title: Pancreatic and pulmonary mast cells activation during experimental acute pancreatitis.
abstract: OBJECTIVE
  To study the activation of pancreatic and pulmonary mast cells and the effect of mast cell inhibition on the activation of peritoneal and alveolar macrophages during acute pancreatitis.
  
  
  METHODS
  Pancreatitis was induced by intraductal infusion of 5% sodium taurodeoxycholate in rats. The mast cell inhibitor cromolyn was administered intraperitoneally (i.p.) 30 min before pancreatitis induction. The pancreatic and pulmonary tissue damage was evaluated histologically and mast cells and their state of activation were evaluated. Peritoneal and alveolar macrophages were obtained and the expression of tumor necrosis factor alpha was determined. Myeloperoxidase activity was measured to evaluate the effect of mast cell inhibition on the progression of the inflammatory process. Finally, the effect of plasma on cultured mast cells or macrophages was evaluated in vitro.
  
  
  RESULTS
  The mast cell stabilizer significantly reduced inflammation in the pancreas and lung and the activation of alveolar macrophages but had no effect on peritoneal macrophages. Mast cell degranulation was observed in the pancreas during pancreatitis but no changes were observed in the lung. Plasma from rats with pancreatitis could activate alveolar macrophages but did not induce degranulation of mast cells in vitro.
  
  
  CONCLUSIONS
  Pancreatic mast cells play an important role in triggering the local and systemic inflammatory response in the early stages of acute pancreatitis. In contrast, lung mast cells are not directly involved in the inflammatory response related to pancreatic damage.
authors.affiliation: Gastroenterology Unit, University General Hospital, Alicante, 03010, Spain.
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Lopez-Font
authors.forename: Sabrina
authors.initials: S
authors.lastname: Gea-Sorlí
authors.forename: Enrique
authors.initials: E
authors.lastname: de-Madaria
authors.forename: Luis M
authors.initials: LM
authors.lastname: Gutiérrez
authors.forename: Miguel
authors.initials: M
authors.lastname: Pérez-Mateo
authors.forename: Daniel
authors.initials: D
authors.lastname: Closa
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000494:pharmacology; D015550:Cell Degranulation / Q000187:drug effects; D002478:Cells, Cultured; D002756:Cholagogues and Choleretics / Q000009:adverse effects; D004205:Cromolyn Sodium / Q000494:pharmacology; D004195:Disease Models, Animal; D008168:Lung / Q000166:cytology* / Q000276:immunology; D016676:Macrophages, Alveolar / Q000166:cytology / Q000276:immunology; D017737:Macrophages, Peritoneal / Q000166:cytology / Q000276:immunology; D008297:Male; D008407:Mast Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D010179:Pancreas / Q000166:cytology* / Q000276:immunology; D010195:Pancreatitis / Q000139:chemically induced / Q000276:immunology*; D051381:Rats; D017208:Rats, Wistar; D013657:Taurodeoxycholic Acid / Q000009:adverse effects; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D018927:Anti-Asthmatic Agents; D002756:Cholagogues and Choleretics; D014409:Tumor Necrosis Factor-alpha; D013657:Taurodeoxycholic Acid; D004205:Cromolyn Sodium