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

腹腔渗出性中性粒细胞作为急性胰腺炎防御机制的动态功能

基本信息

批准号：
15591441
负责人：
SUGIYAMA Masanori
金额：
$ 2.05万
依托单位：
Kyorin University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2005
项目状态：
已结题

项目摘要

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.

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。分别通过腹膜内注射和不腹膜内注射脂多糖七次皮下注射雨蛙素诱导急性胰腺炎的坏死和水肿形式。在诱导胰腺炎后1至24小时，对腹膜渗出性中性粒细胞进行计数并通过流式细胞术连续测定受体表达。腹膜渗出性中性粒细胞计数在水肿状态下高于坏死性胰腺炎。 6~24小时，水肿性胰腺炎腹腔CD 11b阳性渗出性中性粒细胞数量增多，但坏死性胰腺炎的数量低于水肿性胰腺炎。在两种胰腺炎模型中，中性粒细胞上 CD11b 的平均荧光强度相当。细胞计数和平均荧光强度表明水肿性胰腺炎腹膜渗出性中性粒细胞上CD32/CD16表达上调，而坏死性胰腺炎中上调减弱。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调理素受体表达降低，这种差异可能是坏死性胰腺炎局部脓毒症并发症的原因。