Delano Matthew J, Ward Peter A
J Clin Invest. 2016 Jan;126(1):23-31. doi: 10.1172/JCI82224. Epub 2016 Jan 4.
Sepsis is a systemic inflammatory response induced by an infection, leading to organ dysfunction and mortality. Historically, sepsis-induced organ dysfunction and lethality were attributed to the interplay between inflammatory and antiinflammatory responses. With advances in intensive care management and goal-directed interventions, early sepsis mortality has diminished, only to surge later after "recovery" from acute events, prompting a search for sepsis-induced alterations in immune function. Sepsis is well known to alter innate and adaptive immune responses for sustained periods after clinical "recovery," with immunosuppression being a prominent example of such alterations. Recent studies have centered on immune-modulatory therapy. These efforts are focused on defining and reversing the persistent immune cell dysfunction that is associated with mortality long after the acute events of sepsis have resolved.
脓毒症是由感染引起的全身性炎症反应，可导致器官功能障碍和死亡。从历史上看，脓毒症诱导的器官功能障碍和致死率归因于炎症反应和抗炎反应之间的相互作用。随着重症监护管理和目标导向干预措施的进展，早期脓毒症死亡率有所下降，但在从急性事件“恢复”后不久又会激增，这促使人们寻找脓毒症诱导的免疫功能改变。众所周知，脓毒症会在临床“恢复”后的持续时间内改变先天性和适应性免疫反应，免疫抑制就是这种改变的一个突出例子。最近的研究集中在免疫调节治疗上。这些努力的重点是确定并扭转与脓毒症急性事件解决后很长时间的死亡率相关的持续性免疫细胞功能障碍。
