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The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination
The microbiota is now recognized as a key influence on the host immune response in the central nervous system (CNS). As such, there has been some progress toward therapies that modulate the microbiota with the aim of limiting immune-mediated demyelination, as occurs in multiple sclerosis. However, r...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
National Academy of Sciences
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6911206/ https://www.ncbi.nlm.nih.gov/pubmed/31740610 http://dx.doi.org/10.1073/pnas.1905787116 |
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author | McMurran, Christopher E. Guzman de la Fuente, Alerie Penalva, Rosana Ben Menachem-Zidon, Ofra Dombrowski, Yvonne Falconer, John Gonzalez, Ginez A. Zhao, Chao Krause, Fynn N. Young, Adam M. H. Griffin, Julian L. Jones, Clare A. Hollins, Claire Heimesaat, Markus M. Fitzgerald, Denise C. Franklin, Robin J. M. |
author_facet | McMurran, Christopher E. Guzman de la Fuente, Alerie Penalva, Rosana Ben Menachem-Zidon, Ofra Dombrowski, Yvonne Falconer, John Gonzalez, Ginez A. Zhao, Chao Krause, Fynn N. Young, Adam M. H. Griffin, Julian L. Jones, Clare A. Hollins, Claire Heimesaat, Markus M. Fitzgerald, Denise C. Franklin, Robin J. M. |
author_sort | McMurran, Christopher E. |
collection | PubMed |
description | The microbiota is now recognized as a key influence on the host immune response in the central nervous system (CNS). As such, there has been some progress toward therapies that modulate the microbiota with the aim of limiting immune-mediated demyelination, as occurs in multiple sclerosis. However, remyelination—the regeneration of myelin sheaths—also depends upon an immune response, and the effects that such interventions might have on remyelination have not yet been explored. Here, we show that the inflammatory response during CNS remyelination in mice is modulated by antibiotic or probiotic treatment, as well as in germ-free mice. We also explore the effect of these changes on oligodendrocyte progenitor cell differentiation, which is inhibited by antibiotics but unaffected by our other interventions. These results reveal that high combined doses of oral antibiotics impair oligodendrocyte progenitor cell responses during remyelination and further our understanding of how mammalian regeneration relates to the microbiota. |
format | Online Article Text |
id | pubmed-6911206 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | National Academy of Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-69112062019-12-18 The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination McMurran, Christopher E. Guzman de la Fuente, Alerie Penalva, Rosana Ben Menachem-Zidon, Ofra Dombrowski, Yvonne Falconer, John Gonzalez, Ginez A. Zhao, Chao Krause, Fynn N. Young, Adam M. H. Griffin, Julian L. Jones, Clare A. Hollins, Claire Heimesaat, Markus M. Fitzgerald, Denise C. Franklin, Robin J. M. Proc Natl Acad Sci U S A PNAS Plus The microbiota is now recognized as a key influence on the host immune response in the central nervous system (CNS). As such, there has been some progress toward therapies that modulate the microbiota with the aim of limiting immune-mediated demyelination, as occurs in multiple sclerosis. However, remyelination—the regeneration of myelin sheaths—also depends upon an immune response, and the effects that such interventions might have on remyelination have not yet been explored. Here, we show that the inflammatory response during CNS remyelination in mice is modulated by antibiotic or probiotic treatment, as well as in germ-free mice. We also explore the effect of these changes on oligodendrocyte progenitor cell differentiation, which is inhibited by antibiotics but unaffected by our other interventions. These results reveal that high combined doses of oral antibiotics impair oligodendrocyte progenitor cell responses during remyelination and further our understanding of how mammalian regeneration relates to the microbiota. National Academy of Sciences 2019-12-10 2019-11-18 /pmc/articles/PMC6911206/ /pubmed/31740610 http://dx.doi.org/10.1073/pnas.1905787116 Text en Copyright © 2019 the Author(s). Published by PNAS. http://creativecommons.org/licenses/by/4.0/ https://creativecommons.org/licenses/by/4.0/This open access article is distributed under Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | PNAS Plus McMurran, Christopher E. Guzman de la Fuente, Alerie Penalva, Rosana Ben Menachem-Zidon, Ofra Dombrowski, Yvonne Falconer, John Gonzalez, Ginez A. Zhao, Chao Krause, Fynn N. Young, Adam M. H. Griffin, Julian L. Jones, Clare A. Hollins, Claire Heimesaat, Markus M. Fitzgerald, Denise C. Franklin, Robin J. M. The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination |
title | The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination |
title_full | The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination |
title_fullStr | The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination |
title_full_unstemmed | The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination |
title_short | The microbiota regulates murine inflammatory responses to toxin-induced CNS demyelination but has minimal impact on remyelination |
title_sort | microbiota regulates murine inflammatory responses to toxin-induced cns demyelination but has minimal impact on remyelination |
topic | PNAS Plus |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6911206/ https://www.ncbi.nlm.nih.gov/pubmed/31740610 http://dx.doi.org/10.1073/pnas.1905787116 |
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