Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23917400_1.fastq.gz | Fastqsanger.gz | |||
| SRR23917400_2.fastq.gz | Fastqsanger.gz | |||
| SRR23917401_1.fastq.gz | Fastqsanger.gz | |||
| SRR23917401_2.fastq.gz | Fastqsanger.gz | |||
| SRR23917402_1.fastq.gz | Fastqsanger.gz |
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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:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
2025-07-01 | GSE300683 | GEO
Project description:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
2025-07-01 | GSE300684 | GEO
Project description:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
2025-07-01 | GSE300682 | GEO
Project description:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
2025-07-01 | GSE300679 | 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:Analysis of breast cancer survivors' gut microbiota after lifestyle intervention, during the COVID-19 lockdown, by 16S sequencing of fecal samples.
2023-01-13 | E-MTAB-12486 | biostudies-arrayexpress
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: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