Background: Recent genetic investigations into cationic trypsinogen and pancreatic secretory trypsin inhibitor (PSTI) led to the conclusion that mutations in either gene can contribute to the development of (hereditary) chronic pancreatitis. Since genetic animal models are not available yet, we have studied the Wistar-Bonn/Kobori (WBN/Kob) rat, a model for chronic pancreatitis (CP). To explore the possibility that PSTI may be secreted at lower levels or contain a mutation in the WBN/Kob rat, we investigated the masses of PSTI-I and -II and asked whether the ratio of PSTI/trypsinogen is decreased in animals with CP. Methods: We collected pancreatic juice from WBN/Kob and Wistar rats aged 6–36 weeks and measured PSTI-I (ELISA) and trypsin. Results: PSTI-I and -II were identified in Wistar and WBN/Kob rats by mass spectrometry and N-terminal sequencing. Using a newly developed PSTI-I ELISA, we can show that the PSTI-I/trypsinogen ratio is not decreased but rather increased in WBN/Kob rats compared to healthy Wistar rats. No evidence for a PSTI mutation was found. Conclusion: Our data does not support the hypothesis that a dysbalance of PSTI/trypsinogen ratio is a causative factor for CP.

Keywords:
Secretory stress proteins, Pancreas, Acute pancreatitis, Pancreatic stone protein, Immunohistochemistry, Coordinate regulation
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© 2002 S. Karger AG, Basel and IAP
2002
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