Enteropathogenic E. coli Interactions with Host Cells

Finlay, B. Brett; Abe, Akio

doi:10.7883/yoken1952.51.supplement1_s91

Cited by 3 publications

(3 citation statements)

References 19 publications

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“…the cytoskeleton, signaling pathways and intracellular trafficking, to support successful bacterial colonization and survival in the intestinal mucosa [2,3,4]. A prominent hallmark of EPEC infection is the induction of “attaching and effacing” (AE) lesions of the mucosal tissue, characterized by intimate microbial attachment to the apical plasma membrane of the infected epithelial cells, local elimination of brush border microvilli and the formation of a filamentous actin (F-actin)-rich membrane protrusion (often called pedestal) located immediately beneath the attached bacterium [5,6].…”

Section: Introductionmentioning

confidence: 99%

Enteropathogenic Escherichia coli remodels host endosomes to promote endocytic turnover and breakdown of surface polarity

et al. 2019

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Enteropathogenic E . coli (EPEC) is an extracellular diarrheagenic human pathogen which infects the apical plasma membrane of the small intestinal enterocytes. EPEC utilizes a type III secretion system to translocate bacterial effector proteins into its epithelial hosts. This activity, which subverts numerous signaling and membrane trafficking pathways in the infected cells, is thought to contribute to pathogen virulence. The molecular and cellular mechanisms underlying these events are not well understood. We investigated the mode by which EPEC effectors hijack endosomes to modulate endocytosis, recycling and transcytosis in epithelial host cells. To this end, we developed a flow cytometry-based assay and imaging techniques to track endosomal dynamics and membrane cargo trafficking in the infected cells. We show that type-III secreted components prompt the recruitment of clathrin (clathrin and AP2), early (Rab5a and EEA1) and recycling (Rab4a, Rab11a, Rab11b, FIP2, Myo5b) endocytic machineries to peripheral plasma membrane infection sites. Protein cargoes, e.g. transferrin receptors, β1 integrins and aquaporins, which exploit the endocytic pathways mediated by these machineries, were also found to be recruited to these sites. Moreover, the endosomes and cargo recruitment to infection sites correlated with an increase in cargo endocytic turnover (i.e. endocytosis and recycling) and transcytosis to the infected plasma membrane. The hijacking of endosomes and associated endocytic activities depended on the translocated EspF and Map effectors in non-polarized epithelial cells, and mostly on EspF in polarized epithelial cells. These data suggest a model whereby EPEC effectors hijack endosomal recycling mechanisms to mislocalize and concentrate host plasma membrane proteins in endosomes and in the apically infected plasma membrane. We hypothesize that these activities contribute to bacterial colonization and virulence.

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Section: Introductionmentioning

confidence: 99%

Enteropathogenic Escherichia coli remodels host endosomes to promote endocytic turnover and breakdown of surface polarity

et al. 2019

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“…EPEC loosely associate with apical membranes of intestinal epithelial cells and use a specialized secretory apparatus known as a type III secretion system, which has the form of a molecular "syringe", to inject bacterial proteins into the host cell cytosol. These bacterial proteins include a receptor for the bacteria themselves, known as Tir (for translocated intimin receptor), which inserts into the apical membrane and promotes more firm adhesion, as well as several molecules that alter the structure and function of host cell components [93][94][95]. For example, EPEC effectors can remodel cellular actin, resulting in the characteristic "attaching and effacing" lesion seen in EPEC-infected cells [96].…”

