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Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli

Enterohemorrhagic Escherichia coli (EHEC) is a major cause of foodborne gastrointestinal illness. EHEC uses a specialized type III secretion system (T3SS) to form attaching and effacing lesions in the colonic epithelium and outcompete commensal gut microbiota to cause disease. A recent report in mBi...

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Detalles Bibliográficos
Autores principales: Palmer, Lauren D., Skaar, Eric P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Microbiology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391915/
https://www.ncbi.nlm.nih.gov/pubmed/30808700
http://dx.doi.org/10.1128/mBio.00115-19
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author Palmer, Lauren D.
Skaar, Eric P.
author_facet Palmer, Lauren D.
Skaar, Eric P.
author_sort Palmer, Lauren D.
collection PubMed
description Enterohemorrhagic Escherichia coli (EHEC) is a major cause of foodborne gastrointestinal illness. EHEC uses a specialized type III secretion system (T3SS) to form attaching and effacing lesions in the colonic epithelium and outcompete commensal gut microbiota to cause disease. A recent report in mBio (E. A. Cameron, M. M. Curtis, A. Kumar, G. M. Dunny, et al., mBio 9:e02204-18, 2018, https://doi.org/10.1128/mBio.02204-18) describes a new role for gut commensals in potentiating disease caused by EHEC. Proteases produced by EHEC and the prevalent human commensal Bacteroides thetaiotaomicron cleave proteins in the EHEC T3SS translocon that modulate T3SS function. B. thetaiotaomicron protease activity promotes translocation of bacterial effectors required for lesion formation. These results describe a new role for the microbiota in gastrointestinal disease that could uncover future treatments to prevent the spread of gastroenteritis.
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spelling pubmed-63919152019-03-04 Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli Palmer, Lauren D. Skaar, Eric P. mBio Commentary Enterohemorrhagic Escherichia coli (EHEC) is a major cause of foodborne gastrointestinal illness. EHEC uses a specialized type III secretion system (T3SS) to form attaching and effacing lesions in the colonic epithelium and outcompete commensal gut microbiota to cause disease. A recent report in mBio (E. A. Cameron, M. M. Curtis, A. Kumar, G. M. Dunny, et al., mBio 9:e02204-18, 2018, https://doi.org/10.1128/mBio.02204-18) describes a new role for gut commensals in potentiating disease caused by EHEC. Proteases produced by EHEC and the prevalent human commensal Bacteroides thetaiotaomicron cleave proteins in the EHEC T3SS translocon that modulate T3SS function. B. thetaiotaomicron protease activity promotes translocation of bacterial effectors required for lesion formation. These results describe a new role for the microbiota in gastrointestinal disease that could uncover future treatments to prevent the spread of gastroenteritis. American Society for Microbiology 2019-02-26 /pmc/articles/PMC6391915/ /pubmed/30808700 http://dx.doi.org/10.1128/mBio.00115-19 Text en Copyright © 2019 Palmer and Skaar. https://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Commentary
Palmer, Lauren D.
Skaar, Eric P.
Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli
title Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli
title_full Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli
title_fullStr Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli
title_full_unstemmed Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli
title_short Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic Escherichia coli
title_sort cuts both ways: proteases modulate virulence of enterohemorrhagic escherichia coli
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391915/
https://www.ncbi.nlm.nih.gov/pubmed/30808700
http://dx.doi.org/10.1128/mBio.00115-19
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