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

被引:240
作者
Wehkamp, J
Harder, J
Weichenthal, M
Mueller, O
Herrlinger, KR
Fellermann, K
Schroeder, JM
Stange, EF
机构
[1] Robert Bosch Krankenhaus, Dept Internal Med 1, D-70376 Stuttgart, Germany
[2] Univ Kiel, Dept Dermatol, D-2300 Kiel, Germany
关键词
innate immunity; ulcerative colitis; Crohn's disease; defensins; antimicrobial peptides;
D O I
10.1097/00054725-200307000-00001
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 beta-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-tran script ion polymerase chain reaction with primers for HBD-1, HBD-2. HBD-3. tumor necrosis factor a, 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 beta-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 a. The missing induction of both inducible beta-defensins in CD as compared with UC may cause a defect in barrier function that predisposes to bacterial invasion.
引用
收藏
页码:215 / 223
页数:9
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