ArticleACS infectious diseases2018
Fucosylated Molecules Competitively Interfere with Cholera Toxin Binding to Host Cells.
Article in ACS infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Attenuating ETEC virulence using a heat-labile enterotoxin-blocking binding protein.Gut microbes · 2026Article
- Fucosylated hemocyanin regulates ER stress to enhance shrimp antibacterial immunity.Virulence · 2026Article
- Kinetic Insights into Cholera Toxin B-Biomimetic Glycan Interactions.Biomacromolecules · 2026Article
- Gut mucin fucosylation dictates the entry of botulinum toxin complexes.Nature communications · 2025Article
- Gut mucin fucosylation dictates the entry of botulinum toxin complexes.bioRxiv : the preprint server for biology · 2025Article
- Article
- Fucosylation of glycoproteins and glycolipids: opposing roles in cholera intoxication.Nature chemical biology · 2025Article
- Recent advances in the science of human milk oligosaccharides.BBA advances · 2025Article
- Synthesis and screening of a library of LewisNature communications · 2024Article
- Surface Glycans of Microvesicles Derived from Endothelial Cells, as Probed Using Plant Lectins.International journal of molecular sciences · 2024Article
- Cholera intoxication of human enteroids reveals interplay between decoy and functional glycoconjugate ligands.Glycobiology · 2023Article
- Fucosylated glycoproteins and fucosylated glycolipids play opposing roles in cholera intoxication.bioRxiv : the preprint server for biology · 2023Article
- Article
- In silico analysis of the human milk oligosaccharide glycome reveals key enzymes of their biosynthesis.Scientific reports · 2022Article
- Characterization of the ganglioside recognition profile of Escherichia coli heat-labile enterotoxin LT-IIc.Glycobiology · 2022Article
- Glycan-mediated molecular interactions in bacterial pathogenesis.Trends in microbiology · 2022Review
- Review
- Digestion, fermentation, and pathogen anti-adhesive properties of the hMO-mimic di-fucosyl-β-cyclodextrin.Food & function · 2021Article
- Global mapping of glycosylation pathways in human-derived cells.Developmental cell · 2021Article
- Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Cholera toxin (CT) enters host intestinal epithelia cells, and its retrograde transport to the cytosol results in the massive loss of fluids and electrolytes associated with severe dehydration. To initiate this intoxication process, the B subunit of CT (CTB) first binds to a cell surface receptor displayed on the apical surface of the intestinal epithelia. While the monosialoganglioside GM1 is widely accepted to be the sole receptor for CT, intestinal epithelial cell lines also utilize fucosylated glycan epitopes on glycoproteins to facilitate cell surface binding and endocytic uptake of the toxin. Further, l-fucose can competively inhibit CTB binding to intestinal epithelia cells. Here, we use competition binding assays with l-fucose analogs to decipher the molecular determinants for l-fucose inhibition of cholera toxin subunit B (CTB) binding. Additionally, we find that mono- and difucosylated oligosaccharides are more potent inhibitors than l-fucose alone, with the LeY tetrasaccharide emerging as the most potent inhibitor of CTB binding to two colonic epithelial cell lines (T84 and Colo205). Finally, a non-natural fucose-containing polymer inhibits CTB binding two orders of magnitude more potently than the LeY glycan when tested against Colo205 cells. This same polymer also inhibits CTB binding to T84 cells and primary human jejunal epithelial cells in a dose-dependent manner. These findings suggest the possibility that polymeric display of fucose might be exploited as a prophylactic or therapeutic approach to block the action of CT toward the human intestinal epithelium.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.