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Polymeric Binders Block Gliadin-induced Intestinal Cell Toxicity
- By Jefferson Adams
- Published 10/16/2009
- Celiac Disease & Gluten Intolerance Research
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Jefferson Adams
Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
View all articles by Jefferson Adams
Celiac.com 10/16/2009 - A team of researchers recently set out to investigate the ability of a polymeric binder to reverse the toxic effects induced by gliadin in human intestinal cells and gliadin-sensitive HCD4-DQ8 mice. The team was made up of Maud Pinier, Elena F. Verdu, Mohamad Nasser–Eddine, Chella S. David, Anne Vézina, Nathalie Rivard, and Jean–Christophe Leroux.
The team neutralized gliadin through complexation to a linear copolymer of hydroxyethylmethacrylate (HEMA) and sodium 4-styrene sulfonate (SS). They then examined the ability of the polymeric binder to mitigate the damaging effect of gliadin on cell-cell contact in IEC-6, Caco-2/15, and primary cultured differentiated enterocytes.
They used gliadin-sensitive HLA-HCD4/DQ8 transgenic mice to measure the effectiveness of the polymeric binder in averting gliadin-triggered intestinal barrier dysfunction. They found that Poly(hydroxyethylmethacrylate-co-styrene sulfonate) [P(HEMA-co-SS)] complexed with gliadin in a fairly precise manner.
Exposing intestinal cells to gliadin caused major changes in both cell structure and cell to cell contacts. By complexing the gliadin with P(HEMA-co-SS) the researchers were able to prevent these undesirable changes. More importantly, the P(HEMA-co-SS) inhibited gliadin digestion by gastrointestinal enzymes, which minimized the development of peptides that trigger immune adverse immune reactions.
By co-administering P(HEMA-co-SS) with gliadin to HLA-HCD4/DQ8 mice, researchers were able to eliminate gliadin-triggered changes in the gut barrier and lower intraepithelial lymphocyte and macrophage cell counts.
From these results, the team concludes that polymeric binders can prevent in vitro gliadin-induced epithelial toxicity and intestinal barrier dysfunction in HCD4/DQ8 mice. Such polymeric binders might play a significant role in the treating people with gluten-induced disorders.
Source:
GASTROENTEROLOGY 2009;136:288–298
The team neutralized gliadin through complexation to a linear copolymer of hydroxyethylmethacrylate (HEMA) and sodium 4-styrene sulfonate (SS). They then examined the ability of the polymeric binder to mitigate the damaging effect of gliadin on cell-cell contact in IEC-6, Caco-2/15, and primary cultured differentiated enterocytes.
They used gliadin-sensitive HLA-HCD4/DQ8 transgenic mice to measure the effectiveness of the polymeric binder in averting gliadin-triggered intestinal barrier dysfunction. They found that Poly(hydroxyethylmethacrylate-co-styrene sulfonate) [P(HEMA-co-SS)] complexed with gliadin in a fairly precise manner.
Exposing intestinal cells to gliadin caused major changes in both cell structure and cell to cell contacts. By complexing the gliadin with P(HEMA-co-SS) the researchers were able to prevent these undesirable changes. More importantly, the P(HEMA-co-SS) inhibited gliadin digestion by gastrointestinal enzymes, which minimized the development of peptides that trigger immune adverse immune reactions.
By co-administering P(HEMA-co-SS) with gliadin to HLA-HCD4/DQ8 mice, researchers were able to eliminate gliadin-triggered changes in the gut barrier and lower intraepithelial lymphocyte and macrophage cell counts.
From these results, the team concludes that polymeric binders can prevent in vitro gliadin-induced epithelial toxicity and intestinal barrier dysfunction in HCD4/DQ8 mice. Such polymeric binders might play a significant role in the treating people with gluten-induced disorders.
Source:
GASTROENTEROLOGY 2009;136:288–298
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