BACKGROUND: The high mortality rate of severe acute pancreatitis (SAP) is closely associated with secondary infections of pancreatic and peripancreatic tissues. It was reported that granulocyte colony-stimulating factor (G-CSF) increased the number of leukocytes and enhanced their functions. However, an inflammatory response may be enhanced by an increased number of leukocytes. Our purpose was to study the roles of G-CSF in peritoneal-exudate neutrophils and inflammatory cytokines in the early stage of experimental SAP. METHODS: SAP was induced by injecting 0.2 ml of 3% taurocholate acid into the biliopancreatic duct in male Wistar rats. G-CSF (90 microg/kg body weight) or saline was administered 1 h before the SAP induction. The number of neutrophils and their phagocytic and bactericidal activities were evaluated, and the concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-1beta in plasma and ascitic fluid were measured 1 h and 3 h after the SAP induction. RESULTS: The number of peritoneal-exudate neutrophils (PENs) at 3 h was increased by G-CSF administration (81 +/- 50 x 10(5) cells/total exudate), as compared with that shown with saline administration (28 +/- 13 x 10(5) cells/total exudate; P < 0.05). The numbers of phagocytic and bactericidal neutrophils were also elevated by G-CSF administration. G-CSF administration did not increase the concentrations of TNF-alpha, IL-6, and IL-1beta in the plasma and ascitic fluid. CONCLUSIONS: G-CSF increases the numbers of neutrophils and enhances their functions against bacteria, but it does not enhance intraabdominal and systemic inflammatory responses in the early stage of SAP.
BACKGROUND: The high mortality rate of severe acute pancreatitis (SAP) is closely associated with secondary infections of pancreatic and peripancreatic tissues. It was reported that granulocyte colony-stimulating factor (G-CSF) increased the number of leukocytes and enhanced their functions. However, an inflammatory response may be enhanced by an increased number of leukocytes. Our purpose was to study the roles of G-CSF in peritoneal-exudate neutrophils and inflammatory cytokines in the early stage of experimental SAP. METHODS:SAP was induced by injecting 0.2 ml of 3% taurocholate acid into the biliopancreatic duct in male Wistar rats. G-CSF (90 microg/kg body weight) or saline was administered 1 h before the SAP induction. The number of neutrophils and their phagocytic and bactericidal activities were evaluated, and the concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-1beta in plasma and ascitic fluid were measured 1 h and 3 h after the SAP induction. RESULTS: The number of peritoneal-exudate neutrophils (PENs) at 3 h was increased by G-CSF administration (81 +/- 50 x 10(5) cells/total exudate), as compared with that shown with saline administration (28 +/- 13 x 10(5) cells/total exudate; P < 0.05). The numbers of phagocytic and bactericidal neutrophils were also elevated by G-CSF administration. G-CSF administration did not increase the concentrations of TNF-alpha, IL-6, and IL-1beta in the plasma and ascitic fluid. CONCLUSIONS:G-CSF increases the numbers of neutrophils and enhances their functions against bacteria, but it does not enhance intraabdominal and systemic inflammatory responses in the early stage of SAP.