Mechanisms regulating cytokine release from peritoneal macrophages during continuous ambulatory peritoneal dialysis.
The proinflammatory cytokines interleukin-1 (IL-1 beta) and tumor necrosis factor-alpha (TNF alpha) are key mediators of the body's response to infection. Peritoneal macrophages from continuous ambulatory peritoneal dialysis (CAPD) patients isolated during peritonitis have an increased capacity to secrete IL-1 beta and TNF alpha. This peritoneal macrophage activation for IL-1 beta and TNF alpha release is a two-stage process. In contrast, peritonitis macrophages and infection-free macrophages stimulated in vitro with bacteria generate a decreased amount of the anti-inflammatory prostanoids. Exogenous and endogenous prostaglandin E2 (PGE2) was found to inhibit the release of TNF alpha rather than IL-1 beta from peritoneal macrophages, indicating that the synthesis and secretion of these cytokines is distinctly regulated by PGE2. In addition to macrophage products, acting in an autocrine fashion cytokine production and release may be regulated by secretory products of other cells in the peritoneal cavity including lymphocytes and mesothelial cells, which have the capability to produce various mediators. No evidence was found that the NO system is an important part of the antimicrobial arsenal of peritoneal macrophages.
Fieren
M W
MW
Department of Internal Medicine I, University Hospital Dijkzigt, Erasmus University Rotterdam, The Netherlands.
D000818:Animals; D015232:Dinoprostone / Q000502:physiology; D007375:Interleukin-1 / Q000378:metabolism*; D017737:Macrophages, Peritoneal / Q000378:metabolism*; D051379:Mice; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D010531:Peritoneal Dialysis, Continuous Ambulatory; D010538:Peritonitis / Q000503:physiopathology; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D015232:Dinoprostone