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Updated: Feb 27, 2026

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Published on: December 10, 2016

Clostridium difficile Toxin Biology.

Klaus Aktories¹, Carsten Schwan¹, Thomas Jank¹

¹Institute of Experimental and Clinical Pharmacology and Toxicology, University of Freiburg, 79104 Freiburg, Germany; email: klaus.aktories@pharmakol.uni-freiburg.de , carsten.schwan@pharmakol.uni-freiburg.de , thomas.jank@pharmakol.uni-freiburg.de.

Annual Review of Microbiology

|June 29, 2017

Summary

Clostridium difficile toxins A and B (TcdA/TcdB) disrupt host cells by inactivating Rho proteins, leading to cellular damage. C. difficile transferase toxin (CDT) affects actin, causing cytoskeletal changes and disease.

Keywords:

ADP ribosylation CDT Clostridium difficile infection Clostridium difficile toxins Clostridium difficile transferase toxin Rho proteins actin glucosylation microtubules toxin receptors toxin uptake

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Published on: December 10, 2016

Culturing and Maintaining Clostridium difficile in an Anaerobic Environment

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Published on: September 14, 2013

A Protocol to Characterize the Morphological Changes of Clostridium difficile in Response to Antibiotic Treatment

A Protocol to Characterize the Morphological Changes of Clostridium difficile in Response to Antibiotic Treatment

Published on: May 25, 2017

Area of Science:

Microbiology
Cell Biology
Toxicology

Background:

Clostridium difficile causes antibiotic-associated diarrhea and pseudomembranous colitis.
Key virulence factors are TcdA, TcdB, and CDT toxins.
TcdA and TcdB are single-chain toxins; CDT is a binary toxin.

Purpose of the Study:

To elucidate the mechanisms of C. difficile toxin actions.
To understand toxin interaction with host cells.
To detail the functional consequences of toxin activity.

Main Methods:

Analysis of toxin structures.
Investigation of host cell receptor binding.
Study of intracellular toxin activation and function.
Examination of effects on Rho GTPases and actin.

Main Results:

TcdA and TcdB glucosylate and inactivate Rho proteins in the cytosol.
Rho protein inactivation disrupts cytoskeleton, leading to barrier dysfunction, apoptosis, and inflammation.
CDT depolymerizes actin, inducing microtubule-based protrusions.

Conclusions:

C. difficile toxins employ distinct mechanisms to subvert host cell functions.
Understanding these toxins is crucial for developing therapeutic strategies.
Recent advances provide detailed insights into toxin-host interactions.