...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>International immunopharmacology >Prostaglandin E2 blockade enhances the pulmonary anti-Cryptococcus neoformans immune reaction via the induction of TLR-4
【24h】

Prostaglandin E2 blockade enhances the pulmonary anti-Cryptococcus neoformans immune reaction via the induction of TLR-4

机译：前列腺素E2阻滞剂通过诱导TLR-4增强肺部抗隐球菌免疫反应

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

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

摘要

The present study aimed to explore whether the inhibition of prostaglandin E2 enhances pulmonary anti-Cryptococcus neoformans immunity. Lung colony forming unit (CFU) assays demonstrated that the cryptococcal infection was dramatically depressed in mice given EP2 and EP4 or single EP antagonist treatment compared to the untreated wild type mice (p < 0.05), leading to the increased survival of the infected mice by 8-9 days or 2-4 days, respectively. RT-PCR and flow cytometry assays showed that the expression of IFN-gamma, IL-17, IL-22 in M1 macrophages and IL-10 in M2 macrophages increased significantly at 1 week post-infection in mice with either EP2 or EP4 blockade (p < 0.05). The polarization of alveolar macrophages showed that, at 1 week post infection, the alveolar macrophages in untreated wild type mice, TLR4(-/-) mice and TLR4(-/-) mice with EP2 and EP4 blockade were strongly M2 polarized, whereas the alveolar macrophages in wild type mice with EP2 and EP4 blockade were M1 polarized. In conclusion, the blockade of EP2 and EP4 promotes mouse survival after cryptococcus infection by promoting the production of cytokines via TLR4, as well as the enhanced M1 polarization of alveolar macrophages. (C) 2015 Elsevier B.V. All rights reserved.
机译：本研究旨在探讨前列腺素E2的抑制是否增强了肺部新隐隐球菌的免疫力。肺集落形成单位（CFU）分析表明，与未治疗的野生型小鼠相比，在接受EP2和EP4或单次EP拮抗剂治疗的小鼠中，隐球菌感染显着降低了（p <0.05），从而导致感染小鼠的存活率提高。分别为8-9天或2-4天。 RT-PCR和流式细胞仪检测显示，感染EP1或EP4的小鼠感染后1周，M1巨噬细胞中IFN-γ，IL-17，IL-22和M2巨噬细胞中IL-10的表达显着增加（ p ＜0.05）。肺泡巨噬细胞的极化显示，在感染后1周，未经处理的野生型小鼠，TLR4（-/-）小鼠和带有EP2和EP4阻滞的TLR4（-/-）小鼠的肺泡巨噬细胞强烈M2极化，而对具有EP2和EP4阻断作用的野生型小鼠的肺泡巨噬细胞进行M1极化处理。总之，对EP2和EP4的阻断可通过TLR4促进细胞因子的产生以及肺泡巨噬细胞的M1极化增强，从而促进隐球菌感染后的小鼠存活。 （C）2015 Elsevier B.V.保留所有权利。

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