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Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291
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Entry of spores into intestinal epithelial cells contributes to recurrence of Clostridioides difficile infection

Pablo Castro-Córdova1,2, Paola Mora-Uribe1, Rodrigo Reyes-Ramírez1,2

  • 1Microbiota-Host Interactions and Clostridia Research Group, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile.

Nature Communications
|February 19, 2021
PubMed

Insights

Clostridioides difficile spores enter the intestinal lining using host proteins and the BclA3 spore protein. Blocking this entry reduces C. difficile recurrence in mice, suggesting new therapeutic targets.

Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Clostridioides difficile infection (CDI) recurrence is a significant clinical challenge.
  • C. difficile spores are crucial for disease persistence and transmission.
  • Understanding spore-host interactions is key to preventing CDI recurrence.

Purpose of the Study:

  • To elucidate the mechanisms of C. difficile spore entry into the intestinal mucosa.
  • To identify host factors and bacterial components involved in spore invasion.
  • To evaluate therapeutic strategies targeting spore entry to reduce CDI recurrence.

Main Methods:

  • Investigated C. difficile spore interaction with intestinal epithelial cells.
  • Utilized cell-based assays and a mouse model of CDI.
  • Employed genetic deletion of the C. difficile bclA3 gene.
  • Assessed the effect of pharmacological inhibition of endocytosis (nystatin).

Main Results:

  • C. difficile spores utilize host fibronectin-α5β1 and vitronectin-αvβ1 pathways for intestinal entry.
  • The exosporium protein BclA3 is essential for spore adherence and invasion via these pathways.
  • Deletion of bclA3 or inhibition of endocytosis significantly reduced spore entry into the mucosa.
  • Reduced mucosal entry correlated with decreased C. difficile recurrence in a mouse model.

Conclusions:

  • C. difficile spore entry into the intestinal mucosa is a critical step for infection persistence and recurrence.
  • Host fibronectin and vitronectin receptors, along with the bacterial BclA3 protein, mediate this entry.
  • Targeting C. difficile spore-host interactions presents a promising therapeutic strategy for preventing CDI recurrence.

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