» Articles » PMID: 27044305

Pathogenic Effects of Glucosyltransferase from Clostridium Difficile Toxins

Overview
Journal Pathog Dis
Date 2016 Apr 6
PMID 27044305
Citations 4
Authors
Affiliations
Soon will be listed here.
Abstract

The glucosyltransferase domain ofClostridium difficiletoxins modifies guanine nucleotide-binding proteins of Rho family. It is the major virulent domain of the holotoxins. Various pathogenic effects ofC. difficiletoxins in response to Rho glucosylation have been investigated including cytoskeleton damage, cell death and inflammation. The most recent studies have revealed some significant characteristics of the holotoxins that are independent of glucosylating activity. These findings arouse discussion about the role of glucosyltransferase activity in toxin pathogenesis and open up new insights for toxin mechanism study. In this review, we summarize the pathogenic effects of glucosyltransferase domain of the toxins in the past years.

Citing Articles

Advances in the mechanism of metformin with wide-ranging effects on regulation of the intestinal microbiota.

Wang Y, Jia X, Cong B Front Microbiol. 2024; 15:1396031.

PMID: 38855769 PMC: 11157079. DOI: 10.3389/fmicb.2024.1396031.


Exploring the Toxin-Mediated Mechanisms in Infection.

Pourliotopoulou E, Karampatakis T, Kachrimanidou M Microorganisms. 2024; 12(5).

PMID: 38792835 PMC: 11124097. DOI: 10.3390/microorganisms12051004.


The development of live biotherapeutics against infection towards reconstituting gut microbiota.

Zhang Y, Saint Fleur A, Feng H Gut Microbes. 2022; 14(1):2052698.

PMID: 35319337 PMC: 8959509. DOI: 10.1080/19490976.2022.2052698.


Phosphorylation and functionality of CdtR in Clostridium difficile.

Bilverstone T, Minton N, Kuehne S Anaerobe. 2019; 58:103-109.

PMID: 31323291 PMC: 6699598. DOI: 10.1016/j.anaerobe.2019.102074.

References
1.
Genisyuerek S, Papatheodorou P, Guttenberg G, Schubert R, Benz R, Aktories K . Structural determinants for membrane insertion, pore formation and translocation of Clostridium difficile toxin B. Mol Microbiol. 2011; 79(6):1643-54. DOI: 10.1111/j.1365-2958.2011.07549.x. View

2.
Koon H, Ho S, Hing T, Cheng M, Chen X, Ichikawa Y . Fidaxomicin inhibits Clostridium difficile toxin A-mediated enteritis in the mouse ileum. Antimicrob Agents Chemother. 2014; 58(8):4642-50. PMC: 4135997. DOI: 10.1128/AAC.02783-14. View

3.
Na X, Zhao D, Koon H, Kim H, Husmark J, Moyer M . Clostridium difficile toxin B activates the EGF receptor and the ERK/MAP kinase pathway in human colonocytes. Gastroenterology. 2005; 128(4):1002-11. DOI: 10.1053/j.gastro.2005.01.053. View

4.
Giesemann T, Guttenberg G, Aktories K . Human alpha-defensins inhibit Clostridium difficile toxin B. Gastroenterology. 2008; 134(7):2049-58. DOI: 10.1053/j.gastro.2008.03.008. View

5.
Just I, Wilm M, SELZER J, Rex G, von Eichel-Streiber C, Mann M . The enterotoxin from Clostridium difficile (ToxA) monoglucosylates the Rho proteins. J Biol Chem. 1995; 270(23):13932-6. DOI: 10.1074/jbc.270.23.13932. View