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Gut 58:886-887 doi:10.1136/gut.2008.167296
  • Letter
    • PostScript

Is it true that coeliacs do not digest gliadin? Degradation pattern of gliadin in coeliac disease small intestinal mucosa

  1. D Bernardo1,
  2. J A Garrote1,2,
  3. I Nadal3,
  4. A J León1,
  5. C Calvo1,4,
  6. L Fernández-Salazar5,
  7. A Blanco-Quirós1,
  8. Y Sanz3,
  9. E Arranz1
  1. 1
    Mucosal Immunology Laboratory, Department of Paediatrics and Immunology, Universidad de Valladolid, IBGM-CSIC, Spain
  2. 2
    Research Unit, Hospital Clínico Universitario, Valladolid, Spain
  3. 3
    Instituto de Agroquímica y Tecnología de Alimentos, (CSIC), Burjassot, Valencia, Spain
  4. 4
    Paediatrics Service, Hospital Clínico Universitario, Valladolid, Spain
  5. 5
    Gastroenterology Service, Hospital Clínico Universitario, Valladolid, Spain
  1. Dr E Arranz, Mucosal Immunology Laboratory, Department of Paediatrics and Immunology-IBGM, University of Valladolid, C/Ramón y Cajal, 7, 47005 Valladolid, Spain; earranz{at}med.uva.es

    Prolyl-endopeptidase supplementation has been proposed to favour gliadin degradation as an alternative treatment for coeliac disease (CD), although the real usefulness of this therapy in vivo is still under discussion.1 However, our data point to alternative treatments aiming to modify the intestinal microbiota in patients with CD by the use of probiotics and/or prebiotics. We propose that the induction of gliadin proteolysis in the human gut might not be the solution but the origin of CD.

    We have carried out gliadin zymograms using a complete protein solution from duodenal mucosa of patients with CD, both untreated patients with positive serology, genetics and duodenal inflammation (n = 20), and treated patients on a gluten-free diet (GFD) with negative serology and recovering mucosa (n = 9). We have also analysed 18 non-CD controls, without mucosal inflammation and negative serology.

    Figure 1 reveals for the first time to our knowledge, and in contrast to what would be expected, the existence of a specific gliadinase pattern in duodenal samples from patients with CD. This pattern was observed regardless of the phase …