Division of Nephrology and Endocrinology, The University of Tokyo School of Medicine, Tokyo, 113-8655, Japan.
Division of Bacteriology, International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Sci Rep. 2020 Feb 24;10(1):3251. doi: 10.1038/s41598-020-60306-w.
Group A Streptococcus (GAS) secretes deoxyribonucleases and evades neutrophil extracellular killing by degrading neutrophil extracellular traps (NETs). However, limited information is currently available on the interaction between GAS and NETs in the pathogenicity of GAS pharyngitis. In this study, we modified a mouse model of GAS pharyngitis and revealed an essential role for DNase in this model. After intranasal infection, the nasal mucosa was markedly damaged near the nasal cavity, at which GAS was surrounded by neutrophils. When neutrophils were depleted from mice, GAS colonization and damage to the nasal mucosa were significantly decreased. Furthermore, mice infected with deoxyribonuclease knockout GAS mutants (∆spd, ∆endA, and ∆sdaD2) survived significantly better than those infected with wild-type GAS. In addition, the supernatants of digested NETs enhanced GAS-induced cell death in vitro. Collectively, these results indicate that NET degradation products may contribute to the establishment of pharyngeal infection caused by GAS.
A 组链球菌(GAS)分泌脱氧核糖核酸酶,并通过降解中性粒细胞胞外陷阱(NETs)来逃避中性粒细胞的细胞外杀伤。然而,目前关于 GAS 咽炎发病机制中 GAS 与 NETs 之间相互作用的信息有限。在这项研究中,我们修改了 GAS 咽炎的小鼠模型,并揭示了脱氧核糖核酸酶在该模型中的重要作用。鼻内感染后,鼻腔附近的鼻黏膜明显受损,此时 GAS 被中性粒细胞包围。当从小鼠中耗尽中性粒细胞时,GAS 定植和鼻黏膜损伤显著减少。此外,感染脱氧核糖核酸酶缺失突变体(∆spd、∆endA 和 ∆sdaD2)的 GAS 的小鼠比感染野生型 GAS 的小鼠存活得更好。此外,消化后的 NETs 的上清液增强了 GAS 诱导的体外细胞死亡。综上所述,这些结果表明 NET 降解产物可能有助于建立由 GAS 引起的咽感染。