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Tim-3 is a potential regulator that inhibits monocyte inflammation in response to intermittent hypoxia in children with obstructive sleep apnea syndrome
Clinical Immunology ( IF 4.5 ) Pub Date : 2020-11-30 , DOI: 10.1016/j.clim.2020.108641
Wei Wang , Zhifei Xu , Jie Zhang , Shengcai Wang , Wentong Ge , Xiaodan Li , Wenjun Mou , Xiaolin Wang , Wenjia Chai , Jing Zhao , Guixiang Wang , Yue Xi , Yue Qiu , Tingting Ji , Jingang Gui , Jun Tai , Xin Ni

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.



中文翻译:

Tim-3是一种潜在的调节剂,可抑制阻塞性睡眠呼吸暂停综合征患儿间歇性缺氧时的单核细胞炎症

阻塞性睡眠呼吸暂停综合征(OSAS)的特征性间歇性低氧(IH)的单核细胞机制尚不清楚。我们的研究发现,OSAS儿童在循环促炎细胞因子IL-6和IL-12以及内皮损伤标记物VEGF和ICAM1中的表达明显上调。关联分析显示,血浆TNFα,IL-1β,IL-6,IL-10和IL-12浓度与最小SpO 2呈负相关,SpO 2是疾病严重程度的负指标。OSAS单核细胞具有较高的炎症细胞因子mRNA水平的炎症表型。重要的是,我们注意到OSAS单核细胞中T细胞免疫球蛋白和粘蛋白结构域(Tim)-3的表达随血浆促炎细胞因子的增加而显着降低。体外实验证明,IH通过NF-κB依赖性途径诱导的THP-1细胞过度活化被Tim-3信号抑制。我们的结果表明,单核细胞炎症反应的激活与OSAS诱导的IH密切相关,并且由Tim-3信号通路负向介导。

更新日期:2020-12-05
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