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Elevated TNIP3 mRNA Expression in TNF-α-Secreting Cells from Patients with Major Depressive Disorder.
Neuroimmunomodulation ( IF 2.4 ) Pub Date : 2019-07-15 , DOI: 10.1159/000501083
Kai-Wei Huang , Ming-Kung Wu , Yi-Yung Hung

OBJECTIVE Elevated levels of pro-inflammatory cytokines, in particular tumor necrotic factor alpha (TNF-α), and abnormalities in negative regulation in Toll-like receptor (TLR) signaling pathways are associated with major depressive disorder (MDD). Previous research by our group disclosed lower expression of TNF-α-induced protein 3 (TNFAIP3), one of the negative regulators of the TLR4 signaling pathway, in depressive patients than in healthy controls. METHODS In this study, we assessed the mRNA levels of TNFAIP3, TNFAIP3-interacting proteins (TNIP), including TNIP1, TNIP2, and TNIP3, and TNFAIP3-like proteins, such as cezanne1, cezanne2, trabid, and VCIP135, in TNF-α-secreting cells and examined their association with severity of depression using the 17-item Hamilton Depression Rating Scale (HAMD-17) scores from 30 MDD patients and 30 healthy controls. Twenty-six patients received a second assessment after treatment with antidepressants for 4 weeks. RESULTS TNF-α-secreting cells displayed higher TNIP3 mRNA expression in MDD patients than in healthy controls before treatment, which was marginally decreased after antidepressant treatment. In addition, the TNIP2 level could be effectively applied to predict changes in HAMD scores after linear regression analysis. CONCLUSION Our collective findings suggest that molecules associated with negative regulation of innate immunity are aberrantly expressed in patients with MDD and present potential therapeutic targets.

中文翻译:

重度抑郁症患者TNF-α分泌细胞中TNIP3 mRNA表达升高。

目的促炎性细胞因子,特别是肿瘤坏死因子α(TNF-α)水平升高,以及Toll样受体(TLR)信号通路负调控异常与重度抑郁症(MDD)相关。我们小组先前的研究表明,与健康对照组相比,抑郁症患者的TNF-α诱导的蛋白3(TNFAIP3)(TLR4信号通路的负调节剂之一)的表达较低。方法在这项研究中,我们评估了TNFAIP3,TNFAIP3相互作用蛋白(TNIP)(包括TNIP1,TNIP2和TNIP3)以及类似TNFAIP3的蛋白(例如cezanne1,cezanne2,trabid和VCIP135)的mRNA水平,研究人员从30名MDD患者和30名健康对照者的17个项的汉密尔顿抑郁评估量表(HAMD-17)评分中检测了分泌TNF-α的细胞中的抑郁与抑郁症严重程度的关系。26名患者接受抗抑郁药治疗4周后接受了第二次评估。结果MDD患者中分泌TNF-α的细胞比治疗前的健康对照者显示更高的TNIP3 mRNA表达,抗抑郁剂治疗后其表达水平略有下降。此外,在线性回归分析之后,TNIP2水平可以有效地用于预测HAMD分数的变化。结论我们的集体研究结果表明,与先天免疫负调节相关的分子在MDD患者中异常表达,并且具有潜在的治疗靶点。26名患者接受抗抑郁药治疗4周后接受了第二次评估。结果MDD患者中分泌TNF-α的细胞比治疗前的健康对照组显示更高的TNIP3 mRNA表达,抗抑郁剂治疗后其表达水平略有下降。此外,在线性回归分析之后,TNIP2水平可以有效地用于预测HAMD分数的变化。结论我们的集体研究结果表明,与先天免疫负调节相关的分子在MDD患者中异常表达,并且具有潜在的治疗靶点。26名患者接受抗抑郁药治疗4周后接受了第二次评估。结果MDD患者中分泌TNF-α的细胞比治疗前的健康对照者显示更高的TNIP3 mRNA表达,抗抑郁剂治疗后其表达水平略有下降。此外,在线性回归分析之后,TNIP2水平可以有效地用于预测HAMD分数的变化。结论我们的集体研究结果表明,与先天免疫负调节相关的分子在MDD患者中异常表达,并且具有潜在的治疗靶点。抗抑郁药治疗后,其含量略有下降。此外,在线性回归分析之后,TNIP2水平可以有效地用于预测HAMD分数的变化。结论我们的集体研究结果表明,与先天免疫负调节相关的分子在MDD患者中异常表达,并且具有潜在的治疗靶点。抗抑郁药治疗后,其含量略有下降。此外,在线性回归分析之后,TNIP2水平可以有效地用于预测HAMD分数的变化。结论我们的集体研究结果表明,与先天免疫负调节相关的分子在MDD患者中异常表达,并且具有潜在的治疗靶点。
更新日期:2019-11-01
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