Induction of acute pancreatitis in germ-free rats: evidence of a primary role for tumor necrosis factor-alpha. Academic Article uri icon

Overview

abstract

  • BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) has been implicated as a mediator of the systemic manifestations associated with acute pancreatitis. The purpose of this study was to show that TNF-alpha expression in pancreatitis is a primary response and is not the result of endotoxemia. METHODS: Severe acute pancreatitis was induced in germ-free rats, which have no source of endogenous endotoxin, by ductal infusion of artificial bile. Control animals underwent sham operation and ductal infusion of saline solution. TNF-alpha levels were measured by the WEHI bioassay. Endotoxin was measured by the Limulus assay. RESULTS: TNF-alpha levels remained low in the sham group (mean, 24.6 +/- 8.0 pg/ml) but were significantly elevated in normal rats with pancreatitis (181 +/- 26.8 pg/ml; p < 0.001 versus sham group) and in germ-free rats with pancreatitis (213 +/- 90 pg/ml; p < 0.002 versus sham group). No endotoxin was detected in any of the experimental rats. CONCLUSIONS: Our results indicate that TNF-alpha levels are elevated in acute pancreatitis despite the absence of endotoxin, indicating a primary role of TNF-alpha in this disease.

publication date

  • February 1, 1995

Research

keywords

  • Germ-Free Life
  • Pancreatitis
  • Tumor Necrosis Factor-alpha

Identity

Scopus Document Identifier

  • 0028796045

Digital Object Identifier (DOI)

  • 10.1016/s0039-6060(05)80086-8

PubMed ID

  • 7846626

Additional Document Info

volume

  • 117

issue

  • 2