ArticlePLoS pathogens2017
Attaching and effacing (A/E) lesion formation by enteropathogenic E. coli on human intestinal mucosa is dependent on non-LEE effectors.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
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- Why put yourself on a pedestal? The pathogenic role of the A/E pedestal.Infection and immunity · 2024Review
- The pathogen-encoded signalling receptor Tir exploits host-like intrinsic disorder for infection.Communications biology · 2024Article
- Genetic and virulence characteristics of hybrid Shiga toxin-producing and atypical enteropathogenicFrontiers in microbiology · 2024Article
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- Enhanced protein translocation to mammalian cells by expression of EtgA transglycosylase in a synthetic injector E. coli strain.Microbial cell factories · 2022Article
- Efficient markerless integration of genes in the chromosome of probiotic E. coli Nissle 1917 by bacterial conjugation.Microbial biotechnology · 2022Article
- Lymphostatin, a virulence factor of attaching and effacingFrontiers in cellular and infection microbiology · 2022Article
- Neonatal microbiota-epithelial interactions that impact infection.Frontiers in microbiology · 2022Review
- Whole-genome sequence analysis of Shiga toxin-producing Escherichia coli O157 strains isolated from wild deer and boar in Japan.The Journal of veterinary medical science · 2021Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Enteropathogenic E. coli (EPEC) is a human pathogen that causes acute and chronic pediatric diarrhea. The hallmark of EPEC infection is the formation of attaching and effacing (A/E) lesions in the intestinal epithelium. Formation of A/E lesions is mediated by genes located on the pathogenicity island locus of enterocyte effacement (LEE), which encode the adhesin intimin, a type III secretion system (T3SS) and six effectors, including the essential translocated intimin receptor (Tir). Seventeen additional effectors are encoded by genes located outside the LEE, in insertion elements and prophages. Here, using a stepwise approach, we generated an EPEC mutant lacking the entire effector genes (EPEC0) and intermediate mutants. We show that EPEC0 contains a functional T3SS. An EPEC mutant expressing intimin but lacking all the LEE effectors but Tir (EPEC1) was able to trigger robust actin polymerization in HeLa cells and mucin-producing intestinal LS174T cells. However, EPEC1 was unable to form A/E lesions on human intestinal in vitro organ cultures (IVOC). Screening the intermediate mutants for genes involved in A/E lesion formation on IVOC revealed that strains lacking non-LEE effector/s have a marginal ability to form A/E lesions. Furthermore, we found that Efa1/LifA proteins are important for A/E lesion formation efficiency in EPEC strains lacking multiple effectors. Taken together, these results demonstrate the intricate relationships between T3SS effectors and the essential role non-LEE effectors play in A/E lesion formation on mucosal surfaces.
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