Microbiota of MR1 deficient mice confer resistance against Clostridium difficile infection

• DOI: 10.1371/journal.pone.0223025
• Publication Date: 2019-09-27T13:29:10Z
• Authors: Ashley D. Smith; Elissa D. Foss; Irma Zhang; Jessica L. Hastie; Nicole P. Giordano; Lusine Gasparyan; Lam Phuc VinhNguyen; Alyxandria M. Sch...; Deepika Prasad; Hannah L. McMichael; Jinchun Sun; Richard D. Beger; Vahan Simonyan; Siobhán C. Cowley; Paul E. Carlson
• Keywords: 0301 basic medicine; Science; Cefoperazone; Mucosal-Associated Invariant T Cells; Minor Histocompatibility Antigens; Feces; Mice; 03 medical and health sciences; Animals; Humans; Intestinal Mucosa; Disease Resistance; Mice, Knockout; Q; Histocompatibility Antigens Class I; R; Fecal Microbiota Transplantation; Anti-Bacterial Agents; Gastrointestinal Microbiome; Specific Pathogen-Free Organisms; 3. Good health; Disease Models, Animal; Clostridium Infections; Medicine; Research Article

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.