Inflammasome Activation: A Keystone of Proinflammatory Response in Obstructive Sleep Apnea

炎症体 医学 促炎细胞因子 阻塞性睡眠呼吸暂停 缺氧(环境) 间歇性缺氧 半胱氨酸蛋白酶1 炎症 免疫学 上睑下垂 内科学
作者
Elena Díaz-García,Sara García-Tovar,Enrique Alfaro,Ana Jaureguizar,Raquel Casitas,Begoña Sánchez Sánchez,Ester Zamarrón,Juan Fernández-Lahera,Eduardo López-Collazo,Carolina Cubillos-Zapata,Francisco García-Río
出处
期刊:American Journal of Respiratory and Critical Care Medicine [American Thoracic Society]
卷期号:205 (11): 1337-1348 被引量:87
标识
DOI:10.1164/rccm.202106-1445oc
摘要

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.
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