自闭症谱系障碍儿童血浆S100钙结合蛋白B和肿瘤坏死因子α浓度升高

Selin Aktan Guloksuz, O. Abali, E. Cetin, S. Gazioglu, G. Deniz, Abdurrahman Yildirim, I. Kawikova, S. Guloksuz, J. Leckman
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引用次数: 45

摘要

目的:探讨自闭症儿童血浆中S100B(一种主要来源于神经胶质细胞的钙结合蛋白)和炎症因子的浓度及其与细胞因子浓度的关系。方法:测定40例未服药的自闭症儿童和35例正常发育的健康儿童血浆S100B、肿瘤坏死因子α (TNF-α)、干扰素γ、白细胞介素(IL)-1β、IL-4、IL-6、IL-10、IL- 17a水平。使用儿童自闭症评定量表(CARS)评估自闭症的严重程度。结果:在调整优先选择的混杂因素(年龄、性别和体重指数)之前和之后,自闭症儿童的S100B和TNF-α浓度均较高。重度自闭症儿童的S100B浓度高于轻、中度自闭症儿童。然而,在调整混杂因素后,这种关联仍然是一种趋势。S100B浓度与TNF-α浓度呈正相关。结论:我们的研究结果显示外周S100B和TNF-α浓度的增加,为免疫功能改变和S100B在自闭症谱系障碍(ASD)中作用的假设提供了有限的支持。为了阐明免疫系统在这种疾病的病理生理学中的潜在作用,需要对大量具有良好特征的ASD患者进行研究。
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Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders
Objective: To investigate plasma concentrations of S100B (a calcium-binding protein derived primarily from the glia) and inflammatory cytokines in children with autism and the relationship between S100B and cytokine concentrations. Methods: Plasma levels of S100B, tumor necrosis factor alpha (TNF-α), interferon gamma, interleukin (IL)-1β, IL-4, IL-6, IL-10, and IL-17A were measured in 40 unmedicated children with autism and 35 normally developing healthy children. The severity of autism was assessed using the Childhood Autism Rating Scale (CARS). Results: Concentrations of both S100B and TNF-α were higher in children with autism before and after adjusting for a priori-selected confounders (age, sex, and body mass index). S100B concentrations were higher in children with severe autism compared to children with mild-moderate autism. However, this association remained as a trend after adjusting for confounders. S100B concentrations correlated positively with TNF-α concentrations. Conclusion: Our findings showing an increase in peripheral concentrations of S100B and TNF-α provide limited support to the hypothesis about the roles of altered immune function and S100B in autism spectrum disorder (ASD). Studies of larger numbers of well-characterized individuals with ASD are needed to clarify the potential role of the immune system in the pathophysiology of this disorder.
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