Laboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, Department of Internal Medicine and Specialties, University of Genova, IRCCS San Martino Polyclinic Hospital, Genoa, Italy.
Laboratory of Experimental Rheumatology and Academic Division of Clinical Rheumatology, IRCCS San Martino Polyclinic Hospital, Genoa, Italy.
Neuroimmunomodulation. 2023;30(1):185-195. doi: 10.1159/000533286. Epub 2023 Aug 9.
Calcitriol and hydroxyderivatives of lumisterol and tachisterol are secosteroid hormones with immunomodulatory and anti-inflammatory properties. Since the beginning of the COVID-19 pandemic, several studies have correlated deficient serum concentrations of vitamin D3 (calcifediol) with increased severity of the course of SARS-CoV-2 infection. Among systemic complications, subjective (anosmia, ageusia, depression, dizziness) and objective (ischemic stroke, meningoencephalitis, myelitis, seizures, Guillain-Barré syndrome) neurological symptoms have been reported in up to 80% of severe COVID-19 patients. In this narrative review, we will resume the pathophysiology of SARS-CoV-2 infection and the mechanisms of acute and chronic neurological damage. SARS-CoV-2 can disrupt the integrity of the endothelial cells of the blood-brain barrier (BBB) to enter the nervous central system. Invasion of pro-inflammatory cytokines and polarization of astrocytes and microglia cells always in a pro-inflammatory sense together with the pro-coagulative phenotype of cerebral endothelial cells in response to both SARS-CoV-2 and immune cells invasion (immunothrombosis) are the major drivers of neurodamage. Calcitriol and hydroxyderivatives of lumisterol and tachisterol could play an adjuvant role in neuroprotection through mitigation of neuroinflammation and protection of endothelial integrity of the BBB. Dedicated studies on this topic are currently lacking and are desirable to confirm the link between vitamin D3 and neuroprotection in COVID-19 patients.
骨化三醇和 25-羟胆钙化醇及 24-羟他留醇的羟基衍生物是具有免疫调节和抗炎特性的甾体激素。自 COVID-19 大流行开始以来，多项研究表明血清维生素 D3（骨化二醇）浓度不足与 SARS-CoV-2 感染过程严重程度增加有关。在全身并发症中，高达 80%的重症 COVID-19 患者出现主观（嗅觉丧失、味觉丧失、抑郁、头晕）和客观（缺血性中风、脑膜脑炎、脊髓炎、癫痫发作、格林-巴利综合征）神经系统症状。在本叙述性综述中，我们将总结 SARS-CoV-2 感染的病理生理学和急性及慢性神经损伤的机制。SARS-CoV-2 可破坏血脑屏障（BBB）内皮细胞的完整性以进入中枢神经系统。促炎细胞因子的入侵以及星形胶质细胞和小胶质细胞的极化总是表现出促炎的意义，同时脑内皮细胞对 SARS-CoV-2 和免疫细胞入侵的促凝表型（免疫血栓形成）是神经损伤的主要驱动因素。骨化三醇和 25-羟胆钙化醇及 24-羟他留醇的羟基衍生物可以通过减轻神经炎症和保护 BBB 的内皮完整性在神经保护中发挥辅助作用。目前缺乏关于这一主题的专门研究，需要进行这些研究来证实 COVID-19 患者中维生素 D3 与神经保护之间的联系。
