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PLoS One ; 14(9): e0223025, 2019.
Article in English | MEDLINE | ID: mdl-31560732

ABSTRACT

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.


Subject(s)
Clostridium Infections/immunology , Disease Resistance/genetics , Gastrointestinal Microbiome/immunology , Histocompatibility Antigens Class I/genetics , Minor Histocompatibility Antigens/genetics , Animals , Anti-Bacterial Agents/administration & dosage , Anti-Bacterial Agents/adverse effects , Cefoperazone/administration & dosage , Cefoperazone/adverse effects , Clostridium Infections/etiology , Clostridium Infections/microbiology , Clostridium Infections/therapy , Disease Models, Animal , Disease Resistance/immunology , Fecal Microbiota Transplantation , Feces/microbiology , Gastrointestinal Microbiome/drug effects , Histocompatibility Antigens Class I/immunology , Humans , Intestinal Mucosa/cytology , Intestinal Mucosa/immunology , Intestinal Mucosa/microbiology , Mice , Mice, Knockout , Minor Histocompatibility Antigens/immunology , Mucosal-Associated Invariant T Cells/immunology , Specific Pathogen-Free Organisms
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