<i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule Assembly
<i>Escherichia coli</i>, one of the most abundant bacterial species in the human gut microbiota, has developed a mutualistic relationship with its host, regulating immunological responses. In contrast, enterotoxigenic <i>E. coli</i> (ETEC), one of the main etiologic agents of...
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MDPI AG
2020-12-01
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author | Felipe Velásquez Josefina Marín-Rojas Ricardo Soto-Rifo Alexia Torres Felipe Del Canto Fernando Valiente-Echeverría |
author_facet | Felipe Velásquez Josefina Marín-Rojas Ricardo Soto-Rifo Alexia Torres Felipe Del Canto Fernando Valiente-Echeverría |
author_sort | Felipe Velásquez |
collection | DOAJ |
description | <i>Escherichia coli</i>, one of the most abundant bacterial species in the human gut microbiota, has developed a mutualistic relationship with its host, regulating immunological responses. In contrast, enterotoxigenic <i>E. coli</i> (ETEC), one of the main etiologic agents of diarrheal morbidity and mortality in children under the age of five in developing countries, has developed mechanisms to reduce the immune-activator effect to carry out a successful infection. Following infection, the host cell initiates the shutting-off of protein synthesis and stress granule (SG) assembly. This is mostly mediated by the phosphorylation of translation initiator factor 2α (eIF2α). We therefore evaluated the ability of a non-pathogenic <i>E. coli</i> strain (<i>E. coli</i> HS) and an ETEC strain (ETEC 1766a) to induce stress granule assembly, even in response to exogenous stresses. In this work, we found that infection with <i>E. coli</i> HS or ETEC 1766a prevents SG assembly in Caco-2 cells treated with sodium arsenite (Ars) after infection. We also show that this effect occurs through an eIF2α phosphorylation (eIF2α-P)-dependent mechanism. Understanding how bacteria counters host stress responses will lay the groundwork for new therapeutic strategies to bolster host cell immune defenses against these pathogens. |
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institution | Directory Open Access Journal |
issn | 2076-2607 |
language | English |
last_indexed | 2024-03-10T13:50:52Z |
publishDate | 2020-12-01 |
publisher | MDPI AG |
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series | Microorganisms |
spelling | doaj.art-f06403c7d1414a6ebedcc87c20b860a42023-11-21T02:09:54ZengMDPI AGMicroorganisms2076-26072020-12-01911710.3390/microorganisms9010017<i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule AssemblyFelipe Velásquez0Josefina Marín-Rojas1Ricardo Soto-Rifo2Alexia Torres3Felipe Del Canto4Fernando Valiente-Echeverría5Molecular and Cellular Virology Laboratory, Virology Program, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, 8380453 Santiago, ChileMolecular and Cellular Virology Laboratory, Virology Program, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, 8380453 Santiago, ChileMolecular and Cellular Virology Laboratory, Virology Program, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, 8380453 Santiago, ChileMicrobiology and Mycology Program, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, 8380453 Santiago, ChileMicrobiology and Mycology Program, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, 8380453 Santiago, ChileMolecular and Cellular Virology Laboratory, Virology Program, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, 8380453 Santiago, Chile<i>Escherichia coli</i>, one of the most abundant bacterial species in the human gut microbiota, has developed a mutualistic relationship with its host, regulating immunological responses. In contrast, enterotoxigenic <i>E. coli</i> (ETEC), one of the main etiologic agents of diarrheal morbidity and mortality in children under the age of five in developing countries, has developed mechanisms to reduce the immune-activator effect to carry out a successful infection. Following infection, the host cell initiates the shutting-off of protein synthesis and stress granule (SG) assembly. This is mostly mediated by the phosphorylation of translation initiator factor 2α (eIF2α). We therefore evaluated the ability of a non-pathogenic <i>E. coli</i> strain (<i>E. coli</i> HS) and an ETEC strain (ETEC 1766a) to induce stress granule assembly, even in response to exogenous stresses. In this work, we found that infection with <i>E. coli</i> HS or ETEC 1766a prevents SG assembly in Caco-2 cells treated with sodium arsenite (Ars) after infection. We also show that this effect occurs through an eIF2α phosphorylation (eIF2α-P)-dependent mechanism. Understanding how bacteria counters host stress responses will lay the groundwork for new therapeutic strategies to bolster host cell immune defenses against these pathogens.https://www.mdpi.com/2076-2607/9/1/17stress granules<i>E. coli</i>integrated stress response |
spellingShingle | Felipe Velásquez Josefina Marín-Rojas Ricardo Soto-Rifo Alexia Torres Felipe Del Canto Fernando Valiente-Echeverría <i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule Assembly Microorganisms stress granules <i>E. coli</i> integrated stress response |
title | <i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule Assembly |
title_full | <i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule Assembly |
title_fullStr | <i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule Assembly |
title_full_unstemmed | <i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule Assembly |
title_short | <i>Escherichia coli</i> HS and Enterotoxigenic <i>Escherichia coli</i> Hinder Stress Granule Assembly |
title_sort | i escherichia coli i hs and enterotoxigenic i escherichia coli i hinder stress granule assembly |
topic | stress granules <i>E. coli</i> integrated stress response |
url | https://www.mdpi.com/2076-2607/9/1/17 |
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