Emsley Hedley C A, Hopkins Stephen J
Department of Neurology, Royal Preston Hospital,Sharoe Green Lane, Preston, PR2 9HT, UK.
Infect Disord Drug Targets. 2010 Apr;10(2):91-7. doi: 10.2174/187152610790963528.
Infections occur commonly following stroke and adversely influence outcome. Dysphagia, greater stroke severity and increasing age are associated with post-stroke infection, but post-stroke immunodepression is now recognised as an independent factor associated with increased susceptibility. Counter-regulatory responses, triggered by the pro-inflammatory response to stroke, appear to effect systemic immunodepression via suppression of both innate and adaptive immune responses. Experimental and clinical studies have identified a range of anti-inflammatory and immunosuppressive changes, including reduced mononuclear phagocyte and natural killer cell function, induction of anti-inflammatory cytokines, apoptotic lymphocyte loss and altered T lymphocyte activity. A range of mechanisms has been proposed, including hypothalamo-pituitary-adrenal axis (HPAA) and sympathetic nervous system (SNS) activation. The post-stroke balance of pro- and anti- inflammatory mechanisms may be aimed at restricting the extent of inflammation and contributing to the restoration of immune homeostasis. However, severe inflammation in the brain may trigger major systemic, counter-inflammatory responses that ultimately compromise immune mechanisms required to combat pathogens. Although key pathways have been identified, the extent to which the various elements of post-stroke immunodepression are clinically relevant remains to be discovered. The identification of markers of immunodepression in the early post-stroke phase may prove useful for identifying patients that may have increased susceptibility to infection. It also seems likely that post-stroke immunodepression will need to be taken into account where stroke treatments impact upon inflammatory and immune pathways.
中风后感染很常见，且会对预后产生不利影响。吞咽困难、中风严重程度增加以及年龄增长与中风后感染有关，但中风后免疫抑制现在被认为是易感性增加的一个独立因素。由对中风的促炎反应引发的反调节反应，似乎通过抑制先天性和适应性免疫反应来导致全身免疫抑制。实验和临床研究已经确定了一系列抗炎和免疫抑制变化，包括单核吞噬细胞和自然杀伤细胞功能降低、抗炎细胞因子的诱导、凋亡性淋巴细胞损失以及T淋巴细胞活性改变。已经提出了一系列机制，包括下丘脑 - 垂体 - 肾上腺轴（HPAA）和交感神经系统（SNS）激活。中风后促炎和抗炎机制的平衡可能旨在限制炎症程度并有助于免疫稳态的恢复。然而，大脑中的严重炎症可能引发主要的全身反炎症反应，最终损害对抗病原体所需的免疫机制。尽管已经确定了关键途径，但中风后免疫抑制的各个要素在临床上的相关程度仍有待发现。在中风后早期识别免疫抑制标志物可能有助于识别那些可能对感染易感性增加的患者。在中风治疗影响炎症和免疫途径的情况下，似乎也需要考虑中风后免疫抑制。
