Review Article

Interaction of Botulinum Toxin with the Epithelial Barrier

Figure 1

Botulinum neurotoxin complexes and food-borne botulism. (a) Schematic structure of botulinum neurotoxin (BoNT) complexes. (b) The pathway followed by BoNT complexes from the lumen of the intestinal tract to the cytosol of the peripheral nerve terminal in food-borne botulism. Orally ingested BoNT complexes (12S and 16S toxins) must cross the intestinal epithelial barrier to cause the food-borne botulism. After absorption from the small intestine, the botulinum neurotoxin complexes enter the lymphatic system, then the blood stream [3, 8]. In the lymphatic circulation and blood, BoNT exists as a free form dissociated from the complex [3, 9] and binds specifically to neurons [2, 10]. Inhibition of neurotransmitter release occurs via a four-step mechanism, ( 1 ) binding, ( 2 ) endocytosis, ( 3 ) translocation, and ( 4 ) cleavage of the SNARE proteins [2].
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(a) BoNT complex
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(b) Food-borne botulism