Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea

Rationale: As the mechanism that links obstructive sleep apnea (OSA) with the regulation of inflammatory response is not well known, it is important to understand the inflammasome activation, mainly of NLRP3 (nucleotide-binding oligomerization domain-like receptor 3). Objectives: To assess the NLRP3...

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Autores: Díaz García, Elena, García Tovar, Sara, Alfaro, Enrique, Jaureguizar, Ana, Casitas, Raquel, Sánchez Sánchez, Begoña, Zamarrón, Ester, Fernández Lahera, Juan, López Collado, Eduardo, Cubillos Zapata, Carolina, García Rio, Francisco
Formato: artículo
Fecha de publicación:2022
País:España
Recursos:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/737440
Acesso em linha:https://hdl.handle.net/10486/737440
https://dx.doi.org/10.1164/rccm.202106-1445OC
Access Level:acceso abierto
Palavra-chave:NLRP3
OSA
Tissue factor
HIF1α
Intermittent hypoxia
Medicina
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spelling Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apneaDíaz García, ElenaGarcía Tovar, SaraAlfaro, EnriqueJaureguizar, AnaCasitas, RaquelSánchez Sánchez, BegoñaZamarrón, EsterFernández Lahera, JuanLópez Collado, EduardoCubillos Zapata, CarolinaGarcía Rio, FranciscoNLRP3OSATissue factorHIF1αIntermittent hypoxiaMedicinaRationale: As the mechanism that links obstructive sleep apnea (OSA) with the regulation of inflammatory response is not well known, it is important to understand the inflammasome activation, mainly of NLRP3 (nucleotide-binding oligomerization domain-like receptor 3). Objectives: To assess the NLRP3 activity in patients with severe OSA and to identify its role in the systemic inflammatory response of patients with OSA. Methods: We analyzed the NLRP3 activity as well as key components of the inflammasome cascade, such as adaptor molecule apoptosis-associated speck-like protein, caspase-1, Gasdermin D, IL-1β, IL-18, and tissue factor, in monocytes and plasma from patients with severe OSA and control subjects without sleep apnea. We explored the association of the different key markers with inflammatory comorbidities. Measurements and Main Results: Monocytes from patients with severe OSA presented higher NLRP3 activity than those from control subjects, which directly correlated with the apnea–hypopnea index and hypoxemic indices. NLRP3 overactivity triggered inflammatory cytokines (IL-1β and IL-18) via caspase-1 and increased Gasdermin D, allowing for tissue factor to be released. In vitro models confirmed that monocytes increase NLRP3 signaling under intermittent hypoxia in a hypoxia-inducible factor-1α–dependent manner, and/or in combination with plasma from patients with OSA. Plasma concentrations of tissue factor were higher in patients with OSA with systemic inflammatory comorbidities than in those without them. Conclusions: In patients with severe OSA, NLRP3 activation might be a linking mechanism between intermittent hypoxia and other OSA-induced immediate changes with the development of systemic inflammatory responseSupported by grants from Fondo de Investigación Sanitaria (FIS) and European Regional Development Funds (FEDER) (PI13/01512, PI16/00201, and PI19/01612 to F.G.-R. and CP18/00028 and PI19-01363 to C.C.-Z.)American Thoracic Society (ATS)Departamento de MedicinaFacultad de MedicinaGobierno de EspañaInstituto de Salud Carlos III20222022-06-01research articlehttp://purl.org/coar/resource_type/c_2df8fbb1AMhttp://purl.org/coar/version/c_ab4af688f83e57aainfo:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/10486/737440https://dx.doi.org/10.1164/rccm.202106-1445OC35363597reponame:Biblos-e Archivo. Repositorio Institucional de la UAMinstname:Universidad Autónoma de MadridInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:repositorio.uam.es:10486/7374402026-06-23T12:46:27Z
dc.title.none.fl_str_mv Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
title Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
spellingShingle Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
Díaz García, Elena
NLRP3
OSA
Tissue factor
HIF1α
Intermittent hypoxia
