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No mucosal inflammation, basophil activation from gliadin in nonceliac gluten-sensitive patients
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Neither mucosal inflammation nor basophil activation occurred after gliadin incubation in duodenal mucosal samples collected from patients with nonceliac gluten sensitivity compared with samples obtained from patients with celiac disease in a recent study.
Researchers obtained mucosa samples from 34 patients with celiac disease (CD) on gluten-free diets (GFD) for at least 6 months, 35 untreated patients with CD, 16 patients with nonceliac gluten sensitivity (NCGS) and 34 healthy controls between January 2010 and July 2011. Inflammatory markers, including anti-phosphotyrosine-monoclonal antibody (PY99), HLA-DR, intercellular cell adhesion molecule-1 (ICAM-1), CD3, CD25 and CD69, were measured in each biopsy sample after incubation with gliadin. Skin prick tests were administered to identify wheat allergy.
Normal mucosal architecture was observed in 56.3% of patients with NCGS. The remaining seven participants had increased intraepithelial infiltration, but without eosinophils. No patients experienced villous atrophy.
All patients with CD indicated increased immunofluorescence intensity for early and delayed markers of inflammation after gliadin stimulation. Weak levels of some of these markers were also observed in three patients with NCGS and three controls. Investigators said one patient each in the NCGS and control groups whose results indicated only weak PY99 and ICAM-1 positivity also had Helicobacter pylori infection. Basophil challenge via peptic-tryptic gliadin digest and a wheat protein mixture did not significantly increase CD63 or CD203c in the NCGS group.
“In NCGS patients, gliadin fractions do not provoke a clear picture of inflammation upon contact with the duodenal mucosa or with peripheral basophils or, if they do, the inflammation is not comparable with that observed in CD patients,” the researchers concluded. “Furthermore, our study suggests the possibility that wheat components other than proteins, for example, carbohydrates that already had been associated with the appearance of GI symptoms in patients with IBS; also should be investigated for their role in the pathogenesis of NCGS.”
Disclosure: The researchers report no relevant financial disclosures.
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