Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.

Monocyte exposure to mitochondrial Danger Associated Molecular Patterns (DAMPs), including mitochondrial DNA (mtDNA), induces a transient state in which these cells are refractory to further endotoxin stimulation. In this context, IRAK-M up-regulation and impaired p65 activity were observed. This ph...

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Autores principales:	Irene Fernández-Ruiz, Francisco Arnalich, Carolina Cubillos-Zapata, Enrique Hernández-Jiménez, Raúl Moreno-González, Víctor Toledano, María Fernández-Velasco, Maria T Vallejo-Cremades, Laura Esteban-Burgos, Rebeca Pérez de Diego, Miguel A Llamas-Matias, Elena García-Arumi, Ramón Martí, Lisardo Boscá, Antoni L Andreu, José Luis López-Sendón, Eduardo López-Collazo
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/11f38959cab14f00b2cb0de2cbeccdc9
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spelling	oai:doaj.org-article:11f38959cab14f00b2cb0de2cbeccdc92021-11-18T08:20:48ZMitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.1932-620310.1371/journal.pone.0095073https://doaj.org/article/11f38959cab14f00b2cb0de2cbeccdc92014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24797663/?tool=EBIhttps://doaj.org/toc/1932-6203Monocyte exposure to mitochondrial Danger Associated Molecular Patterns (DAMPs), including mitochondrial DNA (mtDNA), induces a transient state in which these cells are refractory to further endotoxin stimulation. In this context, IRAK-M up-regulation and impaired p65 activity were observed. This phenomenon, termed endotoxin tolerance (ET), is characterized by decreased production of cytokines in response to the pro-inflammatory stimulus. We also show that monocytes isolated from patients with myocardial infarction (MI) exhibited high levels of circulating mtDNA, which correlated with ET status. Moreover, a significant incidence of infection was observed in those patients with a strong tolerant phenotype. The present data extend our current understanding of the implications of endotoxin tolerance. Furthermore, our data suggest that the levels of mitochondrial antigens in plasma, such as plasma mtDNA, should be useful as a marker of increased risk of susceptibility to nosocomial infections in MI and in other pathologies involving tissue damage.Irene Fernández-RuizFrancisco ArnalichCarolina Cubillos-ZapataEnrique Hernández-JiménezRaúl Moreno-GonzálezVíctor ToledanoMaría Fernández-VelascoMaria T Vallejo-CremadesLaura Esteban-BurgosRebeca Pérez de DiegoMiguel A Llamas-MatiasElena García-ArumiRamón MartíLisardo BoscáAntoni L AndreuJosé Luis López-SendónEduardo López-CollazoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 5, p e95073 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Irene Fernández-Ruiz Francisco Arnalich Carolina Cubillos-Zapata Enrique Hernández-Jiménez Raúl Moreno-González Víctor Toledano María Fernández-Velasco Maria T Vallejo-Cremades Laura Esteban-Burgos Rebeca Pérez de Diego Miguel A Llamas-Matias Elena García-Arumi Ramón Martí Lisardo Boscá Antoni L Andreu José Luis López-Sendón Eduardo López-Collazo Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.
description	Monocyte exposure to mitochondrial Danger Associated Molecular Patterns (DAMPs), including mitochondrial DNA (mtDNA), induces a transient state in which these cells are refractory to further endotoxin stimulation. In this context, IRAK-M up-regulation and impaired p65 activity were observed. This phenomenon, termed endotoxin tolerance (ET), is characterized by decreased production of cytokines in response to the pro-inflammatory stimulus. We also show that monocytes isolated from patients with myocardial infarction (MI) exhibited high levels of circulating mtDNA, which correlated with ET status. Moreover, a significant incidence of infection was observed in those patients with a strong tolerant phenotype. The present data extend our current understanding of the implications of endotoxin tolerance. Furthermore, our data suggest that the levels of mitochondrial antigens in plasma, such as plasma mtDNA, should be useful as a marker of increased risk of susceptibility to nosocomial infections in MI and in other pathologies involving tissue damage.
format	article
author	Irene Fernández-Ruiz Francisco Arnalich Carolina Cubillos-Zapata Enrique Hernández-Jiménez Raúl Moreno-González Víctor Toledano María Fernández-Velasco Maria T Vallejo-Cremades Laura Esteban-Burgos Rebeca Pérez de Diego Miguel A Llamas-Matias Elena García-Arumi Ramón Martí Lisardo Boscá Antoni L Andreu José Luis López-Sendón Eduardo López-Collazo
author_facet	Irene Fernández-Ruiz Francisco Arnalich Carolina Cubillos-Zapata Enrique Hernández-Jiménez Raúl Moreno-González Víctor Toledano María Fernández-Velasco Maria T Vallejo-Cremades Laura Esteban-Burgos Rebeca Pérez de Diego Miguel A Llamas-Matias Elena García-Arumi Ramón Martí Lisardo Boscá Antoni L Andreu José Luis López-Sendón Eduardo López-Collazo
author_sort	Irene Fernández-Ruiz
title	Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.
title_short	Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.
title_full	Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.
title_fullStr	Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.
title_full_unstemmed	Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.
title_sort	mitochondrial damps induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/11f38959cab14f00b2cb0de2cbeccdc9
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Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.

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