Article Publish Status: FREE
Abstract Title:

Dysbiosis contributes to chronic constipation development via regulation of serotonin transporter in the intestine.

Abstract Source:

Sci Rep. 2017 Sep 4 ;7(1):10322. Epub 2017 Sep 4. PMID: 28871143

Abstract Author(s):

Hailong Cao, Xiang Liu, Yingying An, Guoqiong Zhou, Yanrong Liu, Mengque Xu, Wenxiao Dong, Sinan Wang, Fang Yan, Kui Jiang, Bangmao Wang

Article Affiliation:

Hailong Cao


Chronic constipation is a prevalent functional gastrointestinal disorder accompanied with intestinal dysbiosis. However, causal relationship between dysbiosis and constipation remains poorly understood. Serotonin transporter (SERT) is a transmembrane transport protein which re-uptakes excessive 5-hydroxytryptamine (5-HT) from effective location to terminate its physiological effects and involves in regulating gastrointestinal motility. In this study, fecal microbiota from patients with constipation and healthy controls were transplanted into the antibiotic depletion mice model. The mice which received fecal microbiota from patients with constipation presented a reducing in intestinal peristalsis and abnormal defecation parameters including the frequency of pellet expulsion, fecal weight and fecal water content. After fecal microbiota transplantation, the SERT expression in the colonic tissue was significantly upregulated, and the content of 5-HT was decreased which negatively correlated with the gastrointestinal transit time. Moverover, fecal microbiota from the mice which received fecal microbiota from patients with constipation also upregulated SERT in Caco-2 cells. Besides, this process accompanied with the decreased abundance of Clostridium, Lactobacillus, Desulfovibrio, and Methylobacterium and an increased tend of Bacteroides and Akkermansia, which also involved in the impairment of intestinal barrier after FMT. Taken together, intestinal dysbiosis may upregulate the SERT expression and contribute to the development of chronic constipation.

Study Type : Animal Study

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Sayer Ji
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