The roles of lipoprotein multigene families in pathogenesis of Mycoplasma pneumoniae

脂蛋白多基因家族在肺炎支原体发病机制中的作用

• 批准号: nhmrc : 145789
• 负责人: Prof Glenn Browning
• 金额: $ 17.14万
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2001
• 资助国家: 澳大利亚
• 起止时间: 2001-01-01 至 2003-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/roles-lipoprotein-multigene-mycoplasma-pneumoniae/100555
• 关键词: roles; lipoprotein; multigene; families; pathogenesis

Mycoplasma pneumoniae is one of the most common causes of community acquired pneumonia. Although it can usually be successfully treated with antibiotics, it can result in more severe diseases and can be difficult to diagnose accurately. It has been identified as a target for vaccine development, but this has been hampered by the limited understanding we have of how it causes disease. The attempts at vaccination that have been made have resulted in vaccines which induced more severe, rather than less severe, disease. Investigations of several other related bacteria have shown that they are able to vary their surface proteins and thus may evade the immune system, permitting them to cause more prolonged disease. Better understanding how this occurs, and what this enables the bacteria to do, may assist in developing improved vaccine strategies. This project aims to investigate the six gene families in Mycoplasma pneumoniae which are known to encode surface proteins and establish how and why the bacteria switch from one gene to another during infection. In addition the capacity of bacteria expressing different versions of the six surface proteins to adhere to different tissues will be investigated. Once this is known, these mechanisms may be able to be specifically disrupted to prevent a strain of Mycoplasma pneumoniae from being able to establish prolonged infections. Such a strain might be a useful basis for an effective vaccine.

肺炎支原体是社区获得性肺炎最常见的原因之一。尽管通常可以用抗生素成功治疗，但它可能导致更严重的疾病，并且很难准确诊断。它已被确定为疫苗开发的目标，但由于我们对其如何引起疾病的了解有限，这一目标受到了阻碍。已经进行的疫苗接种尝试导致疫苗诱发更严重的疾病，而不是不太严重的疾病。对其他几种相关细菌的研究表明，它们能够改变其表面蛋白，因此可能逃避免疫系统，从而导致更长时间的疾病。更好地了解这种情况是如何发生的，以及细菌能够做什么，可能有助于开发改进的疫苗策略。该项目旨在研究肺炎支原体中已知编码表面蛋白的六个基因家族，并确定细菌在感染过程中如何以及为何从一个基因转换为另一个基因。此外，还将研究表达不同版本的六种表面蛋白的细菌粘附到不同组织的能力。一旦知道这一点，这些机制可能能够被专门破坏，以防止肺炎支原体菌株建立长期感染。这种菌株可能是有效疫苗的有用基础。