Department of Anesthesia-Critical Care, AZ Sint-Jan Brugge Oostende AV, 8000 Bruges, Belgium.
Department of Anesthesia, Antwerp University Hospital (UZA), 2650 Edegem, Belgium.
Cells. 2023 Apr 4;12(7):1088. doi: 10.3390/cells12071088.
Sepsis-associated encephalopathy (SAE) remains a challenge for intensivists that is exacerbated by lack of an effective diagnostic tool and an unambiguous definition to properly identify SAE patients. Risk factors for SAE development include age, genetic factors as well as pre-existing neuropsychiatric conditions. Sepsis due to certain infection sites/origins might be more prone to encephalopathy development than other cases. Currently, ICU management of SAE is mainly based on non-pharmacological support. Pre-clinical studies have described the role of the alarmin high mobility group box 1 (HMGB1) in the complex pathogenesis of SAE. Although there are limited data available about the role of HMGB1 in neuroinflammation following sepsis, it has been implicated in other neurologic disorders, where its translocation from the nucleus to the extracellular space has been found to trigger neuroinflammatory reactions and disrupt the blood-brain barrier. Negating the inflammatory cascade, by targeting HMGB1, may be a strategy to complement non-pharmacologic interventions directed against encephalopathy. This review describes inflammatory cascades implicating HMGB1 and strategies for its use to mitigate sepsis-induced encephalopathy.
脓毒症相关性脑病（SAE）仍然是重症监护医生面临的挑战，缺乏有效的诊断工具和明确的定义来正确识别 SAE 患者，使这一问题更加恶化。SAE 发展的危险因素包括年龄、遗传因素以及先前存在的神经精神疾病。某些感染部位/起源引起的脓毒症比其他病例更容易发生脑病。目前，重症监护病房（ICU）对 SAE 的管理主要基于非药物支持。临床前研究已经描述了警报素高迁移率族蛋白 1（HMGB1）在 SAE 复杂发病机制中的作用。尽管关于脓毒症后 HMGB1 在神经炎症中的作用的数据有限，但它已被牵连到其他神经疾病中，在这些疾病中，HMGB1 从核内转移到细胞外空间被发现会引发神经炎症反应并破坏血脑屏障。通过针对 HMGB1 来否定炎症级联反应，可能是一种补充针对脑病的非药物干预的策略。这篇综述描述了涉及 HMGB1 的炎症级联反应以及利用其减轻脓毒症引起的脑病的策略。
