**Detection of Cereal Toxic Peptides Based on New Laboratory Methods**

112 Celiac Disease – From Pathophysiology to Advanced Therapies

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**7** 

*Spain* 

**Sensitive Detection of Cereal Fractions** 

**Using Monoclonal Antibodies to a Main** 

**Immunogenic Gluten Peptide** 

*Department of Microbiology and Parasitology, Faculty of Pharmacy, University of Seville, Seville,* 

**that Are Toxic to Coeliac Disease Patients,** 

Carolina Sousa, Ana Real, Mª de Lourdes Moreno and Isabel Comino

Coeliac disease (CD) is a common autoimmune disorder that has genetic, environmental, and immunological components. Though under-diagnosed, it is one of the most prevalent chronic gastrointestinal diseases in humans, and exhibits unusually large clinical, histological, immunological, and genetic heterogeneity (Alaedini & Green, 2005; Sollid & Khosla, 2005). The clinical spectrum of CD has been expanded in recent years, with the identification of asymptomatic patients, patients with minimal symptoms (the most difficult to detect), and patients with extra-intestinal symptoms (Sollid & Khosla, 2005). Regardless of symptomatic presentation, the active disease in virtually all CD patients requires dietary exposure to a common environmental antigen, gluten. The ingestion of gluten proteins contained in wheat, barley, and rye, and in some cases oats (Arentz-Hansen et al., 2004; Comino et al., 2011), leads to characteristic inflammation, villous atrophy, and crypt

Gluten is a complex mixture of polypeptides. The main immunogenic peptides of gluten belong to a family of closely related proline- and glutamine-rich proteins called prolamines (15% proline and 35% glutamine residues). Gliadin, hordein, secalin, and avenin are the

CD is triggered by peptides that result from the fragmentation of prolamines, and are not digested by human proteases because the high proline and glutamine content prevents complete proteolysis by gastric and pancreatic enzymes, and long oligopeptides that are toxic to coeliac sprue patients build up in the small intestine (Sollid & Khosla, 2005). *In vitro* and *in vivo* studies in rats and humans have demonstrated that a 33-mer peptide from gliadin is not digestible by gastric, pancreatic, and intestinal brush-border membrane endoproteases (Shan et al., 2002). This and similar peptides have been identified as the

At present, treatment with a gluten-free diet (GFD) is the only available therapy for CD patients. However, it is not easy to maintain a diet with zero gluten content because gluten

prolamines of wheat, barley, rye, and oats, respectively (Sollid & Khosla, 2005).

**1. Introduction** 

hyperplasia in the CD patient's upper small intestine.

principal contributors to gluten immunotoxicity.
