Inducible and constitutive β‐defensins are differentially expressed in Crohn's disease and ulcerative colitis

Antimicrobial peptides such as defensins provide nonspecific mucosal defense against a multitude of microorganisms. Recently, it has been shown that luminal bacteria may invade the mucosa in inflammatory bowel diseases, suggesting a defect in innate mucosal immunity. The aim of this study was to inv...

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Veröffentlicht in:Inflammatory bowel diseases 2003-07, Vol.9 (4), p.215-223
Hauptverfasser: Wehkamp, Jan, Harder, Juergen, Weichenthal, Michael, Mueller, Oliver, Herrlinger, Klaus R., Fellermann, Klaus, Schroeder, Jens M., Stange, Eduard F.
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Sprache:eng
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Zusammenfassung:Antimicrobial peptides such as defensins provide nonspecific mucosal defense against a multitude of microorganisms. Recently, it has been shown that luminal bacteria may invade the mucosa in inflammatory bowel diseases, suggesting a defect in innate mucosal immunity. The aim of this study was to investigate the expression of human β‐defensins (HBD) in controls, Crohn's disease (CD), ulcerative colitis (UC), and unspecific inflammation. Up to 4 biopsies were taken from 103 patients (33 controls, 24 with Crohn's disease, 36 with ulcerative colitis, 10 with unspecific colitis). Mucosal mRNA was measured using real‐time fluorescence temperature cycler reverse‐transcription polymerase chain reaction with primers for HBD‐1, HBD‐2, HBD‐3, tumor necrosis factor α, and interleukin 8. Mucosal HBD‐1 expression was marginally decreased in both CD and UC. HBD‐2 was increased exclusively in UC but not in CD. The expression of the novel defensin HBD‐3 was strongly correlated with HBD‐2 and also raised predominantly in UC. The expression of both inducible β‐defensins was enhanced in the state of inflammation. Expression of HBD‐2 showed a weak correlation with interleukin 8 only in inflamed CD biopsies but not with tumor necrosis factor α. The missing induction of both inducible β‐defensins in CD as compared with UC may cause a defect in barrier function that predisposes to bacterial invasion.
ISSN:1078-0998
1536-4844
DOI:10.1097/00054725-200307000-00001