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.
Docosahexaenoic 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 patients.