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.

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。