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首页> 外文期刊>Infection and immunity >Role for Streptococcal Collagen-Like Protein 1 in M1T1 Group A Streptococcus Resistance to Neutrophil Extracellular Traps
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Role for Streptococcal Collagen-Like Protein 1 in M1T1 Group A Streptococcus Resistance to Neutrophil Extracellular Traps

机译：链球菌类胶原蛋白1在M1T1 A组链球菌对中性粒细胞胞外诱剂的抗性中的作用

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Streptococcal collagen-like protein 1 (Scl-1) is one of the most highly expressed proteins in the invasive M1T1 serotype group A Streptococcus (GAS), a globally disseminated clone associated with higher risk of severe invasive infections. Previous studies using recombinant Scl-1 protein suggested a role in cell attachment and binding and inhibition of serum proteins. Here, we studied the contribution of Scl-1 to the virulence of the M1T1 clone in the physiological context of the live bacterium by generating an isogenic strain lacking the scl-1 gene. Upon subcutaneous infection in mice, wild-type bacteria induced larger lesions than the Δscl mutant. However, loss of Scl-1 did not alter bacterial adherence to or invasion of skin keratinocytes. We found instead that Scl-1 plays a critical role in GAS resistance to human and murine phagocytic cells, allowing the bacteria to persist at the site of infection. Phenotypic analyses demonstrated that Scl-1 mediates bacterial survival in neutrophil extracellular traps (NETs) and protects GAS from antimicrobial peptides found within the NETs. Additionally, Scl-1 interferes with myeloperoxidase (MPO) release, a prerequisite for NET production, thereby suppressing NET formation. We conclude that Scl-1 is a virulence determinant in the M1T1 GAS clone, allowing GAS to subvert innate immune functions that are critical in clearing bacterial infections.
机译：链球菌胶原样蛋白1（Scl-1）是A1型侵入性M1T1血清型链球菌（GAS）中表达最高的蛋白之一，GAS是一种全球性传播的克隆，与严重的侵袭性感染风险较高相关。先前使用重组Scl-1蛋白的研究表明，在细胞附着，结合和抑制血清蛋白方面发挥了作用。在这里，我们通过产生缺乏scl-1基因的同基因菌株，研究了Scl-1对活细菌生理环境中M1T1克隆的毒力的贡献。在小鼠皮下感染后，野生型细菌比Δscl突变体引起更大的损伤。但是，Scl-1的丢失并没有改变细菌对皮肤角质形成细胞的粘附或侵袭。相反，我们发现Scl-1在GAS对人和鼠吞噬细胞的抗性中起关键作用，使细菌在感染部位持续存在。表型分析表明，Scl-1介导嗜中性白细胞胞外陷阱（NETs）中的细菌存活，并保护GAS免受NETs中的抗菌肽的侵害。此外，Scl-1会干扰髓过氧化物酶（MPO）的释放，这是产生NET的先决条件，从而抑制了NET的形成。我们得出的结论是，Scl-1是M1T1 GAS克隆中的毒力决定因素，它使GAS能够破坏对清除细菌感染至关重要的先天免疫功能。

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