Microbial Butyrate Synthesis Indicates Therapeutic Efficacy of Azathioprine in IBD Patients.


Journal

Journal of Crohn's & colitis
ISSN: 1876-4479
Titre abrégé: J Crohns Colitis
Pays: England
ID NLM: 101318676

Informations de publication

Date de publication:
13 Jan 2021
Historique:
pubmed: 21 7 2020
medline: 14 10 2021
entrez: 21 7 2020
Statut: ppublish

Résumé

The microbial ecosystem seems to be an important player for therapeutic intervenption in inflammatory bowel disease [IBD]. We assessed longitudinal microbiome changes in IBD patients undergoing therapy with either azathioprine [AZA] or anti-tumour necrosis factor [anti-TNF] antibodies. We predicted the metabolic microbial community exchange and linked it to clinical outcome. Faecal and blood samples were collected from 65 IBD patients at baseline and after 12 and 30 weeks on therapy. Clinical remission was defined as Crohn's Disease Activity Index [CDAI] < 150 in Crohn´s disease [CD], partial Mayo score <2 in ulcerative colitis [UC], and faecal calprotectin values <150 µg/g and C-reactive protein <5 mg/dl. 16S rRNA amplicon sequencing was performed. To predict microbial community metabolic processes, we constructed multispecies genome-scale metabolic network models. Paired Bray-Curtis distance between baseline and follow-up time points was significantly different for UC patients treated with anti-TNF antibodies. Longitudinal changes in taxa composition at phylum level showed a significant decrease of Proteobacteria and an increase of Bacteroidetes in CD patients responding to both therapies. At family level, Lactobacilli were associated with persistent disease and Bacteroides abundance with remission in CD. In-silico simulations of microbial metabolite exchange predicted a 1.7-fold higher butyrate production capacity of patients in remission compared with patients without remission [p = 0.041]. In this model, the difference in butyrate production between patients in remission and patients without remission was most pronounced in the CD group treated with AZA [p = 0.008]. In-silico simulation identifies microbial butyrate synthesis predictive of therapeutic efficacy in IBD.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
The microbial ecosystem seems to be an important player for therapeutic intervenption in inflammatory bowel disease [IBD]. We assessed longitudinal microbiome changes in IBD patients undergoing therapy with either azathioprine [AZA] or anti-tumour necrosis factor [anti-TNF] antibodies. We predicted the metabolic microbial community exchange and linked it to clinical outcome.
METHODS METHODS
Faecal and blood samples were collected from 65 IBD patients at baseline and after 12 and 30 weeks on therapy. Clinical remission was defined as Crohn's Disease Activity Index [CDAI] < 150 in Crohn´s disease [CD], partial Mayo score <2 in ulcerative colitis [UC], and faecal calprotectin values <150 µg/g and C-reactive protein <5 mg/dl. 16S rRNA amplicon sequencing was performed. To predict microbial community metabolic processes, we constructed multispecies genome-scale metabolic network models.
RESULTS RESULTS
Paired Bray-Curtis distance between baseline and follow-up time points was significantly different for UC patients treated with anti-TNF antibodies. Longitudinal changes in taxa composition at phylum level showed a significant decrease of Proteobacteria and an increase of Bacteroidetes in CD patients responding to both therapies. At family level, Lactobacilli were associated with persistent disease and Bacteroides abundance with remission in CD. In-silico simulations of microbial metabolite exchange predicted a 1.7-fold higher butyrate production capacity of patients in remission compared with patients without remission [p = 0.041]. In this model, the difference in butyrate production between patients in remission and patients without remission was most pronounced in the CD group treated with AZA [p = 0.008].
CONCLUSIONS CONCLUSIONS
In-silico simulation identifies microbial butyrate synthesis predictive of therapeutic efficacy in IBD.

Identifiants

pubmed: 32687146
pii: 5873836
doi: 10.1093/ecco-jcc/jjaa152
doi:

Substances chimiques

Antimetabolites 0
Butyrates 0
Tumor Necrosis Factor Inhibitors 0
Azathioprine MRK240IY2L

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

88-98

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of European Crohn’s and Colitis Organisation. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Auteurs

M Effenberger (M)

Department of Internal Medicine I, Gastroenterology, Hepatology, Metabolism & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.

S Reider (S)

Department of Internal Medicine I, Gastroenterology, Hepatology, Metabolism & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Christian Doppler Laboratory for Mucosal Immunology, Medical University of Innsbruck, Innsbruck, Austria.

S Waschina (S)

Institute for Human Nutrition and Food Science, Division Nutriinformatics, Christian-Albrechts-University of Kiel, Kiel, Germany.

C Bronowski (C)

Institute of Clinical Molecular Biology, Christian-Albrechts-University and University Hospital Schleswig-Holstein, Kiel, Germany.

B Enrich (B)

Department of Internal Medicine I, Gastroenterology, Hepatology, Metabolism & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.

T E Adolph (TE)

Department of Internal Medicine I, Gastroenterology, Hepatology, Metabolism & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.

R Koch (R)

Department of Internal Medicine I, Gastroenterology, Hepatology, Metabolism & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.

A R Moschen (AR)

Department of Internal Medicine I, Gastroenterology, Hepatology, Metabolism & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Christian Doppler Laboratory for Mucosal Immunology, Medical University of Innsbruck, Innsbruck, Austria.

P Rosenstiel (P)

Institute of Clinical Molecular Biology, Christian-Albrechts-University and University Hospital Schleswig-Holstein, Kiel, Germany.

K Aden (K)

Institute of Clinical Molecular Biology, Christian-Albrechts-University and University Hospital Schleswig-Holstein, Kiel, Germany.
Department of Internal Medicine I, Christian-Albrechts-University and University Hospital Schleswig-Holstein, Kiel, Germany.

H Tilg (H)

Department of Internal Medicine I, Gastroenterology, Hepatology, Metabolism & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.

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Classifications MeSH