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

Autor: Joseph C. Devlin, Stanley L. Hazen, Linchen He, Meifan Zhang, Michelle H. Badri, John Alex Chalk, Wei Vivian Li, Mark Brown, Richard Bonneau, Jincheng Wang, Jamie Morton, Thomas Battaglia, Kelly Needles, Kelly V. Ruggles, Jackie Li, Xue-Song Zhang, Maria Gloria Dominguez-Bello, Martin J. Blaser, Christopher M. Strauch, Yue Sandra Yin, Ina Nemet, Fredrik Bäckhed, Zeneng Wang, Kimberly A. Krautkramer, Nicole J. Altomare, Huilin Li, Julia Mount, Abigail J. S. Armstrong, Viviane Liao
Rok vydání: 2021
Předmět:
Male
type 1 diabetes
Gene Expression
microbiome
Mice
Mice
Inbred NOD
Gene expression
cecal material transfer
2.1 Biological and endogenous factors
histone modification
Aetiology
Cecum
NOD mice
Regulation of gene expression
Pediatric
microRNA
Diabetes
animal models
Anti-Bacterial Agents
Intestines
Histone Code
5.1 Pharmaceuticals
Medical Microbiology
Female
innate immune
Development of treatments and therapeutic interventions
Metabolic Networks and Pathways
Type 1
Immunology
Biology
Autoimmune Disease
Microbiology
Article
Autoimmune Diseases
Immune system
Virology
Diabetes Mellitus
Animals
Microbiome
Metabolic and endocrine
Innate immune system
Bacteria
Animal
autoimmune
Gastrointestinal Microbiome
TLR2
Disease Models
Animal
MicroRNAs
Diabetes Mellitus
Type 1
Good Health and Well Being
Disease Models
Inbred NOD
Metagenome
Parasitology
Zdroj: Cell host & microbe, vol 29, iss 8
Cell Host Microbe
Popis: Early-life antibiotic exposure perturbs the intestinal microbiota and accelerates type 1 diabetes (T1D) development in the NOD mouse model. Here, we found that maternal cecal microbiota transfer (CMT) to NOD mice after early-life antibiotic perturbation largely rescued the induced T1D enhancement. Restoration of the intestinal microbiome was significant and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed metabolites and normalized innate and adaptive immune effectors. CMT restored major patterns of ileal microRNA and histone regulation of gene expression. Further experiments suggest a gut-microbiota-regulated T1D protection mechanism centered on Reg3γ, in an innate intestinal immune network involving CD44, TLR2, and Reg3γ. This regulation affects downstream immunological tone, which may lead to protection against tissue-specific T1D injury.
Databáze: OpenAIRE
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