• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Allergy >Effects of β Agonists, Corticosteroids, and Novel Therapies on Rhinovirus-Induced Cytokine Release and Rhinovirus Replication in Primary Airway Fibroblasts
【24h】

Effects of β Agonists, Corticosteroids, and Novel Therapies on Rhinovirus-Induced Cytokine Release and Rhinovirus Replication in Primary Airway Fibroblasts

机译：β激动剂，皮质类固醇和新疗法对鼻病毒诱导的细胞因子释放和鼻病毒在原发性气道成纤维细胞中复制的影响

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Rhinovirus-(RV-) induced asthma exacerbations account for high asthma-related health costs and morbidity in Australia. The cellular mechanism underlying this pathology is likely the result of RV-induced nuclear-factor-kappa-B-(NF-κB-) dependent inflammation. NF-κB may also be important in RV replication as inhibition of NF-κB inhibits replication of other viruses such as human immunodeficiency virus and cytomegalovirus. To establish the role of NF-κB inhibitors in RV-induced IL- 6 and IL-8 and RV replication, we used pharmacological inhibitors of NF-κB, and steroids and/or β2 agonists were used for comparison. Primary human lung fibroblasts were infected with RV-16 in the presence of NF-κB inhibitors BAY-117085 and dimethyl fumarate; β2 agonist salmeterol; and/or corticosteroids dexamethasone; fluticasone. RV-induced IL-6 and IL-8 and RV replication were assessed using ELISAs and virus titration assays. RV replicated and increased IL-6 and IL-8 release. Salmeterol increased, while dexamethasone and fluticasone decreased RV-induced IL-6 and IL-8 (). The NF-κB inhibitor BAY-117085 inhibited only RV-induced IL-6 () and dimethyl fumarate did not alter RV-induced IL-6 and IL-8. Dimethylfumarate increased RV replication whilst other drugs did not alter RV replication. These data suggest that inhibition of NF-κB alone is unlikely to be an effective treatment compared to current asthma therapeutics.
机译：在澳大利亚，鼻病毒-（RV-）诱发的哮喘加重导致了与哮喘相关的高昂的医疗费用和发病率。导致这种病理的细胞机制可能是RV诱导的核因子-κB-（NF-κB-）依赖性炎症的结果。 NF-κB在RV复制中也可能很重要，因为对NF-κB的抑制会抑制其他病毒的复制，例如人免疫缺陷病毒和巨细胞病毒。为了确定NF-κB抑制剂在RV诱导的IL-6和IL-8和RV复制中的作用，我们使用了NF-κB的药理抑制剂，并使用类固醇和/或β2激动剂进行比较。在NF-κB抑制剂BAY-117085和富马酸二甲酯的存在下，原代人肺成纤维细胞被RV-16感染。 β2激动剂沙美特罗;和/或皮质类固醇地塞米松;氟替卡松。使用ELISA和病毒滴定法评估RV诱导的IL-6和IL-8以及RV复制。 RV复制并增加IL-6和IL-8释放。沙美特罗增加，而地塞米松和氟替卡松减少RV诱导的IL-6和IL-8（）。 NF-κB抑制剂BAY-117085仅抑制RV诱导的IL-6（），而富马酸二甲酯不改变RV诱导的IL-6和IL-8。富马酸二甲酯增加了RV复制，而其他药物并未改变RV复制。这些数据表明，与目前的哮喘治疗剂相比，单独抑制NF-κB不太可能是有效的治疗方法。

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