Intra-acinar trypsinogen activation mediates early stages of pancreatic injury but not inflammation in mice with acute pancreatitis.

ABSTRACT:

Background & aims

The role of trypsinogen activation in the pathogenesis of acute pancreatitis (AP) has not been clearly established.

Methods

We generated and characterized mice lacking trypsinogen isoform 7 (T7) gene (T(-/-)). The effects of pathologic activation of trypsinogen were studied in these mice during induction of AP with cerulein. Acinar cell death, tissue damage, early intra-acinar activation of the transcription factor nuclear factor κB (NF-κB), and local and systemic inflammation were compared between T(-/-) and wild-type mice with AP.

Results

Deletion of T7 reduced the total trypsinogen content by 60% but did not affect physiologic function. T(-/-) mice lacked pathologic activation of trypsinogen, which occurs within acinar cells during early stages of

SUBMITTER: Dawra R 

PROVIDER: S-EPMC3587766 | biostudies-literature | 2011 Dec

REPOSITORIES: biostudies-literature