ArticleInfection and immunity2006
The global regulator Ler is necessary for enteropathogenic Escherichia coli colonization of Caenorhabditis elegans.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- A type III secretion system is required for Bordetella atropi invasion of host cells in vivo.PLoS pathogens · 2026Article
- Mutating bothFrontiers in microbiology · 2023Article
- Adherent-Invasive and Non-InvasiveMicroorganisms · 2021Article
- Caenorhabditis elegans: a model to understand host-microbe interactions.Cellular and molecular life sciences : CMLS · 2020Review
- Animal Models of Type III Secretion System-Mediated Pathogenesis.Pathogens (Basel, Switzerland) · 2019Review
- Enterobacteria and host resistance to infection.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Article
- The bacterial alarmone (p)ppGpp activates the type III secretion system in Erwinia amylovora.Journal of bacteriology · 2015Article
- Biofilm formation protects Escherichia coli against killing by Caenorhabditis elegans and Myxococcus xanthus.Applied and environmental microbiology · 2014Article
- Microarray analysis of the Ler regulon in enteropathogenic and enterohaemorrhagic Escherichia coli strains.PloS one · 2014Article
- Evaluating the pathogenic potential of environmental Escherichia coli by using the Caenorhabditis elegans infection model.Applied and environmental microbiology · 2013Article
- In vitro and in vivo model systems for studying enteropathogenic Escherichia coli infections.Cold Spring Harbor perspectives in medicine · 2013Review
- Genotypic and phenotypic characterisation of enteroaggregative Escherichia coli from children in Rio de Janeiro, Brazil.PloS one · 2013Article
- Burkholderia pseudomallei kills Caenorhabditis elegans through virulence mechanisms distinct from intestinal lumen colonization.Virulence · 2012Article
- Caenorhabditis elegans, a model organism for investigating immunity.Applied and environmental microbiology · 2012Review
- CsrA and TnaB coregulate tryptophanase activity to promote exotoxin-induced killing of Caenorhabditis elegans by enteropathogenic Escherichia coli.Journal of bacteriology · 2011Article
- A role for the RNA chaperone Hfq in controlling adherent-invasive Escherichia coli colonization and virulence.PloS one · 2011Article
- Interkingdom signaling between pathogenic bacteria and Caenorhabditis elegans.Trends in microbiology · 2010Review
- A pathoadaptive deletion in an enteroaggregative Escherichia coli outbreak strain enhances virulence in a Caenorhabditis elegans model.Infection and immunity · 2010Article
- The RNA binding protein CsrA is a pleiotropic regulator of the locus of enterocyte effacement pathogenicity island of enteropathogenic Escherichia coli.Infection and immunity · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enteropathogenic Escherichia coli (EPEC) is an important cause of infant diarrhea in developing countries and is useful for general investigations of the bacterial infection process. However, the study of the molecular pathogenesis of EPEC has been hampered by the lack of genetically tractable, convenient animal models. We have therefore developed the use of the nematode Caenorhabditis elegans as a small animal model of infection for this diarrheal pathogen. We found that nematodes died faster on nematode growth medium in the presence of EPEC pathogens than in the presence of the laboratory control strain MG1655. Increased numbers of pathogens in the gut, determined by standard plate count assays and fluorescence microscopy using green fluorescent protein-expressing bacteria, correlated with killing. Deletion of the gene encoding the global regulator Ler severely reduced the ability of EPEC to colonize the nematode gut and could be complemented by providing the ler gene on a multicopy plasmid in trans. Neither the type III secretion system nor the type IV bundle-forming pilus was required for colonization. Combined, the similarities and distinct differences between EPEC infection of nematodes and that of humans offer a unique opportunity to study several stages of the infection process, namely, attachment, colonization, and persistence, in a genetically tractable, inexpensive, and convenient in vivo system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.