关键词: Affective disorders Chronic fatigue syndrome Inflammation Major depression Neuro-immune Stress

Mesh : Humans Depressive Disorder, Major Fatigue Syndrome, Chronic Fibromyalgia Cytokines Interleukins Chemokines

来  源:   DOI:10.1038/s41598-024-57350-1   PDF(Pubmed)

Abstract:
Major depressive disorder (MDD) is accompanied by activated neuro-immune pathways, increased physiosomatic and chronic fatigue-fibromyalgia (FF) symptoms. The most severe MDD phenotype, namely major dysmood disorder (MDMD), is associated with adverse childhood experiences (ACEs) and negative life events (NLEs) which induce cytokines/chemokines/growth factors. To delineate the impact of ACE + NLEs on physiosomatic and FF symptoms in first episode (FE)-MDMD, and examine whether these effects are mediated by immune profiles. ACEs, NLEs, physiosomatic and FF symptoms, and 48 cytokines/chemokines/growth factors were measured in 64 FE-MDMD patients and 32 normal controls. Physiosomatic, FF and gastro-intestinal symptoms belong to the same factor as depression, anxiety, melancholia, and insomnia. The first factor extracted from these seven domains is labeled the physio-affective phenome of depression. A part (59.0%) of the variance in physiosomatic symptoms is explained by the independent effects of interleukin (IL)-16 and IL-8 (positively), CCL3 and IL-1 receptor antagonist (inversely correlated). A part (46.5%) of the variance in physiosomatic (59.0%) symptoms is explained by the independent effects of interleukin (IL)-16, TNF-related apoptosis-inducing ligand (TRAIL) (positively) and combined activities of negative immunoregulatory cytokines (inversely associated). Partial least squares analysis shows that ACE + NLEs exert a substantial influence on the physio-affective phenome which are partly mediated by an immune network composed of interleukin-16, CCL27, TRAIL, macrophage-colony stimulating factor, and stem cell growth factor. The physiosomatic and FF symptoms of FE-MDMD are partly caused by immune-associated neurotoxicity due to T helper (Th)-1 polarization and M1 macrophage activation and relative lowered compensatory immunoregulatory protection.
摘要:
重度抑郁症(MDD)伴随着激活的神经免疫途径,增加生理和慢性疲劳-纤维肌痛(FF)症状。最严重的MDD表型,即严重情绪障碍(MDMD),与诱导细胞因子/趋化因子/生长因子的不良儿童经历(ACEs)和负面生活事件(NLEs)有关。描述ACE+NLE对首发(FE)-MDMD的生理症状和FF症状的影响,并检查这些作用是否由免疫谱介导。ACE,NLE,生理症状和FF症状,在64例FE-MDMD患者和32例正常对照中测量了48种细胞因子/趋化因子/生长因子。Physiosomatic,FF和胃肠道症状与抑郁症属于同一因素,焦虑,忧郁症,和失眠。从这七个结构域中提取的第一个因子被标记为抑郁症的生理情感表型。一部分(59.0%)的生理症状的变化是由白细胞介素(IL)-16和IL-8的独立作用(正),CCL3和IL-1受体拮抗剂(负相关)。生理症状变化的一部分(46.5%)(59.0%)由白介素(IL)-16,TNF相关的凋亡诱导配体(TRAIL)(正)和负免疫调节的联合活性的独立作用解释。细胞因子(反向相关)。偏最小二乘分析显示,ACE+NLE对生理情感物组产生实质性影响,部分由白细胞介素-16、CCL27、TRAIL、巨噬细胞集落刺激因子,和干细胞生长因子.FE-MDMD的生理症状和FF症状部分是由T辅助细胞(Th)-1极化和M1巨噬细胞激活以及相对降低的代偿性免疫调节保护引起的免疫相关神经毒性引起的。
公众号