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dc.contributorVall d'Hebron Barcelona Hospital Campus
dc.contributor.authorLleal Custey, Marina
dc.contributor.authorSarrabayrouse, Guillaume
dc.contributor.authorWillamil Dos Santos, Joseane
dc.contributor.authorSantiago Badenas, Alba
dc.contributor.authorPozuelo Lopez, Maria Ángeles
dc.contributor.authorManichanh, Chaysavanh
dc.date.accessioned2020-09-02T08:26:00Z
dc.date.available2020-09-02T08:26:00Z
dc.date.issued2019-10-15
dc.identifier.citationLleal M, Sarrabayrouse G, Willamil J, Santiago A, Pozuelo M, Manichanh C. A single faecal microbiota transplantation modulates the microbiome and improves clinical manifestations in a rat model of colitis. EBioMedicine. 2019 Oct 15;48:630–41.
dc.identifier.issn2352-3964
dc.identifier.urihttp://hdl.handle.net/11351/5206
dc.descriptionInflammatory bowel disease; Faecal microbiota transplantation; Rat model of colitis
dc.description.abstractBackground: Faecal microbiota transplantation (FMT) is a novel potential therapy for inflammatory bowel diseases, but it is poorly characterised. Methods: We evaluated the performance of the mouse and rat as a pre-clinical model for human microbiota engraftment. We then characterised the effect of a single human stool transfer (HST) on a humanised model of DSS-induced colitis. Colonic and faecal microbial communities were analysed using the 16S rRNA approach and clinical manifestations were assessed in a longitudinal setting. Findings: The microbial community of rats showed greater similarity to that of humans, while the microbiome of mice showed less similarity to that of humans. Moreover, rats captured more human microbial species than mice after a single HST. Using the rat model, we showed that HST compensated faecal dysbiosis by restoring alpha-diversity and by increasing the relative abundance of health-related microbial genera. To some extent, HST also modulated the microbial composition of colonic tissue. These faecal and colonic microbial communities alterations led to a relative restoration of colon length, and a significant decrease in both epithelium damage and disease severity. Remarkably, stopping inflammation by removing DSS before HST caused a faster and greater recovery of both microbiome and clinical manifestation features. Interpretation: Our results indicate that the rat outperforms the mouse as a model for human microbiota engraftment and show that the efficacy of HST can be enhanced when inflammation stimulation is withdrawn. Finally, our findings support a new therapeutic strategy based on the use FMT combined with anti inflammatory drugs.
dc.language.isoeng
dc.publisherElsevier
dc.relation.ispartofseriesEBioMedicine;48
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.sourceScientia
dc.subjectColitis
dc.subjectIntestins - Microbiologia
dc.subjectModels animals en la investigació
dc.subject.meshColitis
dc.subject.meshFecal Microbiota Transplantation
dc.subject.meshDisease Models, Animal
dc.subject.mesh/methods
dc.titleA single faecal microbiota transplantation modulates the microbiome and improves clinical manifestations in a rat model of colitis
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1016/j.ebiom.2019.10.002
dc.subject.decscolitis
dc.subject.decstrasplante fecal
dc.subject.decsmodelos de enfermedad en animales
dc.subject.decs/métodos
dc.relation.publishversionhttps://www.sciencedirect.com/science/article/pii/S2352396419306668?via%3Dihub
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.audienceProfessionals
dc.contributor.authoraffiliation[Lleal M, Sarrabayrouse G, Willamil J, Santiago A, Pozuelo M] Departament de Fisiologia i Fisiopatologia Digestiva, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. [Manichanh C] Departament de Fisiologia i Fisiopatologia Digestiva, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Centro de Investigación Biomédica en Red en el Área temática de Enfermedades Hepáticas (CIBEREHD), Instituto de Salud Carlos III, Madrid, Spain
dc.identifier.pmid31628021
dc.identifier.wos000493830800061
dc.relation.projectidinfo:eu-repo/grantAgreement/ES/PE2017-2020/PI17%2F00614
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess


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