Gene expression analysis in GATA4fl/flVillin cre+/cre- jejunum
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE118421 | GEO | 2024/08/09
REPOSITORIES: GEO
Similar Datasets
Project description:We compared gene expression in the small intestine (ileum) of mice that were either (i) germ-free, (ii) colonized with a conventional mouse cecal microbiota, (iii) colonized with a conventional zebrafish gut microbiota, or (iv) colonized with Pseudomonas aeruginosa PAO1. Experiment Overall Design: Adult germ-free NMRI mice were colonized with either (i) a conventional mouse cecal microbiota harvested from adult Swiss-Webster mice (5 biological replicates), (ii) a conventional zebrafish intestinal microbiota harvested from adult C32 zebrafish (3 biological replicates), or (iii) a culture of Pseudomonas aeruginosa PAO1 (5 biological replicates). 14 days after colonization, total RNA was prepared from the ileum of each animal, with total RNA prepared from adult germ-free NMRI mouse ileum serving as negative controls (5 biological replicates). RNA was used as template to generate cRNA for hybridization to Affymetrix 430 v2 Mouse GeneChips.
2008-06-13 | E-GEOD-5198 | biostudies-arrayexpress
Project description:We compared gene expression in the small intestine (ileum) of mice that were either (i) germ-free, (ii) colonized with a conventional mouse cecal microbiota, (iii) colonized with a conventional zebrafish gut microbiota, or (iv) colonized with Pseudomonas aeruginosa PAO1. Keywords: response to microbial colonization
2006-07-07 | GSE5198 | GEO
Project description:We compare H3K9Ac enrichment in intestinal epithelial cells from intestine of germ-free and microbiota-replete (conventionally-housed) mice. Intestinal epithelial cells were harvested from the intestine of conventional or germ-free C57Bl6J mice. Chromatin immunoprecipitation was performed with anti-H3K9Ac. Sequencing was performed using the Illumina HiSeq2500. Reads were mapped to the mm10 genome using Bowtie. Microbiota induce loss of H3K9Ac within mulitple sites of the Clec2e gene.
2019-05-26 | GSE128369 | GEO
Project description:We compare transcriptomic profiles of intestinal epithelial cells obtained from the small intestine of germ-free and conventionally-caged mice. Intestinal epithelial cells were harvested from the intestine of conventional or germ-free C57Bl6J mice. Directional polyA RNA-seq was performed on RNA fom cells using standard Illumina protocols. Microbiota induce decreased expression of the Clec2e gene.
2019-05-26 | GSE128362 | GEO
Project description:Gene expression analysis in GATA4fl/flVillin cre+/cre- jejunum
| PRJNA485511 | ENA
Project description:Using a systems biology approach, we discovered and dissected a three-way interaction between the immune system, the intestinal epithelium, and the microbiota. We found that mice lacking B lymphocytes, or lacking IgA, have low intestinal expression of lipid metabolism genes regulated by the transcription factor GATA4, and a consequent decrease in fat absorption in the intestine. The defect disappeared in germ free mice, suggesting that it is dependent on the microbiota; and sequencing analysis of the bacteria showed subtle differences between normal and B-cell deficient mice. Analysis of gene expression of gut biopsies from patients with common variable immunodeficiency and intestinal dysfunction revealed a high similarity to mouse B-cell knockout profiles. These data provide an explanation for a longstanding enigmatic association between immunodeficiency and defective lipid absorption in humans. This series represents the subsection of the study where we address the role of transcription factor Gata4. The data are from conditional KO (Gata4KOvil) and corresponding control mice. Intensity of each channel was extracted from two-color arrays. We used direct dye swap design and performed paired analysis between small intestine of KO and control mice. Corresponding paires of KO and control were hybridized on the same array, except pair X
2011-11-23 | E-GEOD-33885 | biostudies-arrayexpress
Project description:We processed RNA-sequencing on splenic CD11b+ macrophages isolated from 10-week old Mettl3f/f-LysM-Cre KO and littermate WT mice. NO_4-1, NO_4-2 are Mettl3f/f-LysM-Cre KO. NO_5-2, NO_5-3 are WT littermate controls.
2022-01-07 | GSE184318 | GEO
Project description:Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study gut microbiota from young or old conventional mice was transferred to young germ-free mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized germ-free mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here we show by transferring aged microbiota to young germ-free mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the germ-free mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young germ-free mice.
2018-02-14 | GSE104063 | GEO
Project description:Using a systems biology approach, we discovered and dissected a three-way interaction between the immune system, the intestinal epithelium, and the microbiota. We found that mice lacking B lymphocytes, or lacking IgA, have low intestinal expression of lipid metabolism genes regulated by the transcription factor GATA4, and a consequent decrease in fat absorption in the intestine. The defect disappeared in germ free mice, suggesting that it is dependent on the microbiota; and sequencing analysis of the bacteria showed subtle differences between normal and B-cell deficient mice. Analysis of gene expression of gut biopsies from patients with common variable immunodeficiency and intestinal dysfunction revealed a high similarity to mouse B-cell knockout profiles. These data provide an explanation for a longstanding enigmatic association between immunodeficiency and defective lipid absorption in humans. This series represents first part of the study including: 1) B-cell KO mice of different strains and their controls 2) germ free B-cell Ko mice and their controls 3) B lymphocytes Intensity of each channel was extracted from two-color arrays. We used direct dye swap design and performed paired analysis between small intestine of KO and control mice. Corresponding pairs of KO and control were hybridized on the same array and can be matched by the array name. For comparison between B lymphocytes and intestinal tissue we used B-cell KO intestinal samples and B lymphocytes samples balancing the number of Cy5/3 labeled samples in the groups.
2011-11-15 | E-GEOD-23573 | biostudies-arrayexpress
Project description:Using a systems biology approach, we discovered and dissected a three-way interaction between the immune system, the intestinal epithelium, and the microbiota. We found that mice lacking B lymphocytes, or lacking IgA, have low intestinal expression of lipid metabolism genes regulated by the transcription factor GATA4, and a consequent decrease in fat absorption in the intestine. The defect disappeared in germ free mice, suggesting that it is dependent on the microbiota; and sequencing analysis of the bacteria showed subtle differences between normal and B-cell deficient mice. Analysis of gene expression of gut biopsies from patients with common variable immunodeficiency and intestinal dysfunction revealed a high similarity to mouse B-cell knockout profiles. These data provide an explanation for a longstanding enigmatic association between immunodeficiency and defective lipid absorption in humans. This series represents the subsection of the study where we address the role of transcription factor Gata4. The data are from conditional KO (Gata4KOvil) and corresponding control mice.
2011-11-23 | GSE33885 | GEO