title: Human beta-defensin 2 but not beta-defensin 1 is expressed preferentially in colonic mucosa of inflammatory bowel disease.
abstract: OBJECTIVE
  Various antimicrobial peptides such as defensins are part of innate immunity and contribute to the intestinal barrier that may be defective in inflammatory bowel disease (IBD). This study investigated beta-defensin mRNA and peptide expression in the colon from controls and patients with Crohn's disease, ulcerative colitis or unspecific colitis as inflammatory controls.
  
  
  METHODS
  Mucosal mRNA expression was measured by multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) with primers for human beta-defensin 1 (HBD-1) and human beta-defensin 2 (HBD-2) in CaCo-2 cells and in biopsies from 103 patients (33 controls, 24 Crohn's disease patients, 36 ulcerative colitis patients, 10 unspecific colitis patients). Paraffin-embedded tissue from colonic resections was tested for HBD-1 and HBD-2 peptides by immunohistochemistry.
  
  
  RESULTS
  HBD-1 mRNA was expressed constitutively whereas HBD-2 was induced by pro-inflammatory cytokines in CaCo-2 cells. HBD-1 mRNA was detectable in 61% of control and Crohn's disease biopsies and 53% of ulcerative colitis biopsies. HBD-2 transcript was expressed differentially, with 18% of control biopsies positive as opposed to 34% in Crohn's disease and 53% in ulcerative colitis. HBD-2 mRNA but not HBD-1 mRNA was expressed preferentially in inflamed areas. Immunohistochemical investigation demonstrated the presence of defensin peptides in colonic epithelium as well as the differential induction in IBD.
  
  
  CONCLUSIONS
  HBD-1 is expressed constitutively in colonic tissue irrespective of inflammation. HBD-2 is barely present in uninflamed colon but it is induced in inflammation. The lower expression of HBD-2 in Crohn's disease compared with ulcerative colitis indicates different responses of the mucosal innate defence. Defensins may play a crucial role in controlling pathogen invasion in IBD, although the functional significance remains to be established.
authors.affiliation: Department of Internal Medicine I, Division of Gastroenterology, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany.
authors.forename: Jan
authors.initials: J
authors.lastname: Wehkamp
authors.forename: Klaus
authors.initials: K
authors.lastname: Fellermann
authors.forename: Klaus R
authors.initials: KR
authors.lastname: Herrlinger
authors.forename: Steffi
authors.initials: S
authors.lastname: Baxmann
authors.forename: Klaus
authors.initials: K
authors.lastname: Schmidt
authors.forename: Bettina
authors.initials: B
authors.lastname: Schwind
authors.forename: Michael
authors.initials: M
authors.lastname: Duchrow
authors.forename: Charlotte
authors.initials: C
authors.lastname: Wohlschläger
authors.forename: Alfred C
authors.initials: AC
authors.lastname: Feller
authors.forename: Eduard F
authors.initials: EF
authors.lastname: Stange
mesh_terms: D002478:Cells, Cultured; D003093:Colitis, Ulcerative / Q000378:metabolism; D003106:Colon / Q000378:metabolism*; D003424:Crohn Disease / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D015212:Inflammatory Bowel Diseases / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D023083:beta-Defensins / Q000235:genetics / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D023083:beta-Defensins