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Cell Rep. 2017 Oct 24;21(4):994-1008. doi: 10.1016/j.celrep.2017.09.097.

Distinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells.

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Microbial Immune Regulation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Mouse Pathology Platform, Helmholtz Centre for Infection Research, Braunschweig, Germany.
I. Medizinische Klinik und Poliklinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA; Howard Hughes Medical Institute, Yale University, New Haven, CT, USA.
Microbial Immune Regulation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany. Electronic address:


Inflammatory 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.


DSS colitis; IBD; adaptive colitis; colitis pathogenesis; gut microbiota; innate colitis

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