急性卒中后感染的神经免疫机制

Neuroimmunological mechanisms of infection after acute stroke

感染是急性卒中最重要的并发症之一，是导致卒中恶化的一个独立危险因素。越来越多的证据表明，急性卒中患者存在外周免疫反应受损，即卒中诱导的免疫抑制综合征（stroke—induced immtmodepression syndrome，SIDS）。SIDS的特征是急性卒中后出现快速和持续的细胞免疫反应抑制，主要表现为广泛的淋巴细胞凋亡和功能障碍，多重原因激活交感神经并进而引起SIDS。SIDS削弱了机体对入侵病原体的有效防御，导致感染率和病死率增高。然而，SIDS对机体也具有保护作用，可防止损伤脑组织内过度的炎症反应。更好地了解中枢神经系统与免疫系统之问的复杂关系，有望为急性卒中患者带来更有效的治疗方法。

Infection is one of the most important complications of acute stroke, and it is an independent risk factor for resulting in stroke worsening. Growing evidence has indicated that acute stroke patients suffer an impaired peripheral immune response, i.e. stroke-induced immunodepression system （SIDS）. SIDS is characterized by the rapid and sustained cellular immunodepression after acute stroke, vdaieh is mainly presented as wide apoptosis and dysfunction of lymphocyte. Multiple reasons activate the sympathetic nervous system, and thus cause SIDS. SIDS weakens the effective defense against the invasion of pathogens in the human body, resulting in the increased infection and mortality rate. However, SIDS also has protective effect on the humn body. It can prevent the excessive inflammatory response in the injured brain tissue. A better understanding of the complex relationships between the central nervous system and the immune system are promising to provide more effective treatment methods for patients with acute stroke.