REVIEW article
Front. Cell. Infect. Microbiol.
Sec. Clinical Infectious Diseases
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1641564
Mechanisms of Clostridioides difficile Glucosyltransferase Toxins and their Roles in Pathology: Insights and Emerging Therapeutic Strategies
Provisionally accepted
- Medical Center of Hematology, Army Medical University Xinqiao Hospital, Chongqing, China
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Clostridioides difficile infection (CDI) is a significant cause of antibiotic-associated diarrhea and pseudomembranous colitis, manifesting as mild diarrhea, fulminant colitis, and even death. It is typically recognized as a healthcare-associated infection. Glucosyltransferase toxin A (TcdA) and toxin B (TcdB) are two major factors responsible for the pathogenicity of Clostridioides difficile (C. difficile). They bind to cell surface receptors and enter the cytoplasm via pH-dependent pore formation, causing cell death by inactivating GTPase. This review elucidates the pathogenic mechanisms of C. difficile glucosyltransferase toxins and discusses the interactions between the two toxins and host cells. It also summarizes current progresses in CDI therapies, providing a comprehensive understanding of the disease and laying the foundation for developing novel therapies and management strategies.
Keywords: Clostridioides, Difficile, Infection, glucosyltransferase, toxins, TcdA, and, TCDB
Received: 05 Jun 2025; Accepted: 23 Sep 2025.
Copyright: © 2025 Wen, Liu, Wan, Liu, Zhang, Zhang and Qin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Xi Zhang, zhangxxi@sina.com
Wen Qin, qiqi105@sina.com
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