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Plakoglobin and High-Mobility Group Box 1 Mediate Intestinal Epithelial Cell Apoptosis Induced by Clostridioides

Yingxue Li1,2, Wei Xu2, Yutian Ren2

  • 1Division of Natural and Applied Sciences, Duke Kunshan Universitygrid.448631.c, Kunshan, Jiangsu, China.

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|August 31, 2022
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Summary

Clostridioides difficile infection (CDI) toxin TcdB induces apoptosis via plakoglobin (JUP) targeting mitochondria. Inhibiting HMGB1 also protects against TcdB-induced epithelial damage, offering potential therapeutic strategies for CDI.

Keywords:
C. difficileHMGB1JUPRNAi screenTcdBapoptosis

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Area of Science:

  • Microbiology
  • Cell Biology
  • Molecular Biology

Background:

  • Clostridioides difficile infection (CDI) is a major cause of antibiotic-associated diarrhea.
  • The bacterial toxin TcdB triggers host cell apoptosis through poorly understood mechanisms.
  • Understanding host factors involved in TcdB-induced apoptosis is crucial for developing therapeutic interventions.

Purpose of the Study:

  • To identify host factors mediating TcdB-induced apoptosis in intestinal epithelial cells.
  • To elucidate the mechanism by which TcdB induces cell death.
  • To explore potential therapeutic targets for CDI.

Main Methods:

  • RNA interference (RNAi) screen in Caco-2 cells to identify host factors.
  • CRISPR gene editing to validate identified factors.
  • Confocal microscopy to track protein localization.
  • Mitochondrial membrane permeabilization assays.
  • In vitro cell culture and in vivo mouse models for therapeutic evaluation.

Main Results:

  • Plakoglobin (JUP) and high-mobility group box 1 (HMGB1) were identified as key host factors in TcdB-induced apoptosis.
  • Disruption of JUP or HMGB1 conferred resistance to TcdB-mediated apoptosis.
  • JUP translocated to mitochondria, permeabilized the mitochondrial membrane, and promoted cytochrome c release.
  • HMGB1 inhibition using glycyrrhizin protected cultured cells and a mouse model from TcdB-induced damage.

Conclusions:

  • Plakoglobin plays a novel role in promoting mitochondrial apoptosis following TcdB intoxication.
  • HMGB1 is also a critical mediator of TcdB-induced cell death.
  • Targeting JUP or HMGB1 represents a promising therapeutic strategy for managing CDI.