PDF(Pubmed)
Abstract：
UNASSIGNED: Although the contribution of enhanced glial activity in seizure induction is increasingly recognized, the role of glia-induced neuroinflammation in the physiopathology of epileptic encephalopathy (EE) has been scarcely investigated.
UNASSIGNED: To delineate the contribution of glial activity in EE, we measured levels of glia-derived mediators with previously described biomarker value, including glial fibrillary acidic protein (GFAP), high mobility group box 1 (HMGB1), chitinase-3-like protein 1 (CHI3L1), soluble CD163 (sCD163) and triggering receptor expressed on myeloid cells 2 (TREM2) by ELISA in sera of patients with idiopathic West syndrome (WS, n=18), idiopathic Lennox-Gastaut syndrome (LGS, n=13) and healthy controls (n=31).
UNASSIGNED: Patients with EE showed significantly higher CHI3L1 levels compared to healthy controls. Levels of HMGB1, CHI3L1, sCD163 and TREM2 were higher in LGS patients than WS patients and/or healthy controls. One or more of the investigated mediators were associated with treatment responsiveness, disease severity and presence of pathological features on electroencephalography (EEG).
UNASSIGNED: To our knowledge, our findings provide the initial patient-based evidence that astrocyte- and microglia-mediated neuroinflammation might be involved in the pathogenesis of LGS and WS. Moreover, glial mediators may serve as prognostic biomarkers in patients with idiopathic EE.
UNASSIGNED: To delineate the contribution of glial activity in EE, we measured levels of glia-derived mediators with previously described biomarker value, including glial fibrillary acidic protein (GFAP), high mobility group box 1 (HMGB1), chitinase-3-like protein 1 (CHI3L1), soluble CD163 (sCD163) and triggering receptor expressed on myeloid cells 2 (TREM2) by ELISA in sera of patients with idiopathic West syndrome (WS, n=18), idiopathic Lennox-Gastaut syndrome (LGS, n=13) and healthy controls (n=31).
UNASSIGNED: Patients with EE showed significantly higher CHI3L1 levels compared to healthy controls. Levels of HMGB1, CHI3L1, sCD163 and TREM2 were higher in LGS patients than WS patients and/or healthy controls. One or more of the investigated mediators were associated with treatment responsiveness, disease severity and presence of pathological features on electroencephalography (EEG).
UNASSIGNED: To our knowledge, our findings provide the initial patient-based evidence that astrocyte- and microglia-mediated neuroinflammation might be involved in the pathogenesis of LGS and WS. Moreover, glial mediators may serve as prognostic biomarkers in patients with idiopathic EE.
摘要：
■尽管越来越认识到神经胶质活性增强在癫痫发作诱导中的作用，神经胶质诱导的神经炎症在癫痫性脑病（EE）的病理生理学中的作用几乎没有研究。
■为了描述神经胶质活动在EE中的贡献，我们用先前描述的生物标志物值测量了胶质细胞衍生介质的水平，包括胶质纤维酸性蛋白（GFAP），高移动性组盒1(HMGB1)，几丁质酶-3-样蛋白1（CHI3L1），通过ELISA在特发性韦斯特综合征患者血清中的可溶性CD163（sCD163）和在骨髓细胞2上表达的触发受体（TREM2）（WS，n=18),特发性Lennox-Gastaut综合征（LGS，n=13）和健康对照（n=31）。
■与健康对照组相比，EE患者的CHI3L1水平明显更高。LGS患者的HMGB1、CHI3L1、sCD163和TREM2水平高于WS患者和/或健康对照。一个或多个被研究的介质与治疗反应性相关，疾病的严重程度和脑电图（EEG）病理特征的存在。
■据我们所知，我们的发现为基于患者的星形细胞和小胶质细胞介导的神经炎症可能参与LGS和WS的发病机制提供了初步证据.此外，胶质介质可作为特发性EE患者的预后生物标志物.
■为了描述神经胶质活动在EE中的贡献，我们用先前描述的生物标志物值测量了胶质细胞衍生介质的水平，包括胶质纤维酸性蛋白（GFAP），高移动性组盒1(HMGB1)，几丁质酶-3-样蛋白1（CHI3L1），通过ELISA在特发性韦斯特综合征患者血清中的可溶性CD163（sCD163）和在骨髓细胞2上表达的触发受体（TREM2）（WS，n=18),特发性Lennox-Gastaut综合征（LGS，n=13）和健康对照（n=31）。
■与健康对照组相比，EE患者的CHI3L1水平明显更高。LGS患者的HMGB1、CHI3L1、sCD163和TREM2水平高于WS患者和/或健康对照。一个或多个被研究的介质与治疗反应性相关，疾病的严重程度和脑电图（EEG）病理特征的存在。
■据我们所知，我们的发现为基于患者的星形细胞和小胶质细胞介导的神经炎症可能参与LGS和WS的发病机制提供了初步证据.此外，胶质介质可作为特发性EE患者的预后生物标志物.
