title: Acute necrotizing pancreatitis reduces opsonin receptor expression on peritoneal exudative neutrophils in mice.
abstract: OBJECTIVE
  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 G Fc receptor) on local neutrophils in murine acute pancreatitis.
  
  
  METHODS
  The necrotizing and edematous forms of acute pancreatitis were induced by seven subcutaneous injections of cerulein 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.
  
  
  RESULTS
  The peritoneal exudative neutrophil count was greater in edematous than in necrotizing pancreatitis. The number of CD11b-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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Surgery, Kyorin University School of Medicine, Tokyo, Japan.
authors.forename: Masanori
authors.initials: M
authors.lastname: Sugiyama
authors.forename: Nobuhiko
authors.initials: N
authors.lastname: Hatano
authors.forename: Takashi
authors.initials: T
authors.lastname: Watanabe
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Atomi
mesh_terms: D000818:Animals; D039481:CD11b Antigen / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000378:metabolism*; D019283:Pancreatitis, Acute Necrotizing / Q000378:metabolism*; D010537:Peritoneum / Q000166:cytology; D017452:Receptors, IgG / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism*; D015854:Up-Regulation / Q000502:physiology
chemical_list: D039481:CD11b Antigen; D017452:Receptors, IgG; D011971:Receptors, Immunologic; C091196:opsonin receptor