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首页> 外文期刊>Infection and immunity >Cytotoxic Effects of Streptolysin O and Streptolysin S Enhance the Virulence of Poorly Encapsulated Group A Streptococci
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Cytotoxic Effects of Streptolysin O and Streptolysin S Enhance the Virulence of Poorly Encapsulated Group A Streptococci

机译：链球菌溶血素O和链球菌溶血素S的细胞毒性作用增强了A型链球菌的不良包囊性

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Although the toxicity of streptolysin O (SLO) and streptolysin S (SLS) in purified group A streptococci (GAS) has been established, the effect of these molecules in natural infection is not well understood. To identify whether biologically relevant concentrations of SLO and SLS were cytotoxic to epithelial and phagocytic cells that the bacteria would typically encounter during human infection and to characterize the influence of cell injury on bacterial pathogenesis, we derived GAS strains deficient in SLO or SLS in the background of an invasive GAS M3 isolate and determined their virulence in in vitro and in vivo models of human disease. Whereas bacterial production of SLO resulted in lysis of both human keratinocytes and polymorphonuclear leukocytes, GAS expression of SLS was associated only with keratinocyte injury. Expression of SLO but not SLS impaired polymorphonuclear leukocyte killing of GAS in vitro, but this effect could only be demonstrated in the background of acapsular organisms. In mouse invasive soft-tissue infection, neither SLO or SLS expression significantly influenced mouse survival. By contrast, in a mouse model of bacterial sepsis after intraperitoneal inoculation of GAS, SLO expression enhanced the virulence of both encapsulated and acapsular GAS, whereas SLS expression increased the virulence only of acapsular GAS. We conclude that the cytotoxic effects of SLO protect GAS from phagocytic killing and enhance bacterial virulence, particularly of strains that may be relatively deficient in hyaluronic acid capsule. Compared to SLO, SLS in this strain background has a more modest influence on GAS pathogenicity and the effect does not appear to involve bacterial resistance to phagocytosis.
机译：尽管已经建立了链球菌溶血素O（SLO）和链球菌溶血素S（SLS）在纯化的A组链球菌（GAS）中的毒性，但这些分子在自然感染中的作用尚不十分清楚。为了确定生物学相关浓度的SLO和SLS是否对细菌在人类感染过程中通常会遇到的上皮细胞和吞噬细胞具有细胞毒性，并鉴定细胞损伤对细菌发病机理的影响，我们在背景中衍生了GAS菌株，该菌株缺乏SLO或SLS侵袭性GAS M3分离株的分离，并确定其在人类疾病的体外和体内模型中的毒力。 SLO的细菌产生导致人角质形成细胞和多形核白细胞的溶解，而SLS的GAS表达仅与角质形成细胞损伤有关。 SLO的表达而不是SLS的表达在体外损害了GAS的多形核白细胞杀伤，但是这种作用只能在荚膜生物的背景下证明。在小鼠侵袭性软组织感染中，SLO或SLS表达均未显着影响小鼠存活率。相比之下，在腹膜内接种GAS后的细菌性败血症小鼠模型中，SLO表达增强了包囊GAS和荚膜GAS的毒力，而SLS表达仅增强了荚膜GAS的毒力。我们得出的结论是，SLO的细胞毒性作用可以保护GAS免受吞噬作用的杀伤，并增强细菌的毒性，尤其是对于玻尿酸胶囊相对不足的菌株。与SLO相比，此菌株背景中的SLS对GAS的致病性影响较小，并且该作用似乎不涉及细菌对吞噬作用的抗性。

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