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.

急性坏死性胰腺炎通常会因胰腺或周围感染而复杂化。由于坏死性胰腺炎可能会损害免疫功能，从而增加对细菌感染的敏感性，因此我们检查了在鼠类急性胰腺胰腺炎中局部嗜中性粒细胞对局部嗜中性粒细胞的表面反素受体（CD11B，补体受体3; CD32/CD16； CD32/CD16，Remunogolobolin GFC受体）的表达。急性胰腺炎的坏死性和水肿形式分别是塞拉林的七种皮下注射，分别有或不腹膜内给予脂多糖。对腹膜中性粒细胞进行计数，并通过流式细胞仪从胰腺炎诱导后的1到24小时通过流式细胞仪进行测定。腹膜渗出性嗜中性粒细胞计数比坏死性胰腺炎大。在水肿性胰腺炎中，CD 11b阳性腹膜透明性嗜中性粒细胞的数量升高，但在6-24小时时，坏死性的数量低于水肿性胰腺炎。在两个胰腺炎模型中，CD11b在中性粒细胞上的平均荧光强度相当。细胞计数和平均荧光强度表明在水肿性胰腺炎中腹膜渗出性嗜中性粒细胞上CD32/CD16的表达上调，而在坏死性胰腺炎中上调。总之，与水肿性胰腺炎相比，在坏死性胰腺炎中降低了局部嗜中性粒细胞的op子受体表达，并且差异可能导致坏死性胰腺炎的局部败血性并发症。