• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Human airway epithelial cells produce IP-10 (CXCL10) in vitro and in vivo upon rhinovirus infection.
【24h】

Human airway epithelial cells produce IP-10 (CXCL10) in vitro and in vivo upon rhinovirus infection.

机译：鼻病毒感染后，人的气道上皮细胞会在体外和体内产生IP-10（CXCL10）。

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

Human rhinovirus (HRV) infections trigger exacerbations of asthma and chronic obstructive pulmonary disease (COPD) and are associated with lymphocytic infiltration of the airways. We demonstrate that infection of primary cultures of human airway epithelial cells, or of the BEAS-2B human bronchial epithelial cell line, with human rhinovirus type 16 (HRV-16) induces expression of CXCL10 [IFN-gamma-inducible protein 10 (IP-10)], a ligand for the CXCR3 receptor found on activated type 1 T lymphocytes and natural killer cells. IP-10 mRNA reached maximal levels 24 h after HRV-16 infection then declined, whereas protein levels peaked 48 h after infection with no subsequent new synthesis. Cytosolic levels of AU-rich factor 1, a protein associated with mRNA destabilization, increased beginning 24 h after HRV-16 infection. Generation of IP-10 required virus capable of replication but was not dependent on prior induction of type 1 interferons. Transfection of synthetic double-stranded RNA into epithelial cells induced robust production of IP-10, whereas transfection of single-stranded RNA had no effect. Induction of IP-10 gene expression by HRV-16 depended upon activation of NF-kappaB, as well as other transcription factor recognition sequences further upstream in the IP-10 promoter. In vivo infection of human volunteers with HRV-16 strikingly increased IP-10 protein in nasal lavages during symptomatic colds. Levels of IP-10 correlated with symptom severity, viral titer, and numbers of lymphocytes in airway secretions. Thus IP-10 may play a role in the pathogenesis of HRV-induced colds and in HRV-induced exacerbations of COPD and asthma.
机译：人鼻病毒（HRV）感染会引发哮喘和慢性阻塞性肺疾病（COPD）恶化，并与气道淋巴细胞浸润有关。我们证明，人类鼻气道上皮细胞或BEAS-2B人支气管上皮细胞系的原代培养物感染人鼻病毒16型（HRV-16）会诱导CXCL10 [IFN-γ诱导蛋白10（IP- 10）]，这是在活化的1型T淋巴细胞和自然杀伤细胞上发现的CXCR3受体的配体。 IP-10 mRNA在HRV-16感染后24小时达到最高水平，然后下降，而蛋白质水平在感染后48小时达到峰值，没有随后的新合成。富含AU的因子1（一种与mRNA不稳定相关的蛋白）的胞浆水平在HRV-16感染后24小时开始增加。 IP-10的产生需要能够复制但不依赖于先前诱导1型干扰素的病毒。合成双链RNA转染上皮细胞可诱导IP-10的稳定产生，而单链RNA转染则无作用。 HRV-16对IP-10基因表达的诱导依赖于NF-κB以及IP-10启动子上游其他转录因子识别序列的激活。在有症状的感冒过程中，HRV-16的人类志愿者体内感染显着增加了鼻灌洗液中的IP-10蛋白。 IP-10的水平与症状严重程度，病毒滴度和气道分泌物中的淋巴细胞数量相关。因此，IP-10可能在HRV引起的感冒的发病机理以及HRV引起的COPD和哮喘加重中发挥作用。

著录项

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