Division of Infectious Disease, Beverly Hospital, 85 Herrick Street, Beverly, MA, 01915, USA.
Curr Infect Dis Rep. 2012 Oct;14(5):474-83. doi: 10.1007/s11908-012-0276-2.
Marked alterations of the innate and adaptive immune response follow invasive infection and generalized inflammatory states. If left unchecked, this state of immune dysregulation contributes to a myriad of maladaptive cellular responses that culminate in multiple organ dysfunction, septic shock, and lethality. The molecular details of the cell-signaling networks that underlie the pathophysiology of systemic inflammation and sepsis are now increasingly well understood. While a vigorous and effective immune response to invasive pathogens is essential for microbial clearance and host survival, nonresolving, generalized inflammation can induce diffuse endovascular damage, increased capillary permeability, coagulopathy, and widespread tissue damage. Current evidence indicates that a state of relative immune suppression often accompanies sepsis and might provide novel therapeutic options in some patients. An expanding number of potential therapeutic options are now in clinical development to reestablish control and promote resolution over sepsis-induced systemic inflammation and organ dysfunction.
侵袭性感染和全身性炎症状态会导致固有免疫和适应性免疫应答发生明显改变。如果不加以控制，这种免疫失调状态会导致一系列适应性细胞反应，最终导致多器官功能障碍、感染性休克和死亡。目前，人们越来越了解全身性炎症和脓毒症病理生理学中细胞信号转导网络的分子细节。虽然针对侵袭性病原体的强烈有效的免疫应答对于清除微生物和宿主存活至关重要，但持续存在的全身性炎症会导致弥漫性血管损伤、毛细血管通透性增加、凝血功能障碍和广泛的组织损伤。目前的证据表明，相对免疫抑制状态常伴随脓毒症发生，并可能为某些患者提供新的治疗选择。目前有越来越多的潜在治疗选择正在临床开发中，以重新控制和促进脓毒症引起的全身性炎症和器官功能障碍的恢复。
