Special Issue Article
Role of Phospholipid Metabolism and G Protein in the Action Induced by Clostridium Perfringens Alpha-Toxin
- *Corresponding Author:
- Masahiro Nagahama
Department of Microbiology
Faculty of Pharmaceutical Sciences
Tokushima Bunri University, Yamashiro-cho
Tokushima 770-8514, Japan
E-mail: [email protected]
Received date: February 06, 2012; Accepted date: March 20, 2012; Published date: March 23, 2012
Citation: Nagahama M, Oda M, Ochi S, Kobayashi K, Sakurai J (2012) Role of Phospholipid Metabolism and G Protein in the Action Induced by Clostridium Perfringens Alpha-Toxin. J Glycom Lipidom S3:001. doi: 10.4172/2153-0637.S3-001
Copyright: © 2012 Nagahama M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Alpha-toxin (370 residues) of Clostridium perfringens is the key virulence determinant in gas gangrene and has also been implicated in the pathogenesis of sudden death syndrome in young animals. Alpha-toxin possesses phospholipase C (PLC), sphingomyelinase (SMase) and biological activities causing hemolysis and lethality. The structure of the toxin reveals two domains: the N-terminal domain containing the catalytic active site and the C-terminal domain involving the binding to membranes. Recent research data showed that alpha-toxin-induced biological activities are responsible for the activation of phospholipid metabolism via a pertussis toxin (PT)-sensitive GTP-binding protein, Gi. In this review, we summary the role of phospholipid metabolism and G protein in the biological activities induced by alpha-toxin. Discussed are activations of the arachidonic acid cascade (Section 1), the phospholipid metabolism (Section 2), the sphingomeylin metabolism (Section 3) and TrkA signaling (Section 4) induced by alpha-toxin.