The impact of dietary cellulose on transcriptional profiles of colonic epithelial cells during inflammation.
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ABSTRACT:
PROVIDER: PRJNA634852 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11841500.fastq.gz | Fastqsanger.gz | |||
| SRR11841501.fastq.gz | Fastqsanger.gz | |||
| SRR11841502.fastq.gz | Fastqsanger.gz | |||
| SRR11841503.fastq.gz | Fastqsanger.gz | |||
| SRR11841504.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Although dietary cellulose is considered health promoting, there is still a lack of understanding of cellular and molecular mechanisms. The aim of this study was to shed light on possible effects of the fiber on key players in intestinal homeostasis, including intestinal epithelial cells. Method: Mice were fed a diet containing cellulose as the only source of fiber (CD, control diet) or a fiber free diet (FFD, fiber-free diet) for four weeks and then treated with dextran sulphate sodium in the drinking water for five days. To ensure that gene signatures were derived from colonic epithelial cells and not from contaminating lymphocytes, RAG1 KO mice deficient in intraepithelial lymphocytes were used. Results: The analysis of differential expressed genes of colonic epithelial cells revealed multiple effects of dietary cellulose on the transcriptional profiles. In addition, cellulose caused a distinct clustering when comparing signature genes of different epithelial cell types. Conclusion: This study demonstrated that dietary cellulose impacts transcriptional programs in colonic epithelial cells during inflammation.
2021-05-31 | GSE151136 | GEO
Project description:Dietary cellulose prevents gut inflammation by modulating lipid metabolism and gut microbiota
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Project description:To increase our knowledge of the effects of Fructo oligosaccharides (FOS) on Salmonella infection in fats, a controlle rat infection study was performed. Two groups of 12 rats were adapted for 14 days to a cellulose diet and one group of 12 rats to a FOS diet. One cellulose-fed group and the FOS-fed group were infected with Salmonella. Two days post infection mRNA was collected from the mucosa of the colon and changes in gene expression were assessed using an Agilent rat whole genome microarray (G4131A Agilent Technologies). Results indicate that Salmonella affects colonic mucosal gene expression, which is further enhanded by dietary FOS. Keywords: Dietary infection study, colon mucosa, Rat
2007-10-18 | GSE7472 | GEO
Project description:Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARï¡ activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation. Experiment Overall Design: Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0â¢2% curcumin or control + 0â¢1% rutin and monitored from the age of 7 to 24 weeks. As only curcumin significantly reduced colonic HIS, comparison of the gene expression levels in colon was carried out using total RNA from colon tissue of four mdr1a-/- mice from the control group (high HIS) and four mdr1a-/- mice from the curcumin group (low HIS). A reference design with eight arrays was used for this comparison, where each individual RNA sample was hybridized in the array with the reference RNA, totalizing 4 biological replicates per treatment.
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Project description:Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARalpha activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation. Keywords: Colonic inflammation, gene expression, curcumin, rutin, genome-wide microarrays
2008-04-10 | GSE10684 | GEO
Project description:To increase our knowledge of the effects of Fructo oligosaccharides (FOS) on Salmonella infection in fats, a controlle rat infection study was performed. Two groups of 12 rats were adapted for 14 days to a cellulose diet and one group of 12 rats to a FOS diet. One cellulose-fed group and the FOS-fed group were infected with Salmonella. Two days post infection mRNA was collected from the mucosa of the colon and changes in gene expression were assessed using an Agilent rat whole genome microarray (G4131A Agilent Technologies). Results indicate that Salmonella affects colonic mucosal gene expression, which is further enhanded by dietary FOS. Experiment Overall Design: In the present study, large-scale gene expression analysis was performed to reveal whether Salmonella induced changes of colonic mucosal gene expression in rats. Furthermore, we compared the colonic gene expression changes of infected rats fed a diet supplemented with Fructo oligosaccharides (FOS) or cellulose as control. Two groups of Wistar rats (n=12) were adapted for 14 days to a cellulose diet and one group (n=12) to a FOS diet. One cellulose-fed group and the FOS-fed group were infected with Salmonella. RNA was isolated from colonic mucosal scrapings. mRNA samples of 12 rats per group were pooled. Each group-sample was hybridised in duplicate on Agilent rat whole genome microarrays containing 44290 60-mer spots.
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Project description:miR-181 regulates colonic inflammation
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Project description:The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal homeostasis. Intestinal epithelial cells (IECs) have a high turnover rate driven by the death of terminally differentiated cells with concurrent stem cell proliferation, a process critical for maintaining intestinal homeostasis and protecting against mucosal inflammation. The transcriptional programs that regulate IEC quiescence, proliferation, and differentiation have been well-characterized. However, how gene expression networks critical for IEC functions are regulated at the post-transcriptional level during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against the development of severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of gut microbiota composition. As epithelial reconstitution is crucial for restoring intestinal homeostasis after injury, the miR-181 family represents a potential novel therapeutic target in IECs for protection against severe intestinal inflammation.
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Project description:To evaluate the biological impact of cellulose nanofibrils (CNFs) at the transcriptional level, we conducted whole-genome microarray analyses on human bronchial epithelial cells (BEAS-2B) exposed to CNFs with different physicochemical properties. The results were compared with those from exposures to microcrystalline cellulose (MCC).
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Project description:Mature myeloid cells play a crucial role in the pathogenesis of Crohn disease (CD) but the molecular players that regulate their functions in CD are not fully characterized. Here we show that Trim33 mRNA level is decreased in CD patient’s blood monocytes and characterize TRIM33 functions in monocytes during dextran sulfate sodium (DSS) induced colitis. Mice deleted for trim33 only in mature myeloid cells (Trim33-/- mice) display an impaired resolution of colonic inflammation. This deficiency is associated with an increased number of blood and colon neutrophils and monocytes and a decreased number of colonic macrophages. In accordance, Trim33-/- monocytes are less competent that wild type monocytes for recruitment and differentiation into macrophages at the inflammatory site. Furthermore, during resolution of DSS-induced colitis, Trim33-/- colonic macrophages display an impaired M1/M2 switch and express a low level of membrane bound TNFα known to regulate resolution of inflammation. Altogether, these results show an important role of TRIM33 in monocytes/macrophages during the resolution of DSS-induced colonic inflammation and pinpoint TRIM33 as a novel Crohn disease biomarker and as a potential therapeutic target.
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