TT_II_P: Theoretical and Translational Medicine II. Posters
Eszter Lévai 1,2, Csenge Pajtók 1,2, Domonkos Pap 1,2, Apor-Veres-Székely 1,2, Beáta Szebeni 1,2, Ádám Vannay 1,2, Attila J Szabó 1,2
1, 1st Department of Pediatrics, Semmelweis University, Budapest
2,ELKH-SE Pediatrics and Nephrology Research Group, Budapest
Introduction: Peritonitis is the most common complication of peritoneal dialysis (PD). Peritoneal inflammation impaires the peritoneal integrity which leads to decreased ultrafiltration capacity, however the underlying mechanisms mediate the local inflammation are incompletely understood. Previously, the immunmodulatory role of PARK7 has been demonstrated in various organs, however its role in peritoneal inflammation is completely unknown. Therefore our aim was to investigate the role of PARK7 in the inflammatory response of the peritoneal membrane.
Methods: The in vitro effect of pharmacological PARK7 modulation on the oxidative stress (H2O2) and bacterial lipopolisacharide (LPS) induced proinflammatory cytokine production of primary human peritoneal mesothelial cells (HPMC) and peripheral mononuclear cells (PBMC) was investigated by real-time PCR and ELISA.
Results: Pharmacological PARK7 modulation decreased the peritonitis associated oxidative stress H2O2 and LPS induced IL-6 mRNA expression and protein production of HPMCs. Moreover, modulation of PARK7 also resulted in decreased IL-1ß, IL-6 and TNF-a mRNA expression in H2O2 and LPS stimulated PBMCs.
Conclusion: Our study revealed the role of PARK7 in the regulation of peritoneal inflammation suggesting its role in the maintenance of peritoneal integrity. Moreover, our results demonstrated the therapeutic potential of PARK7 in peritonitis.
Funding: Supported by the ÚNKP-20-3-I-SE-49 New National Excellence Program of the Ministry for Innovation and Technology from the source of National Research, Development and Innovation Fund. This study was supported by grant K125470, EFOP-3.6.3-VEKOP-16-2017-0000920382-3/2018 FEKUTSTRAT, 2020-4.1.1- TKP2020 and STIA-KFI-2020.
Semmelweis University, Károly Rácz Doctoral School of Clinical Medicine