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EHEC

  • Open Access
    Probiotic Properties of <span class="named-content genus-species" id="named-content-1">Escherichia coli</span> Nissle in Human Intestinal Organoids
    Editor's Pick Research Article | Host-Microbe Biology
    Probiotic Properties of Escherichia coli Nissle in Human Intestinal Organoids

    Probiotic, or beneficial, bacteria, such as E. coli Nissle, hold promise for the treatment of human disease. More study is needed to fully realize the potential of probiotics. Safety and efficacy studies are critically important; however, mice are poor models for many human intestinal diseases. We used stem cell-derived human intestinal organoid tissues to evaluate...

    Suman Pradhan, Alison Ann Weiss
  • Open Access
    <span class="named-content genus-species" id="named-content-1">Enterococcus faecalis</span> Enhances Expression and Activity of the Enterohemorrhagic <span class="named-content genus-species" id="named-content-2">Escherichia coli</span> Type III Secretion System
    Research Article | Host-Microbe Biology
    Enterococcus faecalis Enhances Expression and Activity of the Enterohemorrhagic Escherichia coli Type III Secretion System

    This work reveals a complex and multifaceted interaction between a human gut commensal, Enterococcus faecalis, and a pathogen, enterohemorrhagic E. coli. We demonstrate that E. faecalis enhances expression of the enterohemorrhagic...

    Elizabeth A. Cameron, Vanessa Sperandio, Gary M. Dunny
  • Open Access
    Reply to Wood and Lee, “Precedence for the Role of Indole with Pathogens”
    Author Reply | Host-Microbe Biology
    Reply to Wood and Lee, “Precedence for the Role of Indole with Pathogens”
    Vanessa Sperandio, Aman Kumar
  • Open Access
    Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic <em>Escherichia coli</em>
    Commentary | Host-Microbe Biology
    Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli

    Enterohemorrhagic Escherichia coli (EHEC) is a major cause of foodborne gastrointestinal illness. EHEC uses a specialized type III secretion system (T3SS) to form attaching and effacing lesions in the colonic epithelium and outcompete commensal gut microbiota to cause disease.

    Lauren D. Palmer, Eric P. Skaar
  • Open Access
    Host-Pathogen Interactions: What the EHEC Are We Learning from Host Genome-Wide Screens?
    Commentary | Host-Microbe Biology
    Host-Pathogen Interactions: What the EHEC Are We Learning from Host Genome-Wide Screens?

    Several genome-wide screens have been conducted to identify host cell factors involved in the pathogenesis of bacterial pathogens whose virulence is dependent on type III secretion systems (T3SSs), nanomachines responsible for the translocation of proteins into host cells. In the most recent of these, Pacheco et al.

    Jason P. Lynch, Cammie F. Lesser
  • Open Access
    Research Article
    CRISPR Screen Reveals that EHEC’s T3SS and Shiga Toxin Rely on Shared Host Factors for Infection

    Enterohemorrhagic Escherichia coli (EHEC) has two critical virulence factors—a type III secretion system (T3SS) and Shiga toxins (Stxs)—that are required for colonizing the intestine and causing diarrheal disease. We screened a genome-wide collection of CRISPR mutants derived from intestinal epithelial cells and identified mutants with enhanced survival following EHEC...

    Alline R. Pacheco, Jacob E. Lazarus, Brandon Sit, Stefanie Schmieder, Wayne I. Lencer, Carlos J. Blondel, John G. Doench, Brigid M. Davis, Matthew K. Waldor
  • Open Access
    Research Article
    Phosphotyrosine-Mediated Regulation of Enterohemorrhagic Escherichia coli Virulence

    Enterohemorrhagic Escherichia coli (EHEC) causes outbreaks of hemorrhagic colitis and the potentially fatal hemolytic-uremic syndrome. Successful host colonization by EHEC relies on the ability to coordinate the expression of virulence factors in response to environmental cues. A complex network that integrates environmental signals at multiple regulatory levels tightly controls virulence gene expression. We demonstrate that...

    Colin D. Robertson, Tracy H. Hazen, James B. Kaper, David A. Rasko, Anne-Marie Hansen
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