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首页> 外文期刊>Infection and immunity >The Ferritin-Like Dps Protein Is Required for Salmonella enterica Serovar Typhimurium Oxidative Stress Resistance and Virulence
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The Ferritin-Like Dps Protein Is Required for Salmonella enterica Serovar Typhimurium Oxidative Stress Resistance and Virulence

机译：肠沙门氏菌血清型鼠伤寒杆菌氧化应激抗性和毒力需要铁蛋白样Dps蛋白

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摘要

Resistance to phagocyte-derived reactive oxygen species is essential for Salmonella enterica serovar Typhimurium pathogenesis. Salmonella can enhance its resistance to oxidants through the induction of specific genetic pathways controlled by SoxRS, OxyR, σS, σE, SlyA, and RecA. These regulons can be found in a wide variety of pathogenic and environmental bacteria, suggesting that evolutionarily conserved mechanisms defend against oxidative stress both endogenously generated by aerobic respiration and exogenously produced by host phagocytic cells. Dps, a ferritin-like protein found in many eubacterial and archaebacterial species, appears to protect cells from oxidative stress by sequestering iron and limiting Fenton-catalyzed oxyradical formation. In Escherichia coli and some other bacterial species, Dps has been shown to accumulate during stationary phase in a σS-dependent fashion, bind nonspecifically to DNA, and form a crystalline structure that compacts and protects chromatin from oxidative damage. In the present study, we provide evidence that Dps protects Salmonella from iron-dependent killing by hydrogen peroxide, promotes Salmonella survival in murine macrophages, and enhances Salmonella virulence. Reduced numbers of dps mutant bacteria in the livers and spleens of infected mice are consistent with a role of Dps in protecting Salmonella from oxidative stress encountered during infection.
机译：对吞噬细胞衍生的活性氧的抗性对于肠沙门氏菌血清鼠伤寒发病机理至关重要。沙门氏菌可以通过诱导SoxRS，OxyR，σ S ，σ E ，SlyA和SlyA控制的特定遗传途径来增强其对氧化剂的抗性。 RecA。这些调节因子可以在多种致病性和环境细菌中找到，这表明进化上保守的机制可以抵抗有氧呼吸内源性和宿主吞噬细胞外源性产生的氧化应激。 Dps是一种在许多真细菌和古细菌物种中发现的类似铁蛋白的蛋白，它似乎可以通过螯合铁并限制Fenton催化的氧自由基形成来保护细胞免受氧化应激。在大肠杆菌和其他一些细菌物种中，Dps已显示出在固定相中以σ S 依赖的方式积累，与DNA特异性结合并形成晶体结构可以压实并保护染色质免受氧化损伤。在本研究中，我们提供证据证明Dps保护沙门氏菌免受过氧化氢铁依赖性杀伤，促进沙门氏菌在鼠巨噬细胞中的存活并增强沙门氏菌毒力。受感染小鼠的肝脏和脾脏中 dps 突变菌数量的减少与Dps在保护沙门氏菌免受感染过程中的氧化应激的作用中是一致的。

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