Barlow Brooke, Ponnaluri Sameer, Barlow Ashley, Roth William
Department of Pharmacy, Memorial Hermann The Woodlands Health System, Houston, TX, United States.
Department of Neurology, University of Florida College of Medicine, Gainesville, FL, United States.
Front Neurol. 2022 Sep 29;13:999035. doi: 10.3389/fneur.2022.999035. eCollection 2022.
Brain injury resulting from sepsis, or sepsis-associated encephalopathy (SAE), occurs due to impaired end-organ perfusion, dysregulated inflammation affecting the central nervous system (CNS), blood-brain barrier (BBB) disruption, mitochondrial dysfunction, oxidative stress, accumulation of toxic neuropeptides and impaired toxin clearance secondary to sepsis-induced hepatic and renal dysfunction. The gut microbiome becomes pathologically altered in sepsis, which likely contributes to the pathogenesis of SAE. Herein, we review the literature detailing dysregulation of microbiota-gut-brain axis (MGBA) in SAE and highlight potential therapeutic strategies to modulate the gut microbiome to mitigate sepsis-induced brain injury.
由脓毒症或脓毒症相关性脑病（SAE）导致的脑损伤，是由于终末器官灌注受损、影响中枢神经系统（CNS）的炎症调节失调、血脑屏障（BBB）破坏、线粒体功能障碍、氧化应激、有毒神经肽的积累以及继发于脓毒症诱导的肝肾功能障碍的毒素清除受损所致。脓毒症时肠道微生物群发生病理性改变，这可能促成了SAE的发病机制。在此，我们综述了详细阐述SAE中微生物群-肠道-脑轴（MGBA）失调的文献，并强调了调节肠道微生物群以减轻脓毒症诱导的脑损伤的潜在治疗策略。
