In major dysmood disorder, physiosomatic, chronic fatigue and fibromyalgia symptoms are driven by immune activation and increased immune-associated neurotoxicity

被引：0
作者：
Michael Maes
Abbas F. Almulla
Bo Zhou
Ali Abbas Abo Algon
Pimpayao Sodsai
机构：
[1] University of Electronic Science and Technology of China,Sichuan Provincial Center for Mental Health, Sichuan Provincial People’s Hospital, School of Medicine
[2] Chinese Academy of Medical Sciences,Key Laboratory of Psychosomatic Medicine
[3] Chulalongkorn University,Department of Psychiatry, Faculty of Medicine
[4] and King Chulalongkorn Memorial Hospital,Department of Psychiatry
[5] The Thai Red Cross Society,Medical Laboratory Technology Department, College of Medical Technology
[6] Medical University of Plovdiv,Research Group of Organic Synthesis and Catalysis
[7] Research Institute,Department of Immunology, Faculty of Medicine, Center of Excellence in Immunology and Immune
[8] Medical University Plovdiv,Mediated Diseases
[9] Kyung Hee University,undefined
[10] The Islamic University,undefined
[11] University of Pannonia,undefined
[12] Chulalongkorn University and King Chulalongkorn Memorial Hospital,undefined
来源：
Scientific Reports | / 14卷
关键词：
Neuro-immune; Inflammation; Stress; Major depression; Affective disorders; Chronic fatigue syndrome;
D O I：
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摘要：
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.
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