Opsonin Receptor Expression on Peritoneal Exudative and Circulatory Neutrophils in Murine Acute Pancreatitis

急性重症（坏死性）胰腺炎常伴有胰腺或胰腺周围感染。由于免疫防御受损，细菌清除率降低，可能引起局部感染。我们研究了小鼠急性胰腺炎中表面调理素受体（CD11b，补体受体3；CD32/CD16，免疫球蛋白G Fc受体）在局部和循环中性粒细胞上的表达。分别皮下注射7次和13次小蛋白诱导轻度和重度急性胰腺炎。在胰腺炎诱导后1-72小时，分别用流式细胞术计数和检测腹腔渗出和循环中性粒细胞的受体表达。组织学上，轻度和重度分别表现为水肿性和坏死性胰腺炎。轻度胰腺炎腹膜渗出中性粒细胞计数高于重度胰腺炎。在轻度胰腺炎早期，局部中性粒细胞CD11b和CD32/CD16表达上调。这种上调在严重胰腺炎中减弱。循环中性粒细胞计数在重症胰腺炎中升高，但在轻度胰腺炎中不变。调理素受体在循环中性粒细胞上的表达在轻度胰腺炎的早期表现出短暂的、适度的上调。受体阳性的循环中性粒细胞在严重胰腺炎过程中持续升高。总之，与轻度（水肿性）胰腺炎相比，严重（坏死性）胰腺炎与局部中性粒细胞的调节素受体表达减少和循环中性粒细胞表达增强有关。在重症胰腺炎中，这些变化可能导致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 7 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 which 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.