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Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection
Synthesis of interferon-β (IFN-β) is an innate response to cytoplasmic infection with bacterial pathogens. Our recent studies showed that Listeria monocytogenes limits immune detection and IFN-β synthesis via deacetylation of its peptidoglycan, which renders the bacterium resistant to lysozyme degra...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303824/ https://www.ncbi.nlm.nih.gov/pubmed/22432012 http://dx.doi.org/10.1371/journal.pone.0033299 |
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author | Aubry, Camille Corr, Sinéad C. Wienerroither, Sebastian Goulard, Céline Jones, Ruth Jamieson, Amanda M. Decker, Thomas O'Neill, Luke A. J. Dussurget, Olivier Cossart, Pascale |
author_facet | Aubry, Camille Corr, Sinéad C. Wienerroither, Sebastian Goulard, Céline Jones, Ruth Jamieson, Amanda M. Decker, Thomas O'Neill, Luke A. J. Dussurget, Olivier Cossart, Pascale |
author_sort | Aubry, Camille |
collection | PubMed |
description | Synthesis of interferon-β (IFN-β) is an innate response to cytoplasmic infection with bacterial pathogens. Our recent studies showed that Listeria monocytogenes limits immune detection and IFN-β synthesis via deacetylation of its peptidoglycan, which renders the bacterium resistant to lysozyme degradation. Here, we examined signaling requirements for the massive IFN-β production resulting from the infection of murine macrophages with a mutant strain of L. monocytogenes, ΔpgdA, which is unable to modify its peptidoglycan. We report the identification of unconventional signaling pathways to the IFN-β gene, requiring TLR2 and bacterial internalization. Induction of IFN-β was independent of the Mal/TIRAP adaptor protein but required TRIF and the transcription factors IRF3 and IRF7. These pathways were stimulated to a lesser degree by wild-type L. monocytogenes. They operated in both resident and inflammatory macrophages derived from the peritoneal cavity, but not in bone marrow-derived macrophages. The novelty of our findings thus lies in the first description of TLR2 and TRIF as two critical components leading to the induction of the IFN-β gene and in uncovering that individual macrophage populations adopt different strategies to link pathogen recognition signals to IFN-β gene expression. |
format | Online Article Text |
id | pubmed-3303824 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-33038242012-03-19 Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection Aubry, Camille Corr, Sinéad C. Wienerroither, Sebastian Goulard, Céline Jones, Ruth Jamieson, Amanda M. Decker, Thomas O'Neill, Luke A. J. Dussurget, Olivier Cossart, Pascale PLoS One Research Article Synthesis of interferon-β (IFN-β) is an innate response to cytoplasmic infection with bacterial pathogens. Our recent studies showed that Listeria monocytogenes limits immune detection and IFN-β synthesis via deacetylation of its peptidoglycan, which renders the bacterium resistant to lysozyme degradation. Here, we examined signaling requirements for the massive IFN-β production resulting from the infection of murine macrophages with a mutant strain of L. monocytogenes, ΔpgdA, which is unable to modify its peptidoglycan. We report the identification of unconventional signaling pathways to the IFN-β gene, requiring TLR2 and bacterial internalization. Induction of IFN-β was independent of the Mal/TIRAP adaptor protein but required TRIF and the transcription factors IRF3 and IRF7. These pathways were stimulated to a lesser degree by wild-type L. monocytogenes. They operated in both resident and inflammatory macrophages derived from the peritoneal cavity, but not in bone marrow-derived macrophages. The novelty of our findings thus lies in the first description of TLR2 and TRIF as two critical components leading to the induction of the IFN-β gene and in uncovering that individual macrophage populations adopt different strategies to link pathogen recognition signals to IFN-β gene expression. Public Library of Science 2012-03-14 /pmc/articles/PMC3303824/ /pubmed/22432012 http://dx.doi.org/10.1371/journal.pone.0033299 Text en Aubry et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Aubry, Camille Corr, Sinéad C. Wienerroither, Sebastian Goulard, Céline Jones, Ruth Jamieson, Amanda M. Decker, Thomas O'Neill, Luke A. J. Dussurget, Olivier Cossart, Pascale Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection |
title | Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection |
title_full | Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection |
title_fullStr | Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection |
title_full_unstemmed | Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection |
title_short | Both TLR2 and TRIF Contribute to Interferon-β Production during Listeria Infection |
title_sort | both tlr2 and trif contribute to interferon-β production during listeria infection |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303824/ https://www.ncbi.nlm.nih.gov/pubmed/22432012 http://dx.doi.org/10.1371/journal.pone.0033299 |
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