Exclusive enteral nutrition mediates gut microbial and metabolic changes that are associated with remission in children with Crohn's disease.
Adolescent
Amino Acids
/ analysis
Bacteria
/ classification
Biodiversity
Cadaverine
/ analysis
Case-Control Studies
Child
Crohn Disease
/ immunology
Enteral Nutrition
/ adverse effects
Feces
/ microbiology
Female
Gastrointestinal Microbiome
/ drug effects
High-Throughput Nucleotide Sequencing
Humans
Interleukin-6
/ metabolism
Lipopolysaccharides
/ adverse effects
Male
Metabolomics
/ methods
Methylamines
/ analysis
Monocytes
/ drug effects
Prospective Studies
RNA, Ribosomal, 16S
/ genetics
Treatment Outcome
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
03 11 2020
03 11 2020
Historique:
received:
25
06
2020
accepted:
13
10
2020
entrez:
4
11
2020
pubmed:
5
11
2020
medline:
10
3
2021
Statut:
epublish
Résumé
A nutritional intervention, exclusive enteral nutrition (EEN) can induce remission in patients with pediatric Crohn's disease (CD). We characterized changes in the fecal microbiota and metabolome to identify the mechanism of EEN. Feces of 43 children were collected prior, during and after EEN. Microbiota and metabolites were analyzed by 16S rRNA gene amplicon sequencing and NMR. Selected metabolites were evaluated in relevant model systems. Microbiota and metabolome of patients with CD and controls were different at all time points. Amino acids, primary bile salts, trimethylamine and cadaverine were elevated in patients with CD. Microbiota and metabolome differed between responders and non-responders prior to EEN. EEN decreased microbiota diversity and reduced amino acids, trimethylamine and cadaverine towards control levels. Patients with CD had reduced microbial metabolism of bile acids that partially normalized during EEN. Trimethylamine and cadaverine inhibited intestinal cell growth. TMA and cadaverine inhibited LPS-stimulated TNF-alpha and IL-6 secretion by primary human monocytes. A diet rich in free amino acids worsened inflammation in the DSS model of intestinal inflammation. Trimethylamine, cadaverine, bile salts and amino acids could play a role in the mechanism by which EEN induces remission. Prior to EEN, microbiota and metabolome are different between responders and non-responders.
Identifiants
pubmed: 33144591
doi: 10.1038/s41598-020-75306-z
pii: 10.1038/s41598-020-75306-z
pmc: PMC7609694
doi:
Substances chimiques
Amino Acids
0
IL6 protein, human
0
Interleukin-6
0
Lipopolysaccharides
0
Methylamines
0
RNA, Ribosomal, 16S
0
Cadaverine
L90BEN6OLL
trimethylamine
LHH7G8O305
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
18879Subventions
Organisme : Wellcome Trust
ID : 098051
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/P002536/1
Pays : United Kingdom
Organisme : Department of Health
ID : II-OL-1116-10027
Pays : United Kingdom
Organisme : NCI NIH HHS
ID : R01 CA204403
Pays : United States
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