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Peritoneal dialysis fluid induces p38-dependent inflammation in human mesothelial cells
Andrea Riesenhuber1, Klaus Kratochwill, Thorsten O Bender
1Department of Pediatrics, Medical University, Vienna, Austria.
Background:
Noninfectious upregulation of proinflammatory pathways in mesothelial cells may represent an integral part of their stress response upon exposure to peritoneal dialysis fluids (PDF).
Objective:
The aim of this study was to evaluate the role of the stress-inducible mitogen-activated protein kinase (MAPK) p38 in regulation of inflammatory and stress responses in mesothelial cells following in vitro exposure to PDF.
Materials And Methods:
Human peritoneal mesothelial cells were exposed to Dianeal PD4 or Physioneal (Baxter AG, Vienna, Austria) containing 1.36% glucose and then allowed to recover. Phosphorylation of p38, induction of heat shock protein-70 (HSP70), release of lactate dehydrogenase (LDH), secretion of interleukin (IL)-8, gene transcription, and mRNA stability were assessed with and without the MAPK p38 inhibitor SB203580.
Results:
Exposure to Dianeal resulted in phosphorylation of p38 within 30 minutes (309% of control, p < 0.05) and increased IL-8 release (370% of control, p < 0.05), HSP70 expression (151% of control, p < 0.05), and LDH release (180% of control, p < 0.05). Exposure to Physioneal resulted in attenuated changes in IL-8, HSP70, and LDH. Addition of the p38 inhibitor SB203580 to Dianeal resulted in dampened IL-8 release (-55%; p < 0.05) and basal HSP70 expression, and unchanged LDH release. Effects of p38 on IL-8 were at transcriptional, posttranscriptional, and translational levels.
Conclusion:
These data confirm concordant p38-dependent upregulation of IL-8 and HSP70 following exposure to bioincompatible PDF. The MAPK p38 pathway therefore links proinflammatory processes and the cellular stress response in human peritoneal mesothelial cells.
Insights
The p38 mitogen-activated protein kinase (MAPK) pathway regulates inflammatory and stress responses in mesothelial cells exposed to peritoneal dialysis fluids (PDF). Inhibiting p38 reduces IL-8 and HSP70 upregulation, linking this pathway to cellular stress.
Area of Science:
- Cellular Biology
- Renal Physiology
- Inflammation Research
Background:
- Peritoneal dialysis fluids (PDF) can induce noninfectious inflammatory responses in mesothelial cells.
- This inflammatory response is part of the cellular stress reaction to PDF exposure.
Purpose of the Study:
- To investigate the role of the stress-inducible mitogen-activated protein kinase (MAPK) p38 pathway.
- To understand how p38 regulates inflammatory and stress responses in mesothelial cells exposed to PDF in vitro.
Main Methods:
- Human peritoneal mesothelial cells were exposed to two types of PDF (Dianeal PD4, Physioneal).
- Key markers including p38 phosphorylation, heat shock protein-70 (HSP70), lactate dehydrogenase (LDH), and interleukin (IL)-8 were measured.
- The effect of a p38 inhibitor (SB203580) on these markers was assessed.
Main Results:
- Dianeal induced significant p38 phosphorylation, IL-8 release, HSP70 expression, and LDH release.
- Physioneal showed less pronounced changes in IL-8, HSP70, and LDH.
- SB203580 treatment dampened IL-8 release and HSP70 expression in Dianeal-exposed cells, while LDH release remained unchanged.
Conclusions:
- The p38 MAPK pathway is critically involved in the upregulation of IL-8 and HSP70 in mesothelial cells exposed to bioincompatible PDF.
- This pathway serves as a crucial link between pro-inflammatory processes and the cellular stress response in human peritoneal mesothelial cells.
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