Ontology highlight
ABSTRACT:
PROVIDER: PRJNA844581 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19521200_1.fastq.gz | Fastqsanger.gz | |||
| SRR19521200_2.fastq.gz | Fastqsanger.gz | |||
| SRR19521201_1.fastq.gz | Fastqsanger.gz | |||
| SRR19521201_2.fastq.gz | Fastqsanger.gz | |||
| SRR19521202_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 54 |
Similar Datasets
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:The aim of this project was to explore the role of gut microbiota in the development of small intestine. The gut microbiota from different groups was used to treat the mice for 1 or 2 weeks. Then the small intestine samples were collected. The RNA was used for the RNA-seq analysis to search the role of gut microbiota in the development of small intestine. Groups: IMA100 mean gut microbiota from Alginate oligosaccharide 100mg/kg treated mice; IMA10 mean gut microbiota from Alginate oligosaccharide 10mg/kg treated mice; IMC mean gut microbiota from control group mice (dosed with water); Sa mean dosed with saline (no gut microbiota). "1" mean dosed for 1 week, "2" means dosed for 2 weeks.
2020-07-29 | GSE137999 | GEO
Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress
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:Gut microbiota comparation of Young mice (n=10), Old mice, Young_yFMT (Young mice 14 days after transplant feces from young mice, n=10) and Young_oFMT (Young mice 14 days after transplant feces from old mice, n=10), Antibiotic group (Cefazolin, n=8).
2023-08-28 | E-MTAB-13206 | biostudies-arrayexpress
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:Intracerebral hemorrhage (ICH) induces alterations in the gut microbiota composition, significantly impacting neuroinflammation post-ICH. However, the impact of gut microbiota absence on neuroinflammation following ICH-induced brain injury remain unexplored. Here, we observed that the gut microbiota absence was associated with reduced neuroinflammation, alleviated neurological dysfunction, and mitigated gut barrier dysfunction post-ICH. In contrast, recolonization of microbiota from ICH-induced SPF mice by transplantation of fecal microbiota (FMT) exacerbated brain injury and gut impairment post-ICH. Additionally, microglia with transcriptional changes mediated the protective effects of gut microbiota absence on brain injury, with Apoe emerging as a hub gene. Subsequently, Apoe deficiency in peri-hematomal microglia was associated with improved brain injury. Finally, we revealed that gut microbiota influence brain injury and gut impairment via gut-derived short-chain fatty acids (SCFA).
2024-05-13 | GSE266602 | GEO
Project description:Chronic diseases arise when pathophysiological processes achieve a steady state by self-reinforcing. Here, we explored the possibility of a self-reinforcement state in a common condition, chronic constipation, where alterations of the gut microbiota have been reported. The functional impact of the microbiota shifts on host physiology remains unclear, however we hypothesized that microbial communities adapted to slow gastrointestinal transit affect host functions in a way that reinforces altered transit, thereby maintaining the advantage for microbial self-selection. To test this, we examined the impact of pharmacologically (loperamide)-induced constipation (PIC) on the structural and functional profile of altered gut microbiota. PIC promoted changes in the gut microbiome, characterized by decreased representation of butyrate-producing Clostridiales, decreased cecal butyrate concentration and altered metabolic profiles of gut microbiota. PIC-associated gut microbiota also impacted colonic gene expression, suggesting this might be a basis for decreased gastrointestinal (GI) motor function. Introduction of PIC-associated cecal microbiota into germ-free (GF) mice significantly decreased GI transit time. Our findings therefore support the concept that chronic diseases like constipation are caused by disease-associated steady states, in this case, caused by reciprocating reinforcement of pathophysiological factors in host-microbe interactions. We used microarrays to detail the global gene expression profile in the proximal colon smooth muscle tissues of germ-free, conventionalized, or specific pathogen free mouse C57Bl/6 female and male specific pathogen free (SPF) mice were bred and housed in the animal care facility at the University of Chicago. Mice of 8–10 weeks of age were treated with 0.1% loperamide in the drinking water for 7 days. Age matched, germ-free (GF) C57Bl/6 mice were gavaged orally with cecal luminal contents harvested from control or loperamide-treated C57Bl/6 donor mice. Recipient mice were sacrificed 4 weeks post-colonization.
2014-07-12 | E-GEOD-59320 | biostudies-arrayexpress