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Effects of dietary tryptophan supplementation in the acetic acid-induced colitis mouse model
Food & Function ( IF 6.1 ) Pub Date : 2018-07-05 , DOI: 10.1039/c8fo01025k
Shuai Chen 1, 2, 3, 4, 5 , Meiwei Wang 1, 2, 3, 4, 5 , Lanmei Yin 1, 2, 3, 4, 5 , Wenkai Ren 1, 2, 3, 4, 5 , Peng Bin 1, 2, 3, 4, 5 , Yaoyao Xia 1, 2, 3, 4, 5 , Gang Liu 1, 2, 3, 4, 5 , Huansheng Yang 1, 2, 3, 4, 5 , Bie Tan 1, 2, 3, 4, 5 , Yulong Yin 1, 2, 3, 4, 5
Affiliation  

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.

中文翻译:

饮食中色氨酸补充对乙酸诱发的结肠炎小鼠模型的影响

炎症性肠病(IBD)的特征是胃肠道的慢性炎症,并且与肠道免疫力和微生物组密切相关。色氨酸(Trp)是肠道菌群的炎性抑制剂和调节剂。我们探讨了氨基酸的血清学特征以及Trp(1.0 g kg -1)对乙酸诱发的结肠炎小鼠模型的肠道免疫力和微生物群的影响。我们分析了存活率,结肠形态学参数,血清氨基酸谱,结肠内容物中的微生物群以及肠道促炎细胞因子的相对基因丰度。尽管饮食中补充Trp不能提高结肠炎小鼠的存活率并不能改善结肠的形态学参数,但是Trp通过降低苏氨酸,蛋氨酸和脯氨酸的氨基酸谱来调节一般的血清氨基酸谱,通过抑制Trp来影响肠道免疫。白介素-22的表达结肠和通过减少的丰度改变了微生物群暂定梭菌Coprococcus在属水平上。总之,在结肠炎小鼠模型中补充饮食中的Trp并不能改善结肠的存活率和形态学参数,但可以调节血清氨基酸谱,肠道免疫力和微生物群。这些发现增强了我们对Trp在血清氨基酸代谢,肠道免疫和微生物群中的作用的理解。
更新日期:2018-08-15
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