Central nervous system injury-induced immune suppression.
Central nervous system injury-induced immune suppression.
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DOI：
10.3171/2021.11.focus21586
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发表时间：
2022-03
影响因子：
4.1
通讯作者：
Hall MW
中科院分区：
文献类型：
--
作者：
Sribnick EA;Popovich PG;Hall MW
中枢神经系统创伤是发病和死亡的常见原因。此外，这些伤害经常发生在年轻人身上，导致患者和护理人员的终身费用以及社会机会的损失。尽管这种流行和设计神经保护剂的多次尝试，用于治疗创伤性脑损伤（TBI）或脊髓损伤（SCI）的药理学试剂的临床试验提供了令人失望的结果。在过去的几十年里，这些疾病过程的结果的改善主要是由于支持性护理的改善。在神经创伤后患者和护理人员面临的诸多挑战中，创伤后医院感染是一个重要且潜在可逆的风险因素。多项动物和临床研究提供了创伤后全身免疫抑制的证据，涉及CNS的损伤可能更容易发生，导致神经创伤后院内感染的风险更高。与未发生感染的患者相比，发生医院感染的神经创伤患者恢复较差，长期发病率和院内死亡率风险较高。因此，神经创伤后免疫抑制的病因学和逆转是一个重要的课题。这些创伤后变化有多种可能的病因，包括损伤相关分子模式的释放、免疫抑制性髓源性抑制细胞的激活和交感神经系统激活。损伤后全身免疫抑制，特别是神经创伤后，为临床医生提供了一个挑战，但也为改善预后提供了机会。在这篇综述中，作者试图概述在TBI、TBI多发伤和SCI的动物模型和临床研究中损伤后全身免疫抑制的证据。
Central nervous system trauma is a common cause of morbidity and mortality. Additionally, these injuries frequently occur in younger individuals, leading to lifetime expenses for patients and caregivers and the loss of opportunity for society. Despite this prevalence and multiple attempts to design a neuroprotectant, clinical trials for a pharmacological agent for the treatment of traumatic brain injury (TBI) or spinal cord injury (SCI) have provided disappointing results. Improvements in outcome from these disease processes in the past decades have been largely due to improvements in supportive care. Among the many challenges facing patients and caregivers following neurotrauma, posttraumatic nosocomial infection is a significant and potentially reversible risk factor. Multiple animal and clinical studies have provided evidence of posttraumatic systemic immune suppression, and injuries involving the CNS may be even more prone, leading to a higher risk for in-hospital infections following neurotrauma. Patients who have experienced neurotrauma with nosocomial infection have poorer recovery and higher risks of long-term morbidity and in-hospital mortality than patients without infection. As such, the etiology and reversal of postneurotrauma immune suppression is an important topic. There are multiple possible etiologies for these posttraumatic changes including the release of damage-associated molecular patterns, the activation of immunosuppressive myeloid-derived suppressor cells, and sympathetic nervous system activation. Postinjury systemic immunosuppression, particularly following neurotrauma, provides a challenge for clinicians but also an opportunity for improvement in outcome. In this review, the authors sought to outline the evidence of postinjury systemic immune suppression in both animal models and clinical research of TBI, TBI polytrauma, and SCI.