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(The FASEB Journal. 2008;22:lb450)
© 2008 FASEB
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lb450

Overexpression of abnormal epithelial glycoprotein MUC1 is associated with pancreatitis and other extraintestinal complications in inflammatory bowel disease (IBD)

Pamela Beatty1, Deepak Kadayakkara2, Michael Turner1, Jelena Janjic2, Eric Ahrens2 and Olivera Finn1

1 Immunology, University of Pittsburgh, Pittsburgh, PA,
2 Biological Sciences, Carnegie Mellon University, Pittsburgh, PA

ABSTRACT

IBD patients are at increased risk for colon cancer and extraintestinal complications including pancreatitis, the mechanisms of which are poorly understood. Earlier studies have shown that overexpression of hypoglycosylated (abnormal) form of epithelial MUC1 in colon accelerates the progression of IBD and colon cancer. Our data suggest that abnormal MUC1 expression is also responsible for the extraintestinal manifestations of IBD. We generated TCR transgenic mice specific for hypoglycosylated MUC1. We transferred T cells labeled with perfluoropolyether (PFPE) nanoemulsions into MUC1 transgenic mice with IBD. Three days later, we quantified the biodistribution of transferred cells in various organs by 19F NMR spectroscopy. The transferred T cells migrated as expected to the colon only in mice with disease. Unexpectedly, large numbers of T cells migrated to pancreas and liver. Immunohistochemistry showed increased expression of abnormal MUC1 in pancreatic acini and ducts in mice with IBD. This change appears sufficient to drive high levels of inflammation causing pancreatitis and liver problems. Thus, we conclude that abnormal expression of MUC1 plays an important role in the intestinal and extraintestinal manifestations of IBD in these animals.

This work is supported by Cancer Research and Prevention Foundation (P.L.B), RO1 56103 (O.J.F.) and NIH R01-EB003453 and P41-EB001977 (E.T.A).





This Article
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