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dc.contributor.authorRoy, Urmi
dc.contributor.authorGálvez, Eric J C
dc.contributor.authorIljazovic, Aida
dc.contributor.authorLesker, Till Robin
dc.contributor.authorBłażejewski, Adrian J
dc.contributor.authorPils, Marina C
dc.contributor.authorHeise, Ulrike
dc.contributor.authorHuber, Samuel
dc.contributor.authorFlavell, Richard A
dc.contributor.authorStrowig, Till
dc.date.accessioned2018-01-19T10:49:13Z
dc.date.available2018-01-19T10:49:13Z
dc.date.issued2017-10-24
dc.identifier.citationDistinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells. 2017, 21 (4):994-1008 Cell Repen
dc.identifier.issn2211-1247
dc.identifier.pmid29069606
dc.identifier.doi10.1016/j.celrep.2017.09.097
dc.identifier.urihttp://hdl.handle.net/10033/621244
dc.description.abstractInflammatory bowel disease comprises a group of heterogeneous diseases characterized by chronic and relapsing mucosal inflammation. Alterations in microbiota composition have been proposed to contribute to disease development, but no uniform signatures have yet been identified. Here, we compare the ability of a diverse set of microbial communities to exacerbate intestinal inflammation after chemical damage to the intestinal barrier. Strikingly, genetically identical wild-type mice differing only in their microbiota composition varied strongly in their colitis susceptibility. Transfer of distinct colitogenic communities in gene-deficient mice revealed that they triggered disease via opposing pathways either independent or dependent on adaptive immunity, specifically requiring antigen-specific CD4+ T cells. Our data provide evidence for the concept that microbial communities may alter disease susceptibility via different immune pathways despite eventually resulting in similar host pathology. This suggests a potential benefit for personalizing IBD therapies according to patient-specific microbiota signatures.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleDistinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells.en
dc.typeArticleen
dc.contributor.departmentHelmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.en
dc.identifier.journalCell reportsen
refterms.dateFOA2018-06-13T19:42:27Z
html.description.abstractInflammatory bowel disease comprises a group of heterogeneous diseases characterized by chronic and relapsing mucosal inflammation. Alterations in microbiota composition have been proposed to contribute to disease development, but no uniform signatures have yet been identified. Here, we compare the ability of a diverse set of microbial communities to exacerbate intestinal inflammation after chemical damage to the intestinal barrier. Strikingly, genetically identical wild-type mice differing only in their microbiota composition varied strongly in their colitis susceptibility. Transfer of distinct colitogenic communities in gene-deficient mice revealed that they triggered disease via opposing pathways either independent or dependent on adaptive immunity, specifically requiring antigen-specific CD4+ T cells. Our data provide evidence for the concept that microbial communities may alter disease susceptibility via different immune pathways despite eventually resulting in similar host pathology. This suggests a potential benefit for personalizing IBD therapies according to patient-specific microbiota signatures.


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