Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness

ABSTRACTDiarrheal diseases are still a significant problem for humankind, causing approximately half a million deaths annually. To cause diarrhea, enteric bacterial pathogens must first colonize the gut, which is a niche occupied by the normal bacterial microbiota. Therefore, the ability of pathogen...

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Main Authors: Jonas Kjellin, Danna Lee, Hans Steinsland, Rachel Dwane, Oda Barth Vedoy, Kurt Hanevik, Sanna Koskiniemi
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Gut Microbes
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/19490976.2023.2295891
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author Jonas Kjellin
Danna Lee
Hans Steinsland
Rachel Dwane
Oda Barth Vedoy
Kurt Hanevik
Sanna Koskiniemi
author_facet Jonas Kjellin
Danna Lee
Hans Steinsland
Rachel Dwane
Oda Barth Vedoy
Kurt Hanevik
Sanna Koskiniemi
author_sort Jonas Kjellin
collection DOAJ
description ABSTRACTDiarrheal diseases are still a significant problem for humankind, causing approximately half a million deaths annually. To cause diarrhea, enteric bacterial pathogens must first colonize the gut, which is a niche occupied by the normal bacterial microbiota. Therefore, the ability of pathogenic bacteria to inhibit the growth of other bacteria can facilitate the colonization process. Although enterotoxigenic Escherichia coli (ETEC) is one of the major causative agents of diarrheal diseases, little is known about the competition systems found in and used by ETEC and how they contribute to the ability of ETEC to colonize a host. Here, we collected a set of 94 fully assembled ETEC genomes by performing whole-genome sequencing and mining the NCBI RefSeq database. Using this set, we performed a comprehensive search for delivered bacterial toxins and investigated how these toxins contribute to ETEC competitiveness in vitro. We found that type VI secretion systems (T6SS) were widespread among ETEC (n = 47). In addition, several closely related ETEC strains were found to encode Colicin Ia and T6SS (n = 8). These toxins provide ETEC competitive advantages during in vitro competition against other E. coli, suggesting that the role of T6SS as well as colicins in ETEC biology has until now been underappreciated.
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spelling doaj.art-2fd5f4aeb735487e9b2c86d088909b852023-12-27T11:11:03ZengTaylor & Francis GroupGut Microbes1949-09761949-09842024-12-0116110.1080/19490976.2023.2295891Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitivenessJonas Kjellin0Danna Lee1Hans Steinsland2Rachel Dwane3Oda Barth Vedoy4Kurt Hanevik5Sanna Koskiniemi6Department of Cell and Molecular Biology, Uppsala University, Uppsala, SwedenDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, SwedenCISMAC, Centre for International Health, Department of Global Public Health and Primary Care, University of Bergen, Bergen, NorwayDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, SwedenDepartment of Clinical Science, University of Bergen, Bergen, NorwayDepartment of Clinical Science, University of Bergen, Bergen, NorwayDepartment of Cell and Molecular Biology, Uppsala University, Uppsala, SwedenABSTRACTDiarrheal diseases are still a significant problem for humankind, causing approximately half a million deaths annually. To cause diarrhea, enteric bacterial pathogens must first colonize the gut, which is a niche occupied by the normal bacterial microbiota. Therefore, the ability of pathogenic bacteria to inhibit the growth of other bacteria can facilitate the colonization process. Although enterotoxigenic Escherichia coli (ETEC) is one of the major causative agents of diarrheal diseases, little is known about the competition systems found in and used by ETEC and how they contribute to the ability of ETEC to colonize a host. Here, we collected a set of 94 fully assembled ETEC genomes by performing whole-genome sequencing and mining the NCBI RefSeq database. Using this set, we performed a comprehensive search for delivered bacterial toxins and investigated how these toxins contribute to ETEC competitiveness in vitro. We found that type VI secretion systems (T6SS) were widespread among ETEC (n = 47). In addition, several closely related ETEC strains were found to encode Colicin Ia and T6SS (n = 8). These toxins provide ETEC competitive advantages during in vitro competition against other E. coli, suggesting that the role of T6SS as well as colicins in ETEC biology has until now been underappreciated.https://www.tandfonline.com/doi/10.1080/19490976.2023.2295891ETECcolicintype VI secretioncompetitive advantagegenome
spellingShingle Jonas Kjellin
Danna Lee
Hans Steinsland
Rachel Dwane
Oda Barth Vedoy
Kurt Hanevik
Sanna Koskiniemi
Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness
Gut Microbes
ETEC
colicin
type VI secretion
competitive advantage
genome
title Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness
title_full Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness
title_fullStr Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness
title_full_unstemmed Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness
title_short Colicins and T6SS-based competition systems enhance enterotoxigenic E. coli (ETEC) competitiveness
title_sort colicins and t6ss based competition systems enhance enterotoxigenic e coli etec competitiveness
topic ETEC
colicin
type VI secretion
competitive advantage
genome
url https://www.tandfonline.com/doi/10.1080/19490976.2023.2295891
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