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Cell Host Microbe. 2017 May 10;21(5):603-610.e3. doi: 10.1016/j.chom.2017.04.010.

Gut Microbiome Function Predicts Response to Anti-integrin Biologic Therapy in Inflammatory Bowel Diseases.

Author information

1
Division of Gastroenterology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
2
Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
3
Division of Gastroenterology, Massachusetts General Hospital, Boston, MA 02114, USA.
4
Harvard Medical School, Boston, MA 02115, USA.
5
Division of Gastroenterology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Center for Microbiome Informatics and Therapeutics, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. Electronic address: xavier@molbio.mgh.harvard.edu.

Abstract

The gut microbiome plays a central role in inflammatory bowel diseases (IBDs) pathogenesis and propagation. To determine whether the gut microbiome may predict responses to IBD therapy, we conducted a prospective study with Crohn's disease (CD) or ulcerative colitis (UC) patients initiating anti-integrin therapy (vedolizumab). Disease activity and stool metagenomes at baseline, and weeks 14, 30, and 54 after therapy initiation were assessed. Community α-diversity was significantly higher, and Roseburia inulinivorans and a Burkholderiales species were more abundant at baseline among CD patients achieving week 14 remission. Several significant associations were identified with microbial function; 13 pathways including branched chain amino acid synthesis were significantly enriched in baseline samples from CD patients achieving remission. A neural network algorithm, vedoNet, incorporating microbiome and clinical data, provided highest classifying power for clinical remission. We hypothesize that the trajectory of early microbiome changes may be a marker of response to IBD treatment.

KEYWORDS:

Microbiome; butyrate; remission; roseburia; treatment response; vedolizumab

PMID:
28494241
PMCID:
PMC5705050
DOI:
10.1016/j.chom.2017.04.010
[Indexed for MEDLINE]
Free PMC Article

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