Microbiota-related changes in bile acid and tryptophan metabolism are associated with gastrointestinal dysfunction in a mouse model of autism

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dc.contributor.authorGolubeva, Anna V.
dc.contributor.authorJoyce, Susan A.
dc.contributor.authorMoloney, Gerard M.
dc.contributor.authorBurokas, Aurelijus
dc.contributor.authorSherwin, Eoin
dc.contributor.authorArboleya, Silvia
dc.contributor.authorFlynn, Ian
dc.contributor.authorKhochanskiy, Dmitry
dc.contributor.authorMoya-Pérez, Angela
dc.contributor.authorPeterson, Veronica L.
dc.contributor.authorRea, Kieran
dc.contributor.authorMurphy, Kiera
dc.contributor.authorMakarova, Olga
dc.contributor.authorBuravkov, Sergey
dc.contributor.authorHyland, Niall P.
dc.contributor.authorStanton, Catherine
dc.contributor.authorClarke, Gerard
dc.contributor.authorGahan, Cormac G.
dc.contributor.authorDinan, Timothy G.
dc.contributor.authorCryan, John F.
dc.contributor.funderEuropean Commission
dc.contributor.funderScience Foundation Ireland
dc.date.accessioned2017-12-08T13:33:41Z
dc.date.available2017-12-08T13:33:41Z
dc.date.issued2017-10-13
dc.description.abstractAutism 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.en
dc.description.sponsorshipScience Foundation Ireland/ European Commission (16/ERAHDHL/3358)en
dc.description.statusPeer revieweden
dc.description.versionPublished Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationGolubeva, A. V., Joyce, S. A., Moloney, G., Burokas, A., Sherwin, E., Arboleya, S., Flynn, I., Khochanskiy, D., Moya-Pérez, A., Peterson, V., Rea, K., Murphy, K., Makarova, O., Buravkov, S., Hyland, N. P., Stanton, C., Clarke, G., Gahan, C. G. M., Dinan, T. G. and Cryan, J. F. (2017) 'Microbiota-related changes in bile acid and tryptophan metabolism are associated with gastrointestinal dysfunction in a mouse model of autism', EBioMedicine, 24, pp. 166-178. doi: 10.1016/j.ebiom.2017.09.020en
dc.identifier.doi10.1016/j.ebiom.2017.09.020
dc.identifier.endpage178
dc.identifier.issn2352-3964
dc.identifier.journaltitleEBioMedicineen
dc.identifier.startpage166
dc.identifier.urihttps://hdl.handle.net/10468/5135
dc.identifier.volume24
dc.language.isoenen
dc.publisherElsevier B.V.en
dc.relation.projectinfo:eu-repo/grantAgreement/SFI/SFI Research Centres/12/RC/2273/IE/Alimentary Pharmabiotic Centre (APC) - Interfacing Food & Medicine/
dc.relation.urihttp://www.sciencedirect.com/science/article/pii/S2352396417303742
dc.rights© 2017, the Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectAutismen
dc.subjectBTBR mouseen
dc.subjectGut microbiotaen
dc.subjectIntestinal permeabilityen
dc.subjectIntestinal transiten
dc.subjectBile acidsen
dc.subjectSerotoninen
dc.subjectTryptophanen
dc.titleMicrobiota-related changes in bile acid and tryptophan metabolism are associated with gastrointestinal dysfunction in a mouse model of autismen
dc.typeArticle (peer-reviewed)en
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