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首页> 外文期刊>Microbial Pathogenesis >The moonlighting peroxiredoxin-glutaredoxin in Neisseria meningitidis binds plasminogen via a C-terminal lysine residue and contributes to survival in a whole blood model
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The moonlighting peroxiredoxin-glutaredoxin in Neisseria meningitidis binds plasminogen via a C-terminal lysine residue and contributes to survival in a whole blood model

机译：脑膜炎脑奈西肝毒素的月亮化过氧杂志 - 戊丙素通过C-末端赖氨酸残基结合纤溶酶原，有助于在整个血液模型中存活

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摘要

Neisseria meningitidis is a human-restricted bacterium that can invade the bloodstream and cross the blood-brain barrier resulting in life-threatening sepsis and meningitis. Meningococci express a cytoplasmic peroxiredoxin-glutaredoxin (Prx5-Grx) hybrid protein that has also been identified on the bacterial surface. Here, recombinant Prx5-Grx was confirmed as a plasminogen (Plg)-binding protein, in an interaction which could be inhibited by the lysine analogue epsilon-aminocapronic acid. rPrx5-Grx derivatives bearing a substituted C-terminal lysine residue (rprx5-Grx(K244A)), but not the active site cysteine residue (rPrx5-Gni(C185A)) or the sub-terminal rPrx5-Grx(K230A) lysine residue, exhibited significantly reduced Plg-binding. The absence of Prx5-Grx did not significantly reduce the ability of whole meningococcal cells to bind Plg, but under hydrogen peroxide-mediated oxidative stress, the N. meningitidis Delta pxn5-grx mutant survived significantly better than the wild-type or complemented strains. Significantly, using human whole blood as a model of meningococcal bacteremia, it was found that the N. meningitidis Delta pxn5-grx mutant had a survival defect compared with the parental or complemented strain, confirming an important role for Prx5-Grx in meningococcal pathogenesis.
机译：Menisseria Meningitidis是一种人类受限制的细菌，可以侵入血液并穿过血脑屏障，导致威胁生命的败血症和脑膜炎。 Meningococci表达了在细菌表面上鉴定的细胞质过氧化嗪 - 戊二糖胺蛋白（PRX5-GRX）杂交蛋白。这里，在赖氨酸类似物ε-氨基己酸抑制的相互作用中，确认重组PRX5-GRX作为纤溶酶原（PLG） - 耦合蛋白。携带取代的C-末端赖氨酸残基的RPRX5-GRX衍生物（RPRX5-GRX（K244A）），但不是活性位点半胱氨酸残基（RPRX5-GNI（C185A））或亚末端RPRX5-GRX（K230A）赖氨酸残基表现出显着减少PLG结合。没有PRX5-GRX没有显着降低整个脑膜炎球菌细胞结合PLG的能力，而是在过氧化氢介导的氧化应激下，N.Meningitidis Delta PXN5-Grx突变体显着优于野生型或互补菌株。值得注意的是，使用人类全血作为脑膜炎球菌菌血症的模型，发现N. Meningitidis Delta PXN5-Grx突变体与亲本或补充菌株相比具有生存缺陷，确认在脑膜炎球菌发病机制中对PRX5-GRX的重要作用。

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