The receptor and transporter for internalization of Clostridium botulinum type C progenitor toxin into HT-29 cells

Orally ingested botulinum toxin enters the circulatory system and eventually reaches the peripheral nerves, where it elicits a response of neurological dysfunction. In this study, we report the important findings concerning the mechanism of Clostridium botulinum type C progenitor toxin (C16S) endocy...

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Published in:Biochemical and biophysical research communications 2004-06, Vol.319 (2), p.327-333
Main Authors: Nishikawa, Atsushi, Uotsu, Nobuo, Arimitsu, Hideyuki, Lee, Jae-Chul, Miura, Yutaka, Fujinaga, Yukako, Nakada, Hiroshi, Watanabe, Toshihiro, Ohyama, Tohru, Sakano, Yoshiyuki, Oguma, Keiji
Format: Article
Language:English
Subjects:
Botulinum Toxins - metabolism
Clostridium botulinum
Endocytic mechanisms
Glycosylation
Hemagglutinin
HT29 Cells
Humans
Microscopy, Fluorescence
Mucin
Neuraminidase - pharmacology
O-linked oligosaccharide
Protein Binding
Protein Transport
Toxin binding
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Summary:Orally ingested botulinum toxin enters the circulatory system and eventually reaches the peripheral nerves, where it elicits a response of neurological dysfunction. In this study, we report the important findings concerning the mechanism of Clostridium botulinum type C progenitor toxin (C16S) endocytic mechanism. C16S toxin bound to high molecular weight proteins on the surface of human colon carcinoma HT-29 cells and was internalized, but not if the cells were pretreated with neuraminidase. Benzyl-GalNAc which inhibited O-glycosylation of glycoproteins also interfered in the toxin’s ability to bind the cell surface. On the other hand, the toxin was internalized in spite of pretreatment of the cells with PPMP, an inhibitor of ganglioside synthesis. These results suggest that the glycoproteins, like mucin, fulfill the important roles of receptor and transporter of C16S toxin.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2004.04.183