首页> 外文学位 >Strain Specificity of Capsular Polysaccharide Production by Staphylococcus aureus
【24h】

Strain Specificity of Capsular Polysaccharide Production by Staphylococcus aureus

机译:金黄色葡萄球菌产生荚膜多糖的菌株特异性

获取原文
获取原文并翻译 | 示例

摘要

Staphylococcus aureus is the leading cause of nosocomial infections in the US and is becoming increasingly difficult to treat due to the limited antibiotics available. Capsular polysaccharides (CP), a virulence factor produced by the bacterium, allows S. aureus to evade the uptake and killing by host neutrophils. It has been shown previously that CP serotype 5 retains more cell-associated CP while type 8 tends to release more CP into the supernatant. This research focused on whether this phenomenon is dependent upon the serotype-specific capHIJK genes that vary between the two serotypes. 6850, a methicillin- sensitive S. aureus (MSSA) serotype 8 strain, is a well characterized clinical isolate that was used in this study. This strain was subjected to two allelic replacement steps: the first step to replace the cap8HIJK genes with an ermB cassette, creating mutant 6850 (CP-); the second step to replace the ermB cassette with the cap5HIJK genes, which resulted in the creation of mutant 6850 (CP5). All 3 strains were characterized genotypically by PCR and phenotypically for growth rate, metabolic profile, and CP production. ELISA inhibition studies revealed that serotype 5 and the serotype 8 variants of S. aureus 6850 produced similar levels of cell-associated CP. These results suggest that cell wall anchoring of S. aureus CP5 and CP8 is not serotype specific, but instead is dependent on the genetic background of the bacterial strain. A better understanding of the anchoring mechanism may allow for development of alternative immunotherapeutics for S. aureus.
机译:金黄色葡萄球菌是美国医院感染的主要原因,由于可用的抗生素有限,因此变得越来越难以治疗。荚膜多糖(CP)是细菌产生的一种致病因子,它使金黄色葡萄球菌能够逃避宿主嗜中性白细胞的摄取和杀死。先前已经显示,CP血清型5保留了更多的细胞相关CP,而8型倾向于将更多的CP释放到上清液中。这项研究集中于这种现象是否取决于在两种血清型之间变化的血清型特异性capHIJK基因。 6850是一种对甲氧西林敏感的金黄色葡萄球菌(MSSA)血清型8株,在本研究中使用的是特征明确的临床分离株。该菌株经历了两个等位基因置换步骤:第一步是用ermB盒替代cap8HIJK基因,从而产生突变体6850(CP-);第二步是用cap5HIJK基因替换ermB盒,从而产生了突变型6850(CP5)。通过PCR在基因型上表征所有3个菌株,并在表型上表征生长速率,代谢谱和CP产生。 ELISA抑制研究表明,金黄色葡萄球菌6850的血清型5和血清型8变体产生相似水平的细胞相关CP。这些结果表明,金黄色葡萄球菌CP5和CP8的细胞壁锚固不是血清型特异性的,而是取决于细菌菌株的遗传背景。对锚定机制的更好的理解可能允许开发金黄色葡萄球菌的替代免疫疗法。

著录项

  • 作者

    Yeh, Anthony J.;

  • 作者单位

    Boston University.;

  • 授予单位 Boston University.;
  • 学科 Microbiology.
  • 学位 M.S.
  • 年度 2017
  • 页码 62 p.
  • 总页数 62
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 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