Microbiota of MR1 deficient mice confer resistance against Clostridium difficile infection
Autoři:
Ashley D. Smith aff001; Elissa D. Foss aff001; Irma Zhang aff001; Jessica L. Hastie aff001; Nicole P. Giordano aff001; Lusine Gasparyan aff002; Lam Phuc VinhNguyen aff002; Alyxandria M. Schubert aff001; Deepika Prasad aff001; Hannah L. McMichael aff001; Jinchun Sun aff003; Richard D. Beger aff003; Vahan Simonyan aff002; Siobhán C. Cowley aff001; Paul E. Carlson, Jr aff001
Působiště autorů:
Laboratory of Mucosal Pathogens and Cellular Immunology, Division of Bacterial Pathogens and Allergenic Products, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, United States Food and Drug Administration, Silver Spri
aff001; Laboratory of Mucosal Pathogens and Cellular Immunology, Division of Bacterial Pathogens and Allergenic Products, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, United States Food and Drug Administration, Silver Spri
aff001; High-performance Integrated Personal Environment, Center for Biologics Evaluation and Research, United States Food and Drug Administration, Silver Spring, Maryland, United States of America
aff002; Division of Systems Biology, National Center for Toxicological Research, United States Food and Drug Administration, Jefferson, Arkansas, United States of America
aff003
Vyšlo v časopise:
PLoS ONE 14(9)
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.pone.0223025
Souhrn
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.
Klíčová slova:
Clostridium difficile – Antibiotics – Gastrointestinal tract – Mouse models – Microbiome – Sequence databases – Antibiotic resistance – Bacterial spores
Zdroje
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