title: Acute pancreatitis in transgenic mice expressing human group IIA phospholipase A2.
abstract: BACKGROUND
  There is circumstantial and contradictory evidence of the role of group IIA phospholipase A2 (PLA2) in acute pancreatitis.
  
  
  OBJECTIVE
  To examine the severity of acute experimental pancreatitis in transgenic mice expressing human PLA2 compared with mice not expressing PLA2.
  
  
  METHODS
  The study involved 12 young female CB57/bl mice not expressing group IIA PLA2 (wild-type mice) and 12 transgenic female CB57/bl mice expressing human group IIA PLA2 (transgenic mice). A choline-deficient, 0.5% ethionine-supplemented diet induced acute pancreatitis for 72 hours after 12 hours of fasting. Mice were killed 4 and 10 days after induction of acute pancreatitis. Pancreas, lung, kidney, and liver were examined histologically, and apoptosis in pancreas and liver was evaluated by DNA nick-end labeling (TUNEL).
  
  
  RESULTS
  On day 4, there were no significant differences in pancreatic apoptosis or total pancreatitis score. Liver damage was similar in both groups. On day 10, pancreatic damage was less but apoptosis more severe than on day 4, and neither hepatic damage nor apoptosis was seen. All mice expressing human group IIA PLA2 but none of the mice not expressing human group IIA PLA2 had marked pancreatic fibrosis. No significant pulmonary or renal damage was found at any time.
  
  
  CONCLUSIONS
  Pancreatitis in mice expressing human group IIA PLA2 is not more severe than in normal mice. Expression of group IIA PLA2 per se is not a major determinant of severity in experimental acute pancreatitis.
authors.affiliation: Department of General Surgery, University of Ulm, Germany.
authors.forename: Jens M
authors.initials: JM
authors.lastname: Mayer
authors.forename: V Jukka O
authors.initials: VJ
authors.lastname: Laine
authors.forename: Susanne
authors.initials: S
authors.lastname: Kolodziej
authors.forename: Timo J
authors.initials: TJ
authors.lastname: Nevalainen
authors.forename: Hans G
authors.initials: HG
authors.lastname: Beger
mesh_terms: D000208:Acute Disease; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006801:Humans; D020287:In Situ Nick-End Labeling; D007668:Kidney / Q000473:pathology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000473:pathology; D051379:Mice; D008822:Mice, Transgenic; D010179:Pancreas / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000201:enzymology / Q000235:genetics / Q000473:pathology*; D010741:Phospholipases A / Q000235:genetics / Q000378:metabolism*; D054467:Phospholipases A2; D012720:Severity of Illness Index
chemical_list: D010741:Phospholipases A; D054467:Phospholipases A2