Peritoneal macrophages from patients on continuous ambulatory peritoneal dialysis show a differential secretion of prostanoids and interleukin-1β

• Published in: Prostaglandins, leukotrienes and essential fatty acids Vol. 47; no. 1; pp. 23 - 28
• Main Authors: Fieren, M.W.J.A., van den Bemd, G.J.C.M., Bonta, I.L.
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01.09.1992; Elsevier
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Dinoprostone - metabolism; Emergency and intensive care: renal failure. Dialysis management; Epoprostenol - metabolism; Female; Humans; In Vitro Techniques; Intensive care medicine; Interleukin-1 - metabolism; Kidney Failure, Chronic - physiopathology; Kidney Failure, Chronic - therapy; Macrophages - metabolism; Male; Medical sciences; Peritoneal Cavity - cytology; Peritoneal Dialysis, Continuous Ambulatory - adverse effects; Peritonitis - etiology; Peritonitis - physiopathology; Prostaglandins - metabolism; Human; Urinary system disease; Prostaglandin; Continuous; Arachidonic acid derivatives; Cytokine; Interleukin 1β; In vitro; Peritoneal dialysis; Extrarenal dialysis; Prostanoid; Ambulatory; Resuscitation; Macrophage
• ISSN: 0952-3278; 1532-2823
• DOI: 10.1016/0952-3278(92)90181-H

In vitro secretion of the prostanoids PGE 2 and PGI 2 and of the cytokine IL-1β by peritoneal macrophages obtained from CAPD patients during episodes of peritonitis and infection free periods, was determined, after culturing with or without 5 μg/ml of LPS. The release of PGE 2 and PGI 2 as measured by its stable metabolite 6-keto-PGFα was determined in 10 episodes of peritonitis and 10 infection free periods. IL-1β release was determined in 14 episodes of peritonitis and 20 infection free periods. PGI 2 release from macrophages declined sharply during peritonitis both in the absence and presence of LPS in the culture medium (p<0.005). A tendency to decreased PGE 2 release was found during peritonitis, when macrophages were cultured in the absence of LPS. In the presence of LPS, the same amounts of PGE 2 were released during peritonitis and during an infection free period. On the other hand, peritoneal macrophages released significantly more IL-1β during peritonitis as compared to an infection free period, provided that the cells were in vitro stimulated with LPS. In view of the interregulatory effects between prostanoids and macrophage cytokines in their production, these findings may indicate that the impaired release of PGI 2 during peritonitis has allowed the macrophages to secrete more IL-1β after in vitro stimulation with LPS. This implies that PGI 2 and PGE 2 may play a distinct role in the regulation of cytokine secretion by these cells.