Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1059631 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27393166_1.fastq.gz | Fastqsanger.gz | |||
| SRR27393166_2.fastq.gz | Fastqsanger.gz | |||
| SRR27393167_1.fastq.gz | Fastqsanger.gz | |||
| SRR27393167_2.fastq.gz | Fastqsanger.gz | |||
| SRR27393168_1.fastq.gz | Fastqsanger.gz |
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Project description:Recent studies in both mice and human have suggested that the gut microbiota could modulate tumor response to chemotherapeutic agents or immunotherapies. However, the underlying mechanism has not been well characterized. Here, we found that disruption of the intestinal microbiota with antibiotics impaired the anti-cancer efficacy of oxaliplatin, which was correlated with the reduction of lots of the intestinal microbial metabolites including butyrate, one of the short chain fatty acids. Re-supplementation of either the whole intestinal microbial metabolites or butyrate could rescue the therapeutic responses of oxaliplatin in the microbiota-destroyed tumor-bearing mice by modulating CD8+ T cell function in the tumor microenvironment. Further experiments showed butyrate boosted the anti-tumor cytotoxic CD8+ T cell responses through ID2, a key transcription regulator highly expressed by tumor-infiltrating CD8+ T cells. Butyrate induced ID2 expression in CD8+ T cells, while ID2 further promoted the proliferation and function of CD8+ T cells through IL-12 signaling. Together, our findings suggest that gut microbial metabolite butyrate could promote the anti-tumor therapeutic efficacy through the ID2-dependent regulation of CD8+ T cell immunity.
2021-03-24 | GSE115426 | GEO
Project description:Recent studies in both mice and human have suggested that the gut microbiota could modulate tumor response to chemotherapeutic agents or immunotherapies. However, the underlying mechanism has not been well characterized. Here, we found that disruption of the intestinal microbiota with antibiotics impaired the anti-cancer efficacy of oxaliplatin, which was correlated with the reduction of lots of the intestinal microbial metabolites including butyrate, one of the short chain fatty acids. Re-supplementation of either the whole intestinal microbial metabolites or butyrate could rescue the therapeutic responses of oxaliplatin in the microbiota-destroyed tumor-bearing mice by modulating CD8+ T cell function in the tumor microenvironment. Further experiments showed butyrate boosted the anti-tumor cytotoxic CD8+ T cell responses through ID2, a key transcription regulator highly expressed by tumor-infiltrating CD8+ T cells. Butyrate induced ID2 expression in CD8+ T cells, while ID2 further promoted the proliferation and function of CD8+ T cells through IL-12 signaling. Together, our findings suggest that gut microbial metabolite butyrate could promote the anti-tumor therapeutic efficacy through the ID2-dependent regulation of CD8+ T cell immunity.
2021-03-24 | GSE115283 | GEO
Project description:Alterations in intestinal microbiota and intestinal short chain fatty acids profiles have been associated with the pathophysiology of obesity and insulin resistance. Whether intestinal microbiota dysbiosis is a causative factor in humans remains to be clarified We examined the effect of fecal microbial infusion from lean donors on the intestinal microbiota composition, glucose metabolism and small intestinal gene expression. Male subjects with metabolic syndrome underwent bowel lavage and were randomised to allogenic (from male lean donors with BMI<23 kg/m2, n=9) or autologous (reinfusion of own feces, n=9) fecal microbial transplant. Insulin sensitivity and fecal short chain fatty acid harvest were measured at baseline and 6 weeks after infusion. Intestinal microbiota composition was determined in fecal samples and jejunal mucosal biopsies were also analyzed for the host transcriptional response. Insulin sensitivity significantly improved six weeks after allogenic fecal microbial infusion (median Rd: from 26.2 to 45.3 μmol/kg.min, p<0.05). Allogenic fecal microbial infusion increased the overall amount of intestinal butyrate producing microbiota and enhanced fecal harvest of butyrate. Moreover, the transcriptome analysis of jejunal mucosal samples revealed an increased expression of genes involved in a G-protein receptor signalling cascade and subsequently in glucose homeostasis. Lean donor microbial infusion improves insulin sensitivity and levels of butyrate-producing and other intestinal microbiota in subjects with the metabolic syndrome. We propose a model wherein these bacteria provide an attractive therapeutic target for insulin resistance in humans. (Netherlands Trial Register NTR1776).
