title: Inflammatory bowel disease is associated with changes of enterocytic junctions.
abstract: Changes of the intestinal mucosal barrier are considered to play a role in the pathogenesis of inflammatory bowel disease (IBD). Our experiments were designed to identify dysregulation of epithelial junctional molecules in the IBD intestinum and to address whether altered expression of these molecules is a primary event in IBD or a phenomenon secondary to the inflammatory process. Noninflamed and inactively and actively inflamed mucosal tissues from patients with ulcerative colitis or Crohn's disease as well as tissues from control subjects were analyzed for the expression of junctional molecules by different methods. Marked downregulation of junctional proteins and their respective mRNAs was observed in actively inflamed IBD tissues. In IBD tissues with inactive inflammation, only a few junctional molecules such as E-cadherin and alpha-catenin were affected, whereas expression of desmosomal or tight junction-associated proteins appeared almost unchanged. In noninflamed IBD tissues, junctional protein expression was not different from that seen in normal control subjects. In IBD, downregulation of junctional molecule expression is apparently associated with the inflammatory process and does not likely represent a primary phenomenon.
authors.affiliation: Pathologisches Institut, Universität Heidelberg, 69120 Heidelberg, Germany.
authors.forename: N
authors.initials: N
authors.lastname: Gassler
authors.forename: C
authors.initials: C
authors.lastname: Rohr
authors.forename: A
authors.initials: A
authors.lastname: Schneider
authors.forename: J
authors.initials: J
authors.lastname: Kartenbeck
authors.forename: A
authors.initials: A
authors.lastname: Bach
authors.forename: N
authors.initials: N
authors.lastname: Obermüller
authors.forename: H F
authors.initials: HF
authors.lastname: Otto
authors.forename: F
authors.initials: F
authors.lastname: Autschbach
mesh_terms: D000328:Adult; D015153:Blotting, Western; D015820:Cadherins / Q000032:analysis / Q000235:genetics; D003093:Colitis, Ulcerative / Q000378:metabolism / Q000473:pathology*; D003424:Crohn Disease / Q000378:metabolism / Q000473:pathology*; D003598:Cytoskeletal Proteins / Q000032:analysis / Q000235:genetics; D051180:Desmoplakins; D020895:Enterocytes / Q000737:chemistry / Q000473:pathology*; D005260:Female; D005455:Fluorescent Antibody Technique; D015870:Gene Expression; D006801:Humans; D007365:Intercellular Junctions / Q000737:chemistry / Q000473:pathology*; D007413:Intestinal Mucosa / Q000737:chemistry / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000032:analysis / Q000235:genetics; D008875:Middle Aged; D062793:Occludin; D051191:Plakophilins; D016133:Polymerase Chain Reaction; D011506:Proteins / Q000032:analysis / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D015534:Trans-Activators; D051178:alpha Catenin; D051176:beta Catenin
chemical_list: C495273:CTNNA1 protein, human; C495270:CTNNB1 protein, human; D015820:Cadherins; D003598:Cytoskeletal Proteins; D051180:Desmoplakins; D008565:Membrane Proteins; C568985:OCLN protein, human; D062793:Occludin; D051191:Plakophilins; D011506:Proteins; D012333:RNA, Messenger; D015534:Trans-Activators; D051178:alpha Catenin; D051176:beta Catenin