{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang XS"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","NNF Center for Basic Metabolic Research","NIGMS NIH HHS"],"pagination":["1249-1265.e9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8370265"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(8)"],"pubmed_abstract":["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 immu"],"journal":["Cell host & microbe"],"pubmed_title":["Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice."],"pmcid":["PMC8370265"],"funding_grant_id":["R01 DK120679","R35 GM139655","Bäckhed Group","R01 GM128955","R01 DK110014","P01 HL147823"],"pubmed_authors":["Needles K","Zhang M","Wang J","Hazen SL","Altomare N","Krautkramer K","Morton JT","Dominguez-Bello MG","Li WV","Wang Z","Nemet I","Li H","Li J","Chalk JA","Ruggles KV","Battaglia T","Liao V","Yin YS","He L","Mount J","Bonneau RA","Brown M","Devlin JC","Blaser MJ","Armstrong AJS","Backhed F","Zhang XS","Badri MH","Strauch CM"],"additional_accession":[]},"is_claimable":false,"name":"Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice.","description":"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 immu","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Aug","modification":"2026-05-29T18:55:05.717Z","creation":"2025-04-06T09:24:41.784Z"},"accession":"S-EPMC8370265","cross_references":{"pubmed":["34289377"],"doi":["10.1016/j.chom.2021.06.014"]}}