Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1036011 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26871857_1.fastq.gz | Fastqsanger.gz | |||
| SRR26871857_2.fastq.gz | Fastqsanger.gz | |||
| SRR26871858_1.fastq.gz | Fastqsanger.gz | |||
| SRR26871858_2.fastq.gz | Fastqsanger.gz | |||
| SRR26871859_1.fastq.gz | Fastqsanger.gz |
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Project description:Gut microbita of CAG rats with colonic mucosal lesions
| PRJNA1036012 | ENA
Project description:To investigate the roles of deoxycholic acid in the regulation of cell function and gene expression of colonic tissue, we treated colitis mice with deoxycholic acid. Then, we performed gene expression profiling analysis using data obtained from RNA-seq of colonic tissue of colitis mice treated with or without deoxycholic acid.
2023-11-13 | GSE247321 | GEO
Project description:Leber2015 - Mucosal immunity and gut
microbiome interaction during C. difficile infection
This model is described in the article:
Systems Modeling of
Interactions between Mucosal Immunity and the Gut Microbiome
during Clostridium difficile Infection.
Leber A, Viladomiu M, Hontecillas R,
Abedi V, Philipson C, Hoops S, Howard B, Bassaganya-Riera
J.
PLoS ONE 2015; 10(7): e0134849
Abstract:
Clostridium difficile infections are associated with the use
of broad-spectrum antibiotics and result in an exuberant
inflammatory response, leading to nosocomial diarrhea, colitis
and even death. To better understand the dynamics of mucosal
immunity during C. difficile infection from initiation through
expansion to resolution, we built a computational model of the
mucosal immune response to the bacterium. The model was
calibrated using data from a mouse model of C. difficile
infection. The model demonstrates a crucial role of T helper 17
(Th17) effector responses in the colonic lamina propria and
luminal commensal bacteria populations in the clearance of C.
difficile and colonic pathology, whereas regulatory T (Treg)
cells responses are associated with the recovery phase. In
addition, the production of anti-microbial peptides by inflamed
epithelial cells and activated neutrophils in response to C.
difficile infection inhibit the re-growth of beneficial
commensal bacterial species. Computational simulations suggest
that the removal of neutrophil and epithelial cell derived
anti-microbial inhibitions, separately and together, on
commensal bacterial regrowth promote recovery and minimize
colonic inflammatory pathology. Simulation results predict a
decrease in colonic inflammatory markers, such as neutrophilic
influx and Th17 cells in the colonic lamina propria, and length
of infection with accelerated commensal bacteria re-growth
through altered anti-microbial inhibition. Computational
modeling provides novel insights on the therapeutic value of
repopulating the colonic microbiome and inducing regulatory
mucosal immune responses during C. difficile infection. Thus,
modeling mucosal immunity-gut microbiota interactions has the
potential to guide the development of targeted fecal
transplantation therapies in the context of precision medicine
interventions.
This model is hosted on
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2024-09-02 | BIOMD0000000583 | BioModels
Project description:Salmonella enteritidis is suggested to translocate in the small intestine. Previously we identified that prebiotics, fermented in the colon, increased Salmonella translocation in rats, suggesting involvement of the colon in translocation. Effects of Salmonella on colonic gene expression in vivo are largely unknown. The aim of this study was to characterize time dependent Salmonella induced changes of colonic mucosal gene expression in rats using whole genome microarrays. Rats were orally infected with Salmonella enteritidis to mimic a foodbore infection and colonic gene expression was determined at day 1, 3 and 6 post-infection (n=8 per timepoint). Agilent rat whole genome microarray (G4131A Agilent Technologies) were used. Results indicate that colon is clearly a target tissue for Salmonella considering the abundant changes in mucosal gene expression observed. 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. Wistar rats were infected with Salmonella enteritidis. Non-infected control rats were sham-treated. Rats were sacrificed on day 1, 3 or 6 post infection or sham-treatment (n=8 rats per treatment and per time point). RNA was isolated from colonic mucosal scrapings. mRNA samples of 8 rats per group were pooled. Each pooled group-sample was hybridised in duplicate on Agilent rat whole genome microarrays containing 44290 60-mer spots. From the 12 arrays one duplicate array (Colon mucosa non-infected day6) did not pass quality control and was left out from further analysis.
2008-06-15 | E-GEOD-7496 | biostudies-arrayexpress
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.
2008-06-15 | E-GEOD-7472 | biostudies-arrayexpress
Project description:Effect of folic acid supplementation on DNA methylation in human colonic mucosal samples.
2009-09-16 | E-MEXP-1323 | biostudies-arrayexpress
Project description:Salmonella enteritidis is suggested to translocate in the small intestine. Previously we identified that prebiotics, fermented in the colon, increased Salmonella translocation in rats, suggesting involvement of the colon in translocation. Effects of Salmonella on colonic gene expression in vivo are largely unknown. The aim of this study was to characterize time dependent Salmonella induced changes of colonic mucosal gene expression in rats using whole genome microarrays. Rats were orally infected with Salmonella enteritidis to mimic a foodbore infection and colonic gene expression was determined at day 1, 3 and 6 post-infection (n=8 per timepoint). Agilent rat whole genome microarray (G4131A Agilent Technologies) were used. Results indicate that colon is clearly a target tissue for Salmonella considering the abundant changes in mucosal gene expression observed. Keywords: Time point infection study, colon mucosa, Rat
2007-10-18 | GSE7496 | GEO
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
2009-07-17 | GSE11022 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE13376: Exposure of Barrett's associated adenocarcinoma cell lines SKGT4 to deoxycholic acid (DCA) GSE13378: Exposure of squamous esophageal cell line HET-1A to deoxycholic acid (DCA) Refer to individual Series
2010-03-02 | E-GEOD-13400 | biostudies-arrayexpress
Project description:Colorectal cancer (CRC) is the third most common cancer in men and the second in women worldwide, with most of the case occurrences in developed regions. CRC can be induced by luminal factors, like dietary components and bile acids. Bile acids are metabolized from cholesterol in the liver, stored in the gallbladder and released into the small intestine upon meal ingestion to facilitate the absorption of dietary lipids and lipid-soluble vitamins. Bile acids are effectively reabsorbed at the distal ileum and returned to the liver, and only a small portion (~2-5%) enters the colon. Here primary bile acids, like cholic acid (CA) and chenodeoxycholic acid (CDCA) are deconjugated by bacteria and secondary bile acids are formed, such as deoxycholic acid (DCA), ursodeoxycholic acid (UDCA) and lithocholic acid. DCA is the major component of the colonic bile acid pool and is found to be increased upon a high fat diet. Moreover, high levels of DCA are known to increase the risk of colorectal cancer by inducing cytotoxicity to epithelial cells. In this study the cytotoxicity of Caco-2 cells to stimulation with cholic acid is investigated.
2021-10-01 | GSE120699 | GEO