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 (ΔlytS and ΔlytT), LTA (ΔdltA and ΔdltD), and insoluble exopolysaccharides (ΔgtfB) 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 ΔgtfB (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.

背景：变形链球菌可协调生物膜的发展，该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：在本研究中，父母亲菌株变形链球菌携带单个基因缺失UA159和衍生菌株被用来研究的eDNA（Δ的作用LYTS和Δ lytT），LTA（Δ DLTA和Δ dltD），和不溶性胞外多糖（Δ GTFB）的毒力在龋齿的啮齿动物模型（大鼠）和全身性感染模型（马勒菌幼虫）。结果：观察到在光滑更少龋损伤和釉质的脑沟表面和牙本质感染Δ大鼠LYTS，Δ dltD，和Δ GTFB（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的失活会损害变形链球菌的体内致癌性和致病性。