Link to the University of Pittsburgh Homepage
Link to the University Library System Homepage Link to the Contact Us Form

Clostridium perfringens epsilon toxin increases the small intestinal permeability in mice and rats

Goldstein, J and Morris, WE and Loidi, CF and Tironi-Farinatti, C and McClane, BA and Uzal, FA and Fernandez Miyakawa, ME (2009) Clostridium perfringens epsilon toxin increases the small intestinal permeability in mice and rats. PLoS ONE, 4 (9).

Published Version
Available under License : See the attached license file.

Download (1MB) | Preview
[img] Plain Text (licence)
Available under License : See the attached license file.

Download (1kB)


Epsilon toxin is a potent neurotoxin produced by Clostridium perfringens types B and D, an anaerobic bacterium that causes enterotoxaemia in ruminants. In the affected animal, it causes oedema of the lungs and brain by damaging the endothelial cells, inducing physiological and morphological changes. Although it is believed to compromise the intestinal barrier, thus entering the gut vasculature, little is known about the mechanism underlying this process. This study characterizes the effects of epsilon toxin on fluid transport and bioelectrical parameters in the small intestine of mice and rats. The enteropooling and the intestinal loop tests, together with the single-pass perfusion assay and in vitro and ex vivo analysis in Ussing's chamber, were all used in combination with histological and ultrastructural analysis of mice and rat small intestine, challenged with or without C. perfringens epsilon toxin. Luminal epsilon toxin induced a time and concentration dependent intestinal fluid accumulation and fall of the transepithelial resistance. Although no evident histological changes were observed, opening of the mucosa tight junction in combination with apoptotic changes in the lamina propria were seen with transmission electron microscopy. These results indicate that C. perfringens epsilon toxin alters the intestinal permeability, predominantly by opening the mucosa tight junction, increasing its permeability to macromolecules, and inducing further degenerative changes in the lamina propria of the bowel. © 2009 Goldstein et al.


Social Networking:
Share |


Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Goldstein, J
Morris, WE
Loidi, CF
Tironi-Farinatti, C
McClane, BAbamcc@pitt.eduBAMCC
Uzal, FA
Fernandez Miyakawa, ME
ContributionContributors NameEmailPitt UsernameORCID
Date: 18 September 2009
Date Type: Publication
Journal or Publication Title: PLoS ONE
Volume: 4
Number: 9
DOI or Unique Handle: 10.1371/journal.pone.0007065
Schools and Programs: School of Medicine > Biochemistry and Molecular Genetics
Refereed: Yes
MeSH Headings: Animals; Bacterial Toxins--metabolism; Electrophysiology; Enterocytes--metabolism; Enterotoxemia--microbiology; Female; Intestinal Mucosa--drug effects; Intestine, Small--drug effects; Male; Mice; Mice, Inbred BALB C; Microscopy, Electron, Transmission--methods; Permeability--drug effects; Rats; Rats, Wistar
Other ID: NLM PMC2739291
PubMed Central ID: PMC2739291
PubMed ID: 19763257
Date Deposited: 03 Aug 2012 16:13
Last Modified: 26 Jan 2019 10:55


Monthly Views for the past 3 years

Plum Analytics

Actions (login required)

View Item View Item