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      Effects of dietary tryptophan supplementation in the acetic acid-induced colitis mouse model

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          Abstract

          Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is strongly associated with intestinal immunity and the microbiome.

          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 (1.0 g kg −1) 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 our understanding of the roles of Trp in the metabolism of serum amino acids, intestinal immunity and microbiota.

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          Most cited references43

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          Inflammatory bowel disease.

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            Current and emerging therapeutic targets for IBD

            The management of IBD has undergone major advances with the development of biologic agents. Here, Markus Neurath provides an overview of current and future therapeutic targets for IBD, including insights into the mechanisms and rationale behind such approaches.
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              The impact of perinatal immune development on mucosal homeostasis and chronic inflammation.

              The mucosal surfaces of the gut and airways have important barrier functions and regulate the induction of immunological tolerance. The rapidly increasing incidence of chronic inflammatory disorders of these surfaces, such as inflammatory bowel disease and asthma, indicates that the immune functions of these mucosae are becoming disrupted in humans. Recent data indicate that events in prenatal and neonatal life orchestrate mucosal homeostasis. Several environmental factors promote the perinatal programming of the immune system, including colonization of the gut and airways by commensal microorganisms. These complex microbial-host interactions operate in a delicate temporal and spatial manner and have an important role in the induction of homeostatic mechanisms.
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                Author and article information

                Journal
                FFOUAI
                Food & Function
                Food Funct.
                Royal Society of Chemistry (RSC)
                2042-6496
                2042-650X
                2018
                2018
                : 9
                : 8
                : 4143-4152
                Affiliations
                [1 ]Laboratory of Animal Nutritional Physiology and Metabolic Process
                [2 ]Key Laboratory of Agro-ecological Processes in Subtropical Region
                [3 ]Institute of Subtropical Agriculture
                [4 ]Chinese Academy of Sciences
                [5 ]National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production
                Article
                10.1039/C8FO01025K
                30042998
                ed913a0c-6b31-4fbb-9def-84f466c05e37
                © 2018

                http://rsc.li/journals-terms-of-use

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