title: Delayed production of IL-18 in lungs and pancreas of rats with acute pancreatitis.
abstract: OBJECTIVE
  During acute pancreatitis, tumor necrosis factor (TNF)-α, interleukin (IL)-1 and IL-6 play a pivotal role in promoting injury in the pancreas and remote organs. IL- 18 is a more recently discovered proinflammatory cytokine whose expression is also increased in serum. However, the profile of IL-18 expression in the pancreas and lung is unknown, and the aim of our study was to investigate such expression in rats with pancreatitis.
  
  
  METHODS
  Acute pancreatitis was induced by taurocholic acid and endotoxin. Pulmonary and pancreatic injury was measured by biological and histological parameters. Lung injury was also evaluated in ex vivo lung preparations.
  
  
  RESULTS
  Pancreatic and pulmonary injury appeared within 2 h after pancreatitis induction and persisted until the end of the protocol (18 h). TNF-α, IL-1 and IL-6 expression increased early in the lungs and pancreas, with a partial recovery by the end of the study. In contrast, IL-18 increased mostly by the end of the protocol (18 h after pancreatitis induction).
  
  
  CONCLUSIONS
  IL-18 may serve as an additional marker to monitor the severity of inflammation during pancreatitis since its tissue production is delayed and appears after that of more commonly investigated cytokines. and IAP.
authors.affiliation: Laboratoire de Physiopathologie Hépatique et Imagerie Moléculaire, Hôpitaux Universitaires de Genève, Genève, Suisse. Catherine.Pastor @ hcuge.ch
authors.forename: Catherine M
authors.initials: CM
authors.lastname: Pastor
authors.forename: Denis R
authors.initials: DR
authors.lastname: Morel
authors.forename: Alain
authors.initials: A
authors.lastname: Vonlaufen
authors.forename: Eduardo
authors.initials: E
authors.lastname: Schiffer
authors.forename: Pierre
authors.initials: P
authors.lastname: Lescuyer
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Frossard
mesh_terms: D000208:Acute Disease; D055371:Acute Lung Injury / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D004731:Endotoxins / Q000633:toxicity; D007375:Interleukin-1 / Q000378:metabolism; D020382:Interleukin-18 / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013656:Taurocholic Acid / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004731:Endotoxins; D007375:Interleukin-1; D020382:Interleukin-18; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D013656:Taurocholic Acid