Ontology highlight
ABSTRACT:
PROVIDER: PRJNA663107 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12628800_1.fastq.gz | Fastqsanger.gz | |||
| SRR12628800_2.fastq.gz | Fastqsanger.gz | |||
| SRR12628801_1.fastq.gz | Fastqsanger.gz | |||
| SRR12628801_2.fastq.gz | Fastqsanger.gz | |||
| SRR12628802_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:TCR sequencing analysis of islets from NOD mice on hydrolyzed casein and hydrolyzed casein + 4% gluten diets
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Project description:Comparative evaluation of tolerogenic effect elicited by the protein/peptide fraction of different formulas available for the dietary treatment of CMA. Peptides from digests of extensively hydrolyzed casein formula (EHCF) elicited tolerogenic effects. Peptides from EHCF and relevant digests (in vitro gastroduodenal simulated digestion with "infant" model) were charaterized by HPLC-MS/MS.
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Project description:Protein source in diet greatly influences the incidence of type-1 diabetes (T1D) in non-obese diabetic (NOD) mouse colonies. NOD mice fed a diet containing hydrolyzed casein (HC) as the sole protein source are protected from T1D. Replacing 1/5th of the HC with gluten restores high T1D to NOD mice. We hypothesized that gluten might promote inflammation in the islets. We used TCR sequencing to characterize the clonal frequency of infiltrating T cells from the pancreatic islets of Langerhans of NOD mice fed a 20% HC diet or a 16% HC + 4% gluten diet.
2023-01-04 | GSE218336 | GEO
Project description:The incidence of Type 1 diabetes (T1D), a T-cell mediated autoimmunity that targets the insulin secreting β-cells, has significantly increased, suggesting greater environmental pressure. In studies of T1D families and the BioBreeding rat model, we have identified a peripheral innate inflammatory state that is associated with diabetes susceptibility, consistent with pattern recognition receptor (PRR) ligation, but independent of disease progression. Here, compared to control strains, islets of spontaneously diabetic BB DRlyp/lyp and nondiatetic BB DR+/+ weanlings provided a standard cereal diet were found to temporally express a proinflammatory transcriptional program consistent with microbial antigen exposure that included numerous cytokines/chemokines. Dependence of this proinflammatory phenotype on the diet and gastrointestinal microbiota was investigated by transitioning DR+/+ weanlings to a hydrolyzed casein diet (HCD) or treating them with antibiotics to respectively alter or reduce PRR ligand exposure. Sequencing of the bacterial 16S rRNA gene revealed that these treatments significantly altered the ileal and cecal microbiota, resulting in increases in the Firmicutes:Bacteriodetes ratio, and abundances of lactobacilli and butyrate producing genera. Both treatments partially normalized the peripheral inflammatory state, reducing plasma cytokine, chemokine and TLR-4 activity levels. The proinflammatory islet transcriptome was more extensively normalized by HCD and immune-fluorescent staining revealed reductions in β-cell chemokine expression. HCD and antibiotic treatment did not normalize BB rat PBMC hyper-responsiveness to ex vivo mitogen stimulation. Combined, these studies link islet-level T1D susceptibility in BB rats to a genetically controlled innate inflammatory state that is influenced by environmental determinants encompassing the diet and the intestinal microbiota.
2018-01-23 | GSE80517 | GEO
Project description:The incidence of Type 1 diabetes (T1D), a T-cell mediated autoimmunity that targets the insulin secreting β-cells, has significantly increased, suggesting greater environmental pressure. In studies of T1D families and the BioBreeding rat model, we have identified a peripheral innate inflammatory state that is associated with diabetes susceptibility, consistent with pattern recognition receptor (PRR) ligation, but independent of disease progression. Here, compared to control strains, islets of spontaneously diabetic BB DRlyp/lyp and nondiatetic BB DR+/+ weanlings provided a standard cereal diet were found to temporally express a proinflammatory transcriptional program consistent with microbial antigen exposure that included numerous cytokines/chemokines. Dependence of this proinflammatory phenotype on the diet and gastrointestinal microbiota was investigated by transitioning DR+/+ weanlings to a hydrolyzed casein diet (HCD) or treating them with antibiotics to respectively alter or reduce PRR ligand exposure. Sequencing of the bacterial 16S rRNA gene revealed that these treatments significantly altered the ileal and cecal microbiota, resulting in increases in the Firmicutes:Bacteriodetes ratio, and abundances of lactobacilli and butyrate producing genera. Both treatments partially normalized the peripheral inflammatory state, reducing plasma cytokine, chemokine and TLR-4 activity levels. The proinflammatory islet transcriptome was more extensively normalized by HCD and immune-fluorescent staining revealed reductions in β-cell chemokine expression. HCD and antibiotic treatment did not normalize BB rat PBMC hyper-responsiveness to ex vivo mitogen stimulation. Combined, these studies link islet-level T1D susceptibility in BB rats to a genetically controlled innate inflammatory state that is influenced by environmental determinants encompassing the diet and the intestinal microbiota.
