ArticleNature communications2015
Botulinum toxin A complex exploits intestinal M cells to enter the host and exert neurotoxicity.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Mucosal immunity: mechanism and application in cancer immunotherapy.Journal of hematology & oncology · 2026Review
- Equine botulism.Equine veterinary journal · 2026Review
- Enteric botulinum neurotoxins facilitate infection byScience advances · 2026Article
- From Gut to Systemic Circulation: Molecular Strategies of Botulinum Neurotoxin Complexes.Toxins · 2026Review
- Advances in Clostridial Neurotoxins: Passage of the Intestinal Barrier and Targeting of Specific Neuronal Cells.Toxins · 2026Review
- Gut mucin fucosylation dictates the entry of botulinum toxin complexes.Nature communications · 2025Article
- Article
- Infant Botulism and Carbohydrate Blood Group Antigens: Preliminary Results from a Discordant Twin Study.Journal of pediatrics. Clinical practice · 2025Article
- Gut mucin fucosylation dictates the entry of botulinum toxin complexes.bioRxiv : the preprint server for biology · 2025Article
- A nut-and-bolt assembly of the bimodular large progenitor botulinum neurotoxin complex.Science advances · 2025Article
- Structure of the complete 14-subunit botulinum neurotoxin B complex reveals a unique anchoring through the narrow central pore of HA70.Science advances · 2025Article
- Observational
- Deciphering the M-cell niche: insights from mouse models on how microfold cells "know" where they are needed.Frontiers in immunology · 2024Review
- Glycoprotein 2 as a gut gate keeper for mucosal equilibrium between inflammation and immunity.Seminars in immunopathology · 2024Review
- Pathogenicity and virulence ofVirulence · 2023Review
- Inhibition of microfold cells ameliorates early pathological phenotypes by modulating microglial functions in Alzheimer's disease mouse model.Journal of neuroinflammation · 2023Article
- Therapeutic Applications of Botulinum Neurotoxins in Veterinary Medicine.Veterinary sciences · 2023Review
- Mucosal Immunity and the Gut-Microbiota-Brain-Axis in Neuroimmune Disease.International journal of molecular sciences · 2022Review
- Review
- Membrane Vesicles Derived FromFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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