Section: Epithelium As Active Interface With Intestinal Pathogens Andmentioning

confidence: 99%

Intestinal epithelial secretion and barrier function: from bench to bedside

Barrett

2005

Eur Surg

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Zusammenfassung. Grundlagen: Flüssigkeitssekre-tion und Barrierefunktion sind wichtige Eigenschaften des intestinalen Epithels. Die experimentellen Modelle, welche maßgeblich unser Verständnis für epitheliale Funktionen und ihre molekularen Mechanismen ermöglicht haben, sind vielen unbekannt.Methodik: Literaturübersicht experimenteller Studien über Grundlagen zur intestinalen Flüssigkeitssekretion und epithelialen Barrierefunktion.Ergebnisse: Ergebnisse von In-vitro-und In-vivo-Studien und deren Bedeutung für das Verständnis der intestinalen Elektrolyttransportmechanismen und der epithelialen Integrität werden diskutiert.Schlussfolgerungen: Experimentelle gastrointestinale Grundlagenforschung liefert Informationen von praktischklinischer Relevanz. Der gegenseitige "bench to bedside"-Dialog zwischen experimenteller und praktischer Medizin trägt wesentlich dazu bei, die den Erkrankungen zugrunde liegenden Prozesse besser zu verstehen und damit unsere Therapiekonzepte gastrointestinaler Erkrankungen zu verbessern.Schlüsselwörter: experimentelle Medizin, UssingKammer, T84-Zellen, Epithelintegrität, intestinale Sekretion.Summary. Background: Fluid secretion and the ability to form a barrier are critical functions of the intestinal epithelium. However, some clinicians may not have an understanding of the model systems that have been used to enhance our knowledge of these important epithelial functions and their molecular regulation.Methods: This article seeks to explain the basis of intestinal fluid secretion and barrier function, and modification of these processes in pathophysiological settings, by reviewing recent basic science literature.Results: Findings from studies conducted both in vivo and in vitro are discussed, with an emphasis on insights that have emerged by applying intestinal epithelial cell lines to investigations of electrolyte transport and the integrity of the epithelial barrier.Conclusions: Even basic observations in reductionist model systems can yield information that is of immediate and practical clinical relevance. Continued bidirectional "bench to bedside" dialogue may enhance the clinician's ability to intervene in gastrointestinal diseases.

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“…On one hand, the observation that the organization and functions of the LEE are conserved among studied E. coli strains (Finlay & Abe, 1998 ;Kaper, 1998 ;Taylor et al, 1998 ;Beltrametti et al, 1999 ;Hartland et al, 1999) and that the locus has a different GjC proportion to the rest of the chromosome (Elliot et al, 1998) suggests that this group of genes was transferred as a cassette from some other bacterial species and was inserted as a whole in the E. coli chromosome. On the other hand, there is increasing evidence of horizontal transfer of some genes of the LEE, recombination within this locus (Finlay & Falkow, 1997 ;Wieler et al, 1997 ;Ismaili et al, 1998 ;McGraw et al, 1999) as well as recombination with other pathogenic genes (Lederberg, 1998).…”

Section: Abbreviationsmentioning

confidence: 99%

The elements of the locus of enterocyte effacement in human and wild mammal isolates of Escherichia coli: evolution by assemblage or disruption?

et al. 2001

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Escherichia coli is an excellent model for studying the evolution of pathogenicity since within one species various genes can be found in pathogenic islands and plasmids causing a wide spectrum of virulence. A collection of 122 strains from different human and wild mammal hosts were analysed by PCR and Southern hybridization for the presence of a subset of the genes included in the LEE (locus of enterocyte effacement). In the PCR analysis, two markers (cesT/eae and espB genes) were found together in more strains (254 %) than either were found alone. The cesT/eae gene was less frequently found alone (82 %) than was the espB gene (156 %). Four regions of the LEE were analysed in a subsample of 25 strains using Southern hybridization. The four regions were all present (44 %), all absent (12 %) or present in different combinations (44 %) in a given strain. The flanking regions of the LEE showed the highest rate of hybridization (in 72 % of the strains). The results indicate that the LEE is a dynamic genetic entity, both the complete gene cluster and the individual genes. The genes that comprise this locus seem to be horizontally acquired (or lost) in an independent way and may control other functions in non-pathogenic E. coli lineages. In this way, horizontal transfer may allow the gradual stepwise construction of gene cassettes facilitating coordinate regulation and expression of novel functions.

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Enteropathogenic E. coli Interactions with Host Cells

Cited by 3 publications

References 19 publications

Enteropathogenic Escherichia coli remodels host endosomes to promote endocytic turnover and breakdown of surface polarity

Enteropathogenic Escherichia coli remodels host endosomes to promote endocytic turnover and breakdown of surface polarity

Intestinal epithelial secretion and barrier function: from bench to bedside

The elements of the locus of enterocyte effacement in human and wild mammal isolates of Escherichia coli: evolution by assemblage or disruption?

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