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Enteropathogenic and enterohaemorrhagic Escherichia coli: even more subversive elements.
Alexander R C Wong1, Jaclyn S Pearson, Michael D Bright
1Centre for Molecular Microbiology and Infection, Division of Cell and Molecular Biology, Imperial College London, London SW7 2AZ, UK.
Molecular Microbiology
|April 15, 2011
Summary
Enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC) use type III secretion systems (T3SS) to inject effector proteins. These proteins manipulate host cell signaling and pathways, contributing to virulence and disease.
Area of Science:
- Microbiology
- Cell Biology
- Pathogen-Host Interactions
Background:
- Enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC) are human pathogens.
- They utilize a type III secretion system (T3SS) for colonization.
- These bacteria induce attaching and effacing (A/E) lesions and subvert host cell signaling.
Purpose of the Study:
- To elucidate the mechanisms by which EPEC and EHEC effector proteins hijack host cell signaling pathways.
- To identify novel activities of effector proteins in mediating virulence.
- To understand the complex interactions of these effectors during infection.
Main Methods:
- Characterization of established and novel effector proteins.
- Investigation of effector protein functions including mimicry of host factors, inhibition of apoptosis, and modulation of inflammatory and phagocytic pathways.
- Analysis of effector protein interactions and their spatiotemporal regulation.
Main Results:
- Identification of novel effector functions, including mimicry of Rho guanine nucleotide exchange factors (Map, EspM).
- Demonstration of effectors inhibiting apoptosis (NleH, NleD) and interfering with inflammatory signaling (NleB, NleC, NleE, NleH).
- Effectors EspF, EspH, and EspJ were shown to interfere with phagocytosis.
Conclusions:
- EPEC and EHEC effector proteins are multifunctional and play critical roles in virulence.
- These effectors exhibit complex relationships (redundant, synergistic, antagonistic) in modulating host cell functions.
- Coordinated action of effectors on host organelles and pathways is crucial for EPEC and EHEC pathogenesis.
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