Versatility of the capsular genes during biofilm formation by Streptococcus pneumoniae
Versatility of the capsular genes during biofilm formation by Streptococcus pneumoniae
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DOI：
10.1111/j.1462-2920.2009.01979.x
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发表时间：
2009-10-01
影响因子：
5.1
通讯作者：
Moscoso, Miriam
中科院分区：
文献类型：
--
作者：
Domenech, Mirian;Garcia, Ernesto;Moscoso, Miriam
肺炎链球菌是鼻咽部自然菌群的一部分。对于肺炎球菌引起感染，需要发生定植，并且该过程由细菌粘附到呼吸道上皮介导。虽然S.已知肺炎对于感染的发生是重要的，但其在定殖中的作用是有争议的。生物膜模型开始成为研究CPS在鼻咽携带过程中作用的一种有前途的工具，鼻咽携带是肺炎球菌感染传播和启动的第一步。使用一个定义明确的模型系统来分析体外肺炎球菌生物膜的形成，在这里，我们探讨了使用3型S的荚膜突变体的出现背后的分子变化。肺炎细胞。自发集落期变体显示启动子突变，以及编码UDP-葡萄糖脱氢酶（UDP-GlcDH）的cap 3A基因的重复、缺失和点突变。增加的生物膜形成能力通常可以与菌落大小和每个菌落变体的细胞表面上存在的CPS的相对量两者的减少相关。然而，导致非常低的CPS产生的Cap 3A Thr 83 Ile（细菌UDP-GlcDH中严格保守的残基）中的突变也导致受损的生物膜形成。我们建议，非封装的3型肺炎球菌菌株的突变体基本上参与在定植/发病过程中的生物膜形成的初始阶段（附着阶段）。
P>Streptococcus pneumoniae forms part of the natural microbiota of the nasopharynx. For the pneumococcus to cause infection, colonization needs to occur and this process is mediated by adherence of bacteria to the respiratory epithelium. Although the capsular polysaccharide (CPS) of S. pneumoniae is known to be important for infection to occur, its role in colonization is controversial. Biofilm models are starting to emerge as a promising tool to investigate the role of CPS during nasopharyngeal carriage, which is the first step in the dissemination and initiation of a pneumococcal infection. Using a well-defined model system to analyse in vitro biofilm formation in pneumococcus, here we explore the molecular changes underlying the appearance of capsular mutants using type 3 S. pneumoniae cells. Spontaneous colony phase variants show promoter mutations, as well as duplications, deletions and point mutations in the cap3A gene, which codes for a UDP-glucose dehydrogenase (UDP-GlcDH). Increased biofilm-forming capacity could usually be correlated with a reduction both in colony size and in the relative amount of CPS present on the cell surface of each colony variant. However, a mutation in Cap3A Thr83Ile (a strictly conserved residue in bacterial UDP-GlcDHs) that resulted in very low CPS production also led to impaired biofilm formation. We propose that non-encapsulated mutants of pneumococcal type 3 strains are essentially involved in the initial stages (the attachment stage) of biofilm formation during colonization/pathogenesis.