Jelena Janjic - Inflammation driven by overexpression of the hypoglycosylated abnormal mucin 1 (MUC1) links inflammatory bowel disease and pancreatitis.

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      Publication Details (including relevant citation   information):

        Kadayakkara DK,   Beatty PL,   Turner MS,   Janjic JM,   Ahrens ET,   Finn OJ.

      Pancreas. 2010 May;39(4):510-5.

      Abstract:

     

     

        OBJECTIVE: Pancreatitis  occurs as an extraintestinal     complication of inflammatory bowel disease  (IBD), but the     cause is poorly understood. Mucin 1 (MUC1) is      overexpressed in an abnormal, hypoglycosylated form on the     colonic  epithelium in human IBD where it contributes to     inflammation. MUC1 is  also expressed on pancreatic ductal     epithelia. We tested the possibility  that in IBD, MUC1     expression on pancreatic ducts is also abnormal  leading     to inflammation and pancreatitis.  

     

        METHODS: We  used MUC1/interleukin-10 mice that develop     IBD. We imaged abnormal MUC1  expression in these mice by     adoptively transferring T cells from T cell  receptor     transgenic mice specific for abnormal MUC1. Cells were     labeled  with a novel perfluorocarbon tracer reagent and     quantified and  visualized in vivo using high-throughput F     nuclear magnetic resonance  spectroscopy and magnetic     resonance imaging.  

     

        RESULTS: MUC1-specific  T cells migrated to the colon in     mice with IBD and also to the  pancreas.     Immunohistochemistry confirmed increased expression on     the  pancreatic ducts of the abnormal MUC1 seen in the     colon and the presence  of cellular infiltrate.  

     

        CONCLUSIONS: Migration  of MUC1-specific T cells to the     colon and the pancreas in diseased mice  suggests that     pancreatitis is an extraintestinal site of IBD,      characterized by proinflammatory abnormal expression of MUC1.     Therapies  directed against abnormal MUC1 have the     potential of targeting the  disease in both sites.  

      Address (URL): http://www.ncbi.nlm.nih.gov/pubmed/20084048