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首页> 外文期刊>Immunology and Cell Biology >IL‐37 alleviates house dust mite‐induced chronic allergic asthma by targeting TSLP through the NF‐κB and ERK1/2 signaling pathways
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IL‐37 alleviates house dust mite‐induced chronic allergic asthma by targeting TSLP through the NF‐κB and ERK1/2 signaling pathways

机译：通过NF-κB和ERK1 / 2信号传导途径靶向TSLP，IL-37通过靶向TSLP减轻了房屋粉尘诱导的慢性过敏性哮喘

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摘要

Abstract Interleukin ( IL )‐37 has been described as a negative regulator of immune responses and is critical for asthma pathogenesis, but the mechanisms behind the protective role of IL ‐37 against allergic asthma are less well understood. We show here that IL ‐37 administered intranasally inhibited house dust mite ( HDM )‐induced chronic airway eosinophilic inflammation, goblet cell hyperplasia, peribronchial collagen deposition and airway hyperresponsiveness ( AHR ) to methacholine. In contrast to a weakened Th2 response in the lung that was characterized by the downregulation of Th2‐associated cytokines and chemokines in IL ‐37‐treated mice, IL ‐37 has no effect on relevant markers of systemic Th2 immune including serum immunoglobulins expression and in?vitro production of Th2‐associated cytokines by splenocytes on HDM recall. We demonstrated that the production of thymic stromal lymphopoietin ( TSLP ) in the lung tissue was associated with IL ‐37. Importantly, compared with IL ‐37 alone, TSLP coadministration with IL ‐37 restored HDM ‐induced airway inflammation and structural alterations, increased AHR to methacholine and promoted Th2‐associated cytokine production. We further found that IL ‐37 inhibited the induction of TSLP expression by the main antigen of house dust mite, Der p1, by suppressing NF ‐κB and extracellular signal regulated kinase 1/2 ( ERK 1/2) activation in human bronchial epithelial (16‐HBE) cells in?vitro . These data highlight the importance of TSLP in IL ‐37‐mediated protective role in asthma. IL ‐37 might represent a useful innovative and alternative therapy to control TSLP production in the airway.
机译：摘要白细胞介素（IL）-37已被描述为免疫应答的负调节剂，对于哮喘发病性至关重要，但IL -37对过敏性哮喘的保护作用背后的机制较小地理解。我们在这里展示IL -37鼻内抑制的房屋粉尘（HDM） - 诱导的慢性气道嗜酸性炎症，血红素细胞增生，血糖高胶原沉积和气道高反应性（AHR）给甲素。与肺中的弱化Th2反应相比，其特征在于IL-37处理的小鼠的Th2相关细胞因子和趋化因子的下调，IL -37对系统性Th2免疫的相关标志物没有影响，包括血清免疫球蛋白表达和通过HDM召回对脾细胞进行TH2相关细胞因子的体外生产。我们证明，肺组织中的胸腺基质淋巴二蛋白（TSLP）与IL -37相关。重要的是，与单独的IL -37相比，TSLP与IL -37恢复的HDM诱导的气道炎症和结构改变，增加AHR与甲素，促进TH2相关的细胞因子产生。我们进一步发现，IL -37通过抑制人支气管上皮中的NF-κB和细胞外信号调节激酶1/2（ERK 1/2）激活（ 16-hbe）体外细胞。这些数据突出了TSLP在IL -37介导的哮喘中的保护作用的重要性。 IL -37可能代表一个有用的创新和替代治疗，可以控制气道中的TSLP生产。

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  • 来源
    《Immunology and Cell Biology》 |2019年第4期|共13页
  • 作者

    Meng Ping; Chen Zhuang‐Gui; Zhang Tian‐Tuo; Liang Zhuo‐Zheng; Zou Xiao‐Ling; Yang Hai‐Ling; Li Hong‐Tao;

  • 作者单位

    Department of Pulmonary DiseasesThe Third Affiliated Hospital of Sun Yat‐Sen UniversityGuangzhou;

    Department of PediatricsThe Third Affiliated Hospital of Sun Yat‐Sen UniversityGuangzhou China;

    Department of Pulmonary DiseasesThe Third Affiliated Hospital of Sun Yat‐Sen UniversityGuangzhou;

    Department of Pulmonary DiseasesThe Third Affiliated Hospital of Sun Yat‐Sen UniversityGuangzhou;

    Department of Pulmonary DiseasesThe Third Affiliated Hospital of Sun Yat‐Sen UniversityGuangzhou;

    Department of Pulmonary DiseasesThe Third Affiliated Hospital of Sun Yat‐Sen UniversityGuangzhou;

    Department of Pulmonary DiseasesThe Third Affiliated Hospital of Sun Yat‐Sen UniversityGuangzhou;

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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

    Asthma; house dust mite; interleukin‐37; TSLP;

    机译：哮喘;房子尘螨;白细胞介素-37;TSLP;

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