In recent years, stroke-induced immunodepression syndrome (SIDS) and the resulting stroke-associated infection (SAI) have become a focus of current research efforts. Inflammatory reactions after stroke promote tissue healing and eliminate necrotic cells, whereas excessive inflammatory reactions may cause secondary damage. Stroke-induced immunodepression not only reduces inflammatory reactions and protects brain tissues but also weakens the resistance of the human body against pathogens and leads to infection. Changes in the local and systemic immune system in stroke patients may play an important role in prognosis. Infection is a leading cause of death in patients following stroke, and an evaluation of the prognosis of stroke patients is associated closely with the presence of infectious complications. Among these complications, pneumonia is the most common type of infection observed after acute stroke, which exhibits the greatest effect on the recovery of neurological function. SIDS is closely related to stroke-associated pneumonia (SAP), and the use of immunodepression as an entry point may provide an efficacious treatment target and drug development strategy. An improved understanding of the pathophysiological mechanisms leading to SAP is essential to develop new treatment strategies for improving the outcomes of stroke patients.

近年来，中风诱发的免疫抑制综合症（SIDS）和中风相关感染（SAI）已成为当前研究工作的重点。中风后的炎症反应可促进组织愈合并消除坏死细胞，而过多的炎症反应则可能引起继发性损伤。中风引起的免疫抑制不仅减少炎症反应并保护脑组织，而且削弱了人体对病原体的抵抗力并导致感染。中风患者局部和全身免疫系统的改变可能在预后中起重要作用。感染是中风患者死亡的主要原因，对中风患者预后的评估与感染性并发症的发生密切相关。在这些并发症中，肺炎是急性中风后最常见的感染类型，对神经功能的恢复作用最大。SIDS与中风相关性肺炎（SAP）密切相关，使用免疫抑制作为切入点可能会提供有效的治疗目标和药物开发策略。更好地理解导致SAP的病理生理机制对于开发新的治疗策略以改善中风患者的结局至关重要。