Dietary emulsifiers disturb mouse microbiota
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ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR706140.fastq.gz | Fastqsanger.gz | |||
| ERR706141.fastq.gz | Fastqsanger.gz | |||
| ERR706142.fastq.gz | Fastqsanger.gz | |||
| ERR706143.fastq.gz | Fastqsanger.gz | |||
| ERR706144.fastq.gz | Fastqsanger.gz |
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Project description:Dietary methionine restriction represses growth and improves therapeutic responses in several pre-clinical settings. However, how this dietary intervention impacts cancer progression in the context of the immune system is unknown. Here we analyzed the CD45+ immune cells from the small intestine of control (CTRL) diet or methionine-restricted (MR) diet fed tumor-free C57BL/6J donor mice and tumor-bearing Apc <min+/-> recipient mice transplanated with feces from these diet-fed tumor-free C57BL/6J mice by scRNA-seq. Our analysis indicate that fecal microbes from methionine-restricted tumor-free C57BL/6J mice are sufficient to represss T cell activation in the small intestine of Apc <min+/-> mice.
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Project description:Background and Aims: We have shown in several controlled rat and human infection studies that dietary calcium improves intestinal resistance and strengthens the mucosal barrier. Reinforcement of gut barrier function is also relevant for inflammatory bowel disease (IBD). Therefore, we investigated the effect of supplemental calcium on spontaneous colitis development in HLA-B27 transgenic rats, an experimental animal model of IBD. Methods: HLA-B27 transgenic rats were fed a purified high-fat diet containing either a low or high calcium content (30 and 120 mmol CaHPO4/kg diet, respectively) for almost 7 weeks. Inert chromium ethylenediamine-tetraacetic acid (CrEDTA) was added to the diets to quantify intestinal permeability by measuring urinary CrEDTA excretion. Relative fecal dry-weight was determined to quantify diarrhea. Colonic inflammation was determined histologically, and by measuring mucosal interleukin-1β. In addition, colonic mucosal gene expression of individual rats was analyzed, using whole genome microarrays. Interesting results were verified by Q-PCR. Results: The high-calcium diet significantly prevented the increase in intestinal permeability and diarrhea with time in HLA-B27 rats developing colitis as compared to the low-calcium group. The histological colitis score and mucosal interleukin-1β levels were lower in high-calcium fed rats. Supplemental calcium prevented the colitis-induced increase in the expression of extracellular matrix remodeling genes (e.g. matrix metalloproteinases, procollagens and fibronectin), which was confirmed by Q-PCR. Conclusions: Dietary calcium inhibits colitis development in HLA-B27 transgenic rats. Calcium prevents the colitis-related increase in intestinal permeability, diminishes diarrhea, and lowers the inflammatory response in the mucosa, resulting in less extracellular matrix breakdown. Keywords: nutritional intervention
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Project description:Excessive intake of dietary fat is known to be a contributing factor in the development of obesity. In this study, we determined the dose-dependent effects of dietary fat on the development of this metabolic condition with a focus on changes in gene expression in the small intestine. C57BL/6J mice were fed diets with either 10, 20, 30 or 45 energy% (E%) derived from fat for four weeks (n=10 mice/diet). We found a significant higher weight gain in mice fed the 30E% and 45E% fat diet compared to mice on the control diet. These data indicate that the main shift towards an obese phenotype lies between a 20E% and 30E% dietary fat intake. Analysis of differential gene expression in the small intestine showed a fat-dose dependent gradient in differentially expressed genes, with the highest numbers in mice fed the 45E% fat diet. The main shift in fat-induced differential gene expression was found between the 30E% and 45E% fat diet. Furthermore, approximately 70% of the differentially expressed genes were regulated in a fat-dose dependent manner. Many of these genes were involved in lipid metabolism-related processes and were already differentially expressed on a 30E% fat diet. Taken together, we conclude that up to 20E% of dietary fat, the small intestine has an effective ‘buffer capacity’ for fat handling. From 30E% of dietary fat, a switch towards an obese phenotype is triggered. We further speculate that especially fat-dose dependently regulated lipid metabolism-related genes are involved in development of obesity. The proximal, middle, and distal parts of the intestine of mice fed 10, 20, 30, or 45E% dietary fat were analyzed. 10 replicates each.
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Project description:Cysteine is a semi-essential amino acid provided by dietary intake of mainly meat, eggs and whole grains or via the amino acid methionine. The majority of dietary cystine is absorbed in the small intestine and can be used for protein synthesis or converted to taurine and glutathione. Since there is a trend towards adopting a vegetarian/vegan diet, which is low in cysteine, in this study, we investigate the effect of dietary cystine restriction on intestinal epithelial layer function. Mice (8/group) received a normal diet or a diet low in cystine for 2 weeks. We observed no changes in plasma methionine, cysteine, taurine or glutathione levels after 2 weeks. Stem cell markers as well as the proliferation marker Ki67 were or tended to be increased upon cystine restriction. Gene set enrichment analysis reveals enrichment of Wnt signaling in the small intestine of mice on the low cystine diet. These proliferative effects were not observed in the colon, and are thus specific for the small intestine. In the colon, we observed that dietary cystine restriction results in an increase in the number of goblet cells but no significant changes in the thickness of the mucus barrier or in its protective capacity. There was no difference in the microbiome between the normal and low cystine diet. Overall, we cannot conclude if dietary cystine restriction is beneficial, since increased proliferation and goblet cells can indicate a potential for damage repair, nevertheless hyperproliferation has the potential to induce cancer as well.
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