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

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

PROVIDER: PRJEB42346 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5043350.fastq.gz	Fastqsanger.gz
	ERR5043351.fastq.gz	Fastqsanger.gz
	ERR5043352.fastq.gz	Fastqsanger.gz
	ERR5043343.fastq.gz	Fastqsanger.gz
	ERR5043353.fastq.gz	Fastqsanger.gz

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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

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

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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

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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

Ileal transcription profiles of NOD mice in Short-term Restoration experiment (Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression)

Project description:Ileal transcription profiles of NOD mice in Short-term Restoration experiment (Cecal microbiota transfer rescues the antibiotic-induced acceleration of type 1 diabetes and alteration of intestinal gene expression)

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

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

CecalTransferT1D

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

| PRJEB42282 | ENA

Cecal contents

Project description:Cecal contents Metagenome

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Postnatal cecal and cecal content luminal miRNA signatures in C57BL/6-VAF/Elite® mice

Project description:The interplay between the intestinal microbiota and host is critical to intestinal ontogeny and homeostasis. MicroRNAs (miRNAs) may be an underlying link. Intestinal miRNAs are microbiota-dependent and when shed in the lumen, affect resident microorganisms. Yet, longitudinal relationships between intestinal tissue miRNAs, luminal miRNAs, and luminal microorganisms have not been elucidated, especially in early life. Here, we investigated the postnatal cecal miRNA and microbiota populations, their relationship, and their impact on intestinal maturation in specific and opportunistic pathogen free mice; we also assessed if they can be modified by an intervention with allochthonous probiotic lactobacilli. We report that cecal and cecal content miRNA and microbiota signatures are temporally regulated, correlated, and modifiable by probiotics with implications for intestinal maturation. These findings help with understanding causal relationships within the gut ecosystem and provide a basis for preventing and managing their alterations in diseases throughout life.

2023-07-08 | GSE149418 | GEO

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