首页> 外文期刊>Proceedings of American Thoracic Society >Airway Epithelia Up-Regulate IL-19 in Response to IL 17A/IL 13
【24h】

Airway Epithelia Up-Regulate IL-19 in Response to IL 17A/IL 13

机译:气道上皮细胞上调IL-19响应IL 17A / IL 13

获取原文
获取原文并翻译 | 示例
           

摘要

Interleukin (IL)-17A and IL-19 are highly expressed in chronic inflammatory diseases, such as psoriasis and asthma. The role of IL-19 in allergic diseases is highlighted by its ability to enhance Th2 cytokine secretion; however, the cell source of IL-19 in individuals with asthma is unknown. Our aims are to determine if the epithelium is one of the major cell sources of mucosal IL-19 in airways, and to elucidate the mechanism of gene expression regulation. By immunofluorescent staining, we found significantly higher IL-19 expression in airway epithelia of subjects with asthma than in subjects with other lung diseases. In cytokine panel treatments, the stimulation of IL-19 expression in well-differentiated human tracheobronchial epithelia is found to be regulated by two Th2 cytokines, IL-4 and -13, in addition to IL-17A. Moreover, the co-treatment of IL-17A and IL-4/13 synergistically up-regulates IL-19. By siRNA and chemical inhibitor treatments, we demonstrated that IL-19 is tran-scriptionally regulated by NF-kB and STAT6. The addition of IL-13 to IL-17A for IL-19 stimulation triggers a shift from NF-KB-dependent to STAT6-based transcriptional regulation. Chromatin-immunoprecipitation assays demonstrated the presence of STAT6-responsive DNA-protein interactions at IL-19 promoter region. We thereby conclude that an IL-17A and IL-4/13-induced synergism in IL-19 stimulation in airway epithelia may play an important role in asthma.
机译:白细胞介素(IL)-17A和IL-19在诸如牛皮癣和哮喘的慢性炎性疾病中高度表达。 IL-19增强Th2细胞因子分泌的能力突显了其在过敏性疾病中的作用。然而,哮喘个体中IL-19的细胞来源尚不清楚。我们的目标是确定上皮是否是气道粘膜IL-19的主要细胞来源之一,并阐明基因表达调控的机制。通过免疫荧光染色,我们发现哮喘患者气道上皮中的IL-19表达明显高于其他肺部疾病患者。在细胞因子组治疗中,发现分化良好的人气管支气管上皮细胞中IL-19表达的刺激除IL-17A外还受两种Th2细胞因子IL-4和-13的调节。而且,IL-17A和IL-4 / 13的共同治疗协同上调IL-19。通过siRNA和化学抑制剂处理,我们证明IL-19受NF-kB和STAT6转录调控。将IL-13添加到IL-17A中以刺激IL-19,从而触发了从依赖NF-KB的转录向基于STAT6的转录调控的转变。染色质免疫沉淀测定法证明在IL-19启动子区域存在STAT6反应性DNA-蛋白质相互作用。因此,我们得出结论,气道上皮细胞中IL-19刺激中的IL-17A和IL-4 / 13诱导的协同作用可能在哮喘中起重要作用。

著录项

  • 来源
    《Proceedings of American Thoracic Society》 |2009年第3期|p.326|共1页
  • 作者单位

    Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, California;

    Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, California;

    Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, California;

    Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, California;

    Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, California;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号