Sepsis is a life-threatening clinical condition caused by a dysregulated host response to infection. Sepsis-associated encephalopathy (SAE) is a common but poorly understood neurological complication of sepsis, which is associated with increased morbidity and mortality. SAE clinical presentation may range from mild confusion and delirium to severe cognitive impairment and deep coma. Important mechanisms associated with SAE include excessive microglial activation, impaired endothelial barrier function, and blood-brain barrier (BBB) dysfunction. Endotoxemia and pro-inflammatory cytokines produced systemically during sepsis lead to microglial and brain endothelial cell activation, tight junction downregulation, and increased leukocyte recruitment. The resulting neuroinflammation and BBB dysfunction exacerbate SAE pathology and aggravate sepsis-induced brain dysfunction. In this mini-review, recent literature surrounding some of the mediators of BBB dysfunction during sepsis is summarized. Modulation of microglial activation, endothelial cell dysfunction, and the consequent prevention of BBB permeability represent relevant therapeutic targets that may significantly impact SAE outcomes.

中文翻译：

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脓毒症相关脑病和血脑屏障功能障碍。

脓毒症是一种危及生命的临床疾病，由宿主对感染的反应失调引起。脓毒症相关脑病 (SAE) 是脓毒症常见但知之甚少的神经系统并发症，与发病率和死亡率增加有关。SAE 的临床表现可能从轻度意识模糊和谵妄到严重的认知障碍和深度昏迷。与 SAE 相关的重要机制包括过度的小胶质细胞激活、内皮屏障功能受损和血脑屏障 (BBB) 功能障碍。脓毒症期间全身产生的内毒素血症和促炎细胞因子导致小胶质细胞和脑内皮细胞活化、紧密连接下调和白细胞募集增加。由此产生的神经炎症和 BBB 功能障碍加剧了 SAE 病理学并加重了败血症引起的脑功能障碍。在这篇小型综述中，总结了有关脓毒症期间 BBB 功能障碍的一些介质的最新文献。小胶质细胞活化的调节、内皮细胞功能障碍以及随之而来的 BBB 通透性的预防代表了可能显着影响 SAE 结果的相关治疗靶点。