Sodium hypochlorite (NaOCl) and its active ingredient, hypochlorous acid (HOCl), are the most commonly used chlorine-based disinfectants. HOCl is a fast-acting and potent antimicrobial agent that interacts with several biomolecules, such as sulfur-containing amino acids, lipids, nucleic acids, and membrane components, causing severe cellular damage. It is also produced by the immune system as a first-line of defense against invading pathogens. In this review, we summarize the adaptive responses of Gram-negative bacteria to HOCl-induced stress and highlight the role of chaperone holdases (Hsp33, RidA, Cnox, and polyP) as an immediate response to HOCl stress. We also describe the three identified transcriptional regulators (HypT, RclR, and NemR) that specifically respond to HOCl. Besides the activation of chaperones and transcriptional regulators, the formation of biofilms has been described as an important adaptive response to several stressors, including HOCl. Although the knowledge on the molecular mechanisms involved in HOCl biofilm stimulation is limited, studies have shown that HOCl induces the formation of biofilms by causing conformational changes in membrane properties, overproducing the extracellular polymeric substance (EPS) matrix, and increasing the intracellular concentration of cyclic-di-GMP. In addition, acquisition and expression of antibiotic resistance genes, secretion of virulence factors and induction of the viable but nonculturable (VBNC) state has also been described as an adaptive response to HOCl. In general, the knowledge of how bacteria respond to HOCl stress has increased over time; however, the molecular mechanisms involved in this stress response is still in its infancy. A better understanding of these mechanisms could help understand host-pathogen interactions and target specific genes and molecules to control bacterial spread and colonization.

中文翻译：

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生存活性氯胁迫：革兰氏阴性细菌对次氯酸的反应。

次氯酸钠（NaOCl）及其活性成分次氯酸（HOCl）是最常用的氯基消毒剂。HOCl 是一种快速作用的强效抗菌剂，可与多种生物分子（例如含硫氨基酸、脂质、核酸和膜成分）相互作用，造成严重的细胞损伤。它也是由免疫系统产生的，作为抵御病原体入侵的第一道防线。在这篇综述中，我们总结了革兰氏阴性细菌对 HOCl 诱导的应激的适应性反应，并强调了分子伴侣保持酶（Hsp33、RidA、Cnox 和 polyP）作为对 HOCl 应激的直接反应的作用。我们还描述了三种已鉴定的对 HOCl 特异性反应的转录调节因子（HypT、RclR 和 NemR）。除了伴侣和转录调节因子的激活之外，生物膜的形成被描述为对包括次氯酸在内的多种应激源的重要适应性反应。尽管对 HOCl 生物膜刺激所涉及的分子机制的了解有限，但研究表明 HOCl 通过引起膜性质的构象变化、过量产生细胞外聚合物 (EPS) 基质以及增加细胞内循环物质浓度来诱导生物膜的形成。 -di-GMP。此外，抗生素抗性基因的获得和表达、毒力因子的分泌以及存活但不可培养（VBNC）状态的诱导也被描述为对次氯酸的适应性反应。总的来说，随着时间的推移，人们对细菌如何应对次氯酸胁迫的了解不断增加。然而，参与这种应激反应的分子机制仍处于起步阶段。更好地了解这些机制可以帮助了解宿主与病原体的相互作用，并针对特定的基因和分子来控制细菌的传播和定植。