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Vancomycin-resistant gut commensal Clostridium innocuum emerges as a pathobiont through synergy with toxigenic

Chia-Jung Kuo1, Tsui-Shan Hsu2, Chin-Ming Hsu2

  • 1School of Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan; Department of Gastroenterology and Hepatology, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan; Chang Gung Microbiota Therapy Center, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.

Microbial Pathogenesis
|May 4, 2026
PubMed

Insights

Clostridium innocuum worsens outcomes in Clostridioides difficile infection (CDI) by enhancing cell damage and barrier disruption. Its vancomycin resistance allows it to thrive during treatment, highlighting its role as a pathobiont.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Host-pathogen interactions

Background:

  • Clostridium innocuum is increasingly found in patients with Clostridioides difficile infection (CDI).
  • Its pathogenic role and cytotoxic mechanisms, especially in conjunction with C. difficile, are not well understood.
  • C. innocuum's intrinsic vancomycin resistance contributes to its persistence during CDI treatment.

Purpose of the Study:

  • To investigate the synergistic interactions between C. difficile and C. innocuum in human intestinal epithelial cells.
  • To elucidate the mechanisms by which C. innocuum influences host cell damage and barrier function during co-infection.

Main Methods:

  • Co-infection models using toxigenic C. difficile and C. innocuum in human intestinal epithelial cells.
  • Assessment of cytotoxicity, epithelial barrier integrity, and host cell apoptosis pathways (p53, BAX/BCL-2, PARP1).

Main Results:

  • C. innocuum alone showed minimal cytotoxicity, but significantly increased cell death and barrier disruption when co-infecting with C. difficile.
  • C. difficile pre-infection facilitated C. innocuum translocation, indicating toxin-mediated barrier damage aids colonization.
  • Co-infection activated p53 signaling and modulated the BAX/BCL-2 ratio, promoting apoptosis via PARP1.

Conclusions:

  • Toxigenic C. difficile facilitates C. innocuum invasion and exacerbates host cell damage through synergistic interactions.
  • C. innocuum acts as a clinically relevant pathobiont in CDI, particularly under vancomycin treatment.
  • Findings underscore the need for improved diagnostics and targeted therapeutic strategies for managing CDI co-infections.
Keywords:
Clostridioides difficileClostridium innocuumCo-infectionPathobiontVancomycin-resistant

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