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Host innate immune responses to sepsis

The immune response to sepsis can be seen as a pattern recognition receptor-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. Invasive infection triggers both pro-inflammatory and anti-inf...

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Detalles Bibliográficos
Autores principales: Wiersinga, Willem Joost, Leopold, Stije J, Cranendonk, Duncan R, van der Poll, Tom
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3916381/
https://www.ncbi.nlm.nih.gov/pubmed/23774844
http://dx.doi.org/10.4161/viru.25436
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author Wiersinga, Willem Joost
Leopold, Stije J
Cranendonk, Duncan R
van der Poll, Tom
author_facet Wiersinga, Willem Joost
Leopold, Stije J
Cranendonk, Duncan R
van der Poll, Tom
author_sort Wiersinga, Willem Joost
collection PubMed
description The immune response to sepsis can be seen as a pattern recognition receptor-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. Invasive infection triggers both pro-inflammatory and anti-inflammatory host responses, the magnitude of which depends on multiple factors, including pathogen virulence, site of infection, host genetics, and comorbidities. Toll-like receptors, the inflammasomes, and other pattern recognition receptors initiate the immune response after recognition of danger signals derived from microorganisms, so-called pathogen-associated molecular patterns or derived from the host, so-called danger-associated molecular patterns. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade, and their multidirectional interactions in sepsis should lead toward the development of new therapeutic strategies in sepsis.
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spelling pubmed-39163812014-03-06 Host innate immune responses to sepsis Wiersinga, Willem Joost Leopold, Stije J Cranendonk, Duncan R van der Poll, Tom Virulence Review The immune response to sepsis can be seen as a pattern recognition receptor-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. Invasive infection triggers both pro-inflammatory and anti-inflammatory host responses, the magnitude of which depends on multiple factors, including pathogen virulence, site of infection, host genetics, and comorbidities. Toll-like receptors, the inflammasomes, and other pattern recognition receptors initiate the immune response after recognition of danger signals derived from microorganisms, so-called pathogen-associated molecular patterns or derived from the host, so-called danger-associated molecular patterns. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade, and their multidirectional interactions in sepsis should lead toward the development of new therapeutic strategies in sepsis. Landes Bioscience 2014-01-01 2013-06-17 /pmc/articles/PMC3916381/ /pubmed/23774844 http://dx.doi.org/10.4161/viru.25436 Text en Copyright © 2014 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Review
Wiersinga, Willem Joost
Leopold, Stije J
Cranendonk, Duncan R
van der Poll, Tom
Host innate immune responses to sepsis
title Host innate immune responses to sepsis
title_full Host innate immune responses to sepsis
title_fullStr Host innate immune responses to sepsis
title_full_unstemmed Host innate immune responses to sepsis
title_short Host innate immune responses to sepsis
title_sort host innate immune responses to sepsis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3916381/
https://www.ncbi.nlm.nih.gov/pubmed/23774844
http://dx.doi.org/10.4161/viru.25436
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