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The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells

Streptococcus mitis (S. mitis) is a pioneer commensal bacterial species colonizing many of the surfaces of the oral cavity in healthy individuals. Yet, not much information is available regarding its interaction with the host. We used examination of its transcriptional regulation in oral keratinocyt...

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Autores principales: Engen, Stian A, Rørvik, Gro H, Schreurs, Olav, Blix, Inger JS, Schenck, Karl
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5709542/
https://www.ncbi.nlm.nih.gov/pubmed/28621325
http://dx.doi.org/10.1038/ijos.2017.17
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author Engen, Stian A
Rørvik, Gro H
Schreurs, Olav
Blix, Inger JS
Schenck, Karl
author_facet Engen, Stian A
Rørvik, Gro H
Schreurs, Olav
Blix, Inger JS
Schenck, Karl
author_sort Engen, Stian A
collection PubMed
description Streptococcus mitis (S. mitis) is a pioneer commensal bacterial species colonizing many of the surfaces of the oral cavity in healthy individuals. Yet, not much information is available regarding its interaction with the host. We used examination of its transcriptional regulation in oral keratinocytes to elucidate some of its potential roles in the oral cavity. Transcription factor analysis of oral keratinocytes predicted S. mitis-mediated activation of aryl hydrocarbon receptor (AhR). Activation and functionality of AhR was confirmed through nuclear translocation determined by immunofluorescence microscopy and real-time polymerase chain reaction with reverse transcription analysis of CYP1A1, the hallmark gene for AhR activation. Addition of Streptococcus mutans or Streptococcus gordonii did not induce CYP1A1 transcription in the keratinocyte cultures. Introduction of an AhR-specific inhibitor revealed that S. mitis-mediated transcription of CXCL2 and CXCL8 was regulated by AhR. Elevated levels of prostaglandin E2 (enzyme-linked immunosorbent assay) in supernatants from S. mitis-treated oral epithelial cells were also attenuated by inhibition of AhR activity. The observed AhR-regulated activities point to a contribution of S. mitis in the regulation of inflammatory responses and thereby to wound healing in the oral cavity. The concept that the oral commensal microbiota can induce AhR activation is important, also in view of the role that AhR has in modulation of T-cell differentiation and as an anti-inflammatory factor in macrophages.
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spelling pubmed-57095422017-12-04 The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells Engen, Stian A Rørvik, Gro H Schreurs, Olav Blix, Inger JS Schenck, Karl Int J Oral Sci Original Article Streptococcus mitis (S. mitis) is a pioneer commensal bacterial species colonizing many of the surfaces of the oral cavity in healthy individuals. Yet, not much information is available regarding its interaction with the host. We used examination of its transcriptional regulation in oral keratinocytes to elucidate some of its potential roles in the oral cavity. Transcription factor analysis of oral keratinocytes predicted S. mitis-mediated activation of aryl hydrocarbon receptor (AhR). Activation and functionality of AhR was confirmed through nuclear translocation determined by immunofluorescence microscopy and real-time polymerase chain reaction with reverse transcription analysis of CYP1A1, the hallmark gene for AhR activation. Addition of Streptococcus mutans or Streptococcus gordonii did not induce CYP1A1 transcription in the keratinocyte cultures. Introduction of an AhR-specific inhibitor revealed that S. mitis-mediated transcription of CXCL2 and CXCL8 was regulated by AhR. Elevated levels of prostaglandin E2 (enzyme-linked immunosorbent assay) in supernatants from S. mitis-treated oral epithelial cells were also attenuated by inhibition of AhR activity. The observed AhR-regulated activities point to a contribution of S. mitis in the regulation of inflammatory responses and thereby to wound healing in the oral cavity. The concept that the oral commensal microbiota can induce AhR activation is important, also in view of the role that AhR has in modulation of T-cell differentiation and as an anti-inflammatory factor in macrophages. Nature Publishing Group 2017-09 2017-06-16 /pmc/articles/PMC5709542/ /pubmed/28621325 http://dx.doi.org/10.1038/ijos.2017.17 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Original Article
Engen, Stian A
Rørvik, Gro H
Schreurs, Olav
Blix, Inger JS
Schenck, Karl
The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells
title The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells
title_full The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells
title_fullStr The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells
title_full_unstemmed The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells
title_short The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells
title_sort oral commensal streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5709542/
https://www.ncbi.nlm.nih.gov/pubmed/28621325
http://dx.doi.org/10.1038/ijos.2017.17
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