title: Lipids generated during acute pancreatitis increase inflammatory status of macrophages by interfering with their M2 polarization.
abstract: BACKGROUND
  Necrosis of adipose tissue is a common complication of acute pancreatitis. The areas of steatonecrosis become a source of inflammatory mediators, including chemically modified fatty acids which could influence the progression of the systemic inflammation. In an experimental model of acute pancreatitis we analyzed the effects of lipids generated by two representative areas of adipose tissue on the switch to the M1 phenotype in macrophages.
  
  
  METHODS
  Pancreatitis was induced in rats by intraductal administration of 5% taurocholate and after 6 h, lipids from retroperitoneal, mesenteric or epididymal adipose tissues were collected. Lipid uptake, phenotype polarization and the activation of PPARγ and NFκB were evaluated in macrophages treated with these lipids.
  
  
  RESULTS
  After induction of pancreatitis, lipids from visceral adipose tissue promote the switch to an increased pro-inflammatory phenotype in macrophages. This effect is not related with a higher activation of NFκB but with an interfering effect on the activation of M2 phenotype.
  
  
  CONCLUSIONS
  During acute pancreatitis, lipids generated by some areas of adipose tissue interfere on the M2 polarization of macrophages, thus resulting in a more intense pro-inflammatory M1 response.
authors.affiliation: Dept. Experimental Pathology, IIBB-CSIC, IDIBAPS, Barcelona, Spain.
authors.forename: Laia
authors.initials: L
authors.lastname: Bonjoch
authors.affiliation: Dept. Experimental Pathology, IIBB-CSIC, IDIBAPS, Barcelona, Spain.
authors.forename: Sabrina
authors.initials: S
authors.lastname: Gea-Sorlí
authors.affiliation: Dept. Experimental Pathology, IIBB-CSIC, IDIBAPS, Barcelona, Spain. Electronic address: daniel.closa@iibb.csic.es.
authors.forename: Daniel
authors.initials: D
authors.lastname: Closa
mesh_terms: D000208:Acute Disease; D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology; D000818:Animals; D002460:Cell Line; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology*; D008049:Lipase / Q000378:metabolism; D008055:Lipids / Q000096:biosynthesis*; D008264:Macrophages / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D047495:PPAR gamma / Q000378:metabolism; D010195:Pancreatitis / Q000378:metabolism* / Q000473:pathology*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D005230:Fatty Acids, Nonesterified; D008055:Lipids; D047495:PPAR gamma; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D009195:Peroxidase; D008049:Lipase
keywords: Adipose tissue; Inflammation; Macrophages; PPARγ; Pancreatitis; Phenotype