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A receptor decoy inhibits the enterotoxic effects of Clostridium difficile toxin A in rat ileum

I Castagliuolo1, J T LaMont, B Qiu

  • 1Division of Gastroenterology, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Gastroenterology
|August 1, 1996
PubMed
Abstract

Insights

Synsorb 90, which carries a specific trisaccharide that binds Clostridium difficile toxin A, effectively sequesters the toxin in the gut. This prevents toxin A-induced intestinal fluid secretion and inflammation, suggesting its therapeutic potential for C. difficile colitis.

Area of Science:

  • Gastroenterology
  • Microbiology
  • Biotechnology

Background:

  • Clostridium difficile toxin A induces intestinal secretion and inflammation by binding to a specific trisaccharide on enterocyte receptors.
  • This trisaccharide is Gal alpha 1-3Gal beta 1-4 GlcNAc.

Purpose of the Study:

  • To evaluate Synsorb 90, an inert support with the trisaccharide, for its ability to bind toxin A in vitro.
  • To assess Synsorb 90's efficacy in inhibiting toxin A's enterotoxic effects in vivo.

Main Methods:

  • Binding assays were performed using radiolabeled toxin A and Synsorb 90, Synsorb 83 (beta-mannose), and Chromosorb P (inert control).
  • In vivo studies utilized rat ileal loops to measure toxin A-mediated fluid secretion, mannitol permeability, and histological damage after treatment with the compounds.

Main Results:

  • Synsorb 90 demonstrated specific binding to toxin A, unlike Synsorb 83 and Chromosorb P.
  • Oral administration of Synsorb 90 significantly reduced toxin A-induced fluid secretion and increased intestinal permeability in rats.

Conclusions:

  • An immobilized toxin A receptor, such as Synsorb 90, can sequester toxin A in the intestinal lumen, thereby inhibiting its detrimental effects on the ileal mucosa.
  • These findings indicate a potential therapeutic application for Synsorb 90 in managing Clostridium difficile colitis.

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