Tim-3 is a potential regulator that inhibits monocyte inflammation in response to intermittent hypoxia in children with obstructive sleep apnea syndrome

Tim-3 is a potential regulator that inhibits monocyte inflammation in response to intermittent hypoxia in children with obstructive sleep apnea syndrome

Copyright © 2020. Published by Elsevier Inc.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 222(2021) vom: 04. Jan., Seite 108641
1. Verfasser: Wang, Wei (VerfasserIn)
Weitere Verfasser: Xu, Zhifei, Zhang, Jie, Wang, Shengcai, Ge, Wentong, Li, Xiaodan, Mou, Wenjun, Wang, Xiaolin, Chai, Wenjia, Zhao, Jing, Wang, Guixiang, Xi, Yue, Qiu, Yue, Ji, Tingting, Gui, Jingang, Tai, Jun, Ni, Xin
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2021
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Inflammation Intermittent hypoxia (IH) Monocytes OSAS Tim-3 HAVCR2 protein, human Hepatitis A Virus Cellular Receptor 2 ICAM1 protein, human mehr... IL12A protein, human IL6 protein, human Interleukin-12 Subunit p35 Interleukin-6 VEGFA protein, human Vascular Endothelial Growth Factor A Intercellular Adhesion Molecule-1 126547-89-5
Beschreibung
Zusammenfassung:Copyright © 2020. Published by Elsevier Inc.
The mechanism of the characteristic intermittent hypoxia (IH) of obstructive sleep apnea syndrome (OSAS) on monocyte remain unclear. Our study found that OSAS children had a significantly upregulated expression in circulating proinflammatory cytokines IL-6 and IL-12, and endothelial injury markers VEGF and ICAM1. Association analysis revealed that the plasma TNFα, IL-1β, IL-6, IL-10 and IL-12 concentration were negatively associated with the minimal SpO2, a negative index for disease severity. OSAS monocytes presented an inflammatory phenotype with higher mRNA levels of inflammatory cytokines. Importantly, we noted a significant decrease in T-cell immunoglobulin and mucin domain (Tim)-3 expression in OSAS monocytes with the increase of the plasma proinflammatory cytokines. In vitro assay demonstrated that IH induced THP-1 cell overactivation via NF-κB dependent pathway was inhibited by the Tim-3 signal. Our results indicated that activation of monocyte inflammatory responses is closely related to OSAS-induced IH, and negatively mediated by a Tim-3 signaling pathway
Beschreibung:Date Completed 16.06.2021
Date Revised 16.06.2021
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2020.108641