AI Article Synopsis
- The study aimed to assess how C. difficile's toxin TcdB affects human neutrophils (PMNs) by evaluating its glucosyltransferase activity.
- PMNs were exposed to TcdB to investigate its impact on GTPase glucosylation, their phagocytic/bactericidal function, and activation markers.
- Findings revealed that TcdB does not glucosylate key GTPases or impair PMN functions significantly, but it slightly inhibits the production of certain inflammatory markers when PMNs are stimulated by E. coli-LPS.
Article Abstract
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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| http://dx.doi.org/10.1016/j.anaerobe.2022.102553 | DOI Listing |
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