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Microbiota of MR1 deficient mice confer resistance against Clostridium difficile infection.

Ashley D SmithElissa D FossIrma ZhangJessica L HastieNicole P GiordanoLusine GasparyanLam Phuc VinhNguyenAlyxandria M SchubertDeepika PrasadHannah L McMichaelJinchun SunRichard D BegerVahan SimonyanSiobhán C CowleyPaul E Carlson
Published in: PloS one (2019)
Clostridium difficile (Cd) infection (CDI) typically occurs after antibiotic usage perturbs the gut microbiota. Mucosa-associated invariant T cells (MAIT) are found in the gut and their development is dependent on Major histocompatibility complex-related protein 1 (MR1) and the host microbiome. Here we were interested in determining whether the absence of MR1 impacts resistance to CDI. To this end, wild-type (WT) and MR1-/- mice were treated with antibiotics and then infected with Cd spores. Surprisingly, MR1-/- mice exhibited resistance to Cd colonization. 16S rRNA gene sequencing of feces revealed inherent differences in microbial composition. This colonization resistance was transferred from MR1-/- to WT mice via fecal microbiota transplantation, suggesting that MR1-dependent factors influence the microbiota, leading to CDI susceptibility.
Keyphrases
  • contrast enhanced
  • wild type
  • magnetic resonance
  • clostridium difficile
  • computed tomography
  • single cell
  • metabolic syndrome
  • microbial community
  • mesenchymal stem cells
  • cell therapy
  • genome wide analysis