Infectivity of a glucan synthesis-defective mutant of Streptococcus gordonii (Challis) in a rat endocarditis model.

Infectivity of a glucan synthesis-defective mutant of Streptococcus gordonii (Challis) in a rat endocarditis model.
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戈登链球菌 (Challis) 葡聚糖合成缺陷突变体在大鼠心内膜炎模型中的感染性。

DOI:
10.1111/j.1574-6968.1993.tb06466.x
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发表时间:
1993
影响因子:
2.1
通讯作者:
Macrina,FL
Macrina,FL
中科院分区:
生物学4区
文献类型:
--
作者:
Wells,VD;Munro,CL;Sulavik,MC;Clewell,DB;Macrina,FL

文献摘要

被引文献

相似文献

戈登链球菌是人类口腔固有菌群的一员,在光滑的牙齿表面定植并促进牙菌斑的形成。虽然它不被认为是一种致龋病原体,但它可能会在侵入血流后引起心内膜炎。利用等位基因交换诱变技术,我们构建了一个突变株。gordonii(查利斯),其单功能葡糖基转移酶基因有缺陷,因此不能从蔗糖合成葡聚糖外聚物。当在大鼠心内膜炎模型中检测时,蔗糖生长的突变体与S. gordonii野生型,表明葡聚糖聚合物对感染性没有贡献。这一结果与先前用聚合物缺陷的观察到的结果形成鲜明对比。突变体
Streptococcus gordonii, a member of the human indigenous oral microflora, colonizes smooth tooth surfaces and contributes to dental plaque formation. Although it is not recognized as being a cariogenic pathogen, it may cause endocarditis following invasion of the bloodstream. Using allelic exchange mutagenesis, we have constructed a mutant ofS. gordonii(Challis) which is defective in its single functional glucosyltransferase gene and, hence, is unable to synthesize glucan exopolymers from sucrose. When examined in a rat endocarditis model, the sucrose-grown mutant did not differ significantly fromS. gordoniiwild-type, suggesting that glucan polymers did not contribute to infectivity. This result was in striking contrast to that previously observed with a polymer-defectiveS. mutansmutant.