• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文学位 >The role of pneumococcal surface protein A in virulence of a capsular serotype 3 Streptococcus pneumoniae: Complement attack versus bacterial evasion.
【24h】

The role of pneumococcal surface protein A in virulence of a capsular serotype 3 Streptococcus pneumoniae: Complement attack versus bacterial evasion.

机译：肺炎球菌表面蛋白A在荚膜血清3型肺炎链球菌的毒性中的作用：补体攻击与细菌逃逸。

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

Complement plays an important role in host immunity against pneumococcal infections. Pneumococcal surface protein A (PspA) is a virulence factor of pneumococci, and also a promising candidate for pneumococcal protein-based vaccine. Based on their sequence homology, PspA molecules have been divided into three major families. Previous studies have shown that family 1 PspA is important for the virulence of WU2, a capsular serotype 3 strain, and it inhibits complement deposition on the pneumococcal surface. PspAs of family 1 and 2 share 40% homology in their N-terminal alpha-helical region. To determine whether these two family PspAs play similar roles in virulence, a family 2 PspA from the TIGR4 strain (capsular type 4) was introduced into WU2 to replace the original family 1 PspA. Our results showed that on the WU2 background, both family 1 and 2 PspAs have the same influence on complement deposition and virulence in a murine bacteremia model.; Complement activation can be triggered by two major pathways: the classical/MBL and alternative pathways. It was revealed that mainly the classical pathway initiates the deposition of C3 on the surface of the capsular type 3 strain, while the alter native pathway is important for amplifying C3 activation and deposition triggered via the classical pathway. The difference in C3 deposition onto strains WU2 (pspA+) and JY1119 ( pspA-) in the presence of antibodies to capsular type 3 and factor-B-deficient mouse serum suggests that PspA may interfere with the classical-pathway-mediated C3 deposition. Both human and mouse antibodies to PspA significantly increased the C3 deposition on the surface of WU2.; The roles of complement receptors in the pneumococcal infection were investigated using mutant mice deficient in complement receptors. Our results suggest that complement receptor 1, 3 and 4 play essential roles in elimination of bacteria from the host blood stream. Our results also confirmed the important role of the alternative pathway in host defense against pneumococcal infection, since factor-D-deficient mice challenged with either WU2 or JY1119 showed significantly decreased survival time as compared to wild-type mice.
机译：补体在宿主抵抗肺炎球菌感染的免疫中起重要作用。肺炎球菌表面蛋白A（PspA）是肺炎球菌的致病因子，也是基于肺炎球菌蛋白的疫苗的有希望的候选者。基于其序列同源性，PspA分子已分为三个主要家族。先前的研究表明，家族1 PspA对于荚膜血清型3株WU2的毒力很重要，并且它抑制补体在肺炎球菌表面的沉积。家族1和家族2的PspA在其N末端的α螺旋区具有40％的同源性。为了确定这两个家族PspA在毒力中是否发挥相似的作用，将来自TIGR4菌株（荚膜类型4）的家族2 PspA引入WU2，以取代原始的家族1 PspA。我们的结果表明，在WU2背景下，在鼠菌血症模型中，家族1和2 PspAs对补体沉积和毒力的影响相同。补体激活可以通过两种主要途径触发：经典/ MBL途径和替代途径。结果表明，经典途径主要引起C3在3型荚膜菌株表面的沉积，而天然途径的改变对于放大经典途径触发的C3活化和沉积很重要。在存在针对荚膜类型3和缺乏因子B的小鼠血清的抗体的情况下，将C3沉积到菌株WU2（pspA +）和JY1119（pspA-）上的差异表明，PspA可能会干扰经典途径介导的C3沉积。人和小鼠的PspA抗体均显着增加了WU2表面的C3沉积。使用缺乏补体受体的突变小鼠研究了补体受体在肺炎球菌感染中的作用。我们的结果表明，补体受体1、3和4在消除宿主血流中的细菌方面起着至关重要的作用。我们的研究结果还证实了替代途径在宿主对抗肺炎球菌感染的防御中的重要作用，因为与野生型小鼠相比，用WU2或JY1119攻击的缺乏D因子的小鼠均显示存活时间大大缩短。

著录项

  • 作者

    Ren, Bing.;

  • 作者单位

    The University of Alabama at Birmingham.;

  • 授予单位 The University of Alabama at Birmingham.;
  • 学科 Biology Microbiology.; Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2003
  • 页码 139 p.
  • 总页数 139
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 微生物学;预防医学、卫生学;
  • 关键词

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