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，我们研究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。分别通过皮下注射雨蛙肽和腹腔注射脂多糖诱导急性胰腺炎的坏死和水肿形式。诱导胰腺炎后1 - 24小时，连续计数腹膜渗出性中性粒细胞，并通过流式细胞术测定受体表达。腹膜渗出性中性粒细胞计数大于坏死性胰腺炎。在6 - 24小时，水肿性胰腺炎中CD 11b阳性腹膜渗出性中性粒细胞的数量增加，但坏死性胰腺炎中的数量低于水肿性胰腺炎。中性粒细胞上CD11b的平均荧光强度在两种胰腺炎模型中相当。细胞计数和平均荧光强度表明，在水肿性胰腺炎腹膜渗出性中性粒细胞上的CD 32/CD 16表达上调，而在坏死性胰腺炎中上调减弱。总之，与水肿型胰腺炎相比，坏死型胰腺炎局部中性粒细胞上调理素受体表达减少，这种差异可能是坏死型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.