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Peritoneal macrophages from patients on continuous ambulatory peritoneal dialysis show a differential secretion of
M W Fieren1, G J van den Bemd, I L Bonta
1Department of Internal Medicine I, University Hospital Dijkzigt, Rotterdam, The Netherlands.
Abstract:
In vitro secretion of the prostanoids PGE2 and PGI2 and of the cytokine IL-1 beta by peritoneal macrophages obtained from CAPD patients during episodes of peritonitis and infection free periods, was determined, after culturing with or without 5 micrograms/ml of LPS. The release of PGE2 and PGI2 as measured by its stable metabolite 6-keto-PGF alpha was determined in 10 episodes of peritonitis and 10 infection free periods. IL-1 beta release was determined in 14 episodes of peritonitis and 20 infection free periods. PGI2 release from macrophages declined sharply during peritonitis both in the absence and presence of LPS in the culture medium (p less than 0.005). A tendency to decreased PGE2 release was found during peritonitis, when macrophages were cultured in the absence of LPS. In the presence of LPS, the same amounts of PGE2 were released during peritonitis and during an infection free period. On the other hand, peritoneal macrophages released significantly more IL-1 beta 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 PGI2 during peritonitis has allowed the macrophages to secrete more IL-1 beta after in vitro stimulation with LPS. This implies that PGI2 and PGE2 may play a distinct role in the regulation of cytokine secretion by these cells.
Insights
During peritonitis in CAPD patients, peritoneal macrophages show reduced prostaglandin I2 (PGI2) and prostaglandin E2 (PGE2) release. This impairment may lead to increased interleukin-1 beta (IL-1 beta) secretion, highlighting a distinct regulatory role for prostanoids in macrophage cytokine production.
Area of Science:
- Immunology
- Cell Biology
- Peritoneal Dialysis
Background:
- Peritoneal macrophages play a crucial role in the immune response during peritonitis in Continuous Ambulatory Peritoneal Dialysis (CAPD) patients.
- Prostanoids (PGE2, PGI2) and cytokines (IL-1 beta) are key mediators in inflammatory processes.
- Understanding their interplay is vital for managing CAPD-related infections.
Purpose of the Study:
- To investigate the in vitro secretion of PGE2, PGI2, and IL-1 beta by peritoneal macrophages from CAPD patients.
- To compare mediator release during peritonitis episodes versus infection-free periods.
- To explore the regulatory role of prostanoids in macrophage cytokine secretion.
Main Methods:
- Peritoneal macrophages were obtained from CAPD patients during peritonitis and infection-free periods.
- Macrophages were cultured in vitro with or without lipopolysaccharide (LPS).
- Secretion of PGE2, PGI2 (measured as 6-keto-PGF alpha), and IL-1 beta was quantified.
Main Results:
- Prostaglandin I2 (PGI2) release significantly decreased during peritonitis, irrespective of LPS stimulation.
- Prostaglandin E2 (PGE2) release showed a tendency to decrease during peritonitis without LPS, but remained unchanged with LPS.
- Interleukin-1 beta (IL-1 beta) release was significantly higher during peritonitis when macrophages were stimulated with LPS.
Conclusions:
- Impaired PGI2 release during peritonitis may contribute to increased IL-1 beta secretion by peritoneal macrophages upon LPS stimulation.
- PGE2 and PGI2 likely play distinct roles in regulating cytokine production by macrophages in CAPD patients.
- These findings suggest a complex interplay between prostanoids and cytokines in the immune response to peritonitis.