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Regulation of pancreatic inflammation by connective tissue growth factor (CTGF/CCN2)*

Posted by on in 2014
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  1. Alyssa Charrier1,2
  3. Ruju Chen1
  5. Sherri Kemper1 and
  7. David R. Brigstock1,2,3,* 2014. Immunology 141:564-576.

    Author Information

  8. 1

    Center for Clinical and Translational Research, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA

  9. 2

    Molecular, Cellular and Developmental Biology Program, The Ohio State University, Columbus, OH, USA

  10. 3

    Department of Surgery, The Ohio State University, Columbus, OH, USA

    * Correspondence: David R. Brigstock, Center for Clinical and Translational Research, The Research Institute at Nationwide Children's Hospital, Room WA2011, 700 Children's Drive, Columbus, OH 43205, USA. 
    Email: David.Brigstock@NationwideChildrens.Org
    Senior author: David R. Brigstock



    Pancreatitis is caused by long-term heavy alcohol consumption, which results in injury and death of pancreatic acinar cells (PAC). The PAC play a pivotal role in mediating early inflammatory responses but the underlying mechanisms remain poorly understood. Treatment of C57BL/6 mice with ethanol and cerulein resulted in increased staining for acinar interleukin-1β (IL-1β), chemokine (C-C motif) ligand 3 (CCL3), or connective tissue growth factor (CTGF/CCN2) by Day 16 and this was associated with increased infiltration of F4/80-positive macrophages and increased expression of pancreatic CTGF/CCN2 mRNA. Compared with wild-type Swiss Webster mice, ethanol treatment of pan-green fluorescent protein (GFP)-CTGF/CCN2 transgenic mice caused enhanced acinar staining for GFP or CTGF/CCN2 and a significant increase in pancreatic infiltration of F4/80-positive macrophages or NIMP-R14-positive neutrophils. Treatment of primary mouse PAC or the rat AR42J PAC line with ethanol or CTGF/CCN2 resulted in enhanced expression of IL-1β or CCL3. Conditioned medium from CTGF/CCN2-treated AR42J cells induced chemotaxis in NR8383 macrophages and this response was abrogated in a dose-dependent manner by addition of BX471, an inhibitor of chemokine (C-C motif) receptor 1. These results reveal that acinar CTGF/CCN2 plays a novel role in alcohol-induced inflammatory processes in the pancreas by increasing infiltration of macrophages and neutrophils and increasing acinar production of inflammatory mediators such as IL-1β or CCL3. The early production of CTGF/CCN2 by PAC to drive inflammation is distinct from its previously reported production by pancreatic stellate cells to drive fibrosis at later stages of pancreatic injury.

    *Note: The Normal Chicken IgY used in this publication was produced by Gallus Immunotech Inc.

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