Transfer of dysbiotic gut microbiota
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ABSTRACT:
PROVIDER: PRJEB19465 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gut microbiota dysbiosis characterizes systemic metabolic alteration, yet its causality is debated. To address this issue, we transplanted antibiotic-free conventional wild-type mice with either dysbiotic (“obese”) or eubiotic (“lean”) gut microbiota and fed them either a NC or a 72%HFD. We report that, on NC, obese gut microbiota transplantation reduces hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non-transplanted mice. Of note, this phenotype is blunted in conventional NOD2KO mice. By contrast, lean microbiota transplantation did not affect hepatic gluconeogenesis. In addition, obese microbiota transplantation changed both gut microbiota and microbiome of recipient mice. Interestingly, hepatic gluconeogenesis, PEPCK and G6Pase activity were reduced even once mice transplanted with the obese gut microbiota were fed a 72%HFD, together with reduced fed glycaemia and adiposity compared to non-transplanted mice. Notably, changes in gut microbiota and microbiome induced by the transplantation were still detectable on 72%HFD. Finally, we report that obese gut microbiota transplantation may impact on hepatic metabolism and even prevent HFD-increased hepatic gluconeogenesis. Our findings may provide a new vision of gut microbiota dysbiosis, useful for a better understanding of the aetiology of metabolic diseases. all livers are from NC-fed mice only.
2017-03-16 | GSE81318 | GEO
Project description:Antibiotics have long-lasting consequences on the gut microbiota with the potential to impact host physiology and health. However, little is known about the transgenerational impact of an antibiotic-perturbed microbiota. Here we demonstrated that adult pregnant female mice inoculated with a gut microbial community shaped by antibiotic exposure passed on their dysbiotic microbiota to their offspring. This dysbiotic microbiota remained distinct from controls for at least 5 months in the offspring without any continued exposure to antibiotics. By using IL-10 deficient mice, which are genetically susceptible to colitis, we showed mice that received an antibiotic-perturbed gut microbiota from their mothers had increased risk of colitis. Taken together, our findings indicate that the consequences of antibiotic exposure affecting the gut microbiota can extend to a second generation.
2017-12-01 | GSE92623 | 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:The higher susceptibility of the germ-free (GF) mice to bacterial infection has been proposed to be due to a lack of host immune defense. We hypothesized that this lower efficiency to mount a proficient defense might correlate with an aberrant miRNA expression, leading to the host failure to adapt its gene transcriptomic response to infection. To explore this hypothesis, we undertook a thorough transcriptional analysis of the host intestine in uninfected conventional (CV0) and germ-free (GF0) mice, by monitoring both the miRNA and mRNA expression levels. Crossing of the intestinal epithelial barrier is the first step of L. monocytogenes oral infection. Total eukaryotic RNAs were extracted from the ileum of uninfected conventional (CV0) and germ-free (GF0) mice and from L. monocytogenes infected conventional and germ-free mice 24h p.i (CV24 and GF24, respectively) and 72h p.i (CV72 and GF72, respectively). From these samples, transcriptome profiles were generated using Illumina sequencing for miRNA expression or microarrays for mRNA expression.
2013-10-15 | E-MTAB-1800 | biostudies-arrayexpress
Project description:The higher susceptibility of the germ-free (GF) mice to bacterial infection has been proposed to be due to a lack of host immune defense. We hypothesized that this lower efficiency to mount a proficient defense might correlate with an aberrant miRNA expression, leading to the host failure to adapt its gene transcriptomic response to infection. To explore this hypothesis, we undertook a thorough transcriptional analysis of the host intestine in uninfected conventional (CV0) and germ-free (GF0) mice, by monitoring both the miRNA and mRNA expression levels. Crossing of the intestinal epithelial barrier is the first step of L. monocytogenes oral infection. Total eukaryotic RNAs were extracted from the ileum of uninfected conventional (CV0) and germ-free (GF0) mice and from L. monocytogenes infected conventional and germ-free mice 24h p.i (CV24 and GF24, respectively) and 72h p.i (CV72 and GF72, respectively). From these samples, transcriptome profiles were generated using Illumina sequencing for miRNA expression or microarrays for mRNA expression. Results from this experiment are from the sequencing assays. The microarray data set has also been deposited at ArrayExpress under accession number E-MTAB-1800 (https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1800/).
2013-10-15 | E-MTAB-1877 | 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. 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 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:Germ-free mice are an indispensable tool in studying the gut microbiome and its effects on host physiology, though they are phenotypically different than their conventional counterparts. While antibiotic mediated microbiota depletion in conventional mice mimics the germ-free state, the scope of these reversible changes is unknown. We demonstrate robust hepatic transcriptomic alterations after antibiotic-mediated microbiota depletion together with depletion of luminal and portal vein levels of SCFAs though hepatic histone acetylation states remained largely unchanged.
2023-01-25 | GSE144266 | 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:To more directly understand the mechanisms by which CMT reduced 1PAT-induced T1D development, we examined P23 ileal gene expression profile of Non-obese diabetic mice by RNAseq. There 3 treatments C, 1P and CMT, and each treatment has 4 mice.
2021-09-02 | E-MTAB-9981 | biostudies-arrayexpress