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    Exclusive enteral nutrition mediates gut microbial and metabolic changes that are associated with remission in children with Crohn's disease.

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    Author
    Diederen, K; Li, JV; Donachie, GE; de Meij, TG; de Waart, DR; Hakvoort, TBM; Kindermann, A; Wagner, J; Auyeung, V; Te Velde, AA; ...
    Date
    2020-11-03
    Source Title
    Scientific Reports
    Publisher
    Springer Science and Business Media LLC
    University of Melbourne Author/s
    Wagner, Josef
    Affiliation
    Paediatrics (RCH)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Diederen, K., Li, J. V., Donachie, G. E., de Meij, T. G., de Waart, D. R., Hakvoort, T. B. M., Kindermann, A., Wagner, J., Auyeung, V., Te Velde, A. A., Heinsbroek, S. E. M., Benninga, M. A., Kinross, J., Walker, A. W., de Jonge, W. J. & Seppen, J. (2020). Exclusive enteral nutrition mediates gut microbial and metabolic changes that are associated with remission in children with Crohn's disease.. Sci Rep, 10 (1), pp.18879-. https://doi.org/10.1038/s41598-020-75306-z.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/252994
    DOI
    10.1038/s41598-020-75306-z
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7609694
    Abstract
    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.

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