Nuclear expression of mu-opioid receptors in a human mesothelial cell line.
BACKGROUND Many of the effector mechanisms that characterize peritonitis are generated by neutrophils and macrophages. However, it is now appreciated that peritoneal mesothelial cells can also produce mediators of inflammation when grown in culture. This study tested the hypothesis that peritoneal mesothelial cells produce inflammation-related cytokines in a murine model of peritonitis. METHODS Fifty Wistar rats were randomized to either a control group or a peritonitis group. Groups of five animals were sacrificed at 4, 18, 24, 48, and 96 h after the induction of peritonitis, which was induced by the administration of 5 mg zymosan intra-peritoneally. Control animals received an equal volume of phosphate-buffered saline. Monolayers of peritoneal mesothelial cells were obtained using an imprint technique. The expression and production of TNFalpha, IL-1beta, IL-10, and ICAM-I were determined using semi-quantitative reverse transcription- polymerase chain reaction, immunocytochemistry, and Western blotting. RESULTS The mesothelial cells significantly expressed TNFalpha, IL-1beta, IL-10, and ICAM-I in a time-dependent manner. We were able to demonstrate increased production for each of these cytokines, and this coincided with the initial shedding of mesothelial cells and their regeneration within 96 h. CONCLUSIONS Peritoneal mesothelial cells play a role in peritonitis by producing inflammation- associated cytokines. This implies that they may be suitable targets for molecular interventions aimed at modulating the effects of peritonitis.