| Nutrients | |
| Lectin Staining Shows no Evidence of Involvement of Glycocalyx/Mucous Layer Carbohydrate Structures in Development of Celiac Disease | |
| Henrik Toft-Hansen1  Christian Nielsen3  Matteo Biagini2  Steffen Husby1  | |
| [1] Hans Christian Andersen Children’s Hospital, Odense University Hospital, Sdr. Boulevard 29, Odense 5000, Denmark; E-Mail:;Department of Pathology, Odense University Hospital, J.B. Winsløws Vej 15, 2., Odense 5000, Denmark; E-Mail:;Department of Clinical Immunology, Odense University Hospital, Sdr. Boulevard 29, Odense 5000, Denmark; E-Mails: | |
| 关键词: pediatric celiac disease; type 1 diabetes; duodenal biopsies; glycosylation; lectin staining; | |
| DOI : 10.3390/nu5114540 | |
| 来源: mdpi | |
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【 摘 要 】
The presence of unique carbohydrate structures in the glycocalyx/mucous layer of the intestine may be involved in a susceptibility to celiac disease (CD) by serving as attachment sites for bacteria. This host-microbiota interaction may influence the development of CD and possibly other diseases with autoimmune components. We examined duodenal biopsies from a total of 30 children, of which 10 had both celiac disease (CD) and type 1 diabetes (T1D); 10 had CD alone; and 10 were suspected of having gastrointestinal disease, but had normal duodenal histology (non-CD controls). Patients with both CD and T1D were examined before and after remission following a gluten-free diet. We performed lectin histochemistry using peanut agglutinin (PNA) and Ulex europaeus agglutinin (UEA) staining for Gal-β(1,3)-GalNAc and Fucα1-2Gal-R, respectively, of the glycocalyx/mucous layer. The staining was scored based on dissemination of stained structures on a scale from 0 to 3. Evaluation of the scores revealed no difference between biopsies obtained before and after remission in the group of children with both CD and T1D. A comparison of this pre-remission group with the children who had CD alone or the non-CD controls also showed no significant differences. Based on our material, we found no indication that the presence of Gal-β(1,3)-GalNAc or Fucα1-2Gal-R is involved in the susceptibility to CD, or that the disease process affects the expression of these carbohydrates.
【 授权许可】
CC BY
© 2013 by the authors; licensee MDPI, Basel, Switzerland.
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO202003190031357ZK.pdf | 1055KB |
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