Low expression of human β-defensin 1 in duodenum of celiac patients is partially restored by a gluten-free diet
Clinical Chemistry and Laboratory Medicine, ISSN: 1434-6621, Vol: 48, Issue: 4, Page: 489-492
2010
- 8Citations
- 25Captures
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Metrics Details
- Citations8
- Citation Indexes8
- CrossRef5
- Captures25
- Readers25
- 25
Article Description
Background: Human β-defensins (hBDs) are small cationic, widely expressed proteins involved in innate immunity that exert strong bactericidal activity toward various pathogens. However, the role of hBDs in various diseases to which bacterial infection add severity, as it is in celiac disease (CD), is not yet clear. We analyzed the expression of the hBD1, hBD2, hBD3 and hBD4 genes in patients with CD during the active phase and after remission following a gluten-free diet to determine their role in development and relapse of CD. Methods: We studied 21 unrelated adults with CD (confirmed by anti-thyroglobulin antibodies and intestinal biopsy); 14 were evaluated at diagnosis, before diet modification, and seven after 2 years of a gluten-free diet. Thirty-six unrelated adults served as controls. We analyzed the mRNA expression of hBD1, 2, 3 and 4 on biopsy samples of duodenum obtained from all patients during endoscopy for diagnostic purposes. We used real-time polymerase chain reaction with TaqMan probes and obtained gene expression data using the delta-Ct method. Results: hBD1 mRNA was significantly lower in patients with active CD compared with patients on diet modification, whereas the mRNA levels of the other three defensins did not differ significantly between the two subgroups. Interestingly, the gluten-free diet restored only partially hBD1 expression as compared to a normal group of celiac-free subjects. Conclusions: Our data reinforce the evidence that hBD1 expression is greatly reduced in the duodenum of patients with active CD. It also strengthens the concept that reduced activity of immune peptides may predispose individuals to bacterial proliferation that contributes to the pathogenesis of CD. © 2010 by Walter de Gruyter Berlin New York.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77949856336&origin=inward; http://dx.doi.org/10.1515/cclm.2010.098; http://www.ncbi.nlm.nih.gov/pubmed/20128731; https://www.degruyter.com/view/j/cclm.2010.48.issue-4/cclm.2010.098/cclm.2010.098.xml; https://www.degruyter.com/view/j/cclm.2010.48.issue-4/cclm.2010.098/cclm.2010.098.pdf; https://www.degruyter.com/document/doi/10.1515/CCLM.2010.098/html
Walter de Gruyter GmbH
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