Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor Activity
Peritoneal dialysis (PD) is an essential daily life-saving treatment for end-stage renal failure. PD therapy is limited by peritoneal inflammation, which leads to peritoneal membrane failure as a result of progressive fibrosis. Peritoneal infections, with the concomitant acute inflammatory response...
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2018-11-01
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Series: | Frontiers in Physiology |
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Online Access: | https://www.frontiersin.org/article/10.3389/fphys.2018.01692/full |
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author | Anne-Catherine Raby Mario O. Labéta |
author_facet | Anne-Catherine Raby Mario O. Labéta |
author_sort | Anne-Catherine Raby |
collection | DOAJ |
description | Peritoneal dialysis (PD) is an essential daily life-saving treatment for end-stage renal failure. PD therapy is limited by peritoneal inflammation, which leads to peritoneal membrane failure as a result of progressive fibrosis. Peritoneal infections, with the concomitant acute inflammatory response and membrane fibrosis development, worsen PD patient outcomes. Patients who remain infection-free, however, also show evidence of inflammation-induced membrane damage and fibrosis, leading to PD cessation. In this case, uraemia, prolonged exposure to bio-incompatible PD solutions and surgical catheter insertion have been reported to induce sterile peritoneal inflammation and fibrosis as a result of cellular stress or tissue injury. Attempts to reduce inflammation (either infection-induced or sterile) and, thus, minimize fibrosis development in PD have been hampered because the immunological mechanisms underlying this PD-associated pathology remain to be fully defined. Toll-like receptors (TLRs) are central to mediating inflammatory responses by recognizing a wide variety of microorganisms and endogenous components released following cellular stress or generated as a consequence of extracellular matrix degradation during tissue injury. Given the close link between inflammation and fibrosis, recent investigations have evaluated the role that TLRs play in infection-induced and sterile peritoneal fibrosis development during PD. Here, we review the findings and discuss the potential of reducing peritoneal TLR activity by using a TLR inhibitor, soluble TLR2, as a therapeutic strategy to prevent PD-associated peritoneal fibrosis. |
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institution | Directory Open Access Journal |
issn | 1664-042X |
language | English |
last_indexed | 2024-12-24T13:00:11Z |
publishDate | 2018-11-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Physiology |
spelling | doaj.art-887a071616044d9c9489dd91903dd11d2022-12-21T16:54:10ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2018-11-01910.3389/fphys.2018.01692418841Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor ActivityAnne-Catherine RabyMario O. LabétaPeritoneal dialysis (PD) is an essential daily life-saving treatment for end-stage renal failure. PD therapy is limited by peritoneal inflammation, which leads to peritoneal membrane failure as a result of progressive fibrosis. Peritoneal infections, with the concomitant acute inflammatory response and membrane fibrosis development, worsen PD patient outcomes. Patients who remain infection-free, however, also show evidence of inflammation-induced membrane damage and fibrosis, leading to PD cessation. In this case, uraemia, prolonged exposure to bio-incompatible PD solutions and surgical catheter insertion have been reported to induce sterile peritoneal inflammation and fibrosis as a result of cellular stress or tissue injury. Attempts to reduce inflammation (either infection-induced or sterile) and, thus, minimize fibrosis development in PD have been hampered because the immunological mechanisms underlying this PD-associated pathology remain to be fully defined. Toll-like receptors (TLRs) are central to mediating inflammatory responses by recognizing a wide variety of microorganisms and endogenous components released following cellular stress or generated as a consequence of extracellular matrix degradation during tissue injury. Given the close link between inflammation and fibrosis, recent investigations have evaluated the role that TLRs play in infection-induced and sterile peritoneal fibrosis development during PD. Here, we review the findings and discuss the potential of reducing peritoneal TLR activity by using a TLR inhibitor, soluble TLR2, as a therapeutic strategy to prevent PD-associated peritoneal fibrosis.https://www.frontiersin.org/article/10.3389/fphys.2018.01692/fullperitoneal dialysisinflammationperitoneal fibrosistoll-like receptorssoluble toll-like receptor 2 |
spellingShingle | Anne-Catherine Raby Mario O. Labéta Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor Activity Frontiers in Physiology peritoneal dialysis inflammation peritoneal fibrosis toll-like receptors soluble toll-like receptor 2 |
title | Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor Activity |
title_full | Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor Activity |
title_fullStr | Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor Activity |
title_full_unstemmed | Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor Activity |
title_short | Preventing Peritoneal Dialysis-Associated Fibrosis by Therapeutic Blunting of Peritoneal Toll-Like Receptor Activity |
title_sort | preventing peritoneal dialysis associated fibrosis by therapeutic blunting of peritoneal toll like receptor activity |
topic | peritoneal dialysis inflammation peritoneal fibrosis toll-like receptors soluble toll-like receptor 2 |
url | https://www.frontiersin.org/article/10.3389/fphys.2018.01692/full |
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