Medicina
title_short Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
title_full Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
title_fullStr Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
title_full_unstemmed Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
title_sort Inflammasome activation: A keystone of proinflammatory response in obstructive sleep apnea
dc.creator.none.fl_str_mv Díaz García, Elena
García Tovar, Sara
Alfaro, Enrique
Jaureguizar, Ana
Casitas, Raquel
Sánchez Sánchez, Begoña
Zamarrón, Ester
Fernández Lahera, Juan
López Collado, Eduardo
Cubillos Zapata, Carolina
García Rio, Francisco
author Díaz García, Elena
author_facet Díaz García, Elena
García Tovar, Sara
Alfaro, Enrique
Jaureguizar, Ana
Casitas, Raquel
Sánchez Sánchez, Begoña
Zamarrón, Ester
Fernández Lahera, Juan
López Collado, Eduardo
Cubillos Zapata, Carolina
García Rio, Francisco
author_role author
author2 García Tovar, Sara
Alfaro, Enrique
Jaureguizar, Ana
Casitas, Raquel
Sánchez Sánchez, Begoña
Zamarrón, Ester
Fernández Lahera, Juan
López Collado, Eduardo
Cubillos Zapata, Carolina
García Rio, Francisco
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Departamento de Medicina
Facultad de Medicina
Gobierno de España
Instituto de Salud Carlos III
dc.subject.none.fl_str_mv NLRP3
OSA
Tissue factor
HIF1α
Intermittent hypoxia
Medicina
topic NLRP3
OSA
Tissue factor
HIF1α
Intermittent hypoxia
Medicina
description Rationale: As the mechanism that links obstructive sleep apnea (OSA) with the regulation of inflammatory response is not well known, it is important to understand the inflammasome activation, mainly of NLRP3 (nucleotide-binding oligomerization domain-like receptor 3). Objectives: To assess the NLRP3 activity in patients with severe OSA and to identify its role in the systemic inflammatory response of patients with OSA. Methods: We analyzed the NLRP3 activity as well as key components of the inflammasome cascade, such as adaptor molecule apoptosis-associated speck-like protein, caspase-1, Gasdermin D, IL-1β, IL-18, and tissue factor, in monocytes and plasma from patients with severe OSA and control subjects without sleep apnea. We explored the association of the different key markers with inflammatory comorbidities. Measurements and Main Results: Monocytes from patients with severe OSA presented higher NLRP3 activity than those from control subjects, which directly correlated with the apnea–hypopnea index and hypoxemic indices. NLRP3 overactivity triggered inflammatory cytokines (IL-1β and IL-18) via caspase-1 and increased Gasdermin D, allowing for tissue factor to be released. In vitro models confirmed that monocytes increase NLRP3 signaling under intermittent hypoxia in a hypoxia-inducible factor-1α–dependent manner, and/or in combination with plasma from patients with OSA. Plasma concentrations of tissue factor were higher in patients with OSA with systemic inflammatory comorbidities than in those without them. Conclusions: In patients with severe OSA, NLRP3 activation might be a linking mechanism between intermittent hypoxia and other OSA-induced immediate changes with the development of systemic inflammatory response
publishDate 2022
dc.date.none.fl_str_mv 2022
2022-06-01
dc.type.none.fl_str_mv research article
http://purl.org/coar/resource_type/c_2df8fbb1
AM
http://purl.org/coar/version/c_ab4af688f83e57aa
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/10486/737440
https://dx.doi.org/10.1164/rccm.202106-1445OC
35363597
url https://hdl.handle.net/10486/737440
https://dx.doi.org/10.1164/rccm.202106-1445OC
identifier_str_mv 35363597
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv American Thoracic Society (ATS)
publisher.none.fl_str_mv American Thoracic Society (ATS)
dc.source.none.fl_str_mv reponame:Biblos-e Archivo. Repositorio Institucional de la UAM
instname:Universidad Autónoma de Madrid
instname_str Universidad Autónoma de Madrid
reponame_str Biblos-e Archivo. Repositorio Institucional de la UAM
collection Biblos-e Archivo. Repositorio Institucional de la UAM
repository.name.fl_str_mv
repository.mail.fl_str_mv
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