Biofilm formation by Streptococcus pneumoniae:: Role of choline, extracellular DNA, and capsular polysaccharide in microbial accretion
Biofilm formation by Streptococcus pneumoniae:: Role of choline, extracellular DNA, and capsular polysaccharide in microbial accretion
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DOI：
10.1128/jb.00673-06
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发表时间：
2006-11-01
影响因子：
3.2
通讯作者：
Lopez, Rubens
中科院分区：
文献类型：
--
作者：
Moscoso, Miriam;Garcia, Ernesto;Lopez, Rubens
肺炎链球菌在人上呼吸道定植，这种无症状的定植是肺炎球菌疾病的先兆。在这份报告中，化学成分和半合成的媒体被用来确定生物膜形成的初始步骤，肺炎球菌在非生物表面，如聚苯乙烯或玻璃生长。通过共聚焦激光扫描显微镜和低温扫描电子显微镜观察到，未封装的肺炎球菌粘附在非生物表面，并形成约25 μ m深的三维结构。研究发现细胞壁磷壁酸的胆碱残基在肺炎球菌生物膜的发育中发挥着重要作用。胆碱结合蛋白，其中锚的磷壁酸的细胞被膜的形成中的作用，确定使用明确特征的突变体。结果表明，LytA酰胺酶，LytC溶菌酶，LytB氨基葡萄糖苷酶，CbpA粘附素，PcpA假定的粘附素，和PspA（肺炎球菌表面蛋白A）突变体的能力下降，形成生物膜，而没有观察到这样的减少在Pce磷酸胆碱酯酶或CbpD假定的酰胺酶突变体。此外，胶囊化的临床肺炎球菌分离株形成生物膜的能力受损。此外，还对胞外DNA和蛋白质在S. pneumoniae生物膜。总之，这些观察结果提供了有利于S。肺炎。这里描述的实验方法应该有助于研究生物膜形成所需的细菌基因。这些结果，反过来，可以提供洞察战略，以防止肺炎球菌定植的人类宿主。
Streptococcus pneumoniae colonizes the human upper respiratory tract, and this asymptomatic colonization is known to precede pneumococcal disease. In this report, chemically defined and semisynthetic media were used to identify the initial steps of biofilm formation by pneumococcus during growth on abiotic surfaces such as polystyrene or glass. Unencapsulated pneumococci adhered to abiotic surfaces and formed a three-dimensional structure about 25 mu m deep, as observed by confocal laser scanning microscopy and low-temperature scanning electron microscopy. Choline residues of cell wall teichoic acids were found to play a fundamental role in pneumococcal biofilm development. The role in biofilm formation of choline-binding proteins, which anchor to the teichoic acids of the cell envelope, was determined using unambiguously characterized mutants. The results showed that LytA amidase, LytC lysozyme, LytB glucosaminidase, CbpA adhesin, PcpA putative adhesin, and PspA (pneumococcal surface protein A) mutants had a decreased capacity to form biofilms, whereas no such reduction was observed in Pce phosphocholinesterase or CbpD putative amidase mutants. Moreover, encapsulated, clinical pneumococcal isolates were impaired in their capacity to form biofilms. In addition, a role for extracellular DNA and proteins in the establishment of S. pneumoniae biofilms was demonstrated. Taken together, these observations provide information on conditions that favor the sessile mode of growth by S. pneumoniae. The experimental approach described here should facilitate the study of bacterial genes that are required for biofilm formation. Those results, in turn, may provide insight into strategies to prevent pneumococcal colonization of its human host.