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Project description:Intestinal epithelial cells and the intestinal microbiota are in a mutualistic relationship that is dependent on communication. This communication is multifaceted, but one aspect is communication through compounds produced by the microbiota such as the short-chain fatty acids (SCFAs) butyrate, propionate and acetate. Studying the effects of SCFAs and especially butyrate in intestinal epithelial cell lines like Caco-2 cells has been proven problematic. In contrast to the in vivo intestinal epithelium, Caco-2 cells do not use butyrate as an energy source, leading to a build-up of butyrate. Therefore, we used human induced pluripotent stem cell derived intestinal epithelial cells, grown as a cell layer, to study the effects of butyrate, propionate and acetate on whole genome gene expression in the cells. For this, cells were exposed to concentrations of 1 and 10 mM of the individual short-chain fatty acids for 24 hours. Unique gene expression profiles were observed for each of the SCFAs in a concentration-dependent manner. Evaluation on both an individual gene level and pathway level showed that butyrate induced the biggest effects followed by propionate and then acetate. Several known effects of SCFAs on intestinal cells were confirmed, such as effects on metabolism and immune responses. The changes in metabolic pathways in the intestinal epithelial cell layers in this study demonstrate that there is a switch in energy source from glucose to SCFAs, thus induced pluripotent stem cell derived intestinal epithelial cell are responding in a similar manner to SCFAs as in vivo intestinal tissues.
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Project description:Intestinal macrophages were isolated from the intestine of mice that had been administered antibiotics for 7 days, prior to 7 days or re-exposure to the microbiota (recolonisation). In some experiments, the short-chain fatty acid butyrate was administered alongside antibiotics prior to recolonisation.
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Project description:The consumption of fermented food has been linked to positive health outcomes due to a variety of functional properties. Fermented dairy constitutes a major dietary source and contains lactoseas main carbohydrate and living starter cultures. To investigate whether nutritional and microbial modulation impacted intestinal microbiota composition and activity, we employed fecal microbiota fermentations and a dairy model system consisting of lactose and β-galactosidase positive and negative Streptococcus thermophilus. Based on 16S rRNA gene based microbial community analysis, we observed that lactose addition increased the abundance of Bifidobacteriaceae, and of Veillonellaceae and Enterobacteraceae in selected samples. The supplied lactose was hydrolysed within 24 h of fermentation and led to higher expression of community indigenous β-galactosidases. Targeted protein analysis confirmed that bifidobacteria contributed most β-galactosidases together with other taxa including Escherichia coli and Anaerobutyricum hallii. Lactose addition led to 1.1-1.8 fold higher levels of butyrate compared to controls likely due to (i) lactate-crossfeeding and (ii) direct lactose metabolism by butyrate producing Anaerobutyricum and Faecalibacterium spp. Representatives of both genera used lactose to produce butyrate in single cultures. When supplemented at around 5.5 log cells mL-1, S. thermophilus or its beta-galactosidase negative mutant outnumbered the indigenous Streptococcaceae population at the beginning of fermentation but had no impact on lactose utilisation and final SCFA profiles. This study brings forward new fundamental insight into interactions of major constituents of fermented dairy with the intestinal microbiota. We provide evidence that lactose addition increases fecal microbiota production of butyrate through cross-feeding and direct metabolism without contribution of starter cultures.
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Project description:Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences [30_week_Liver]
2014-09-08 | E-GEOD-58086 | ExpressionAtlas
Project description:Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences [8_week_ileal]
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Project description:Dry eye is a common ocular inflammatory disorder characterized by tear film instability and reduced tear production. There is increasing evidence that homeostasis of the ocular surface is impacted by the intestinal microbiome. We are interested in investigating the potential role of microbially produced small molecules in mediating the interaction between the intestinal microbiota and the ocular surface. One such molecule is butyrate, a short-chain fatty acid (SCFA) produced by certain members of the gut microbiota through fermentation of dietary fiber. We have shown that oral administration of tributyrin, a prodrug form of butyrate, is protective of the ocular surface in mice undergoing desiccating stress. To gain insight into the mechanism, we analyzed gene expression in conjunctival tissue from mice treated with either tributyrgn or vehicle control.
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Project description:Gene expression accompanying the promotion of hepatocellular carcinoma by intestinal microbiota and Tlr4 in mice.
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