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

急性坏死性胰腺炎常并发胰腺或胰周感染。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控素受体（CD11b，补体受体3；CD32/CD16，免疫球蛋白GFc受体）的表达。急性胰腺炎的坏死性和水肿形式分别由皮下注射七次蛋白并腹腔注射和不腹腔注射脂多糖引起。在胰腺炎诱导后1 ~ 24小时，流式细胞术对腹膜渗出中性粒细胞进行计数和受体表达测定。腹膜渗出性中性粒细胞计数大于坏死性胰腺炎。腹膜渗出性中性粒细胞CD 11b阳性的数量在水肿性胰腺炎中升高，但在6-24小时坏死性胰腺炎中的数量低于水肿性胰腺炎。在两种胰腺炎模型中，CD11b对中性粒细胞的平均荧光强度具有可比性。细胞计数和平均荧光强度显示，水肿性胰腺炎腹膜渗出性中性粒细胞CD32/CD16表达上调，而坏死性胰腺炎腹膜渗出性中性粒细胞CD32/CD16表达下调。总之，与水肿性胰腺炎相比，坏死性胰腺炎局部中性粒细胞上的opsonin受体表达减少，这种差异可能是坏死性胰腺炎局部脓毒性并发症的原因。

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.