Mucin-1 is required for Coxsackie Virus B3-induced inflammation in pancreatitis

Xiang Liu, Dahn L. Clemens, James A. Grunkemeyer, Jeffrey D. Price, Kelly O’Connell, Nora M Chapman, Peter Storz, Haitao Wen, Jesse L. Cox, Whitney L. Reid, Michael A. Hollingsworth, Sarah P Thayer

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

The Muc-1 oncoprotein is a tumor-associated mucin often overexpressed in pancreatic cancer. We report that knockout of Muc-1 reduced the degree of pancreatic inflammation that resulted from infection with Coxsackievirus B3 (CVB3) in a mouse model. CVB3-infected Muc-1-deficient (Muc-1KO) mice had significantly reduced infiltration of macrophages into the murine pancreas. We found that Muc-1 signaling through NF-κB increased expression of ICAM-1, a pro-inflammatory mediator that recruits macrophages. Further investigation revealed that bone marrow derived macrophages (BMDM) from the Muc-1KO mice exhibited defective migration properties, in part due to low expression of the C-C motif chemokine receptor (CCR2) and the integrin Very Late Antigen 4 (VLA-4). The results presented here provide novel insight into the role of Muc-1 in regulating the inflammatory response and the cellular microenvironment in pancreatitis.

Original languageEnglish (US)
Article number10656
JournalScientific reports
Volume9
Issue number1
DOIs
StatePublished - Dec 1 2019

ASJC Scopus subject areas

  • General

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