Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism

Autism spectrum disorder (ASD) is one of the most prevalent neurodevelopmental conditions worldwide. There is growing awareness that ASD is highly comorbid with gastrointestinal distress and altered intestinal microbiome, and that host-microbiome interactions may contribute to the disease symptoms....

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Autores: Golubeva, Anna V., Joyce, Susan A., Moloney, Gerard, Burokas, Aurelijus, Sherwin, Eoin, Arboleya, Silvia, Flynn, Ian, Khochanskiy, Dmitry, Moya-Pérez, Angela, Peterson, Veronica, Rea, Kieran, Murphy, Kiera, Makarova, Olga, Buravkov, Sergey, Hyland, Niall P., Stanton, Catherine, Clarke, Gerard, Gahan, Cormac G. M., Dinan, Timothy G., Cryan, John F.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/346039
Acceso en línea:http://hdl.handle.net/10261/346039
Access Level:acceso abierto
Palabra clave:Autism
BTBR mouse
Gut microbiota
Intestinal permeability
Intestinal transit
Bile acids
Serotonin
Tryptophan
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spelling Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of AutismGolubeva, Anna V.Joyce, Susan A.Moloney, GerardBurokas, AurelijusSherwin, EoinArboleya, SilviaFlynn, IanKhochanskiy, DmitryMoya-Pérez, AngelaPeterson, VeronicaRea, KieranMurphy, KieraMakarova, OlgaBuravkov, SergeyHyland, Niall P.Stanton, CatherineClarke, GerardGahan, Cormac G. M.Dinan, Timothy G.Cryan, John F.AutismBTBR mouseGut microbiotaIntestinal permeabilityIntestinal transitBile acidsSerotoninTryptophanAutism spectrum disorder (ASD) is one of the most prevalent neurodevelopmental conditions worldwide. There is growing awareness that ASD is highly comorbid with gastrointestinal distress and altered intestinal microbiome, and that host-microbiome interactions may contribute to the disease symptoms. However, the paucity of knowledge on gut-brain axis signaling in autism constitutes an obstacle to the development of precision microbiota-based therapeutics in ASD. To this end, we explored the interactions between intestinal microbiota, gut physiology and social behavior in a BTBR T+ Itpr3tf/J mouse model of ASD. Here we show that a reduction in the relative abundance of very particular bacterial taxa in the BTBR gut – namely, bile-metabolizing Bifidobacterium and Blautia species, - is associated with deficient bile acid and tryptophan metabolism in the intestine, marked gastrointestinal dysfunction, as well as impaired social interactions in BTBR mice. Together these data support the concept of targeted manipulation of the gut microbiota for reversing gastrointestinal and behavioral symptomatology in ASD, and offer specific plausible targets in this endeavor.The APC Microbiome Institute is a research institute funded by Science Foundation Ireland (SFI) through the Irish Government's National Development Plan. J.F·C, T.G.D, C.S., S.A.J. and C.G.M.G. are supported by SFI (Grant Nos. SFI/12/RC/2273). S.A.J is also funded by SFI-EU 16/ERA-HDHL/3358. J.F·C, C.S. and T.G.D have research support from Mead Johnson, Cremo, 4D Pharma, Suntory Wellness, and Nutricia. J.F.C, C.S., T.G.D and G.C. have spoken at meetings sponsored by food and pharmaceutical companies.Peer reviewedElsevierScience Foundation IrelandIrish GovernmentEuropean CommissionMead Johnson Nutrition202420242017info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501Publisher's versioninfo:eu-repo/semantics/publishedVersionapplication/pdfhttp://hdl.handle.net/10261/346039reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Ingléshttps://doi.org/10.1016/j.ebiom.2017.09.020Noinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/3460392026-05-22T06:33:51Z
dc.title.none.fl_str_mv Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
title Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
spellingShingle Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
Golubeva, Anna V.
Autism
BTBR mouse
Gut microbiota
Intestinal permeability
Intestinal transit
Bile acids
Serotonin
Tryptophan
title_short Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
title_full Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
title_fullStr Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
title_full_unstemmed Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
title_sort Microbiota-related Changes in Bile Acid & Tryptophan Metabolism are Associated with Gastrointestinal Dysfunction in a Mouse Model of Autism
dc.creator.none.fl_str_mv Golubeva, Anna V.
Joyce, Susan A.
Moloney, Gerard
Burokas, Aurelijus
Sherwin, Eoin
Arboleya, Silvia
Flynn, Ian
Khochanskiy, Dmitry
Moya-Pérez, Angela
Peterson, Veronica
Rea, Kieran
Murphy, Kiera
Makarova, Olga
Buravkov, Sergey
Hyland, Niall P.
Stanton, Catherine
Clarke, Gerard
Gahan, Cormac G. M.
Dinan, Timothy G.
Cryan, John F.
author Golubeva, Anna V.
author_facet Golubeva, Anna V.
Joyce, Susan A.
Moloney, Gerard
Burokas, Aurelijus
Sherwin, Eoin
Arboleya, Silvia
Flynn, Ian
Khochanskiy, Dmitry
Moya-Pérez, Angela
Peterson, Veronica
Rea, Kieran
Murphy, Kiera
Makarova, Olga
Buravkov, Sergey
Hyland, Niall P.
Stanton, Catherine
Clarke, Gerard
Gahan, Cormac G. M.
Dinan, Timothy G.
Cryan, John F.
author_role author
author2 Joyce, Susan A.
Moloney, Gerard
Burokas, Aurelijus
Sherwin, Eoin
Arboleya, Silvia
Flynn, Ian
Khochanskiy, Dmitry
Moya-Pérez, Angela
Peterson, Veronica
Rea, Kieran
Murphy, Kiera
Makarova, Olga
Buravkov, Sergey
Hyland, Niall P.
Stanton, Catherine
Clarke, Gerard
Gahan, Cormac G. M.
Dinan, Timothy G.
Cryan, John F.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Science Foundation Ireland
Irish Government
European Commission
Mead Johnson Nutrition
dc.subject.none.fl_str_mv Autism
BTBR mouse
Gut microbiota
Intestinal permeability
Intestinal transit
Bile acids
Serotonin
Tryptophan
topic Autism
BTBR mouse
Gut microbiota
Intestinal permeability
Intestinal transit
Bile acids
Serotonin
Tryptophan
description Autism spectrum disorder (ASD) is one of the most prevalent neurodevelopmental conditions worldwide. There is growing awareness that ASD is highly comorbid with gastrointestinal distress and altered intestinal microbiome, and that host-microbiome interactions may contribute to the disease symptoms. However, the paucity of knowledge on gut-brain axis signaling in autism constitutes an obstacle to the development of precision microbiota-based therapeutics in ASD. To this end, we explored the interactions between intestinal microbiota, gut physiology and social behavior in a BTBR T+ Itpr3tf/J mouse model of ASD. Here we show that a reduction in the relative abundance of very particular bacterial taxa in the BTBR gut – namely, bile-metabolizing Bifidobacterium and Blautia species, - is associated with deficient bile acid and tryptophan metabolism in the intestine, marked gastrointestinal dysfunction, as well as impaired social interactions in BTBR mice. Together these data support the concept of targeted manipulation of the gut microbiota for reversing gastrointestinal and behavioral symptomatology in ASD, and offer specific plausible targets in this endeavor.
publishDate 2017
dc.date.none.fl_str_mv 2017
2024
2024
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
Publisher's version
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/346039
url http://hdl.handle.net/10261/346039
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv https://doi.org/10.1016/j.ebiom.2017.09.020
No
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15.811543

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