Department of Orthopaedic Surgery, University of Colorado School of Medicine, Denver Health Medical Center, 777 Bannock Street, Denver, CO 80204, USA.
Crit Care. 2010;14(3):165. doi: 10.1186/cc9035. Epub 2010 Jun 16.
The exact cellular and molecular mechanisms of sepsis-induced encephalopathy remain elusive. The breakdown of the blood-brain barrier (BBB) is considered a focal point in the development of sepsis-induced brain damage. Contributing factors for the compromise of the BBB include cytokines and chemokines, activation of the complement cascade, phagocyte-derived toxic mediators, and bacterial products. To date, we are far from fully understanding the neuropathology that develops as a secondary remote organ injury as a consequence of sepsis. However, recent studies suggest that bacterial proteins may readily cross the functional BBB and trigger an inflammatory response in the subarachnoid space, in absence of a bacterial invasion. A better understanding of the pathophysiological events leading to septic encephalopathy appears crucial to advance the clinical care for this vulnerable patient population.
败血症性脑病的确切细胞和分子机制仍不清楚。血脑屏障 (BBB) 的破坏被认为是败血症性脑损伤发展的一个关键点。破坏 BBB 的促成因素包括细胞因子和趋化因子、补体级联的激活、吞噬细胞衍生的毒性介质和细菌产物。迄今为止，我们远未完全了解败血症作为继发性远程器官损伤而发展的神经病理学。然而，最近的研究表明，细菌蛋白可能很容易穿过功能正常的 BBB，并在没有细菌入侵的情况下在蛛网膜下腔引发炎症反应。更好地了解导致败血症性脑病的病理生理事件对于改善这一脆弱患者群体的临床护理似乎至关重要。
