Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intestinal expression in murine antibiotic-induced acceleration of Type 1 diabetes

ABSTRACT: Intestinal expression in murine antibiotic-induced acceleration of Type 1 diabetes

PROVIDER: PRJEB28151 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2732010.fastq.gz	Fastqsanger.gz
	ERR2732020.fastq.gz	Fastqsanger.gz
	ERR2732030.fastq.gz	Fastqsanger.gz
	ERR2732040.fastq.gz	Fastqsanger.gz
	ERR2732050.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 66

Similar Datasets

Intestinal expression in murine antibiotic-induced acceleration of Type 1 diabetes

Project description:Here we asked whether the single early-life (pup day of life P5-P10) antibiotic pulse was sufficient to enhance Type-1 Diabetes (T1D) in Non Obese Diabetic (NOD) mice. Two sets of experimental samples were analyzed for changes in intestinal pathway expression using the NOD mouse model and Pulsed Antibiotic Therapy (PAT). NODPAT sought to describe the intestinal changes related to early life PAT treatment while the RESTORE experiment sought to restore an antibiotic-perturbed host and measure the intestinal expression changes over time. We provide evidence that maternal microbiota provides partial restoration of both the altered pup microbiota and its immunological phenotypes.

2018-08-19 | E-MTAB-6826 | biostudies-arrayexpress

Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression II

Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury

2020-12-28 | GSE163888 | GEO

Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression I

Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model. Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration. The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors. CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing. Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota. This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury.

2020-12-28 | GSE163887 | GEO

Antibiotic-induced acceleration of type 1 diabetes alters maturation of innate intestinal immunity

Project description:The early-life intestinal microbiota plays a key role in shaping host immune system development. We found that a single early-life antibiotic course (1PAT) accelerated Type 1 diabetes (T1D) development in male NOD mice. The single course had strong and persistent effects on the intestinal microbiome, selecting for a highly metabolically active metagenome, with altered hepatic and serum metabolites. The exposure led to differential ileal and hepatic histone modification, and perturbed ileal gene expression, strongly affecting the normal maturational pattern. Earliest effects involved specific genes in innate immune pathways, with later effects on adaptive immunity. Microbiome analysis revealed four potential T1D-protective taxa and four T1D-accelerating taxa, and a network linking specific microbial taxa to differences in ileal gene expression was identified. This simplified animal model has improved understanding of the mechanisms by which early-life gut microbiome perturbations alter host intestinal responses, contributing to T1D.

2018-08-03 | GSE101721 | GEO

Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice-the long term restoration

Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model. Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration. The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors. CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing. Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota. This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury.

2021-09-02 | E-MTAB-9982 | biostudies-arrayexpress

E-MTAB-6826

Project description:Intestinal expression in murine antibiotic-induced acceleration of Type 1 diabetes

2018-09-17 | E-MTAB-6826 | ExpressionAtlas

Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression

Project description:Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression

| PRJEB42346 | ENA

Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression I

Project description:Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression I

| PRJNA688076 | ENA

Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression II

Project description:Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression II

| PRJNA688077 | ENA

Transcriptional profiling of mouse intestinal tissue, with or without antibiotic or sulindac treatment

Project description:Loss of APC or activation of Braf V600E mutation in combination with Alk5 loss in the intestinal epithelium under the control of VilCreER, with or without antibiotic/sulindac treatment

2021-04-01 | GSE168478 | 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