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Updated: Sep 28, 2025

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291
Published on: December 10, 2016
Human neutrophils are resistant to Clostridioides difficile toxin B
Catalina Chaves-Cordero1, Carlos Quesada-Gómez2, Esteban Chaves-Olarte2
1Programa de Investigación en Enfermedades Tropicales, Escuela de Medicina Veterinaria, Universidad Nacional de Costa Rica, Heredia, Costa Rica.
Objective:
The main objective of this study was to evaluate the glucosyltransferase activity of C. difficile TcdB on the activity of human PMNs.
Methods:
To better understand the interaction between PMNs and TcdB, PMNs were treated with sub-lethal concentrations of TcdB. We evaluated: (i) the glucosylation of GTPases, (ii) the phagocytic and bactericidal activity, and (iii) PMNs activation (through quantification of TNF-α, IL-8, and expression of CD11b cell surface activation marker).
Results:
We found that TcdB did not glucosylate RhoA and Rac1 GTPases and did not affect the phagocytic or bactericidal capacity of PMNs. Moreover, TcdB did not increase the production of TNF-α, IL-8, or the expression of activation marker CD11b. The only significant effect of TcdB on PMNs was the partial inhibition of TNF-α and IL-8 production and the diminished expression of CD11b induced by E. coli-LPS.
Conclusion:
Our results show that human PMNs are resistant to TcdB GTPase glucosyltransferase activity against RhoA and Rac1.
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