...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Allergy >Tumor necrosis factor family member LIGHT LIGHT acts with IL IL ‐1β and TGF TGF ‐β to promote airway remodeling during rhinovirus infection
【24h】

Tumor necrosis factor family member LIGHT LIGHT acts with IL IL ‐1β and TGF TGF ‐β to promote airway remodeling during rhinovirus infection

机译：肿瘤坏死因子家庭成员轻光用IL IL-1β和TGF TGF-β促进鼻病毒感染期间的气道重塑

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abstract Background Rhinovirus ( RV ) can exacerbate allergen‐driven asthma. However, it has been suggested that serial infections with RV may also lead to asthma‐like features in childhood without prior allergen exposure. Aim We sought to test the effects of RV infection in the absence of allergen challenge on lung tissue remodeling and to understand whether RV induced factors in common with allergen that promote remodeling. Methods We infected C57 BL /6 mice multiple times with RV in the absence or presence of allergen to assess airway remodeling. We used knockout mice and blocking reagents to determine the participation of LIGHT ( TNFSF 14), as well as IL ‐1β and TGF ‐β, each previously shown to contribute to lung remodeling driven by allergen. Results Recurrent RV infection without allergen challenge induced an increase in peribronchial smooth muscle mass and subepithelial fibrosis. Rhinovirus ( RV ) induced LIGHT expression in mouse lungs after infection, and alveolar epithelial cells and neutrophils were found to be potential sources of LIGHT . Accordingly, LIGHT ‐deficient mice, or mice where LIGHT was neutralized, displayed reduced smooth muscle mass and lung fibrosis. Recurrent RV infection also exacerbated the airway remodeling response to house dust mite allergen, and this was significantly reduced in LIGHT ‐deficient mice. Furthermore, neutralizing IL ‐1β or TGF ‐β also limited subepithelial fibrosis and/or smooth muscle thickness induced by RV . Conclusion Rhinovirus can promote airway remodeling in the absence of allergen through upregulating common factors that also contribute to allergen‐associated airway remodeling.
机译：摘要背景鼻病毒（RV）可以加剧过敏原驱动的哮喘。然而，已经提出，具有RV的序列感染也可能导致儿童时期的哮喘状特征，而没有先前过敏原暴露。目的我们试图在没有过敏原对肺组织重塑的攻击中的影响，了解RV诱导促进重塑的过敏原的因素是否造成过敏原的影响。方法在缺乏或存在过敏原的情况下多次感染C57 BL / 6小鼠，以评估气道重塑。我们使用敲除小鼠和阻断试剂来确定光（TNFSF 14）的参与，以及IL-1β和TGF-β，每个先前所示有助于通过过敏原驱动的肺部重塑。结果反复性RV感染没有过敏原攻击诱导血浆平滑肌肉质量和耻骨上纤维化的增加。鼻病毒（RV）感染后小鼠肺中的光表达，发现肺泡上皮细胞和中性粒细胞是潜在的光源。因此，光 - 缺光小鼠或光被中和的小鼠，显示出平滑的肌肉质量和肺纤维化。复发性RV感染也加剧了气道重塑对房屋粉尘螨过敏原的反应，并且在光的小鼠中显着降低。此外，中和IL-1β或TGF-β还限于诸如RV诱导的耻骨纤维化和/或平滑肌厚度。结论rhinovirus可以通过上调常见因素来促进气道重塑，这些常见因素也有助于过敏原相关气道重塑。

著录项

  • 来源
    《Allergy》 |2018年第7期|共10页
  • 作者

    Mehta A. K.; Doherty T.; Broide D.; Croft M.;

  • 作者单位

    Division of Immune RegulationLa Jolla Institute for Allergy and ImmunologyLa Jolla CA USA;

    Department of MedicineUniversity of California San DiegoLa Jolla CA USA;

    Department of MedicineUniversity of California San DiegoLa Jolla CA USA;

    Division of Immune RegulationLa Jolla Institute for Allergy and ImmunologyLa Jolla CA USA;

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

    asthma; collagen; rhinovirus; smooth muscle; TNFSF 14;

    机译：哮喘;胶原蛋白;鼻病毒;平滑肌;TNFSF 14;

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