Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Bvul restores Am-depleted dysbiosis: mouse feces

PROVIDER: PRJEB42595 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR5166540.fastq.gz	Fastqsanger.gz
	ERR5166540_1.fastq.gz	Fastqsanger.gz
	ERR5166540_2.fastq.gz	Fastqsanger.gz
	ERR5166550.fastq.gz	Fastqsanger.gz
	ERR5166550_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 671

Similar Datasets

Project description:Bvul restores Am-depleted dysbiosis: mouse cecum

| PRJEB42594 | ENA

Project description:Bvul restores Am-depleted dysbiosis: mouse shotgun

| PRJEB42634 | ENA

Project description:EMG produced TPA metagenomics assembly of PRJEB42634 data set (Bvul restores Am-depleted dysbiosis: mouse shotgun).

| PRJEB58310 | ENA

Gut microbiota analysis in WT and Il17d-deficient mice treated with or without colitis

Project description:Microbiota dysbiosis has been reported to contribute to the pathogenesis of colitis, to demonstrate whether IL-17D protects against DSS-induced colitis through regulation of microflora, we performed 16S rRNA sequencing in feces from WT and Il17d-deficient mice. Our data indicate that Il17d deficiency results in microbiota dysibiosis in both steady state and DSS-induced colitis.

2021-05-20 | GSE165789 | GEO

Intestinal tumor expression data from Apcmin/+ mice gavaged by feces from healthy controls or colorectal cancer patients

Project description:Colorectal cancer (CRC) is closely related to gut dysbiosis. We investigated the effects of imbalanced gut microbiota on the progression of intestinal adenoma in Apcmin/+ mice model using fecal microbiota transplantation (FMT). Administration of feces from CRC patients increased tumor proliferation and decreased apoptosis in tumor cells. Abnormal expression of genes related to Wnt-protein binding and lipid metabolic process was observed.

2019-09-16 | GSE136682 | GEO

Extracellular miRNAs in serum and feces of mice exposed to high-dose radiation

Project description:Exposure to high-dose radiation causes life-threatening serious intestinal damage. Histological analysis is the most accurate method for judging the extent of intestinal damage after death. However, it is difficult to predict the extent of intestinal damage to body samples. Here we focused on extracellular microRNAs (miRNAs) released from cells and investigated miRNA species that increased or decreased in serum and feces using a radiation-induced intestinal injury mouse model. A peak of small RNA of 25–200 nucleotides was detected in mouse serum and feces 72 h after radiation exposure, and miRNA presence in serum and feces was inferred. MiRNAs expressed in the small intestine and were increased by more than 2.0-fold in serum or feces following a 10 Gy radiation exposure were detected by microarray analysis and were 4 in serum and 19 in feces. In this study, miR-375-3p, detected in serum and feces, was identified as the strongest candidate for a high-dose radiation biomarker in serum and/or feces using a radiation-induced intestinal injury model.

2023-12-15 | GSE247876 | GEO

16s rRNA-young and old mouse gut microbiota-stroke

Project description:To explore the effects of gut microbiota of young (8 weeks) or old mice (18～20 months) on stroke, feces of young (Y1-Y9) and old mice (O6-O16) were collected and analyzed by 16s rRNA sequencing. Then stroke model was established on young mouse receive feces from old mouse (DOT1-15) and young mouse receive feces from young mouse (DYT1-15). 16s rRNA sequencing were also performed for those young mice received feces from young and old mice.

2021-10-15 | E-MTAB-10837 | biostudies-arrayexpress

The effects of obesity microbiota produced metabolites on colorectal carcinogenesis in murine models

Project description:Obesity is a risk factor for colorectal cancer (CRC). We aim to study the effects and mechanisms of gut microbiota of obese subjects in contributing to CRC progression. Conventional AOM-treated and ApcMin/+ mice receiving feces from obese individuals showed significantly increased colon tumor formation compared with those receiving feces from control subjects. AOM-treated mice receiving feces from obese (OB-M) exhibited microbiota dysbiosis with enriched potential pathobionts Erysipelotrichaceae bacterium GAM147, Turicibacter sp. H121, Mucinivorans hirudinis, and depleted symbionts Bacteroides vulgatus, Faecalibaculum rodentium, Bifidobacterium spp. and Lactobacillus delbrueckii. The OB-M group also showed altered gut metabolites including elevated phenylacetic acid, and depleted genipin. Moreover, OB-M group showed impaired intestinal barrier function and significant upregulation of pro-inflammatory cytokines and activation of oncogenic Wnt signaling pathway. In conclusion, gut microbiota from obese individuals promotes colorectal carcinogenesis. Microbiota modulation in obese individuals may provide new insight into obesity-driven CRC prevention and therapy.

2022-05-18 | ST002193 | MetabolomicsWorkbench

Project description:CRAMP Restores Citrobacter rodentium-induced Gut Microbial Dysbiosis

| PRJNA555462 | ENA

Lysophosphatidylserines derived from microbiota in Crohn’s disease elicit pathological Th1 response

Project description:Microbiota alteration and IFN-γ-producing CD4+ T cell overactivation are implicated in Crohn's disease (CD) pathogenesis. However, it remains unclear how dysbiosis enhances Th1 responses, leading to intestinal inflammation. Here, we identified key metabolites that are derived from dysbiotic microbiota and induce enhanced Th1 responses and severe colitis in mouse models. Patients with CD showed elevated lysophosphatidylserine (LysoPS) concentration in their feces, accompanied with a higher relative abundance of microbiota possessing a gene encoding the phospholipid-hydrolyzing enzyme phospholipase A. LysoPS induced metabolic reprograming, thereby eliciting aberrant effector responses in both human and mouse IFN-?-producing CD4+ T cells. Administration of LysoPS into T cell-dependent mouse colitis models induced severe inflammation. LysoPS-induced aggravation of colitis was impaired in mice lacking P2ry10 and P2ry10b, and their CD4+ T cells were hypo-responsive to LysoPS. Thus, our findings elaborate on the mechanism by which metabolites elevated in patients with CD harboring dysbiotic microbiota induce intestinal pathology.

2022-05-03 | GSE169006 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data