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

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Distinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells. / Roy, Urmi; Gálvez, Eric J C; Iljazovic, Aida; Lesker, Till Robin; Błażejewski, Adrian J; Pils, Marina C; Heise, Ulrike; Huber, Samuel; Flavell, Richard A; Strowig, Till.

in: CELL REP, Jahrgang 21, Nr. 4, 24.10.2017, S. 994-1008.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Roy, U, Gálvez, EJC, Iljazovic, A, Lesker, TR, Błażejewski, AJ, Pils, MC, Heise, U, Huber, S, Flavell, RA & Strowig, T 2017, 'Distinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells', CELL REP, Jg. 21, Nr. 4, S. 994-1008. https://doi.org/10.1016/j.celrep.2017.09.097

APA

Roy, U., Gálvez, E. J. C., Iljazovic, A., Lesker, T. R., Błażejewski, A. J., Pils, M. C., Heise, U., Huber, S., Flavell, R. A., & Strowig, T. (2017). Distinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells. CELL REP, 21(4), 994-1008. https://doi.org/10.1016/j.celrep.2017.09.097

Vancouver

Roy U, Gálvez EJC, Iljazovic A, Lesker TR, Błażejewski AJ, Pils MC et al. Distinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells. CELL REP. 2017 Okt 24;21(4):994-1008. https://doi.org/10.1016/j.celrep.2017.09.097

Bibtex

@article{89bbf3bf9d284284b11568d8b703cc3f,
title = "Distinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells",
abstract = "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.",
keywords = "Journal Article",
author = "Urmi Roy and G{\'a}lvez, {Eric J C} and Aida Iljazovic and Lesker, {Till Robin} and B{\l}a{\.z}ejewski, {Adrian J} and Pils, {Marina C} and Ulrike Heise and Samuel Huber and Flavell, {Richard A} and Till Strowig",
note = "Copyright {\textcopyright} 2017 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2017",
month = oct,
day = "24",
doi = "10.1016/j.celrep.2017.09.097",
language = "English",
volume = "21",
pages = "994--1008",
journal = "CELL REP",
issn = "2211-1247",
publisher = "Elsevier",
number = "4",

}

RIS

TY - JOUR

T1 - Distinct Microbial Communities Trigger Colitis Development upon Intestinal Barrier Damage via Innate or Adaptive Immune Cells

AU - Roy, Urmi

AU - Gálvez, Eric J C

AU - Iljazovic, Aida

AU - Lesker, Till Robin

AU - Błażejewski, Adrian J

AU - Pils, Marina C

AU - Heise, Ulrike

AU - Huber, Samuel

AU - Flavell, Richard A

AU - Strowig, Till

N1 - Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2017/10/24

Y1 - 2017/10/24

N2 - 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.

AB - 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.

KW - Journal Article

U2 - 10.1016/j.celrep.2017.09.097

DO - 10.1016/j.celrep.2017.09.097

M3 - SCORING: Journal article

C2 - 29069606

VL - 21

SP - 994

EP - 1008

JO - CELL REP

JF - CELL REP

SN - 2211-1247

IS - 4

ER -