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Effects of Dietary Tryptophan Supplementation in the Acetic Acid-Induced Colitis Mouse Model

Abstract

Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is strongly associated with intestinal immunity and the microbiome. Tryptophan (Trp) is an inflammatory inhibitor and modulator of the intestinal microflora. We explored the serum profile of amino acids and the effects of diet supplementation with Trp (1.0g/kg) on intestinal immunity and microbiota in the acetic acid-induced colitis mouse model. We analyzed the survival rate, colonic morphological parameters, profiles of serum amino acids, microbiota in colonic contents and the relative gene abundance of intestinal proinflammatory cytokines. Although the dietary Trp supplementation failed to improve the survival rate and ameliorate the morphological parameters of colon in mice with colitis, Trp modulated the general serum amino acid profile by reducing the amino acid profiles of threonine, methionine and proline, affected intestinal immunity by inhibiting the colonic expression of interleukin-22 and changed the microbiota by reducing the abundance of Candidatus, Clostridium and Coprococcus at the genus level. In conclusion, dietary Trp supplementation in a mouse model of colitis did not ameliorate the survival rate and morphological parameters of colon but did modulate the serum amino acid profiles, intestinal immunity and microbiota. These findings enhance the understanding of the roles of Trp in the metabolism of serum amino acids, intestinal immunity and microbiota.

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Publication details

The article was received on 23 May 2018, accepted on 05 Jul 2018 and first published on 05 Jul 2018


Article type: Paper
DOI: 10.1039/C8FO01025K
Citation: Food Funct., 2018, Accepted Manuscript
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    Effects of Dietary Tryptophan Supplementation in the Acetic Acid-Induced Colitis Mouse Model

    S. chen, M. wang, L. yin, W. Ren, P. bin, Y. Xia, G. Liu, H. yang, B. Tan and Y. Yin, Food Funct., 2018, Accepted Manuscript , DOI: 10.1039/C8FO01025K

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