title: Peritoneal mesothelial cells produce inflammatory related cytokines.
abstract: BACKGROUND
  Peritonitis involves cascading interactions between cytokines that initiate robust signalling processes via the interferon-g and nuclear factor kappa B pathways. The present study evaluates the interplay between various putative inducers of peritonitis and a battery of inflammation-related cytokines.
  
  
  METHODS
  Cultures of peritoneal mesothelial cells were isolated from omenta harvested from male Wistar rats. These cultures were exposed to tumour necrosis factor (TNF)-alpha, lipopolysaccharide, zymosan, myeloperoxidase, peritoneal fluid from rats with zymosan-induced peritonitis, and peritoneal fluid from control animals. The production of TNF-alpha, interleukin (IL)-1beta, IL-6, and IL-10 was assessed after 4, 12 and 24 h.
  
  
  RESULTS
  Lipopolysaccharide and zymosan stimulated TNF-alpha, IL-1beta, and IL-10 production; and peritoneal fluids from both control animals and animals with zymosan-induced peritonitis stimulated the production of TNF-alpha, IL-1RII, and IL-6. Expression and secretion of TNF-alpha occurred in a constitutive manner and was regulation at the protein level. The decoy molecule IL-1 receptor type II (IL-1RII) was produced at the same time as IL-1beta and production of the anti-inflammatory cytokine IL-10 was evident within 4 h. IL-6 was constitutively expressed and regulated at the transcriptional level as indicated by a marked discontinuity between the amount of IL-6 produced and the extent IL-6 messenger ribonucleic acid (mRNA) expression.
  
  
  CONCLUSIONS
  Tumour necrosis factor-alpha might not be the sole primary mediator of peritonitis. The anti-inflammatory molecules IL-1RII and IL-10 are induced at the same time as the pro-inflammatory cytokines TNF-alpha, IL-1beta, and IL-6. This suggests that complex control systems are set in place by the factors that stimulate peritoneal mesothelial cells and might have the potential to cause peritonitis.
authors.affiliation: School of Surgery and Pathology, The University of Western Australia, Perth, Western Australia, Australia.
authors.forename: Veronica
authors.initials: V
authors.lastname: Yao
authors.forename: Cameron
authors.initials: C
authors.lastname: Platell
authors.forename: John C
authors.initials: JC
authors.lastname: Hall
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis*; D018836:Inflammation Mediators / Q000378:metabolism*; D007375:Interleukin-1 / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D010537:Peritoneum / Q000378:metabolism; D010538:Peritonitis / Q000209:etiology; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D015054:Zymosan / Q000494:pharmacology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015054:Zymosan