Peritoneal mesothelial cells produce inflammatory related cytokines.

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.