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Epithelial maturity influences EPEC-induced desmosomal alterations.

Jennifer Lising Roxas1, Gayatri Vedantam1,2,3,4, V K Viswanathan1,2,3

  • 1a School of Animal and Comparative Biomedical Sciences , University of Arizona , Tucson , AZ , USA.

Gut Microbes
|September 6, 2018
PubMed
Summary
This summary is machine-generated.

Enteropathogenic Escherichia coli (EPEC) disrupts intestinal cell adhesion by damaging desmosomes. The EPEC effector protein EspH causes keratin retraction, leading to desmosome loss and weakened epithelial barriers.

Keywords:
DSG2EPECEspHRho GTPasedesmogleindesmosomekeratin

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Area of Science:

  • Cell biology
  • Microbiology
  • Epithelial biology

Background:

  • Desmosomes are crucial for strong cell-cell adhesion in epithelial tissues.
  • Enteropathogenic Escherichia coli (EPEC) infection can compromise intestinal barrier function.
  • Previous work identified EPEC's disruption of desmosomes and cell adhesion.

Purpose of the Study:

  • To elucidate the mechanism by which EPEC disrupts desmosomes.
  • To investigate the role of the EPEC effector protein EspH in desmosome damage.
  • To examine the impact of epithelial cell monolayer maturity on desmosome integrity during EPEC infection.

Main Methods:

  • Immunofluorescence microscopy to visualize keratin and desmoglein-2 (DSG2) distribution.
  • Analysis of EPEC effector protein EspH's effect on Rho GTPases.
  • Assessment of cell-cell adhesion and barrier function in C2BBe cells.

Main Results:

  • EPEC infection, mediated by EspH, inactivates Rho GTPases, causing keratin intermediate filament retraction.
  • Keratin retraction leads to the cytoplasmic redistribution and loss of anchoring of desmoglein-2 (DSG2) from cell junctions.
  • Epithelial cell monolayer maturity influences the extent of desmosome damage during EPEC infection.

Conclusions:

  • EPEC-induced keratin retraction is a key mechanism for desmosome disruption and loss of cell adhesion.
  • EspH is a critical EPEC virulence factor targeting host cell junctional integrity.
  • The epithelial barrier's susceptibility to EPEC may be modulated by its developmental stage.