title: Opsonin receptor expression on peritoneal exudative and circulatory neutrophils in murine acute pancreatitis.
abstract: 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.
authors.affiliation: The First Department of Surgery, Kyorin University School of Medicine, Mitaka, Tokyo, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Hatano
authors.forename: M
authors.initials: M
authors.lastname: Sugiyama
authors.forename: T
authors.initials: T
authors.lastname: Watanabe
authors.forename: Y
authors.initials: Y
authors.lastname: Atomi
mesh_terms: D000208:Acute Disease; D000818:Animals; D001202:Ascitic Fluid / Q000139:chemically induced / Q000378:metabolism*; D002108:Ceruletide / Q000008:administration & dosage / Q000633:toxicity; D003167:Complement Activation; D018450:Disease Progression; D004334:Drug Administration Schedule; D004487:Edema / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005260:Female; D007958:Leukocyte Count; D016177:Macrophage-1 Antigen / Q000096:biosynthesis / Q000235:genetics; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000378:metabolism*; D010195:Pancreatitis / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D010587:Phagocytosis; D011961:Receptors, Fc / Q000096:biosynthesis / Q000235:genetics; D017452:Receptors, IgG / Q000096:biosynthesis / Q000235:genetics; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D016177:Macrophage-1 Antigen; D011961:Receptors, Fc; D017452:Receptors, IgG; D011971:Receptors, Immunologic; C091196:opsonin receptor; D002108:Ceruletide