Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation
Infectious agents have been long considered to play a role in the pathogenesis of neurological diseases as part of the interaction between genetic susceptibility and the environment. The role of bacteria in CNS autoimmunity has also been highlighted by changes in the diversity of gut microbiota in p...
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sg-ntu-dr.10356-1710542023-10-15T15:38:52Z Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation Elkjaer, Maria L. Simon, Lukas Frisch, Tobias Bente, Lisa-Marie Kacprowski, Tim Thomassen, Mads Reynolds, Richard Baumbach, Jan Röttger, Richard Illes, Zsolt Lee Kong Chian School of Medicine (LKCMedicine) Centre for Molecular Neuropathology Science::Medicine Gut-brain Axis Microbiome Infectious agents have been long considered to play a role in the pathogenesis of neurological diseases as part of the interaction between genetic susceptibility and the environment. The role of bacteria in CNS autoimmunity has also been highlighted by changes in the diversity of gut microbiota in patients with neurological diseases such as Parkinson's disease, Alzheimer disease and multiple sclerosis, emphasizing the role of the gut-brain axis. We discuss the hypothesis of a brain microbiota, the BrainBiota: bacteria living in symbiosis with brain cells. Existence of various bacteria in the human brain is suggested by morphological evidence, presence of bacterial proteins, metabolites, transcripts and mucosal-associated invariant T cells. Based on our data, we discuss the hypothesis that these bacteria are an integral part of brain development and immune tolerance as well as directly linked to the gut microbiome. We further suggest that changes of the BrainBiota during brain diseases may be the consequence or cause of the chronic inflammation similarly to the gut microbiota. Published version MLE is grateful for financial support from Lundbeckfonden (no. R347-2020-2454). ZI is grateful for financial support from Independent Research Fund Denmark (DFF 9039-00370B), Lundbeckfonden (R118-A11472), Scleroseforeningen (A25341, A29926, A31829, A33600), University of Southern Denmark (14/24200), Odense University Hospital (5798002573633). JB is grateful for financial support from the Center for Data and Computing in Natural Sciences (CDCS), and by his VILLUM Young Investigator Grant nr.13154. Furthermore, this project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 777111. 2023-10-10T08:42:42Z 2023-10-10T08:42:42Z 2022 Journal Article Elkjaer, M. L., Simon, L., Frisch, T., Bente, L., Kacprowski, T., Thomassen, M., Reynolds, R., Baumbach, J., Röttger, R. & Illes, Z. (2022). Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation. Frontiers in Immunology, 13, 1043579-. https://dx.doi.org/10.3389/fimmu.2022.1043579 1664-3224 https://hdl.handle.net/10356/171054 10.3389/fimmu.2022.1043579 36532064 2-s2.0-85144209280 13 1043579 en Frontiers in Immunology © 2022 Elkjaer, Simon, Frisch, Bente, Kacprowski, Thomassen, Reynolds, Baumbach, Röttger and Illes. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. application/pdf |
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Science::Medicine Gut-brain Axis Microbiome Elkjaer, Maria L. Simon, Lukas Frisch, Tobias Bente, Lisa-Marie Kacprowski, Tim Thomassen, Mads Reynolds, Richard Baumbach, Jan Röttger, Richard Illes, Zsolt Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation |
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Infectious agents have been long considered to play a role in the pathogenesis of neurological diseases as part of the interaction between genetic susceptibility and the environment. The role of bacteria in CNS autoimmunity has also been highlighted by changes in the diversity of gut microbiota in patients with neurological diseases such as Parkinson's disease, Alzheimer disease and multiple sclerosis, emphasizing the role of the gut-brain axis. We discuss the hypothesis of a brain microbiota, the BrainBiota: bacteria living in symbiosis with brain cells. Existence of various bacteria in the human brain is suggested by morphological evidence, presence of bacterial proteins, metabolites, transcripts and mucosal-associated invariant T cells. Based on our data, we discuss the hypothesis that these bacteria are an integral part of brain development and immune tolerance as well as directly linked to the gut microbiome. We further suggest that changes of the BrainBiota during brain diseases may be the consequence or cause of the chronic inflammation similarly to the gut microbiota. |
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Lee Kong Chian School of Medicine (LKCMedicine) |
author_facet |
Lee Kong Chian School of Medicine (LKCMedicine) Elkjaer, Maria L. Simon, Lukas Frisch, Tobias Bente, Lisa-Marie Kacprowski, Tim Thomassen, Mads Reynolds, Richard Baumbach, Jan Röttger, Richard Illes, Zsolt |
format |
Article |
author |
Elkjaer, Maria L. Simon, Lukas Frisch, Tobias Bente, Lisa-Marie Kacprowski, Tim Thomassen, Mads Reynolds, Richard Baumbach, Jan Röttger, Richard Illes, Zsolt |
author_sort |
Elkjaer, Maria L. |
title |
Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation |
title_short |
Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation |
title_full |
Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation |
title_fullStr |
Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation |
title_full_unstemmed |
Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation |
title_sort |
hypothesis of a potential brainbiota and its relation to cns autoimmune inflammation |
publishDate |
2023 |
url |
https://hdl.handle.net/10356/171054 |
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1781793901305135104 |