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ABSTRACT: Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice

PROVIDER: PRJEB46735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6388540.fastq.gz	Fastqsanger.gz
	ERR6388550.fastq.gz	Fastqsanger.gz
	ERR6388560.fastq.gz	Fastqsanger.gz
	ERR6388570.fastq.gz	Fastqsanger.gz
	ERR6388580.fastq.gz	Fastqsanger.gz

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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

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

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

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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

CecalTransferT1D

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

| PRJEB42282 | ENA

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

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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

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Maternal antibiotic exposure enhances neonatal ILC2 responses and aggravates allergic airway inflammation in adults

Project description:The maternal microbiota plays an important role in shaping and priming infant immunity, although the cellular and molecular mechanisms underlying these effects remain obscure. Here we report that prenatal antibiotic exposure caused significant elevation of group 2 innate lymphoid cells (ILC2s) in neonatal lungs, in both cell numbers and functionality. Downregulation of type 1 interferon signaling in ILC2s caused by diminished production of microbiota-derived metabolite butyrate represents the underlying mechanism. Mice lacking butyrate receptor GPR41 (GPR41-/-) or type 1 interferon receptor (Ifnar1-/-) recapitulated the phenotype of neonatal ILC2s upon maternal antibiotic exposure. Furthermore, prenatal antibiotic exposure induced persistent epigenetic changes in ILC2s and had a long-lasting deteriorative effect on allergic airway inflammation in adulthood. Prenatal supplementation with butyrate ameliorated airway inflammation in adult offspring born to antibiotic-exposed dams. These observations demonstrate an essential role for the maternal microbiota in the control of type 2 innate immunity at the neonatal stage, which provides a therapeutic window for treating asthma in early life.

2023-05-08 | GSE231887 | GEO

The effect of antibiotic mediated gut microbiome perturbation on ileal gene expression in NOD mice.

Project description:The early life microbiome plays important roles in host immunological and metabolic development. Because type 1 diabetes (T1D) incidence has been increasing substantially in recent decades, we hypothesized that early-life antibiotic use alters gut microbiota that predisposes to disease. Using NOD mice that are genetically susceptible to T1D, we examined the effects of exposure to either continuous low-dose antibiotics or pulsed therapeutic antibiotics (PAT) early in life, mimicking childhood exposures. We found that in mice receiving PAT, T1D incidence was significantly higher, microbial community composition and structure differed compared with controls. In pre-diabetic male PAT mice, the intestinal lamina propria had lower Th17 and T reg proportions and intestinal SAA expression than in controls, suggesting key roles in transducing the altered microbiota signals. PAT affected microbial lipid metabolism and host cholesterol biosynthetic gene expression. These findings show that early-life antibiotic treatments alter the gut microbiota and its metabolic capacities, intestinal gene expression, and T-cell populations, accelerating T1D onset in NOD mice.

2016-05-20 | GSE81648 | GEO

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