Loss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization

ABSTRACT Enterococcus faecalis is paradoxically a dangerous nosocomial pathogen and a normal constituent of the human gut microbiome, an environment rich in ethanolamine. E. faecalis carries the eut (ethanolamine utilization) genes, which enable the catabolism of ethanolamine (EA) as a valuable sour...

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Autores principales: Karan Gautam Kaval, Kavindra V. Singh, Melissa R. Cruz, Sruti DebRoy, Wade C. Winkler, Barbara E. Murray, Danielle A. Garsin
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Publicado: American Society for Microbiology 2018
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spelling oai:doaj.org-article:64653fa2c8f942b09a46ef17c1a58a572021-11-15T16:00:27ZLoss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization10.1128/mBio.00790-182150-7511https://doaj.org/article/64653fa2c8f942b09a46ef17c1a58a572018-07-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.00790-18https://doaj.org/toc/2150-7511ABSTRACT Enterococcus faecalis is paradoxically a dangerous nosocomial pathogen and a normal constituent of the human gut microbiome, an environment rich in ethanolamine. E. faecalis carries the eut (ethanolamine utilization) genes, which enable the catabolism of ethanolamine (EA) as a valuable source of carbon and/or nitrogen. EA catabolism was previously shown to contribute to the colonization and growth of enteric pathogens, such as Salmonella enterica serovar Typhimurium and enterohemorrhagic Escherichia coli (EHEC), in the gut environment. We tested the ability of eut mutants of E. faecalis to colonize the gut using a murine model of gastrointestinal (GI) tract competition and report the surprising observation that these mutants outcompete the wild-type strain. IMPORTANCE Some bacteria that are normal, harmless colonizers of the human body can cause disease in immunocompromised patients, particularly those that have been heavily treated with antibiotics. Therefore, it is important to understand the factors that promote or negate these organisms’ ability to colonize. Previously, ethanolamine, found in high concentrations in the GI tract, was shown to promote the colonization and growth of bacteria associated with food poisoning. Here, we report the surprising, opposite effect of ethanolamine utilization on the commensal colonizer E. faecalis, namely, that loss of this metabolic capacity made it a better colonizer.Karan Gautam KavalKavindra V. SinghMelissa R. CruzSruti DebRoyWade C. WinklerBarbara E. MurrayDanielle A. GarsinAmerican Society for MicrobiologyarticleEnterococcusethanolamineintestinal colonizationMicrobiologyQR1-502ENmBio, Vol 9, Iss 3 (2018)
institution DOAJ
collection DOAJ
language EN
topic Enterococcus
ethanolamine
intestinal colonization
Microbiology
QR1-502
spellingShingle Enterococcus
ethanolamine
intestinal colonization
Microbiology
QR1-502
Karan Gautam Kaval
Kavindra V. Singh
Melissa R. Cruz
Sruti DebRoy
Wade C. Winkler
Barbara E. Murray
Danielle A. Garsin
Loss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization
description ABSTRACT Enterococcus faecalis is paradoxically a dangerous nosocomial pathogen and a normal constituent of the human gut microbiome, an environment rich in ethanolamine. E. faecalis carries the eut (ethanolamine utilization) genes, which enable the catabolism of ethanolamine (EA) as a valuable source of carbon and/or nitrogen. EA catabolism was previously shown to contribute to the colonization and growth of enteric pathogens, such as Salmonella enterica serovar Typhimurium and enterohemorrhagic Escherichia coli (EHEC), in the gut environment. We tested the ability of eut mutants of E. faecalis to colonize the gut using a murine model of gastrointestinal (GI) tract competition and report the surprising observation that these mutants outcompete the wild-type strain. IMPORTANCE Some bacteria that are normal, harmless colonizers of the human body can cause disease in immunocompromised patients, particularly those that have been heavily treated with antibiotics. Therefore, it is important to understand the factors that promote or negate these organisms’ ability to colonize. Previously, ethanolamine, found in high concentrations in the GI tract, was shown to promote the colonization and growth of bacteria associated with food poisoning. Here, we report the surprising, opposite effect of ethanolamine utilization on the commensal colonizer E. faecalis, namely, that loss of this metabolic capacity made it a better colonizer.
format article
author Karan Gautam Kaval
Kavindra V. Singh
Melissa R. Cruz
Sruti DebRoy
Wade C. Winkler
Barbara E. Murray
Danielle A. Garsin
author_facet Karan Gautam Kaval
Kavindra V. Singh
Melissa R. Cruz
Sruti DebRoy
Wade C. Winkler
Barbara E. Murray
Danielle A. Garsin
author_sort Karan Gautam Kaval
title Loss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization
title_short Loss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization
title_full Loss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization
title_fullStr Loss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization
title_full_unstemmed Loss of Ethanolamine Utilization in <named-content content-type="genus-species">Enterococcus faecalis</named-content> Increases Gastrointestinal Tract Colonization
title_sort loss of ethanolamine utilization in <named-content content-type="genus-species">enterococcus faecalis</named-content> increases gastrointestinal tract colonization
publisher American Society for Microbiology
publishDate 2018
url https://doaj.org/article/64653fa2c8f942b09a46ef17c1a58a57
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