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Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease

The gut microbiota regulates the host immune and nervous systems and plays an important role in the pathogenesis of autoimmune neurological disease multiple sclerosis (MS). There are considerable efforts currently being undertaken to develop therapies for MS based on the modulation of microbiota. Ev...

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Autores principales: Gödel, Clemens, Kunkel, Birgit, Kashani, Alireza, Lassmann, Hans, Arumugam, Manimozhiyan, Krishnamoorthy, Gurumoorthy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060541/
https://www.ncbi.nlm.nih.gov/pubmed/32143718
http://dx.doi.org/10.1186/s12974-020-01766-9
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author Gödel, Clemens
Kunkel, Birgit
Kashani, Alireza
Lassmann, Hans
Arumugam, Manimozhiyan
Krishnamoorthy, Gurumoorthy
author_facet Gödel, Clemens
Kunkel, Birgit
Kashani, Alireza
Lassmann, Hans
Arumugam, Manimozhiyan
Krishnamoorthy, Gurumoorthy
author_sort Gödel, Clemens
collection PubMed
description The gut microbiota regulates the host immune and nervous systems and plays an important role in the pathogenesis of autoimmune neurological disease multiple sclerosis (MS). There are considerable efforts currently being undertaken to develop therapies for MS based on the modulation of microbiota. Evidence from experimental models suggests that the manipulation of microbiota through diet or antibiotics prior to the disease development limits disease susceptibility. However, it is currently unclear if microbiota manipulation therapies would also have an impact on ongoing neurological disease. Here, we examined the effect of antibiotic-based microbiota modulation in spontaneous experimental autoimmune encephalomyelitis (EAE) mouse models of MS before and after the onset of autoimmune disease. Prophylactic antibiotic treatment led to a significant reduction of susceptibility to spontaneous EAE. In contrast, antibiotic treatment after the onset of spontaneous EAE did not show a significant amelioration. These results reveal that the perturbation of gut bacteria alters disease susceptibility but has minimal impact on the ongoing neurological disease.
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spelling pubmed-70605412020-03-12 Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease Gödel, Clemens Kunkel, Birgit Kashani, Alireza Lassmann, Hans Arumugam, Manimozhiyan Krishnamoorthy, Gurumoorthy J Neuroinflammation Short Report The gut microbiota regulates the host immune and nervous systems and plays an important role in the pathogenesis of autoimmune neurological disease multiple sclerosis (MS). There are considerable efforts currently being undertaken to develop therapies for MS based on the modulation of microbiota. Evidence from experimental models suggests that the manipulation of microbiota through diet or antibiotics prior to the disease development limits disease susceptibility. However, it is currently unclear if microbiota manipulation therapies would also have an impact on ongoing neurological disease. Here, we examined the effect of antibiotic-based microbiota modulation in spontaneous experimental autoimmune encephalomyelitis (EAE) mouse models of MS before and after the onset of autoimmune disease. Prophylactic antibiotic treatment led to a significant reduction of susceptibility to spontaneous EAE. In contrast, antibiotic treatment after the onset of spontaneous EAE did not show a significant amelioration. These results reveal that the perturbation of gut bacteria alters disease susceptibility but has minimal impact on the ongoing neurological disease. BioMed Central 2020-03-06 /pmc/articles/PMC7060541/ /pubmed/32143718 http://dx.doi.org/10.1186/s12974-020-01766-9 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Short Report
Gödel, Clemens
Kunkel, Birgit
Kashani, Alireza
Lassmann, Hans
Arumugam, Manimozhiyan
Krishnamoorthy, Gurumoorthy
Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease
title Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease
title_full Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease
title_fullStr Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease
title_full_unstemmed Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease
title_short Perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease
title_sort perturbation of gut microbiota decreases susceptibility but does not modulate ongoing autoimmune neurological disease
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060541/
https://www.ncbi.nlm.nih.gov/pubmed/32143718
http://dx.doi.org/10.1186/s12974-020-01766-9
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