Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation

Maria L. Elkjaer; Lukas Simon; Tobias Frisch; Lisa Marie Bente; Tim Kacprowski; Mads Thomassen; Richard Reynolds; Jan Baumbach; Richard Röttger; Zsolt Illes

doi:10.3389/fimmu.2022.1043579

Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation

Maria L. Elkjaer^*, Lukas Simon, Tobias Frisch, Lisa Marie Bente, Tim Kacprowski, Mads Thomassen, Richard Reynolds, Jan Baumbach, Richard Röttger, Zsolt Illes

^*Kontaktforfatter

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

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Abstrakt

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.

Originalsprog	Engelsk
Artikelnummer	1043579
Tidsskrift	Frontiers in Immunology
Vol/bind	13
ISSN	1664-3224
DOI	https://doi.org/10.3389/fimmu.2022.1043579
Status	Udgivet - 2. dec. 2022

Bibliografisk note

Funding Information:
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. This publication reflects only the authors’ view and the European Commission is not responsible for any use that may be made of the information it contains.

Publisher Copyright:
Copyright © 2022 Elkjaer, Simon, Frisch, Bente, Kacprowski, Thomassen, Reynolds, Baumbach, Röttger and Illes.

Dokumenter og links

10.3389/fimmu.2022.1043579Licens: CC BY

Open access versionForlagets udgivne version, 1,66 MBLicens: CC BY

Citationsformater

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abstract = "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{\textquoteright}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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author = "Elkjaer, {Maria L.} and Lukas Simon and Tobias Frisch and Bente, {Lisa Marie} and Tim Kacprowski and Mads Thomassen and Richard Reynolds and Jan Baumbach and Richard R{\"o}ttger and Zsolt Illes",

note = "Funding Information: 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{\textquoteright}s Horizon 2020 research and innovation programme under grant agreement No 777111. This publication reflects only the authors{\textquoteright} view and the European Commission is not responsible for any use that may be made of the information it contains. Publisher Copyright: Copyright {\textcopyright} 2022 Elkjaer, Simon, Frisch, Bente, Kacprowski, Thomassen, Reynolds, Baumbach, R{\"o}ttger and Illes.",

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T1 - Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation

AU - Elkjaer, Maria L.

AU - Simon, Lukas

AU - Frisch, Tobias

AU - Bente, Lisa Marie

AU - Kacprowski, Tim

AU - Thomassen, Mads

AU - Reynolds, Richard

AU - Baumbach, Jan

AU - Röttger, Richard

AU - Illes, Zsolt

N1 - Funding Information: 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. This publication reflects only the authors’ view and the European Commission is not responsible for any use that may be made of the information it contains. Publisher Copyright: Copyright © 2022 Elkjaer, Simon, Frisch, Bente, Kacprowski, Thomassen, Reynolds, Baumbach, Röttger and Illes.

PY - 2022/12/2

Y1 - 2022/12/2

N2 - 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.

AB - 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.

KW - bacterial transcripts

KW - brainbiome

KW - brainbiota

KW - CNS autoimmunity

KW - gut-brain axis

KW - microbiome

KW - microbiota

KW - smoldering MS

U2 - 10.3389/fimmu.2022.1043579

DO - 10.3389/fimmu.2022.1043579

M3 - Journal article

C2 - 36532064

AN - SCOPUS:85144209280

VL - 13

JO - Frontiers in Immunology

JF - Frontiers in Immunology

SN - 1664-3224

M1 - 1043579

ER -

Hypothesis of a potential BrainBiota and its relation to CNS autoimmune inflammation

Abstrakt

Bibliografisk note

Dokumenter og links

Fingeraftryk

Citationsformater