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Updated: Mar 19, 2026
09:12
A Protein Microarray Assay for Serological Determination of Antigen-specific Antibody Responses Following Clostridium difficile Infection
Published on: June 15, 2018
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Glucosylation Drives the Innate Inflammatory Response to Clostridium difficile Toxin A
Carrie A Cowardin1, Brianna M Jackman2, Zannatun Noor1
1Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, Virginia, USA.
Infection and Immunity
|June 9, 2016
Summary
Clostridium difficile toxins cause severe colitis by damaging tissue and triggering inflammation. Inhibiting their enzymatic activity may offer a new treatment for this infection.
Area of Science:
- Microbiology
- Immunology
- Pathogen Research
Background:
- Clostridium difficile is a significant cause of hospital-acquired infections, leading to colitis.
- The Rho-glucosylating toxins A and B are key factors in C. difficile infection (CDI) pathogenesis.
- These toxins induce epithelial cell death, inflammation via NF-κB activation, and IL-1β secretion through inflammasome activation.
Purpose of the Study:
- To investigate the role of Rho glucosylation by Toxin A in inflammasome activation.
- To determine the dependence of tissue destruction and inflammation on Toxin A's enzymatic activity in vivo.
Main Methods:
- Utilized a glucosylation-deficient Toxin A mutant.
- Assessed inflammasome activation.
- Evaluated tissue destruction and inflammatory cytokine production in vivo.
Main Results:
- Inflammasome activation by Toxin A is dependent on Rho glucosylation, similar to Toxin B.
- Tissue damage and in vivo inflammatory cytokine production are critically dependent on Toxin A's enzymatic activity.
Conclusions:
- The enzymatic activity of Clostridium difficile Toxin A is essential for causing tissue destruction and inflammation.
- Inhibiting the glucosyltransferase activity of Toxin A presents a potential therapeutic strategy against CDI.
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