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1 Pathologisches Institut, Universität Heidelberg, 69120 Heidelberg; 2 BASF-LYNX Bioscience AG, 69120 Heidelberg; 3 Deutsches Krebsforschungszentrum, 69120 Heidelberg; 4 Universität Heidelberg, ZMF, Klinikum Mannheim, 68167 Mannheim; and 5 Universität Frankfurt, Abteilung Nephrologie, IV. Medizinische Klinik, 60590 Frankfurt, Germany
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 
-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.
junctional proteins; Crohn's disease; ulcerative colitis
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