Abstract

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.

Highlights

  • Epsilon toxin (ETX) produced by Clostridium perfringens types B and D is responsible for a highly fatal enterotoxaemia in livestock [1]

  • Effects of ETX on intestinal fluid Intestinal fluid accumulation in the mouse small intestine was initially determined by the enteropooling assay

  • This study aimed to clarify the physiopathology of fluid accumulation and toxin absorption in the rodent small intestine exposed to ETX

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Summary

Introduction

Epsilon toxin (ETX) produced by Clostridium perfringens types B and D is responsible for a highly fatal enterotoxaemia in livestock [1]. This toxin is secreted in the gut lumen as a prototoxin which becomes fully active by the action of either the host’s intestinal trypsin or a C. perfringens metalloproteinase [2]. In mice, lethal effects were observed 2 hours after oral administration of ETX [6] This evidence indicates that ETX is promptly absorbed from the gut lumen into the blood circulation, the mechanism involving this process is yet unknown

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