by enteropathogenic is believed to have contributed to the evolution of EHEC, and consequently some virulence factors are conserved in both pathotypes. A key requirement for to colonize the intestines and produce disease is the ability to adhere to epithelial cells lining the gastrointestinal tract. Here, we review knowledge of the adhesins produced by EHEC and other Stx-producing , with emphasis on genetic, structural, and mechanistic aspects and their contribution to pathogenesis.

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Figures

Image of Figure 1
Figure 1

Scale bar = 1 μm. Reprinted from reference 19 with permission from the publisher.

Citation: Stevens M, Wallis T. 2005. Adhesins of Enterohemorrhagic , EcoSal Plus 2005; doi:10.1128/ecosalplus.8.3.2.3
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Image of Figure 2
Figure 2

Open reading frames (Orfs) are represented by thick arrows; putative polycistronic operons are designated by thin arrows. Clear arrows represent Orfs of unknown function and are designated or , depending on the direction of transcription relative to .

Citation: Stevens M, Wallis T. 2005. Adhesins of Enterohemorrhagic , EcoSal Plus 2005; doi:10.1128/ecosalplus.8.3.2.3
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Figure 3

Translocation of EHEC effectors requires the function of the LEE-encoded type III secretion apparatus and depends on the assembly of EspA filaments and insertion of EspB and EspD into the host cell plasma membrane, putatively creating a translocation pore. EspA filaments act as a conduit for the delivery of Tir and other secreted effectors into the enterocyte membrane and cytoplasm. Binding of the EHEC outer membrane adhesin intimin to Tir results in intimate bacterial contact. Intimin also interacts with cellular coreceptors and this may occur before Tir binding and influence tissue tropism. In the case of EHEC O157:H7 a type III secreted protein (EspF/T ccP) is required for recruitment and activation of N-WASP. N-WASP stimulates the cellular Arp2/3 complex resulting in the nucleation of filamentous actin under adherent bacteria.

Citation: Stevens M, Wallis T. 2005. Adhesins of Enterohemorrhagic , EcoSal Plus 2005; doi:10.1128/ecosalplus.8.3.2.3
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