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首页> 外文期刊>Infection and immunity >Streptococcal Erythrogenic Toxin B Abrogates Fibronectin-Dependent Internalization of Streptococcus pyogenes by Cultured Mammalian Cells
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Streptococcal Erythrogenic Toxin B Abrogates Fibronectin-Dependent Internalization of Streptococcus pyogenes by Cultured Mammalian Cells

机译：链球菌促红细胞生成素B废除纤连蛋白依赖的化脓性链球菌培养的哺乳动物细胞的内在化。

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摘要

Streptococcus pyogenes secretes several proteins that influence host-pathogen interactions. A tissue-culture model was used to study the influence of the secreted cysteine protease streptococcal erythrogenic toxin B (SPE B) on the interaction between S. pyogenes strain NZ131 (serotype M49) and mammalian cells. Inactivation of the speB gene enhanced fibronectin-dependent uptake of the pathogen by Chinese hamster ovary (CHO-K1) cells compared to that in the isogenic wild-type strain. Preincubation of the NZ131 speB mutant with purified SPE B protease significantly inhibited fibronectin-dependent uptake by both CHO-K1 and CHO-pgs745 cells. The effect was attributed to an abrogation of fibronectin binding to the surface of the bacteria that did not involve either the M49 protein or the streptococcal fibronectin-binding protein SfbI. In contrast, pretreatment of the NZ131 speB mutant with SPE B did not influence sulfated polysaccharide-mediated uptake by CHO-pgs745 cells. The results indicate that the SPE B protease specifically alters bacterial cell surface proteins and thereby influences pathogen uptake.
机译：化脓性链球菌分泌几种影响宿主与病原体相互作用的蛋白质。使用组织培养模型研究分泌的半胱氨酸蛋白酶链球菌促红细胞生成素B（SPE B）对化脓性链球菌菌株NZ131（血清型M49）与哺乳动物细胞之间相互作用的影响。与同基因野生型菌株相比，speB基因的失活增强了中国仓鼠卵巢（CHO-K1）细胞对病原体纤连蛋白依赖性的吸收。 NZ131 speB突变体与纯化的SPE B蛋白酶的预温育可显着抑制CHO-K1和CHO-pgs745细胞对纤连蛋白的摄取。该作用归因于纤连蛋白与不涉及M49蛋白或链球菌纤连蛋白结合蛋白SfbI的细菌表面结合的结合被消除。相反，用SPE B预处理NZ131 speB突变体不会影响CHO-pgs745细胞对硫酸化多糖介导的摄取。结果表明，SPE B蛋白酶特异性改变细菌细胞表面蛋白，从而影响病原体的摄取。

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