Format

Send to

Choose Destination
Toxicon. 2013 Dec 1;75:122-35. doi: 10.1016/j.toxicon.2013.04.003. Epub 2013 Apr 27.

Attack of the nervous system by Clostridium perfringens Epsilon toxin: from disease to mode of action on neural cells.

Author information

1
Centre National de la Recherche Scientifique (CNRS) and Université de Strasbourg, Institut des Neurosciences Cellulaires et Intégratives (INCI), UPR 3212, Strasbourg, France.

Abstract

Epsilon toxin (ET), produced by Clostridium perfringens types B and D, ranks among the four most potent poisonous substances known so far. ET-intoxication is responsible for enterotoxaemia in animals, mainly sheep and goats. This disease comprises several manifestations indicating the attack of the nervous system. This review aims to summarize the effects of ET on central nervous system. ET binds to endothelial cells of brain capillary vessels before passing through the blood-brain barrier. Therefore, it induces perivascular oedema and accumulates into brain. ET binding to different brain structures and to different component in the brain indicates regional susceptibility to the toxin. Histological examination has revealed nerve tissue and cellular lesions, which may be directly or indirectly caused by ET. The naturally occurring disease caused by ET-intoxication can be reproduced experimentally in rodents. In mice and rats, ET recognizes receptor at the surface of different neural cell types, including certain neurons (e.g. the granule cells in cerebellum) as well as oligodendrocytes, which are the glial cells responsible for the axons myelination. Moreover, ET induces release of glutamate and other transmitters, leading to firing of neural network. The precise mode of action of ET on neural cells remains to be determined.

KEYWORDS:

Brain; Clostridial toxins; Glutamate; Neuron; Pore-forming toxin; White matter

PMID:
23632158
DOI:
10.1016/j.toxicon.2013.04.003
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center