Entry of spores into intestinal epithelial cells contributes to recurrence of Clostridioides difficile infection.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 33602902.
- Also identified by DOI 10.1038/s41467-021-21355-5 and PMC identifier 7893008.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Clostridioides difficile spores produced during infection are important for the recurrence of the disease. Here, we show that C. difficile spores gain entry into the intestinal mucosa via pathways dependent on host fibronectin-α<sub>5</sub>β<sub>1</sub> and vitronectin-α<sub>v</sub>β<sub>1</sub>. The exosporium protein BclA3, on the spore surface, is required for both entry pathways. Deletion of the bclA3 gene in C. difficile, or pharmacological inhibition of endocytosis using nystatin, leads to reduced entry into the intestinal mucosa and reduced recurrence of the disease in a mouse model. Our findings indicate that C. difficile spore entry into the intestinal barrier can contribute to spore persistence and infection recurrence, and suggest potential avenues for new therapies.
Medical subject headings
- Clostridioides difficile
- Clostridium Infections
- Epithelial Cells
- Intestines
- Spores, Bacterial