A. actinomycetemcomitans LPS and Biofilm Formation

A.放线菌LPS和生物膜形成

• 批准号: 6886621
• 负责人: Casey CHEN
• 金额: $ 5.83万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-02-15 至 2006-02-14
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6886621
• 关键词: Actinobacillus actinomycetemcomitans; bacterial genetics; biofilm; carbohydrate structure; cell adhesion; chemical synthesis; gene deletion mutation; lipopolysaccharides; microorganism growth; microorganism metabolism; mutant; oral bacteria

DESCRIPTION (provided by applicant): Gram-negative facultative bacillus A. actinomycetemcomitans (Aa) is a major periodontal pathogen. The mechanism of Aa colonization was not fully understood. Aa has been observed to form tenacious biofilms on abiotic surfaces. This F33 application will test the hypothesis that LPS core mediates the adherence of Aa biofilms to abiotic surfaces. Specific Aim I will examine the genetics and the structure of Aa LPS core. A working model of the structure of Aa LPS and its biosynthesis pathway will be proposed. The LPS core synthesis genes will be mutated individually. The structure of the LPS of Aa wildtype and mutants will be determined. The results will be used to revise the proposed model until it is in agreement with the experimental data. Specific Aim II will identify the minimal LPS core structure required for the adherence and biofilm formation of Aa. Specific gene deletion LPS mutants of Aa will be constructed based on information obtained from Aim 1. The specific LPS core mutants will be tested for their adherence and, biofilm formation on abiotic surfaces. The long term goal of this research plan is to identify novel strategy to prevent colonization of Aa. Understanding the role of LPS in Aa biofilm formation may help fulfill this goal.

性状（申请人提供）：革兰氏阴性兼性芽孢杆菌A。伴放线菌（actinomycetemcomitans，Aa）是牙周病的主要致病菌。Aa定殖的机制尚未完全了解。已观察到Aa在非生物表面上形成坚韧的生物膜。该F33应用将测试LPS核心介导Aa生物膜粘附到非生物表面的假设。具体目的我将研究Aa LPS核心的遗传学和结构。我们将提出一个Aa LPS结构及其生物合成途径的工作模型。LPS核心合成基因将单独突变。将确定Aa野生型和突变体的LPS的结构。结果将被用来修改所提出的模型，直到它是与实验数据一致。特异性目标II将确定Aa粘附和生物膜形成所需的最小LPS核心结构。将基于从Aim 1获得的信息构建Aa的特异性基因缺失LPS突变体。将测试特定LPS核心突变体在非生物表面上的粘附和生物膜形成。这项研究计划的长期目标是确定新的策略，以防止Aa的殖民化。了解LPS在Aa生物膜形成中的作用可能有助于实现这一目标。