Aim: 

Coeliac disease (CD) is an autoimmune enteropathy caused, in genetically susceptible individuals, by ingestion of wheat gliadins and prolamins. This leads to villous atrophy, crypt hyperplasia and heavy inflammatory infiltrate of both epithelium and lamina propria. Malabsorption, diarrhea and weight loss are frequent disease symptoms. The aim of this study was to investigate the possible alteration in the expression and localization of water channels (aquaporins, AQP) and of some solute transporters in duodenal mucosa of CD patients.

Methods: 

Four groups were considered: 1) patients with untreated CD, 2) patients with treated CD, following a gluten-free diet, 3) healthy volunteers (control subjects), 4) patients affected by other intestinal diseases served as pathological controls. The expression and the localization of some aquaporins and transporters in duodenal biospies was determined by semiquantitative RT-PCR and immunohistochemistry.

Results: 

AQP-3, -7, -10, -11, Na⁺/glucose cotransporter, H⁺/oligopeptide transporter, Na⁺/H⁺ exchanger, cystic fibrosis transmembrane conductance regulator (CFTR) and Na-K-2Cl cotransporter (NKCC1) mRNAs were similarly expressed in duodenal biopsies from control subjects, treated CD patients and pathological controls. The expression of transcripts was virtually absent in duodenal biopsies of active CD patients except for CFTR and NKCC1 that was unchanged. A strong labeling of the apical membrane of crypt epithelial cells of duodenal mucosa in control subjects at immunohistochemistry was observed. The staining was greatly reduced or absent in untreated CD patients but recovered after a gluten free diet (treated CD patients).

Conclusion: 

Results indicate that the main routes for water and solute absorption are deficient in CD and likely responsible for malabsorption-linked symptoms.