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)‐α, lipopolysaccharide, zymosan, myeloperoxidase, peritoneal fluid from rats with zymosan‐induced peritonitis, and peritoneal fluid from control animals. The production of TNF‐α, interleukin (IL)‐1β, IL‐6, and IL‐10 was assessed after 4, 12 and 24 h. Results: Lipopolysaccharide and zymosan stimulated TNF‐α, IL‐1β, and IL‐10 production; and peritoneal fluids from both control animals and animals with zymosan‐induced peritonitis stimulated the production of TNF‐α, IL‐1RII, and IL‐6. Expression and secretion of TNF‐α 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‐1β 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‐α 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‐α, IL‐1β, 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.