Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes

Acute coronary syndrome (ACS) groups different cardiac diseases whose development is associated with inflammation. Here we have analyzed the levels of inflammatory cytokines and of members of the TLR/IRAK pathway including IRAK-M in monocytes from ACS patients classified as either UA (unstable angin...

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Author: López Collazo, Eduardo
Format: article
Publication Date:2007
Country:España
Institution:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repository:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/212822
Online Access:http://hdl.handle.net/2445/212822
Access Level:Open access
Keyword:Inflamació
Malalties cardiovasculars
Inflammation
Cardiovascular diseases
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spelling Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytesLópez Collazo, EduardoInflamacióMalalties cardiovascularsInflammationCardiovascular diseasesAcute coronary syndrome (ACS) groups different cardiac diseases whose development is associated with inflammation. Here we have analyzed the levels of inflammatory cytokines and of members of the TLR/IRAK pathway including IRAK-M in monocytes from ACS patients classified as either UA (unstable angina), STEMI (ST-elevation myocardial infarction) or NSTEMI (non-ST-elevation myocardial infarction). Circulating monocytes from all patients, but not from healthy individuals, showed high levels of pro-inflammatory cytokines, TNF-α and IL-6, as well as of IRAK-M and IL-10. TLR4 was also up-regulated, but IRAK-1, IRAK-4 and MyD88 levels were similar in patients and controls. Further, we investigated the consequences of cytokines/IRAK-M expression on the innate immune response to endotoxin. Ex vivo responses to LPS were markedly attenuated in patient monocytes compared to controls. Control monocytes cultured for 6 h in supplemented medium (10% serum from ACS patients) expressed IRAK-M, and LPS stimulation failed to induce TNF-α and IL-6 in these cultures. Pre-incubation of the serum with a blocking anti-TNF-α antibody reduced this endotoxin tolerance effect, suggesting that TNF-α controls this phenomenon, at least partially. We show for the first time that inflammatory responses associated with ACS induce an unresponsiveness state to endotoxin challenge in circulating monocytes, which correlates with expression of IRAK-M, TLR4 and IL-10. The magnitude of this response varies according to the clinical condition (UA, STEMI or NSTEMI), and is regulated by TNF-α.2024202420072024info:eu-repo/semantics/articleinfo:eu-repo/semantics/14 p.application/pdfhttp://hdl.handle.net/2445/212822http://hdl.handle.net/2445/212822Articles publicats en revistes (Biologia, Sanitat i Medi Ambient)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)https://doi.org/10.1177/09680519070786232007, vol. 13, num.1, p. 39-52https://doi.org/10.1177/0968051907078623, 2007info:eu-repo/semantics/openAccessoai:recercat.cat:2445/2128222026-05-29T05:05:01Z
dc.title.none.fl_str_mv Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
title Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
spellingShingle Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
López Collazo, Eduardo
Inflamació
Malalties cardiovasculars
Inflammation
Cardiovascular diseases
title_short Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
title_full Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
title_fullStr Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
title_full_unstemmed Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
title_sort Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes
dc.creator.none.fl_str_mv López Collazo, Eduardo
author López Collazo, Eduardo
author_facet López Collazo, Eduardo
author_role author
dc.subject.none.fl_str_mv Inflamació
Malalties cardiovasculars
Inflammation
Cardiovascular diseases
topic Inflamació
Malalties cardiovasculars
Inflammation
Cardiovascular diseases
description Acute coronary syndrome (ACS) groups different cardiac diseases whose development is associated with inflammation. Here we have analyzed the levels of inflammatory cytokines and of members of the TLR/IRAK pathway including IRAK-M in monocytes from ACS patients classified as either UA (unstable angina), STEMI (ST-elevation myocardial infarction) or NSTEMI (non-ST-elevation myocardial infarction). Circulating monocytes from all patients, but not from healthy individuals, showed high levels of pro-inflammatory cytokines, TNF-α and IL-6, as well as of IRAK-M and IL-10. TLR4 was also up-regulated, but IRAK-1, IRAK-4 and MyD88 levels were similar in patients and controls. Further, we investigated the consequences of cytokines/IRAK-M expression on the innate immune response to endotoxin. Ex vivo responses to LPS were markedly attenuated in patient monocytes compared to controls. Control monocytes cultured for 6 h in supplemented medium (10% serum from ACS patients) expressed IRAK-M, and LPS stimulation failed to induce TNF-α and IL-6 in these cultures. Pre-incubation of the serum with a blocking anti-TNF-α antibody reduced this endotoxin tolerance effect, suggesting that TNF-α controls this phenomenon, at least partially. We show for the first time that inflammatory responses associated with ACS induce an unresponsiveness state to endotoxin challenge in circulating monocytes, which correlates with expression of IRAK-M, TLR4 and IL-10. The magnitude of this response varies according to the clinical condition (UA, STEMI or NSTEMI), and is regulated by TNF-α.
publishDate 2007
dc.date.none.fl_str_mv 2007
2024
2024
2024
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/2445/212822
http://hdl.handle.net/2445/212822
url http://hdl.handle.net/2445/212822
dc.language.none.fl_str_mv
language_invalid_str_mv
dc.relation.none.fl_str_mv https://doi.org/10.1177/0968051907078623
2007, vol. 13, num.1, p. 39-52
https://doi.org/10.1177/0968051907078623
dc.rights.none.fl_str_mv , 2007
info:eu-repo/semantics/openAccess
rights_invalid_str_mv , 2007
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 14 p.
application/pdf
dc.source.none.fl_str_mv Articles publicats en revistes (Biologia, Sanitat i Medi Ambient)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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