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Cytokine dysregulation persists in childhood post Neonatal Encephalopathy.
BMC Neurology ( IF 2.6 ) Pub Date : 2020-03-30 , DOI: 10.1186/s12883-020-01656-w
Zunera Zareen 1, 2, 3, 4 , Tammy Strickland 1, 2 , Victoria Mc Eneaney 1, 2 , Lynne A Kelly 1, 2, 5 , Denise McDonald 1, 3 , Deirdre Sweetman 4 , Eleanor J Molloy 1, 2, 3, 4, 5, 6
Affiliation  

Cytokines are possible mediators of neuroinflammation and associated with adverse outcome in neonatal encephalopathy (NE). Our aim was to explore cytokine response in children with Neonatal Encephalopathy (NE) at school age compared to age-matched controls. Follow up at school age, children who had NE and age-matched controls were assessed for their cytokine responses and neurodevelopment outcome. Pro- and anti-inflammatory cytokines in the serum, [Interleukin (IL)-1α, IL-1β, IL-2, IL-6, IL-8, IL-18, Tumor necrosis factor (TNF)-α, TNF β, Interferon (IFN)-γ, granulocyte-macrophage colony-stimulating factor (GM-CSF), vascular endothelial growth factor (VEGF), erythropoietin (EPO), IL-10 & IL-1RA] were measured at baseline and in response to in vitro stimulation with lipopolysaccharide (LPS: endotoxin). GM-CSF, TNF-β, IL-2 IL-6 and IL-8 were significantly elevated at school age following NE (n = 40) compared to controls (n = 37). A rise in GM-CSF, IL-8, TNF-α, IL-1β, & IL-6 were seen in NE group following LPS stimulation. Relative LPS hypo-responsiveness was also noted in children with severe NE with IL-10, VEGF, EPO and TNF-β. Elevated TNF-β was associated with low gross motor scores on assessment at school age. School-age children post-NE had significantly altered cytokine responses to endotoxin compared to controls. TNF-β was associated with adverse developmental outcomes. This suggests the inflammatory process may persist into childhood and a longer therapeutic window may be available for neuroprotection therapies.

中文翻译:

细胞因子失调在新生儿脑病后的儿童时期持续存在。

细胞因子可能是神经炎症的介质,并与新生儿脑病(NE)的不良结局有关。我们的目的是探讨与年龄相匹配的对照组相比,学龄期新生儿脑病(NE)儿童的细胞因子反应。在学龄期进行随访,评估患有NE和年龄匹配的对照的儿童的细胞因子反应和神经发育结果。血清中的促炎和抗炎细胞因子[白介素(IL)-1α,IL-1β,IL-2,IL-6,IL-8,IL-18,肿瘤坏死因子(TNF)-α,TNFβ ,基线时和响应时,测量干扰素(IFN)-γ,粒细胞巨噬细胞集落刺激因子(GM-CSF),血管内皮生长因子(VEGF),促红细胞生成素(EPO),IL-10和IL-1RA]。脂多糖(LPS:内毒素)体外刺激。GM-CSF,TNF-β,与对照组(n = 37)相比,NE后学龄儿童的IL-2 IL-6和IL-8显着升高(n = 40)。LPS刺激后,NE组的GM-CSF,IL-8,TNF-α,IL-1β和IL-6升高。在患有IL-10,VEGF,EPO和TNF-β的重症NE患儿中也发现了相对的LPS低反应性。在学龄期评估中,TNF-β升高与总运动评分低有关。与对照组相比,NE后的学龄儿童的细胞因子对内毒素的反应明显改变。TNF-β与不良的发育结果相关。这表明炎症过程可能会持续到儿童期,并且更长的治疗窗口可用于神经保护疗法。LPS刺激后NE组可见IL-6。在患有IL-10,VEGF,EPO和TNF-β的重症NE患儿中也发现了相对的LPS低反应性。在学龄期评估中,TNF-β升高与总运动评分低有关。与对照组相比,NE后的学龄儿童的细胞因子对内毒素的反应明显改变。TNF-β与不良的发育结果相关。这表明炎症过程可能会持续到儿童期,并且更长的治疗窗口可用于神经保护治疗。LPS刺激后NE组可见IL-6。在患有IL-10,VEGF,EPO和TNF-β的重症NE患儿中也发现了相对的LPS低反应性。在学龄期评估中,TNF-β升高与总运动评分低有关。与对照组相比,NE后的学龄儿童的细胞因子对内毒素的反应明显改变。TNF-β与不良的发育结果相关。这表明炎症过程可能会持续到儿童期,并且更长的治疗窗口可用于神经保护疗法。与对照组相比,NE后的学龄儿童的细胞因子对内毒素的反应明显改变。TNF-β与不良的发育结果相关。这表明炎症过程可能会持续到儿童期,并且更长的治疗窗口可用于神经保护治疗。与对照组相比,NE后的学龄儿童的细胞因子对内毒素的反应明显改变。TNF-β与不良的发育结果相关。这表明炎症过程可能会持续到儿童期,并且更长的治疗窗口可用于神经保护治疗。
更新日期:2020-04-22
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