...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Microbiology >Delayed association of the NADPH oxidase complex with macrophage vacuoles containing the opportunistic pathogen Burkholderia cenocepacia
【24h】

Delayed association of the NADPH oxidase complex with macrophage vacuoles containing the opportunistic pathogen Burkholderia cenocepacia

机译：延迟NADPH氧化酶复合物与含有机会病原体Burkowneria Cenocepacia的巨噬细胞液泡

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

摘要

Burkholderia cenocepacia causes chronic lung infections in patients suffering from cystic fibrosis and chronic granulomatous disease. We have previously shown that B. cenocepacia survives intracellularly in macrophages within a membrane vacuole (BcCV) that delays acidification. Here, we report that after macrophage infection with live B. cenocepacia there is a ～6?h delay in the association of NADPH oxidase with BcCVs, while heat-inactivated bacteria are normally trafficked into NADPH oxidase-positive vacuoles. BcCVs in macrophages treated with a functional inhibitor of the cystic fibrosis transmembrane conductance regulator exhibited a further delay in the assembly of the NADPH oxidase complex at the BcCV membrane, but the inhibitor did not affect NADPH oxidase complex assembly onto vacuoles containing heat-inactivated B. cenocepacia or live Escherichia coli. Macrophages produced less superoxide following B. cenocepacia infection as compared to heat-inactivated B. cenocepacia and E. coli controls. Reduced superoxide production was associated with delayed deposition of cerium perhydroxide precipitates around BcCVs of macrophages infected with live B. cenocepacia, as visualized by transmission electron microscopy. Together, our results demonstrate that intracellular B. cenocepacia resides in macrophage vacuoles displaying an altered recruitment of the NADPH oxidase complex at the phagosomal membrane. This phenomenon may contribute to preventing the efficient clearance of this opportunistic pathogen from the infected airways of susceptible patients.
机译：Cenocepacia伯克德利亚宫颈切割导致患有囊性纤维化和慢性肉芽肿疾病的患者的慢性肺部感染。我们之前已经表明，B. Cenocepacia在延迟酸化的膜液泡（BCCV）内的巨噬细胞内部存活。在这里，我们报道，在巨噬细胞感染与活体B. cenocepacia有一个〜6？h延迟NADPH氧化酶与BCCVs的延迟，而热灭活的细菌通常被贩运成NADPH氧化酶阳性水渣。用囊性纤维化跨膜电导调节器的功能性抑制剂处理的巨噬细胞中的BCCV在BCCV膜组装中显示出NADPH氧化酶复合物的进一步延迟，但抑制剂没有影响NADPH氧化酶复合组件在含有热灭活B的真空上。 Cenocepacia或Live Escherichia Coli。巨噬细胞在B. cenocepacia感染后产生较少的超氧化物与热灭活的B. cenocepacia和大肠杆菌对照相比。通过透射电子显微镜可视化，降低过量的超氧化物产生与血红蛋白羟基氧化物沉淀物的延迟沉淀有关。我们的结果一起表明，细胞内B. Cenocepacia在巨噬细胞液泡中纳入显示在吞噬膜膜处的NADPH氧化酶复合物的改变募集。这种现象可能有助于防止来自受感染的患者的感染的气道有效地清除这种机会主义病原体。

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