Celiac.com 04/13/2011 - When people with celiac disease consume gluten, their intraepithelial
lymphocytes (IELs) wreak havoc in their guts by promoting inflammation
and attacking the epithelial cells lining the intestines. This
autoimmune activity is mediated by arachidonic acid (AA), a cytokine
produced by the IELs. But there is data that the enterocytes
"the very intestinal epithelial cells attacked by the IELs" can also produce and secrete AA in response to inflammation.
Do they do so in celiac disease?
A recent study reported in
Clinical Nutrition set out to determine just that. Using Caco-2 cells, a
human intestinal epithelial cell line commonly used as an in vitro
model of celiac disease, Vincentini et al. are the first to find that
when these enterocytes were exposed to gliadin peptides, they did in
fact generate and release arachidonic acid.
(DHA) is a long chain polyunsaturated fatty acid that counteracts many
of the inflammatory effects precipitated by AA. When Caco-2 cells were
treated with gliadin peptides and DHA, they produced much less AA
(although they still made more than untreated cells). Treatment with
DHA also reduced the production of other molecules involved in
inflammation that were increased by exposure to gliadin, including
cyclooxygenase (COX)-2, prostaglandin E2 (PGE2), and interleukin (IL)-8.
PGE2 is particularly interesting, as it can increase the intestinal
paracellular permeability that has been suggested to be the initial
event in the pathogenesis of celiac disease.
The authors suggest
that by blocking the release of AA, DHA might be a tenable therapeutic
option for modulating mucosal inflammation in newly diagnosed celiac