Dataset Information

Gut microbiota composition and functional prediction in diarrhea-predominant irritable bowel syndrome.

ABSTRACT:

Background

Irritable bowel syndrome (IBS) is common and difficult to treat and its pathogenesis is closely related to gut microbiota. However, differences in gut microbiota of patients in different regions make it more difficult to elucidate the mechanism of IBS. We performed an analysis of gut microbiota composition and functional prediction in Chinese patients with diarrhea-predominant IBS (IBS-D).

Methods

Fecal samples were obtained from 30 IBS-D patients and 30 healthy controls (HCs) in Nanchang, China. Using 16S gene sequence profiles, we analyzed the abundance of dominant microbiota at different taxonomy levels. Based on 16S information, Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) was used to predicting the function of gut microbiota.

Results

Compared to HCs, gut microbiota richness but not diversity was decreased in IBS-D patients. The abundant phyla Firmicutes, Fusobacteria and Actinobacteria decreased significantly, and Proteobacteria increased significantly in IBS-D patients. PICRUSt indicated that function expression of gut microbiota in IBS-D patients was up-regulated in metabolism of cofactors and vitamins, xenobiotics biodegradation and metabolism, and down-regulated in environmental adaptation, cell growth and death.

Conclusions

Compared with the normal population in China, IBS-D patients are characterized by complex and unstable gut microbiota, which may influence inflammation and metabolism of the host.

SUBMITTER: Mei L

PROVIDER: S-EPMC7934555 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature

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Publications

Gut microbiota composition and functional prediction in diarrhea-predominant irritable bowel syndrome.

Mei Lijun L Zhou Jiaoli J Su Yimo Y Mao Kunhong K Wu Jing J Zhu Caicai C He Ling L Cui Ying Y

BMC gastroenterology 20210305 1

<h4>Background</h4>Irritable bowel syndrome (IBS) is common and difficult to treat and its pathogenesis is closely related to gut microbiota. However, differences in gut microbiota of patients in different regions make it more difficult to elucidate the mechanism of IBS. We performed an analysis of gut microbiota composition and functional prediction in Chinese patients with diarrhea-predominant IBS (IBS-D).<h4>Methods</h4>Fecal samples were obtained from 30 IBS-D patients and 30 healthy control ...[more]

PMID: 33663411

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Project description:Altered gut microbiota are assumed to be involved in the pathogenesis of irritable bowel syndrome (IBS). However, gut microbiota alterations reported in different studies are divergent and sometimes even contradictory. To better elucidate the relationship between altered gut microbiota and IBS, we characterized fecal microbiota of diarrhea-predominant IBS (IBS-D) patients and further explored the effect of rifaximin on gut microbiota using bacterial 16S rRNA gene-targeted pyrosequencing. In our study, IBS-D patients defined by Rome III criteria and age-and-gender matched healthy controls (HC) were enrolled to investigate the fecal microbiota alterations. These IBS-D patients were then treated with rifaximin for 2 weeks and followed up for 10 weeks. Fecal microbiota alterations, small intestine bacterial overgrowth (SIBO) and gastrointestinal (GI) symptoms of IBS-D patients were analyzed before and after treatment. Our results showed fecal microbiota richness but not diversity was decreased in IBS-D patients as compared to HC and there were alterations of fecal microbiota at different taxonomy levels. The abundant phyla Firmicutes was significantly decreased and Bacteroidetes was increased in IBS-D patients. Moreover, the alterations of predominant fermenting bacteria such as Bacteroidales and Clostridiales might be involved in the pathophysiology of IBS-D. In addition, rifaximin was effective in terms of SIBO eradication and even GI symptoms of IBS-D patients achieved at least 10-week improvement after treatment. Furthermore, rifaximin induced alterations of some special bacteria rather than affected the overall composition of microbiota in IBS-D patients. Meanwhile, a potential decrease in propanoate and butanoate metabolism was found in these IBS-D patients after rifaximin treatment. Taken together, there were alterations of gut microbiota in IBS-D patients as compared to HC. Rifaximin could relieve GI symptoms, modify gut microbiota in IBS-D patients and eradicate SIBO in those patients with SIBO, suggesting an additional therapeutic mechanism of rifaximin in the treatment of IBS-D. Our findings of compositional gut microbiota alterations in IBS-D and the effect of rifaximin on the gut microbiota implied that altered gut microbiota were associated with the pathogenesis of IBS.

Project description:ObjectiveFructose malabsorption is a common digestive disorder in which absorption of fructose in the small intestine is impaired. An abnormality of the main intestinal fructose transporter proteins has been proposed as a cause for fructose malabsorption. However the underlying molecular mechanism for this remains unclear. In this study, we investigated whether carbohydrate response element-binding protein (ChREBP) plays a role in intestinal fructose absorption through the regulation of genes involved in fructose transport and metabolism and ion transport.MethodsWild type (WT) and Chrebp knockout (KO) mice (6 or 8 weeks old) were fed a control diet (55% starch, 15% maltodextrin 10) or high-fructose diet (HFrD, 60% fructose, 10% starch) for 3-12 days. Body weight and food intake were measured, signs of fructose malabsorption were monitored, and the expression of genes involved in fructose transport/metabolism and ion transport was evaluated. Furthermore, transient transfection and chromatin immunoprecipitation were performed to show the direct interaction between ChREBP and carbohydrate response elements in the promoter of Slc2A5, which encodes the fructose transporter GLUT5.ResultsChrebp KO mice fed the control diet maintained a constant body weight, whereas those fed a HFrD showed significant weight loss within 3-5 days. In addition, Chrebp KO mice fed the HFrD exhibited a markedly distended cecum and proximal colon containing both fluid and gas, suggesting incomplete fructose absorption. Fructose-induced increases of genes involved in fructose transport (GLUT5), fructose metabolism (fructokinase, aldolase B, triokinase, and lactate dehydrogenase), and gluconeogenesis (glucose-6-phosphatase and fructose-1,6-bisphosphatase) were observed in the intestine of WT but not of Chrebp KO mice. Moreover the Na+/H+ exchanger NHE3, which is involved in Na+ and water absorption in the intestine, was significantly decreased in HFrD-fed Chrebp KO mice. Consistent with this finding, the high-fructose diet-fed Chrebp KO mice developed severe diarrhea. Results of chromatin immunoprecipitation assays showed a direct interaction of ChREBP with the Glut5 promoter, but not the Nhe3 promoter, in the small intestine. Ectopic co-expression of ChREBP and its heterodimer partner Max-like protein X activated the Glut5 promoter in Caco-2BBE cells.ConclusionsChREBP plays a key role in the dietary fructose transport as well as conversion into lactate and glucose through direct transcriptional control of genes involved in fructose transport, fructolysis, and gluconeogenesis. Moreover, ablation of Chrebp results in a severe diarrhea in mice fed a high-fructose diet, which is associated with the insufficient induction of GLUT5 in the intestine.

Dataset Information

Gut microbiota composition and functional prediction in diarrhea-predominant irritable bowel syndrome.

Background

Methods

Results

Conclusions

Publications

Gut microbiota composition and functional prediction in diarrhea-predominant irritable bowel syndrome.

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