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Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons
Listeria monocytogenes (L. monocytogenes) is a food-borne bacterial pathogen. Innate immunity to L. monocytogenes is profoundly affected by type I interferons (IFN-I). Here we investigated host metabolism in L. monocytogenes-infected mice and its potential control by IFN-I. Accordingly, we used anim...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8266069/ https://www.ncbi.nlm.nih.gov/pubmed/34237114 http://dx.doi.org/10.1371/journal.ppat.1009697 |
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author | Demiroz, Duygu Platanitis, Ekaterini Bryant, Michael Fischer, Philipp Prchal-Murphy, Michaela Lercher, Alexander Lassnig, Caroline Baccarini, Manuela Müller, Mathias Bergthaler, Andreas Sexl, Veronika Dolezal, Marlies Decker, Thomas |
author_facet | Demiroz, Duygu Platanitis, Ekaterini Bryant, Michael Fischer, Philipp Prchal-Murphy, Michaela Lercher, Alexander Lassnig, Caroline Baccarini, Manuela Müller, Mathias Bergthaler, Andreas Sexl, Veronika Dolezal, Marlies Decker, Thomas |
author_sort | Demiroz, Duygu |
collection | PubMed |
description | Listeria monocytogenes (L. monocytogenes) is a food-borne bacterial pathogen. Innate immunity to L. monocytogenes is profoundly affected by type I interferons (IFN-I). Here we investigated host metabolism in L. monocytogenes-infected mice and its potential control by IFN-I. Accordingly, we used animals lacking either the IFN-I receptor (IFNAR) or IRF9, a subunit of ISGF3, the master regulator of IFN-I-induced genes. Transcriptomes and metabolite profiles showed that L. monocytogenes infection induces metabolic rewiring of the liver. This affects various metabolic pathways including fatty acid (FA) metabolism and oxidative phosphorylation and is partially dependent on IFN-I signaling. Livers and macrophages from Ifnar1(-/-) mice employ increased glutaminolysis in an IRF9-independent manner, possibly to readjust TCA metabolite levels due to reduced FA oxidation. Moreover, FA oxidation inhibition provides protection from L. monocytogenes infection, explaining part of the protection of Irf9(-/-) and Ifnar1(-/-) mice. Our findings define a role of IFN-I in metabolic regulation during L. monocytogenes infection. Metabolic differences between Irf9(-/-) and Ifnar1(-/-) mice may underlie the different susceptibility of these mice against lethal infection with L. monocytogenes. |
format | Online Article Text |
id | pubmed-8266069 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-82660692021-07-19 Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons Demiroz, Duygu Platanitis, Ekaterini Bryant, Michael Fischer, Philipp Prchal-Murphy, Michaela Lercher, Alexander Lassnig, Caroline Baccarini, Manuela Müller, Mathias Bergthaler, Andreas Sexl, Veronika Dolezal, Marlies Decker, Thomas PLoS Pathog Research Article Listeria monocytogenes (L. monocytogenes) is a food-borne bacterial pathogen. Innate immunity to L. monocytogenes is profoundly affected by type I interferons (IFN-I). Here we investigated host metabolism in L. monocytogenes-infected mice and its potential control by IFN-I. Accordingly, we used animals lacking either the IFN-I receptor (IFNAR) or IRF9, a subunit of ISGF3, the master regulator of IFN-I-induced genes. Transcriptomes and metabolite profiles showed that L. monocytogenes infection induces metabolic rewiring of the liver. This affects various metabolic pathways including fatty acid (FA) metabolism and oxidative phosphorylation and is partially dependent on IFN-I signaling. Livers and macrophages from Ifnar1(-/-) mice employ increased glutaminolysis in an IRF9-independent manner, possibly to readjust TCA metabolite levels due to reduced FA oxidation. Moreover, FA oxidation inhibition provides protection from L. monocytogenes infection, explaining part of the protection of Irf9(-/-) and Ifnar1(-/-) mice. Our findings define a role of IFN-I in metabolic regulation during L. monocytogenes infection. Metabolic differences between Irf9(-/-) and Ifnar1(-/-) mice may underlie the different susceptibility of these mice against lethal infection with L. monocytogenes. Public Library of Science 2021-07-08 /pmc/articles/PMC8266069/ /pubmed/34237114 http://dx.doi.org/10.1371/journal.ppat.1009697 Text en © 2021 Demiroz et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Demiroz, Duygu Platanitis, Ekaterini Bryant, Michael Fischer, Philipp Prchal-Murphy, Michaela Lercher, Alexander Lassnig, Caroline Baccarini, Manuela Müller, Mathias Bergthaler, Andreas Sexl, Veronika Dolezal, Marlies Decker, Thomas Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons |
title | Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons |
title_full | Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons |
title_fullStr | Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons |
title_full_unstemmed | Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons |
title_short | Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons |
title_sort | listeria monocytogenes infection rewires host metabolism with regulatory input from type i interferons |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8266069/ https://www.ncbi.nlm.nih.gov/pubmed/34237114 http://dx.doi.org/10.1371/journal.ppat.1009697 |
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