Dynamic Function of Peritoneal Exudative Neutrophils As a Defense Mechanism in Acute Pancreatitis

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Acute necrotizing pancreatitis is often complicated by pancreatic or peripancreatic infection. Since necrotizing pancreatitis may impair immune function, thereby increasing susceptibility to bacterial infection, we examined the expression of surface opsonin receptors (CD11b, complement receptor 3; CD32/CD16, immunoglobulin GFc receptor) on local neutrophils in murine acute pancreatitis. The necrotizing and edematous forms of acute pancreatitis were induced by seven subcutaneous injections of caerulein with and without intraperitoneal administration of lipopolysaccharide, respectively. Peritoneal exudative neutrophils were counted and assayed for receptor expression by flow cytometry, serially, from 1 to 24 hours after induction of pancreatitis. The peritoneal exudative neutrophil count was greater inedematous than in necrotizing pancreatitis. The number of CD 11b-positive peritoneal exudative neutrophils was elevated in edematous pancreatitis, but the number was lower in necrotizing than in edematous pancreatitis at 6-24 hours. The mean fluorescence intensity of CD11b on neutrophils was comparable in both pancreatitis models. The cell count and mean fluorescence intensity indicated upregulated expression of CD32/CD16 on peritoneal exudative neutrophils in edematous pancreatitis, whereas the upregulation was attenuated in necrotizing pancreatitis. In conclusion, opsonin receptor expression on local neutrophils was reduced in necrotizing pancreatitis, compared to edematous pancreatitis, and the difference may be responsible for the local septic complications in necrotizing pancreatitis.