4.3 Article

Defensin-mRNA Expression in the Upper Gastrointestinal Tract Is Modulated in Children With Celiac Disease and Helicobacter pylori-positive Gastritis

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MPG.0b013e3181cd26cd

Keywords

celiac disease; defensins; gastrointestinal tract; Helicobacter pylori; innate immunity

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Objectives: Defensins are expressed in epithelial cells as cationic peptides with antimicrobial properties. Because of their role as immunologically important effector molecules, their contribution in maintaining a stable microenvironment in the gastrointestinal tract has recently received much attention. The present study was designed to further characterize expression patterns of defensins in diseases of the upper gastrointestinal tract in children, particularly in Helicobacter pylori (Hp)-associated gastritis or celiac disease (CD). Patients and Methods: Semiquantitative real-time reverse transcriptase-polymerase chain reaction (PCR) was carried out with gene-specific primers for human beta-defensin 1 to 6 (hBD1 to 6) and human alpha-defensin 5 and 6 (hD5 and 6) in mucosal biopsies of children diagnosed as having CD (n = 11; 4.2 - 16.2 years) or Hp gastritis (n = 18; 3.2 - 16.7 years). Levels of expression were compared with those of healthy individuals (n = 21; 2.8 - 14.6 years). Expression levels in Hp-infected specimens were furthermore compared with those with histologic inflammation not associated with Hp infection (n = 30; 3.6 - 15.7 years). Results: Expression of hBD2 was upregulated in the antrum and corpus of patients with Hp gastritis, whereas inflammation without detection of Hp was not associated with any change in defensin gene expression. In patients with CD, expression of hBD2 was upregulated in the antrum, whereas hBD1 and 4 were downregulated in duodenal biopsies. Conclusions: Different pathological conditions of the upper gastrointestinal tract lead to specific modulations of defensin gene expression in children. Especially the pathophysiological role of hBD2 in Hp infection and hBD1 and 4 in CD warrant further attention.

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