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Detection of Enterohemorrhagic Escherichia Coli Colonization in Murine Host by Non-invasive In Vivo Bioluminescence System
Published on: April 9, 2018
Enteropathogenic Escherichia coli: a pathogen that inserts its own receptor into host cells
R DeVinney1, A Gauthier, A Abe
1Biotechnology Laboratory, University of British Columbia, Vancouver, Canada.
Cellular and Molecular Life Sciences : CMLS
|July 21, 1999
Summary
Enteropathogenic Escherichia coli (EPEC) causes infant diarrhea by intimately attaching to host cells. This review details the discovery and role of the translocated intimin receptor (Tir) in EPEC pathogenesis and disease.
Area of Science:
- Microbiology
- Pathogenesis
- Cell Biology
Background:
- Enteropathogenic Escherichia coli (EPEC) is a significant cause of infant diarrhea globally.
- EPEC pathogenesis involves intimate attachment to host cells, forming actin-rich pedestals.
- This attachment is mediated by the outer membrane adhesin intimin.
Purpose of the Study:
- To review the discovery and characterization of the translocated intimin receptor (Tir).
- To elucidate the role of Tir in EPEC-mediated pedestal formation.
- To discuss the delivery of Tir via type III secretion systems and the relevance of in vitro and in vivo models.
Main Methods:
- Literature review focusing on EPEC adherence and pathogenesis.
- Analysis of the role of intimin and Tir in bacterial-host cell interactions.
- Critical evaluation of animal models for EPEC infection studies.
Main Results:
- Tir is identified as the host cell receptor for EPEC's intimate adherence.
- Tir is translocated into the host cell membrane by EPEC's type III secretion system.
- Understanding Tir's function is crucial for elucidating EPEC disease mechanisms.
Conclusions:
- The translocated intimin receptor (Tir) is a key virulence factor in EPEC infections.
- Tir's translocation and function are central to EPEC's ability to cause disease.
- Further research into Tir will advance our understanding of EPEC pathogenesis and inform therapeutic strategies.
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