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Inactivation of Streptococcus mutans genes lytST and dltAD impairs its pathogenicity in vivo

机译:变形链球菌基因 lytST dltAD 的失活削弱了其在体内的致病性

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ABSTRACT Background: Streptococcus mutans orchestrates the development of a biofilm that causes dental caries in the presence of dietary sucrose, and, in the bloodstream, S. mutans can cause systemic infections. The development of a cariogenic biofilm is dependent on the formation of an extracellular matrix rich in exopolysaccharides, which contains extracellular DNA (eDNA) and lipoteichoic acids (LTAs). While the exopolysaccharides are virulence markers, the involvement of genes linked to eDNA and LTAs metabolism in the pathogenicity of S. mutans remains unclear. Objective and Design: In this study, a parental strain S. mutans UA159 and derivative strains carrying single gene deletions were used to investigate the role of eDNA (Δ lytS and Δ lytT ), LTA (Δ dltA and Δ dltD ), and insoluble exopolysaccharides (Δ gtfB ) in virulence in a rodent model of dental caries (rats) and a systemic infection model ( Galleria mellonella larvae). Results: Fewer carious lesions were observed on smooth and sulcal surfaces of enamel and dentin of the rats infected with ? lytS , ? dltD , and Δ gtfB (vs. the parental strain). Moreover, strains carrying gene deletions prevented the killing of larvae (vs. the parental strain). Conclusions: Altogether, these findings indicate that inactivation of lytST and dltAD impaired S. mutans cariogenicity and virulence in vivo .
机译:摘要背景:变形链球菌可协调生物膜的发展,这种生物膜在饮食中存在蔗糖时会引起龋齿,并且在血液中,变形链球菌会引起全身感染。致龋生物膜的形成取决于富含胞外多糖的胞外基质的形成,该胞外基质含有胞外DNA(eDNA)和脂蛋白酸(LTAs)。虽然胞外多糖是毒力标记,但尚不清楚与eDNA和LTA代谢相关的基因是否参与变形链球菌的致病性。目的与设计:在这项研究中,使用了带有单基因缺失的亲本菌株变形链球菌UA159和衍生菌株来研究eDNA(ΔlytS和ΔlytT),LTA(ΔdltA和ΔdltD)以及不溶性胞外多糖的作用。龋齿(大鼠)的啮齿动物模型和全身感染模型(蜜环菌幼虫)的毒力(ΔgtfB)。结果:在被感染的大鼠的牙釉质和牙本质的光滑和沟渠表面观察到更少的龋损。 lytS ,? dltD和ΔgtfB(相对于亲本菌株)。此外,携带基因缺失的菌株阻止了幼虫的杀死(相对于亲本菌株)。结论:总而言之,这些发现表明lytST和dltAD的失活会破坏变形链球菌的体内致癌性和致病性。

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