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

Publication date: 24 October 2017
Source:Cell Reports, Volume 21, Issue 4
Author(s): Urmi Roy, Eric J.C. Gálvez, Aida Iljazovic, Till Robin Lesker, Adrian J. Błażejewski, Marina C. Pils, Ulrike Heise, Samuel Huber, Richard A. Flavell, Till Strowig
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.

Graphical abstract

Teaser

Alterations in the microbiota contribute to the development of intestinal inflammation. Roy et al. demonstrate that distinct intestinal microbial communities cause colitis via opposing effector mechanisms independent or dependent on adaptive immunity. Their findings suggest that personalized immunomodulatory treatment according to distinct microbial signatures may be beneficial for IBD patients.


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