Neutrophils, not complement, mediate the mortality of experimental hemorrhagic pancreatitis

Chemoactivation of the neutrophil (PMN) via the complement system has been observed in many inflammatory conditions and is thought to play a pathogeni c role in acute pancreatitis. This study examined the effects of PMN deplet ion in experimental hemorrhagic pancreatitis and tested the role played by complement. Severe pancreatitis was induced by a choline-deficient, 0.5% et hionine-supplemented diet in female Institute of Cancer Research (ICR) mice weighing 11-13 g. Neutropenia was induced by an antibody injection. Total complement depletion was achieved by tail vein injections of cobra venom fa ctor (CVF). Serum amylase levels and local pancreatic injury were not signi ficantly modulated by either PMN or complement depletion at 72 hours. Syste mic and remote organ injury, assessed by the formation of ascites, hematocr it, and serum alanine aminotransferase levels, was significantly reduced in neutropenic mice but failed to be moderated by complement depletion. In ad dition, liver and lung myeloperoxidase activity was independent of compleme nt depletion. At 5 days, mortality was zero in PMN-depleted mice. There was no improvement in survival in the CVF-treated group. Neutrophils are impor tant in the systemic injury and mortality of severe pancreatitis. PMN chemo activation involves mechanisms other than complement.