Our organism is exposed to pathogens on a daily basis. Owing to this age-old interaction, both pathogen and host evolved strategies to cope with these encounters. Here, we focus on the consequences of the direct encounter of cells of the innate immune system with bacteria. First, we will discuss the bacterial strategies to counteract powerful reactive species. Our emphasis lies on the effects of hypochlorous acid (HOCl), arguably the most powerful oxidant produced inside the phagolysosome of professional phagocytes. We will highlight individual examples of proteins in gram-negative bacteria activated by HOCl via thiol-disulfide switches, methionine sulfoxidation, and N-chlorination of basic amino acid side chains. Second, we will discuss the effects of HOCl on proteins of the host. Recent studies have shown that both host and bacteria address failing protein homeostasis by activation of chaperone-like holdases through N-chlorination. After discussing the role of individual proteins in the HOCl-defense, we will turn our attention to the examination of effects on host and pathogen on a systemic level. Recent studies using genetically encoded redox probes and redox proteomics highlight differences in redox homeostasis in host and pathogen and give first hints at potential cellular HOCl signaling beyond thiol-disulfide switch mechanisms.

中文翻译：

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宿主-病原体相互作用中的氧化还原调节：硫醇开关及其他

我们的机体每天都会接触到病原体。由于这种古老的相互作用，病原体和宿主都进化出应对这些遭遇的策略。在这里，我们关注先天免疫系统细胞与细菌直接接触的后果。首先，我们将讨论抵消强大活性物种的细菌策略。我们的重点在于次氯酸 (HOCl) 的影响，次氯酸可以说是专业吞噬细胞的吞噬溶酶体内产生的最强大的氧化剂。我们将重点介绍由 HOCl 通过硫醇-二硫化物开关、甲硫氨酸亚硫氧化和碱性氨基酸侧链的 N-氯化激活的革兰氏阴性菌中蛋白质的个别例子。其次，我们将讨论 HOCl 对宿主蛋白质的影响。最近的研究表明，宿主和细菌都通过 N-氯化作用激活伴侣蛋白样酶来解决蛋白质稳态失衡。在讨论了单个蛋白质在 HOCl 防御中的作用之后，我们将把注意力转向在系统水平上检查对宿主和病原体的影响。最近使用基因编码氧化还原探针和氧化还原蛋白质组学的研究突出了宿主和病原体氧化还原稳态的差异，并首次提示了潜在的细胞 HOCl 信号传导，而不是硫醇-二硫化物转换机制。