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首页> 外文期刊>Infectious disorders drug targets >Post-stroke immunodepression and infection: an emerging concept.
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Post-stroke immunodepression and infection: an emerging concept.

机译：卒中后免疫抑制和感染：一个新兴的概念。

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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.
机译：感染通常发生在卒中后，并对预后产生不利影响。吞咽困难、卒中严重程度加重和年龄增长与卒中后感染有关，但卒中后免疫抑制现在被认为是与易感性增加相关的独立因素。由卒中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影响全身性免疫抑制。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、抗炎细胞因子诱导、凋亡淋巴细胞丢失和 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。卒中后促炎和抗炎机制的平衡可能旨在限制炎症的程度并有助于恢复免疫稳态。然而，大脑中的严重炎症可能会引发主要的全身性抗炎反应，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，但卒中后免疫抑制的各种因素在多大程度上具有临床相关性仍有待发现。在卒中后早期识别免疫抑制标志物可能有助于识别可能对感染易感性增加的患者。在中风治疗对炎症和免疫通路的影响下，似乎还需要考虑中风后免疫抑制。

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