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Microbiota of MR1 deficient mice confer resistance against Clostridium difficile infection

Ashley D Smith1, Elissa D Foss1, Irma Zhang1

  • 1Laboratory 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 Spring, Maryland, United States of America.

Plos One
|September 28, 2019
PubMed

Insights

Mice lacking Major histocompatibility complex-related protein 1 (MR1) showed resistance to Clostridium difficile infection (CDI). This resistance was linked to gut microbiota changes, transferable via fecal microbiota transplantation, indicating MR1 influences CDI susceptibility.

Area of Science:

  • Immunology
  • Microbiome research
  • Infectious diseases

Background:

  • Clostridium difficile infection (CDI) commonly follows antibiotic use, disrupting the gut microbiota.
  • Mucosa-associated invariant T cells (MAIT) are gut-resident immune cells dependent on Major histocompatibility complex-related protein 1 (MR1) and the microbiome.
  • The role of MR1 in CDI pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the impact of MR1 absence on resistance to Clostridium difficile colonization.
  • To determine if MR1 influences the gut microbiota composition in a manner relevant to CDI.

Main Methods:

  • Wild-type (WT) and MR1-/- mice were subjected to antibiotic treatment followed by Clostridium difficile spore infection.
  • Fecal samples were analyzed using 16S rRNA gene sequencing to assess microbial composition.
  • Fecal microbiota transplantation (FMT) was performed from MR1-/- to WT mice.

Main Results:

  • MR1-/- mice demonstrated significant resistance to Clostridium difficile colonization compared to WT mice.
  • 16S rRNA gene sequencing revealed distinct baseline gut microbial compositions between WT and MR1-/- mice.
  • Transfer of microbiota from MR1-/- mice conferred colonization resistance to WT recipients.

Conclusions:

  • The absence of MR1 confers resistance to Clostridium difficile colonization in mice.
  • MR1-dependent factors significantly shape the gut microbiota, influencing susceptibility to CDI.
  • Targeting MR1-mediated pathways could offer novel strategies for CDI prevention or treatment.

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