Opsonin receptor expression on peritoneal exudative and circulatory neutrophils in murine acute pancreatitis
Opsonin receptor expression on peritoneal exudative and circulatory neutrophils in murine acute pancreatitis
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DOI：
10.1097/00006676-200107000-00008
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发表时间：
2001-07-01
期刊：
影响因子：
2.9
通讯作者：
Atomi, Y
中科院分区：
文献类型：
--
作者：
Hatano, N;Sugiyama, M;Atomi, Y
急性重症(坏死性)胰腺炎常伴有胰腺或胰周感染。由于免疫防御受损导致细菌清除减少，可能会导致局部感染。我们研究了小鼠急性胰腺炎局部和循环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G Fc受体)的表达。轻型和重型急性胰腺炎分别由7次和13次皮下注射雨蛙素诱发。在胰腺炎诱导后1-72小时连续取腹膜渗出液和循环中性粒细胞，用流式细胞仪检测中性粒细胞受体的表达。组织学上，轻度和重度分别表现为水肿性和坏死性胰腺炎。轻度胰腺炎患者的腹膜渗出液中性粒细胞计数明显高于重症胰腺炎患者。轻度胰腺炎早期局部中性粒细胞CD11b和CD32/CD16表达上调。这种上调在重症胰腺炎中减弱。重症胰腺炎患者循环中性粒细胞计数升高，轻度胰腺炎患者中性粒细胞计数无明显变化。在轻型胰腺炎的早期阶段，循环中性粒细胞上调色素受体的表达显示出一过性的、适度的上调。受体阳性的循环中性粒细胞显着升高，并持续整个重症胰腺炎的病程。总而言之，与轻度(水肿性)胰腺炎相比，重症(坏死性)胰腺炎与局部中性粒细胞调色素受体表达减少和循环中性粒细胞表达增强有关。这些改变可能导致重症胰腺炎的局部感染并发症和多器官衰竭。
Acute severe (necrotizing) pancreatitis is often associated with pancreatic or peripancreatic infection. Decreased bacterial clearance due to impaired immune defense may cause local infection. We investigated expressions of surface opsonin receptors (CD11b, complement receptor 3; CD32/CD16, immunoglobulin G Fc receptor) on local and circulatory neutrophils, in murine acute pancreatitis. The mild and severe forms of acute pancreatitis were induced by seven and 13 subcutaneous injections of caerulein, respectively. Peritoneal exudative and circulatory neutrophils were counted and assayed for receptor expressions by flow cytometry, serially at 1-72 hours after pancreatitis induction. Histologically, mild and severe forms showed edematous and necrotizing pancreatitis, respectively. The peritoneal exudative neutrophil count was greater in mild than in severe pancreatitis. Expressions of CD11b and CD32/CD16 on Local neutrophils were upregulated early in mild pancreatitis. This upregulation was attenuated in severe pancreatitis. The circulatory neutrophil count was elevated in severe pancreatitis but was unchanged in mild pancreatitis. Opsonin receptor expression on circulatory neutrophils showed a transient, modest upregulation in the early phase of mild pancreatitis. Receptor-positive circulatory neutrophils showed a marked elevation that persisted throughout the course of severe pancreatitis. In conclusion, severe (necrotizing) pancreatitis is associated with reduced opsonin receptor expression on local neutrophils and enhanced expression on circulatory neutrophils, as compared with mild (edematous) pancreatitis. These changes may contribute to local infectious complications and multiple organ failure, in severe pancreatitis.