Microbiota changes induced by microencapsulated sodium butyrate in patients with inflammatory bowel disease.


Journal

Neurogastroenterology and motility
ISSN: 1365-2982
Titre abrégé: Neurogastroenterol Motil
Pays: England
ID NLM: 9432572

Informations de publication

Date de publication:
10 2020
Historique:
received: 17 01 2020
revised: 06 04 2020
accepted: 11 05 2020
pubmed: 2 6 2020
medline: 12 8 2021
entrez: 2 6 2020
Statut: ppublish

Résumé

Butyrate has shown anti-inflammatory and regenerative properties, providing symptomatic relief when orally supplemented in patients suffering from various colonic diseases. We investigated the effect of a colonic-delivery formulation of butyrate on the fecal microbiota of patients with inflammatory bowel diseases (IBDs). In this double-blind, placebo-controlled, pilot study, 49 IBD patients (n = 19 Crohn's disease, CD and n = 30 ulcerative colitis, UC) were randomized to oral administration of microencapsulated-sodium-butyrate (BLM) or placebo for 2 months, in addition to conventional therapy. Eighteen healthy volunteers (HVs) were recruited to provide a healthy microbiota model of the local people. Fecal microbiota from stool samples was assessed by 16S sequencing. Clinical disease activity and quality of life (QoL) were evaluated before and after treatment. At baseline, HVs showed a different microbiota composition compared with IBD patients. Sodium-butyrate altered the gut microbiota of IBD patients by increasing bacteria able to produce SCFA in UC patients (Lachnospiraceae spp.) and the butyrogenic colonic bacteria in CD patients (Butyricicoccus). In UC patients, QoL was positively affected by treatment. Sodium-butyrate supplementation increases the growth of bacteria able to produce SCFA with potentially anti-inflammatory action. The clinical impact of this finding requires further investigation.

Sections du résumé

BACKGROUND
Butyrate has shown anti-inflammatory and regenerative properties, providing symptomatic relief when orally supplemented in patients suffering from various colonic diseases. We investigated the effect of a colonic-delivery formulation of butyrate on the fecal microbiota of patients with inflammatory bowel diseases (IBDs).
METHODS
In this double-blind, placebo-controlled, pilot study, 49 IBD patients (n = 19 Crohn's disease, CD and n = 30 ulcerative colitis, UC) were randomized to oral administration of microencapsulated-sodium-butyrate (BLM) or placebo for 2 months, in addition to conventional therapy. Eighteen healthy volunteers (HVs) were recruited to provide a healthy microbiota model of the local people. Fecal microbiota from stool samples was assessed by 16S sequencing. Clinical disease activity and quality of life (QoL) were evaluated before and after treatment.
KEY RESULTS
At baseline, HVs showed a different microbiota composition compared with IBD patients. Sodium-butyrate altered the gut microbiota of IBD patients by increasing bacteria able to produce SCFA in UC patients (Lachnospiraceae spp.) and the butyrogenic colonic bacteria in CD patients (Butyricicoccus). In UC patients, QoL was positively affected by treatment.
CONCLUSIONS AND INFERENCES
Sodium-butyrate supplementation increases the growth of bacteria able to produce SCFA with potentially anti-inflammatory action. The clinical impact of this finding requires further investigation.

Identifiants

pubmed: 32476236
doi: 10.1111/nmo.13914
pmc: PMC7583468
doi:

Substances chimiques

Capsules 0
Histamine Antagonists 0
Butyric Acid 107-92-6

Types de publication

Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13914

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2020 The Authors. Neurogastroenterology & Motility published by John Wiley & Sons Ltd.

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Auteurs

Sonia Facchin (S)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

Nicola Vitulo (N)

Department of Biotechnology, University of Verona, Verona, Italy.

Matteo Calgaro (M)

Department of Biotechnology, University of Verona, Verona, Italy.

Andrea Buda (A)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

Chiara Romualdi (C)

Department of Biology, University of Padua, Padua, Italy.

Daniel Pohl (D)

Department of Gastroenterology, University Hospital Zurich, Zurich, Switzerland.

Barbara Perini (B)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

Greta Lorenzon (G)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

Carla Marinelli (C)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

Renata D'Incà (R)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

Giacomo Carlo Sturniolo (GC)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

Edoardo Vincenzo Savarino (EV)

Department of Surgery, Oncology and Gastroenterology (DISCOG), University Hospital of Padua, Padua, Italy.

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