Characterization and allergic role of IL-33-induced neutrophil polarization
Characterization and allergic role of IL-33-induced neutrophil polarization
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IL-33 诱导的中性粒细胞极化的特征和过敏作用
DOI：
10.1038/cmi.2017.163
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发表时间：
2018-03
影响因子：
24.1
通讯作者：
Zhao Yong
中科院分区：
文献类型：
--
作者：
Sun Bo;Zhu Linnan;Tao Yaling;Sun Hai Xi;Li Yang;Wang Peng;Hou Yuzhu;Zhao Yang;Zhang Xiaodong;Zhang Lianfeng;Na Ning;Zhao Yong
中性粒细胞参与过敏的发病机制。然而，不同功能极化的中性粒细胞在过敏中的作用需要澄清。我们试图确定白细胞介素 (IL)-33 诱导的中性粒细胞的特征以及极化中性粒细胞亚群在过敏发病机制中的参与。用不同的细胞因子处理新鲜分离的中性粒细胞，并通过实时PCR检测细胞因子的表达水平。通过微阵列测定测定IL-33诱导的中性粒细胞的基因表达谱。过继转移测定用于研究卵清蛋白 (OVA) 诱导的过敏性哮喘模型中 IL-33 诱导的中性粒细胞的功能。 IL-33 处理的中性粒细胞选择性产生 IL-4、IL-5、IL-9 和 IL-13（称为 N (IL-33) 细胞），并表现出独特的基因表达谱，与静息和脂多糖 (LPS) 处理的中性粒细胞形成鲜明对比。 IL-33 诱导的中性粒细胞在细胞表面表达高水平的 IL-1R2，而静息和 LPS 处理的中性粒细胞则不然，表明 IL-1R2 可能用作 N (IL-33) 细胞的生物标志物。重要的是，N (IL-33) 中性粒细胞存在于 OVA 诱导的过敏性哮喘小鼠的肺部。在该模型中，N (IL-33) 中性粒细胞的过继转移显着促进了肺部发病机制的严重程度。 IL-33 通过 c-Jun N 末端激酶和核因子 κB 依赖性途径诱导中性粒细胞极化。定义了一种先前未被认识到的由 IL-33 驱动的中性粒细胞极化，具有独特的细胞表面标记和产生细胞因子/趋化因子的基因谱。新发现的 N (IL-33) 亚群可能对 IL-33 相关发病机制有重要贡献。
Neutrophils are involved in the pathogenesis of allergy. However, the contribution of the different functionally polarized neutrophils in allergy needs to be clarified. We sought to define the characteristics of interleukin (IL)-33-induced neutrophils and the involvement of this subset of polarized neutrophils in allergic pathogenesis. Freshly isolated neutrophils were treated with different cytokines and the cytokine expression levels were detected by real-time PCR. The gene expression profile of IL-33-induced neutrophils was determined by microarray assay. Adoptive transfer assay was used to investigate the function of IL-33-induced neutrophils in an ovalbumin (OVA)-induced allergic asthma model. IL-33-treated neutrophils selectively produced IL-4, IL-5, IL-9 and IL-13 (referred as to N (IL-33) cells) and displayed a distinctive gene expression profile in sharp contrast to resting and lipopolysaccharide (LPS)-treated neutrophils. IL-33-induced neutrophils expressed high Levels of IL-1R2 on cell surface, whereas resting and LPS-treated neutrophils did not, indicating IL-1R2 might be used as a biomarker for N (IL-33) cells. Importantly, N (IL-33) neutrophils exist in the lungs of OVA-induced allergic asthma mice. Adoptive transfer of N (IL-33) neutrophils significantly promotes the severity of the lung pathogenesis in this model. IL-33 induces neutrophil polarization through c-Jun N-terminal kinase-and nuclear factor-κB-dependent pathways. A previously unappreciated neutrophil polarization driven by IL-33 with unique cell surface markers and cytokine/chemokine-producing gene profile was defined. The newly identified N (IL-33) subpopulation may have significant contribution to IL-33-related pathogenesis.
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作者：
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