論文

査読有り 国際誌
2015年2月

Botulinum toxin A complex exploits intestinal M cells to enter the host and exert neurotoxicity

NATURE COMMUNICATIONS
  • Takuhiro Matsumura
  • ,
  • Yo Sugawara
  • ,
  • Masahiro Yutani
  • ,
  • Sho Amatsu
  • ,
  • Hideo Yagita
  • ,
  • Tomoko Kohda
  • ,
  • Shin-Ichi Fukuoka
  • ,
  • Yutaka Nakamura
  • ,
  • Shinji Fukuda
  • ,
  • Koji Hase
  • ,
  • Hiroshi Ohno
  • ,
  • Yukako Fujinaga

6
開始ページ
6255
終了ページ
6255
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/ncomms7255
出版者・発行元
NATURE PUBLISHING GROUP

To cause food-borne botulism, botulinum neurotoxin (BoNT) in the gastrointestinal lumen must traverse the intestinal epithelial barrier. However, the mechanism by which BoNT crosses the intestinal epithelial barrier remains unclear. BoNTs are produced along with one or more non-toxic components, with which they form progenitor toxin complexes (PTCs). Here we show that serotype A1 L-PTC, which has high oral toxicity and makes the predominant contribution to causing illness, breaches the intestinal epithelial barrier from microfold (M) cells via an interaction between haemagglutinin (HA), one of the non-toxic components, and glycoprotein 2 (GP2). HA strongly binds to GP2 expressed on M cells, which do not have thick mucus layers. Susceptibility to orally administered L-PTC is dramatically reduced in M-cell-depleted mice and GP2-deficient (Gp2(-/-)) mice. Our finding provides the basis for the development of novel antitoxin therapeutics and delivery systems for oral biologics.


リンク情報
DOI
https://doi.org/10.1038/ncomms7255
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/25687350
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4339894
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000350202800005&DestApp=WOS_CPL
ID情報
  • DOI : 10.1038/ncomms7255
  • ISSN : 2041-1723
  • PubMed ID : 25687350
  • PubMed Central 記事ID : PMC4339894
  • Web of Science ID : WOS:000350202800005

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