2018-01-23 | GSE80516 | GEO
Project description:The incidence of Type 1 diabetes (T1D), a T-cell mediated autoimmunity that targets the insulin secreting β-cells, has significantly increased, suggesting greater environmental pressure. In studies of T1D families and the BioBreeding rat model, we have identified a peripheral innate inflammatory state that is associated with diabetes susceptibility, consistent with pattern recognition receptor (PRR) ligation, but independent of disease progression. Here, compared to control strains, islets of spontaneously diabetic BB DRlyp/lyp and nondiatetic BB DR+/+ weanlings provided a standard cereal diet were found to temporally express a proinflammatory transcriptional program consistent with microbial antigen exposure that included numerous cytokines/chemokines. Dependence of this proinflammatory phenotype on the diet and gastrointestinal microbiota was investigated by transitioning DR+/+ weanlings to a hydrolyzed casein diet (HCD) or treating them with antibiotics to respectively alter or reduce PRR ligand exposure. Sequencing of the bacterial 16S rRNA gene revealed that these treatments significantly altered the ileal and cecal microbiota, resulting in increases in the Firmicutes:Bacteriodetes ratio, and abundances of lactobacilli and butyrate producing genera. Both treatments partially normalized the peripheral inflammatory state, reducing plasma cytokine, chemokine and TLR-4 activity levels. The proinflammatory islet transcriptome was more extensively normalized by HCD and immune-fluorescent staining revealed reductions in β-cell chemokine expression. HCD and antibiotic treatment did not normalize BB rat PBMC hyper-responsiveness to ex vivo mitogen stimulation. Combined, these studies link islet-level T1D susceptibility in BB rats to a genetically controlled innate inflammatory state that is influenced by environmental determinants encompassing the diet and the intestinal microbiota.
2018-01-23 | GSE80515 | GEO
Project description:Protein source in diet greatly influences the incidence of type-1 diabetes (T1D) in non-obese diabetic (NOD) mouse colonies. NOD mice fed a diet containing hydrolyzed casein (HC) as the sole protein source are protected from T1D. Replacing 1/5th of the HC with gluten restores high T1D to NOD mice. We hypothesized that gluten might promote inflammation in the islets. We used single cell RNA sequencing (scRNAseq) to characterize and contrast the transcriptional profiles of endocrine cells and islet infiltrating leukocytes from the pancreatic islets of Langerhans of NOD mice fed a 20% HC diet or a 16% HC + 4% gluten diet.
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Project description:We used microarray to determine the differences in hepatic gene expression for diet-induced obese Sprague-Dawley rats consuming different dietary proteins. Proteins of interest included skim milk powder (dairy), casein, and the branched-chain amino acid, leucine. The primary aims of this study were: (i) to compare the effects of diets with protein derived from casein, casein supplemented with leucine, and complete dairy on body composition and insulin sensitivity; and (ii) to determine if there is a synergistic effect of dietary Ca and protein source on body composition and insulin sensitivity. Secondarily, we used microarray analysis to examine the effect of casein, leucine, or complete dairy containing diets on the expression of hepatic genes related to lipid and glucose metabolism. Diet induced obese rats consumed ad libitum, a high fat, high sucrose diet for 8 weeks (n=4). All diets had an energy density of 4.6 kcal/gram and provided 10% of total energy from protein [casein, complete dairy (skim milk powder), or leucine-supplemented casein (7.1% from casein plus 2.9% from leucine)]. The casein treatment was the control diet.
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Project description:We used microarray to determine the differences in hepatic gene expression for diet-induced obese Sprague-Dawley rats consuming different dietary proteins. Proteins of interest included skim milk powder (dairy), casein, and the branched-chain amino acid, leucine. The primary aims of this study were: (i) to compare the effects of diets with protein derived from casein, casein supplemented with leucine, and complete dairy on body composition and insulin sensitivity; and (ii) to determine if there is a synergistic effect of dietary Ca and protein source on body composition and insulin sensitivity. Secondarily, we used microarray analysis to examine the effect of casein, leucine, or complete dairy containing diets on the expression of gastrocnemius muscle genes related to lipid and glucose metabolism. Diet induced obese rats consumed ad libitum, a high fat, high sucrose diet for 8 weeks (n=4). All diets had an energy density of 4.6 kcal/gram and provided 10% of total energy from protein [casein, complete dairy (skim milk powder), or leucine-supplemented casein (7.1% from casein plus 2.9% from leucine)]. The casein treatment was the control diet.
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Project description:Protein source in diet greatly influences the incidence of type-1 diabetes (T1D) in non-obese diabetic (NOD) mouse colonies. NOD mice fed a diet containing hydrolyzed casein (HC) as the sole protein source are protected from T1D. Exposure to HC also reduced beta-cell insulin secretion during glucose challenge suggesting that beneficial changes to beta-cell physiology might protect NOD mice from T1D. We used single cell RNA sequencing (scRNAseq) to contrast the transcriptional profiles of beta-cells and from the pancreatic islets of Langerhans of NOD mice with the scid mutation (scid mice were used to avoid confouding influence of infiltrating leukocytes) fed a 20% HC diet or a standard chow diet.
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