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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Interleukin‐16 aggravates ovalbumin‐induced allergic inflammation by enhancing Th2 and Th17 cytokine production in a mouse model
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Interleukin‐16 aggravates ovalbumin‐induced allergic inflammation by enhancing Th2 and Th17 cytokine production in a mouse model

机译：白细胞介素-16通过在小鼠模型中提高TH2和TH17细胞因子产生来加剧卵霉蛋白诱导的过敏性炎症

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摘要

Summary Asthma is a chronic inflammatory disease that involves a variety of cytokines and cells. Interleukin‐16 (IL‐16) is highly expressed during allergic airway inflammation and is involved in its development. However, its specific mechanism of action remains unclear. In the present study, we used an animal model of ovalbumin (OVA)‐induced allergic asthma with mice harboring an IL‐16 gene deletion to investigate the role of this cytokine in asthma, in addition to its underlying mechanism. Increased IL‐16 expression was observed during OVA‐induced asthma in C57BL/6J mice. However, when OVA was used to induce asthma in IL‐16 ?/? mice, a diminished inflammatory reaction, decreased bronchoalveolar lavage fluid (BALF) eosinophil numbers, and the suppression of OVA‐specific IgE levels in the serum and BALF were observed. The results also demonstrated decreased levels of T helper type 2 (Th2) and Th17 cytokines upon OVA‐induced asthma in IL‐16 ?/? mice. Hence, we confirmed that IL‐16 enhances the lung allergic inflammatory response and suggest a mechanism possibly associated with the up‐regulation of IgE and the promotion of Th2 and Th17 cytokine production. This work explored the mechanism underlying the regulation of IL‐16 in asthma and provides a new target for the clinical treatment of asthma.
机译：发明内容哮喘是一种慢性炎症疾病，涉及各种细胞因子和细胞。白细胞介素-16（IL-16）在过敏气道炎症期间高度表达，涉及其发展。然而，其特定的行动机制仍然不清楚。在本研究中，我们使用卵烧（OVA）的动物模型 - 诱导患IL-16基因缺失的小鼠的过敏性哮喘，除了其潜在的机制外，还研究该细胞因子在哮喘中的作用。在C57BL / 6J小鼠中，在OVA诱导的哮喘期间观察IL-16表达增加。但是，当OVA用于在IL-16中诱导哮喘？/？小鼠，炎症反应减少，降低支气管肺泡灌洗液（BALF）嗜酸性粒细胞数，并且观察到血清和BALF中的卵子特异性IgE水平。结果还证明了在IL-16中OVA诱导的哮喘患者的T辅助型2（TH2）和Th17细胞因子的水平降低？/？老鼠。因此，我们证实IL-16增强了肺部过敏性炎症反应，并提出了一种可能与IgE的上调和促进Th2和Th17细胞因子产生相关的机制。这项工作探索了哮喘患者IL-16调节的机制，为哮喘的临床治疗提供了新的靶标。

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  • 作者

    Li Chunxia; Dai Jun; Dong Guanjun; Ma Qun; Li Zhihua; Zhang Hui; Yan Fenglian; Zhang Junfeng; Wang Bo; Shi Hui; Zhu Yuzhen; Yao Xiaoying; Si Chuanping; Xiong Huabao;

  • 作者单位

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Institute of Immunology and Molecular MedicineJining Medical UniversityShandong China;

    Department of MedicineIcahn School of Medicine at Mount SinaiNew York NY USA;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医学免疫学;
  • 关键词

    IgE; interleukin‐16; ovalbumin‐induced asthma; T helper type 2 cytokines; T helper type 17 cytokines;

    机译：IgE;白细胞介素-16;卵泡诱导的哮喘;T辅助型细胞因子;T辅助17型细胞因子;

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