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Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis
Despite a decrease in mortality over the last decade, sepsis remains the tenth leading causes of death in western countries and one of the most common cause of death in intensive care units. The recent discovery of Toll-like receptors and their downstream signalling pathways allowed us to better und...
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855078/ https://www.ncbi.nlm.nih.gov/pubmed/20396414 http://dx.doi.org/10.1155/2010/568396 |
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author | Wittebole, X. Castanares-Zapatero, D. Laterre, P. F. |
author_facet | Wittebole, X. Castanares-Zapatero, D. Laterre, P. F. |
author_sort | Wittebole, X. |
collection | PubMed |
description | Despite a decrease in mortality over the last decade, sepsis remains the tenth leading causes of death in western countries and one of the most common cause of death in intensive care units. The recent discovery of Toll-like receptors and their downstream signalling pathways allowed us to better understand the pathophysiology of sepsis-related disorders. Particular attention has been paid to Toll-like receptor 4, the receptor for Gram-negative bacteria outer membrane lipopolysaccharide or endotoxin. Since most of the clinical trial targeting single inflammatory cytokine in the treatment of sepsis failed, therapeutic targeting of Toll-like receptor 4, because of its central role, looks promising. The purpose of this paper is to focus on the recent data of various drugs targeting TLR4 expression and pathway and their potential role as adjunctive therapy in severe sepsis and septic shock. |
format | Text |
id | pubmed-2855078 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-28550782010-04-15 Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis Wittebole, X. Castanares-Zapatero, D. Laterre, P. F. Mediators Inflamm Review Article Despite a decrease in mortality over the last decade, sepsis remains the tenth leading causes of death in western countries and one of the most common cause of death in intensive care units. The recent discovery of Toll-like receptors and their downstream signalling pathways allowed us to better understand the pathophysiology of sepsis-related disorders. Particular attention has been paid to Toll-like receptor 4, the receptor for Gram-negative bacteria outer membrane lipopolysaccharide or endotoxin. Since most of the clinical trial targeting single inflammatory cytokine in the treatment of sepsis failed, therapeutic targeting of Toll-like receptor 4, because of its central role, looks promising. The purpose of this paper is to focus on the recent data of various drugs targeting TLR4 expression and pathway and their potential role as adjunctive therapy in severe sepsis and septic shock. Hindawi Publishing Corporation 2010 2010-04-14 /pmc/articles/PMC2855078/ /pubmed/20396414 http://dx.doi.org/10.1155/2010/568396 Text en Copyright © 2010 X. Wittebole et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Wittebole, X. Castanares-Zapatero, D. Laterre, P. F. Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis |
title | Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis |
title_full | Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis |
title_fullStr | Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis |
title_full_unstemmed | Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis |
title_short | Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis |
title_sort | toll-like receptor 4 modulation as a strategy to treat sepsis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855078/ https://www.ncbi.nlm.nih.gov/pubmed/20396414 http://dx.doi.org/10.1155/2010/568396 |
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