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蛛网膜下腔出血后血管痉挛的免疫特征。

Immunological Profile of Vasospasm after Subarachnoid Hemorrhage.

机构信息

Neurology and Stroke Unit, Department of Neuroscience, Bufalini Hospital, 47521 Cesena, Italy.

Translational Molecular Medicine and Surgery, Department of Biomedical, Dental Science and Morphological and Functional Images, University of Messina, 98122 Messina, Italy.

出版信息

Int J Mol Sci. 2023 May 16;24(10):8856. doi: 10.3390/ijms24108856.

DOI:10.3390/ijms24108856
PMID:37240207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10218712/
Abstract

Subarachnoid hemorrhage (SAH) carries high mortality and disability rates, which are substantially driven by complications. Early brain injury and vasospasm can happen after SAH and are crucial events to prevent and treat to improve prognosis. In recent decades, immunological mechanisms have been implicated in SAH complications, with both innate and adaptive immunity involved in mechanisms of damage after SAH. The purpose of this review is to summarize the immunological profile of vasospasm, highlighting the potential implementation of biomarkers for its prediction and management. Overall, the kinetics of central nervous system (CNS) immune invasion and soluble factors' production critically differs between patients developing vasospasm compared to those not experiencing this complication. In particular, in people developing vasospasm, a neutrophil increase develops in the first minutes to days and pairs with a mild depletion of CD45+ lymphocytes. Cytokine production is boosted early on after SAH, and a steep increase in interleukin-6, metalloproteinase-9 and vascular endothelial growth factor (VEGF) anticipates the development of vasospasm after SAH. We also highlight the role of microglia and the potential influence of genetic polymorphism in the development of vasospasm and SAH-related complications.

摘要

蛛网膜下腔出血 (SAH) 死亡率和致残率高,其主要原因是并发症。SAH 后可发生早期脑损伤和血管痉挛,这是预防和治疗以改善预后的关键事件。近几十年来,免疫机制被认为与 SAH 并发症有关,固有免疫和适应性免疫都参与了 SAH 后的损伤机制。本文旨在总结血管痉挛的免疫学特征,重点介绍预测和管理血管痉挛的生物标志物的潜在应用。总的来说,与未发生该并发症的患者相比,发生血管痉挛的患者中枢神经系统 (CNS) 免疫入侵和可溶性因子产生的动力学有显著差异。特别是在发生血管痉挛的患者中,中性粒细胞在最初几分钟到几天内增加,并伴有 CD45+淋巴细胞轻度耗竭。SAH 后早期细胞因子产生增加,白细胞介素-6、基质金属蛋白酶-9 和血管内皮生长因子 (VEGF) 的急剧增加预示着 SAH 后血管痉挛的发生。我们还强调了小胶质细胞的作用以及遗传多态性在血管痉挛和与 SAH 相关并发症发展中的潜在影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2460/10218712/987d860529e3/ijms-24-08856-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2460/10218712/be18d8456647/ijms-24-08856-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2460/10218712/987d860529e3/ijms-24-08856-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2460/10218712/be18d8456647/ijms-24-08856-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2460/10218712/987d860529e3/ijms-24-08856-g002.jpg

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Front Immunol. 2022 Nov 23;13:1027756. doi: 10.3389/fimmu.2022.1027756. eCollection 2022.
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A Review of Genetic Polymorphisms and Susceptibilities to Complications after Aneurysmal Subarachnoid Hemorrhage.颅内动脉瘤性蛛网膜下腔出血后并发症的遗传多态性和易感性研究综述
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TLR4-Pathway-Associated Biomarkers in Subarachnoid Hemorrhage (SAH): Potential Targets for Future Anti-Inflammatory Therapies.
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