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

Xue Song Zhang, Yue Sandra Yin, Jincheng Wang, Thomas Battaglia, Kimberly Krautkramer, Wei Vivian Li, Jackie Li, Mark Brown, Meifan Zhang, Michelle H. Badri, Abigail J.S. Armstrong, Christopher M. Strauch, Zeneng Wang, Ina Nemet, Nicole Altomare, Joseph C. Devlin, Linchen He, Jamie T. Morton, John Alex Chalk, Kelly NeedlesViviane Liao, Julia Mount, Huilin Li, Kelly V. Ruggles, Richard A. Bonneau, Maria Gloria Dominguez-Bello, Fredrik Bäckhed, Stanley L. Hazen, Martin J. Blaser

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)1249-1265.e9
JournalCell Host and Microbe
Issue number8
StatePublished - Aug 11 2021


  • NOD mice
  • animal models
  • autoimmune
  • cecal material transfer
  • gene expression
  • histone modification
  • innate immune
  • microRNA
  • microbiome
  • type 1 diabetes

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Virology


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