Increased expression of Siglec-9 in chronic obstructive pulmonary disease.
Increased expression of Siglec-9 in chronic obstructive pulmonary disease.
复制标题
慢性阻塞性肺疾病中 Siglec-9 表达增加
DOI：
10.1038/s41598-017-09120-5
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发表时间：
2017-08-31
影响因子：
4.6
通讯作者：
Xie J
中科院分区：
文献类型：
--
作者：
Zeng Z;Li M;Wang M;Wu X;Li Q;Ning Q;Zhao J;Xu Y;Xie J
慢性阻塞性肺疾病(COPD)是一种常见的炎症性肺部疾病。唾液酸结合免疫球蛋白型凝集素9(Siglec-9)主要表达在天然免疫细胞上，并通过识别糖蛋白对免疫细胞发挥调节作用。可溶性Siglec-9(sSiglec-9)是Siglec-9的胞外区，可能通过竞争性抑制Siglec-9与其配体的结合来实现其部分功能，但Siglec-9和sSiglec-9在COPD发病机制中的作用尚不清楚。在本研究中，我们分别用免疫荧光法和流式细胞术检测了COPD患者肺泡和外周血中性粒细胞中Siglec-9的表达。在体外，香烟烟雾提取物(CSE)、脂多糖(LPS)、某些细胞因子和地塞米松(DEX)可上调sSiglelc-9的表达和/或sSiglelc-9的水平。重组sSiglce-9可增加中性粒细胞氧化爆发，增强中性粒细胞对IL-8的趋化作用，而不依赖于CXCR1和CXCR2的表达，但不影响中性粒细胞凋亡或炎性细胞因子的分泌。综上所述，Siglec-9在COPD中互补增加，诱导负反馈环限制中性粒细胞的激活，sSiglec-9可能通过竞争性抑制与Siglec-9的配体结合而增强中性粒细胞ROS和对IL-8的趋化作用。
Chronic obstructive pulmonary disease (COPD) is a common inflammatory lung disease. Sialic acid-binding immunoglobulin-type lectins 9 (Siglec-9) is predominantly expressed on innate immune cells and has been shown to exert regulatory effect on immune cells through glycan recognition. Soluble Siglec-9 (sSiglec-9), the extracellular region of Siglec-9, might fulfill its function partly by competitive inhibiting siglec-9 binding to its ligands; however, the role of Siglec-9 and sSiglec-9 in the pathogenesis COPD remain largely unknown. In this study, we showed that Siglec-9 expression in alveolar and peripheral blood neutrophil were increased in COPD patients by immunofluorescence and flow cytometry, respectively. Plasma levels of sSiglelc-9 were elevated in COPD patients by ELISA.In vitro, Siglec-9 expression and/or sSiglelc-9 levels were up-regulated by cigarette smoke extract (CSE), lipopolysaccharide (LPS), some cytokines, and dexamethasone (DEX). Recombinant sSiglce-9 increased oxidative burst in neutrophil and enhanced neutrophil chemotaxis toward IL-8 independent on CXCR1 and CXCR2 expression, but it did not affect neutrophil apoptosis or secretions of inflammatory cytokines. In conclusion, Siglec-9 was complementarily increased to induce a negative feedback loop to limit neutrophil activation in COPD, sSiglce-9 enhanced neutrophil ROS and chemotaxis toward IL-8 likely via competitively inhibiting ligands binding to Siglec-9.
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