IL-17 in peritoneal dialysis-associated inflammation and angiogenesis: conclusions and perspectives
- 1Department of Pathophysiology, Poznan University of Medical Sciences, Poland
- 2Medizinische Abteilung, Abteilung für Nephrologie und Innere Intensivmedizin CVK / CCM, Charité Universitätsmedizin Berlin, Germany
- 3Abteilung für Transfusionsmedizin, Charité Universitätsmedizin Berlin, Germany
- 4Universität Witten/Herdecke, Germany
Long-term peritoneal dialysis (PD) is associated with peritoneal membrane remodelling. This includes changes in peritoneal vasculature, which may ultimately lead to inadequate solute and water removal and treatment failure. The potential cause of such alterations is chronic inflammation caused by repeated episodes of infectious peritonitis and/or exposure to bioincompatible PD fluids. While these factors may jeopardize the peritoneal membrane integrity, it is not clear why adverse peritoneal remodelling develops only in some PD patients. Increasing evidence point to the differences that occur between patients in response to the same invading microorganism and/or the differences in the course of inflammatory reaction triggered by different species. Such differences may be related to the involvement of different inflammatory mediators. Here, we discuss the potential role of IL-17 in these processes with emphasis on its impact on peritoneal mesothelial cells and peritoneal vascularity.
Keywords: IL-17, Inflammation, Peritonitis, Angiogeneis, Fibrosis, VEGF, Peritoneal Dialysis
Received: 07 Sep 2018;
Accepted: 09 Nov 2018.
Edited by:Ovidiu C. Baltatu, Anhembi Morumbi University - Laureate International Universities, Brazil
Reviewed by:Abdel R. Hamad, Johns Hopkins University, United States
Shai Efrati, Tel Aviv University, Israel
Copyright: © 2018 Witowski, Kamhieh-Milz, Kawka, Catar and Joerres. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Prof. Janusz Witowski, Department of Pathophysiology, Poznan University of Medical Sciences, Poznan, 60-512, Poland, firstname.lastname@example.org