Microbiota of MR1 deficient mice confer resistance against Clostridium difficile infection.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 31560732.
- Also identified by DOI 10.1371/journal.pone.0223025 and PMC identifier 6764671.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
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.
Medical subject headings
- Clostridium Infections
- Disease Resistance
- Gastrointestinal Microbiome
- Histocompatibility Antigens Class I
- Minor Histocompatibility Antigens