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The Effect of Inulin Supplementation on Colorectal Surgery Outcomes

ABSTRACT: Colorectal cancer (CRC) is the third most diagnosed cancer in Canada. The most common surgical procedure in patients with CRC is an intestinal resection followed by a reconnection to rejoin the ends of the remaining bowel. Among the postoperative complications, leaking of this intestinal connection is notably feared, affecting up to 20% of patients. These leaks are characterized by impaired intestinal healing and are associated with severe infections and even death. Various studies have shown that gut microbiota, the bacteria that live in the digestive tract, plays an essential role in intestinal healing following surgery. These results support the possibility of enhancing intestinal healing through supplements that act as an energy source for gut bacteria. Indeed, animal studies have shown that inulin supplementation, a fiber commonly found in plants, improves intestinal healing following bowel surgery. However, no studies in humans have evaluated its effects on CRC surgery patients. This study aims to determine feasibility of a randomized controlled trial that assesses the effects of inulin supplementation before elective colorectal surgery.

DISEASE(S): Colorectal Cancer,Anastomotic Complication

PROVIDER: 60182 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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The effect of probiotic Lactobacilli strains, inulin-type fructans and oligofructose on gene expression profiles in intestinal Caco-2 cells

Project description:Background: Beneficial microbes can be actors in maintaining or stimulating barrier function, and may counteract pathogen-infection. Lactobacilli are particularly recognized for enhancing intestinal barrier function and to confer protective effects against multiresistant pathogens. Various L. acidophilus strains support intestinal immune barrier function and have been shown to improve resistance to pathogens. Although less extensively studied than beneficial bacteria, other food-based ingredients that can contribute to strengthening barrier function are dietary fibers. For instance, inulin and fructooligosaccharides (FOS) have recently been shown to enhance barrier function and protect against barrier dysfunction. Effects of these ingredients on intestinal barrier function were evaluated by quantifying regulation of gene expression by microarray. Methods: Caco-2 cells were incubated with probiotic strains or inulin-type fibers for 6 hours, total RNA was extracted and Affymterix Human Gene 1.1 ST arrays were used to analyze the gene expression profiles. Results: Only L. acidophilus modulated a group of 26 genes related to tight-junctions. Inulin-type fructans, L. brevis W63 and L. casei W56 regulated other genes, unrelated to tight junctions. L. acidophilus also had unique effects on a group of 6 genes regulating epithelial phenotype towards follicle-associated epithelium. L. acidophilus W37 was therefore selected for a challenge with STM and prevented STM-induced barrier disruption and decreased secretion of IL-8. L. acidophilus W37 increases TEER and can protect against STM induced disruption of gut epithelial cells integrity in vitro. Conclusion: Our results suggest that selection of specific bacterial strains for enforcing barrier function may be a promising strategy to reduce or prevent STM infections.

2018-07-19 | GSE115022 | GEO

Transcriptional response of Pseudomonas aeruginosa to the prebiotic Fructooligosaccharide

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2020-01-17 | GSE124468 | GEO

Gut Microbiota, Anastomotic Leak and Colorectal Cancer

Project description:This is a prospective study evaluating the relation between the gut microbiota composition, intestinal healing after colorectal surgery and colorectal cancer behavior. Our hypothesis is that the gut microbiota composition could predict poor intestinal healing in colorectal surgery, and that the gut microbiota might have an impact on colorectal cancer clinical behavior and may predict disease outcomes.

| 2314926 | ecrin-mdr-crc

An integrative multi-omics approach to characterize prebiotic inulin effects on Faecalibacterium prausnitzii

Project description:Faecalibacterium prausnitzii, a major commensal bacterium in the human gut, is well known for its anti-inflammatory effects, which improve host intestinal health. Although several studies have reported that inulin, a well-known prebiotic, increases the abundance of F. prausnitzii in the intestine, the mechanism underlying this effect remains unclear. In this study, we applied liquid chromatography tandem mass spectrometry (LC-MS/MS)-based multi-omics approaches to identify biological and enzymatic mechanisms of F. prausnitzii involved in the selective digestion of inulin. An LC-MS/MS-based intracellular proteomic and metabolic profiling was performed to determine the quantitative changes in specific proteins and metabolites of F. prausnitzii when grown on inulin. Interestingly, proteomic analysis revealed that the putative proteins involved in inulin-type fructan utilization by F. prausnitzii, particularly b-fructosidase and amylosucrase were upregulated in the presence of inulin. To investigate the function of these proteins, we overexpressed bfrA and ams, genes encoding beta-fructosidase and amylosucrase, respectively, in Escherichia coli, and observed their ability to degrade fructan. In addition, the enzyme activity assay demonstrated that intracellular fructan hydrolases degrade the inulin-type fructans taken up by fructan ATP-binding cassette transporters. Furthermore, we showed that the fructose uptake activity of F. prausnitzii was enhanced by the fructose phosphotransferase system transporter when inulin was used as a carbon source.

2022-04-04 | PXD030078 | Pride

Faecalibacterium prausnitzii promotes intestinal epithelial IL-18 production through activation of the HIF1A pathway

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2023-11-30 | GSE248806 | GEO

Contributions of microbiome and mechanical deformation to intestinal bacterial overgrowth and inflammation in a human gut-on-a-chip.

Project description:A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1Î², and TNF-Î±) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models. 6 samples, 2 biological replicates for each 3 conditions.

2015-12-16 | E-GEOD-65790 | biostudies-arrayexpress

Expression data from colon epithelium of STAT3IEC-KO in acute DSS colitis

Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing. 4 samples of colon epithelium were analyzed from 4 mice (2 per group Stat3flfl VillinCre- and Stat3flfl VillinCre+, respectively) after they had been treated with DSS (2.5%) for 5 days

2009-05-08 | E-GEOD-15955 | biostudies-arrayexpress

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Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.

2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress

mouse gut metagenome

Project description:Inulin supplementation globally changed gut microbial community

| PRJDB8684 | ENA

Effect of inulin on extracellular vesicles microRNAs in milk from dairy cows with sub-clinical mastitis

Project description:Milk contains microRNAs (miRNAs) that are protected by extracellular vesicles (EV). Beyond variations among individuals, the nutritional conditions of cattle play a role in shaping these milk miRNA profiles. This study explored milk-derived EV-miRNA variations induced by inulin supplementation and analyzed involved pathways. Fourteen lactating cows with sub-clinical mastitis were equally and randomly divided into an inulin and a control group. Cows in the inulin group received 300 g/d inulin, while the control group did not. After one week of adaptation and five weeks of treatment, milk-derived EV-miRNAs from cows were isolated. Differentially expressed (DE) miRNAs were identified via high-throughput sequencing. Functional enrichment analyses, including Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, were conducted to examine the target genes of DE miRNAs. Inulin supplementation did not significantly alter miRNA length, the number of known miRNAs, or the read number of small RNAs.

2024-05-31 | GSE256521 | GEO

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