• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Clearance of Pseudomonas aeruginosa from a Healthy Ocular Surface Involves Surfactant Protein D and Is Compromised by Bacterial Elastase in a Murine Null-Infection Model
【24h】

Clearance of Pseudomonas aeruginosa from a Healthy Ocular Surface Involves Surfactant Protein D and Is Compromised by Bacterial Elastase in a Murine Null-Infection Model

机译：从健康的眼表清除铜绿假单胞菌涉及表面活性剂蛋白D，并在鼠空感染模型中被细菌弹性蛋白酶破坏。

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

摘要

Our previous studies showed that surfactant protein D (SP-D) is present in human tear fluid and that it can protect corneal epithelial cells against bacterial invasion. Here we developed a novel null-infection model to test the hypothesis that SP-D contributes to the clearance of viable Pseudomonas aeruginosa from the healthy ocular surface in vivo. Healthy corneas of Black Swiss mice were inoculated with 107 or 109 CFU of invasive (PAO1) or cytotoxic (6206) P. aeruginosa. Viable counts were performed on tear fluid collected at time points ranging from 3 to 14 h postinoculation. Healthy ocular surfaces cleared both P. aeruginosa strains efficiently, even when 109 CFU was used: e.g., <0.01% of the original inoculum was recoverable after 3 h. Preexposure of eyes to bacteria did not enhance clearance. Clearance of strain 6206 (low protease producer), but not strain PAO1 (high protease producer), was delayed in SP-D gene-targeted (SP-D?/?) knockout mice. A protease mutant of PAO1 (PAO1 lasA lasB aprA) was cleared more efficiently than wild-type PAO1, but this difference was negligible in SP-D?/? mice, which were less able to clear the protease mutant. Experiments to study mechanisms for these differences revealed that purified elastase could degrade tear fluid SP-D in vivo. Together, these data show that SP-D can contribute to the clearance of P. aeruginosa from the healthy ocular surface and that proteases can compromise that clearance. The data also suggest that SP-D degradation in vivo is a mechanism by which P. aeruginosa proteases could contribute to virulence.
机译：我们以前的研究表明，人泪液中存在表面活性剂蛋白D（SP-D），它可以保护角膜上皮细胞免受细菌侵袭。在这里，我们开发了一种新型的无效感染模型，以测试SP-D有助于从体内健康眼表清除活的铜绿假单胞菌的假说。用侵袭性（PAO1）或细胞毒性（6206） P的10 7 或10 9 CFU接种黑瑞士小鼠的健康角膜。铜绿。在接种后3至14小时的时间点对收集的泪液进行了活计数。健康的眼表清除了两个 P。即使使用10 9 CFU，铜绿假单胞菌菌株也能有效分离：例如，3小时后可恢复<0.01％的原始接种物。眼睛接触细菌不会增加清除率。在靶向SP-D基因的（SP-D ？/？）基因敲除小鼠中，菌株6206（低蛋白酶产生者）而不是PAO1（高蛋白酶产生者）的清除被延迟。与野生型PAO1相比，PAO1的蛋白酶突变体（PAO1 lasA lasB aprA ）清除效率更高，但在SP- D ？/？小鼠清除蛋白酶突变体的能力较弱。研究这些差异机制的实验表明，纯化的弹性蛋白酶可以在体内降解泪液SP-D。这些数据加在一起表明SP-D可以有助于清除 P。可以从健康的眼表看到铜绿假单胞菌，而蛋白酶会破坏该清除率。数据还表明体内SP-D降解是 P的机制。铜绿蛋白酶可能会增加毒力。

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