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The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway
The essential first step in bacterial colonization is adhesion to the host epithelial cells. The early host-responses post-bacterial adhesions are still poorly understood. Early growth response 1 (EGR1) is an early response transcriptional regulator that can be rapidly induced by various environment...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5264520/ https://www.ncbi.nlm.nih.gov/pubmed/28180113 http://dx.doi.org/10.3389/fcimb.2017.00016 |
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author | de Klerk, Nele Saroj, Sunil D. Wassing, Gabriela M. Maudsdotter, Lisa Jonsson, Ann-Beth |
author_facet | de Klerk, Nele Saroj, Sunil D. Wassing, Gabriela M. Maudsdotter, Lisa Jonsson, Ann-Beth |
author_sort | de Klerk, Nele |
collection | PubMed |
description | The essential first step in bacterial colonization is adhesion to the host epithelial cells. The early host-responses post-bacterial adhesions are still poorly understood. Early growth response 1 (EGR1) is an early response transcriptional regulator that can be rapidly induced by various environmental stimuli. Several bacteria can induce EGR1 expression in host cells, but the involved bacterial characteristics and the underlying molecular mechanisms of this response are largely unknown. Here, we show that EGR1 can be induced in host epithelial cells by different species of bacteria independent of the adherence level, Gram-staining type and pathogenicity. However, bacterial viability and contact with host cells is necessary, indicating that an active interaction between bacteria and the host is important. Furthermore, the strongest response is observed in cells originating from the natural site of the infection, suggesting that the EGR1 induction is cell type specific. Finally, we show that EGFR–ERK1/2 and β1-integrin signaling are the main pathways used for bacteria-mediated EGR1 upregulation. In conclusion, the increase of EGR1 expression in epithelial cells is a common stress induced, cell type specific response upon host-bacteria interaction that is mediated by EGFR–ERK1/2 and β1-integrin signaling. |
format | Online Article Text |
id | pubmed-5264520 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-52645202017-02-08 The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway de Klerk, Nele Saroj, Sunil D. Wassing, Gabriela M. Maudsdotter, Lisa Jonsson, Ann-Beth Front Cell Infect Microbiol Microbiology The essential first step in bacterial colonization is adhesion to the host epithelial cells. The early host-responses post-bacterial adhesions are still poorly understood. Early growth response 1 (EGR1) is an early response transcriptional regulator that can be rapidly induced by various environmental stimuli. Several bacteria can induce EGR1 expression in host cells, but the involved bacterial characteristics and the underlying molecular mechanisms of this response are largely unknown. Here, we show that EGR1 can be induced in host epithelial cells by different species of bacteria independent of the adherence level, Gram-staining type and pathogenicity. However, bacterial viability and contact with host cells is necessary, indicating that an active interaction between bacteria and the host is important. Furthermore, the strongest response is observed in cells originating from the natural site of the infection, suggesting that the EGR1 induction is cell type specific. Finally, we show that EGFR–ERK1/2 and β1-integrin signaling are the main pathways used for bacteria-mediated EGR1 upregulation. In conclusion, the increase of EGR1 expression in epithelial cells is a common stress induced, cell type specific response upon host-bacteria interaction that is mediated by EGFR–ERK1/2 and β1-integrin signaling. Frontiers Media S.A. 2017-01-25 /pmc/articles/PMC5264520/ /pubmed/28180113 http://dx.doi.org/10.3389/fcimb.2017.00016 Text en Copyright © 2017 de Klerk, Saroj, Wassing, Maudsdotter and Jonsson. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology de Klerk, Nele Saroj, Sunil D. Wassing, Gabriela M. Maudsdotter, Lisa Jonsson, Ann-Beth The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway |
title | The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway |
title_full | The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway |
title_fullStr | The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway |
title_full_unstemmed | The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway |
title_short | The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR–ERK1/2 Pathway |
title_sort | host cell transcription factor egr1 is induced by bacteria through the egfr–erk1/2 pathway |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5264520/ https://www.ncbi.nlm.nih.gov/pubmed/28180113 http://dx.doi.org/10.3389/fcimb.2017.00016 |
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