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

急性坏死性胰腺炎常合并胰腺或胰周感染。由于坏死性胰腺炎可能损害免疫功能，从而增加对细菌感染的易感性，我们检测了小鼠急性胰腺炎局部中性粒细胞表面调理素受体(CD11b，补体受体3；CD32/CD16，免疫球蛋白GFC受体)的表达。急性胰腺炎的坏死型和水肿型分别由7次皮下注射雨蛙素加或不加内毒素诱导。在胰腺炎诱导后1~24小时连续检测腹膜渗出液中性粒细胞的数量，并用流式细胞仪检测其受体的表达。腹膜渗出性中性粒细胞计数水肿性胰腺炎多于坏死性胰腺炎。CD11b阳性中性粒细胞在水肿性胰腺炎6~24小时明显高于水肿性胰腺炎，坏死性胰腺炎CD11b阳性中性粒细胞数低于水肿性胰腺炎。在两种胰腺炎模型中，中性粒细胞表面CD11b的平均荧光强度相似。细胞计数和平均荧光强度显示腹膜渗出性中性粒细胞CD32/CD16在水肿性胰腺炎中表达上调，而在坏死性胰腺炎中表达减弱。结论：与水肿性胰腺炎相比，坏死性胰腺炎局部中性粒细胞上调理素受体的表达减少，这种差异可能是坏死性胰腺炎局部败血症并发症的原因。

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.