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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...

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Autores principales: 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.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Academy of Sciences 2019
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.
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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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