关键词: Affective disorders Biomarkers Cytokines Inflammation Major depression Neuro-immune

Mesh : Humans Depression Suicidal Ideation Adverse Childhood Experiences Depressive Disorder, Major / genetics Cytokines Chemokines

来  源:   DOI:10.1016/j.psychres.2024.115812

Abstract:
This research assessed the effects of adverse childhood experiences (ACEs) and negative life events (NLEs) on forty-eight cytokines/chemokines/growth factors, in 71 FE-MDMD patients and forty heathy controls. ACEs are highly significantly associated with the classical M1 macrophage, T helper (Th)-1, Th-1 polarization, IRS, and neurotoxicity immune profiles, and not with the alternative M2, and Th-2 immune profiles. There are highly significant correlations between ACEs and NLEs and different cytokines/chemokines/growth factors, especially with interleukin (IL)-16, CCL27, stem cell growth factor, and platelet-derived growth factor. Partial Least Squares analysis showed that 62.3 % of the variance in the depression phenome (based on severity of depression, anxiety and suicidal behaviors) was explained by the regression on IL-4 (p = 0.001, inversely), the sum of ACEs + NLEs (p < 0.0001), and a vector extracted from 10 cytokines/chemokines/growth factors (p < 0.0001; both positively associated). The latter partially mediated (p < 0.0001) the effects of ACE + NLEs on the depression phenome. In conclusion, part of the effects of ACEs and NLEs on the depression phenome is mediated via activation of immune and growth factor networks. These pathways have a stronger impact in subjects with lowered activities of the compensatory immune-regulatory system.
摘要:
这项研究评估了不良儿童经历(ACEs)和负面生活事件(NLEs)对48种细胞因子/趋化因子/生长因子的影响。71例FE-MDMD患者和40例健康对照。ACE与经典的M1巨噬细胞高度显着相关,T辅助(Th)-1,Th-1极化,国税局,和神经毒性免疫谱,而不是替代M2和Th-2免疫谱。ACEs和NLEs与不同细胞因子/趋化因子/生长因子之间存在高度显著的相关性,特别是白细胞介素(IL)-16,CCL27,干细胞生长因子,和血小板衍生生长因子。偏最小二乘分析显示,抑郁现象组的方差为62.3%(基于抑郁的严重程度,焦虑和自杀行为)由IL-4的回归解释(p=0.001,反之亦然),ACE+NLE的总和(p<0.0001),和从10种细胞因子/趋化因子/生长因子中提取的载体(p<0.0001;两者正相关)。后者部分介导(p<0.0001)ACE+NLEs对抑郁症表型的影响。总之,ACEs和NLE对抑郁症表型的部分影响是通过激活免疫和生长因子网络介导的。这些途径对补偿性免疫调节系统活性降低的受试者具有更强的影响。
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