首页> 外文期刊>Progress in Neuro-Psychopharmacology & Biological Psychiatry: An International Research, Review and News Journal >Activation of cell-mediated immunity in depression: Association with inflammation, melancholia, clinical staging and the fatigue and somatic symptom cluster of depression
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Activation of cell-mediated immunity in depression: Association with inflammation, melancholia, clinical staging and the fatigue and somatic symptom cluster of depression

机译:抑郁症中细胞介导的免疫的激活:与炎症,忧郁症,临床分期以及抑郁症的疲劳和躯体症状群相关

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Background: Depression is characterized by activation of cell-mediated immunity (CMI), including increased neopterin levels, and increased pro-inflammatory cytokines (PICs), such as interleukin-1 (IL-1) and tumor necrosis factor-α (TNFα). These PICs may induce depressive, melancholic and chronic fatigue (CF) symptoms. Methods: We examined serum neopterin and plasma PIC levels in depressive subgroups in relation to the depressive subtypes and the melancholic and CF symptoms of depression. Participants were 85 patients with depression and in 26 normal controls. Severity of depression was assessed with the Hamilton Depression Rating Scale (HDRS) and severity of CF with the Fibromyalgia and Chronic Fatigue Syndrome (FF) Rating Scale. Results: Serum neopterin was significantly higher in depressed patients and in particular in those with melancholia. There were positive correlations between serum neopterin, the plasma PICs and the number of previous depressive episodes. Neopterin and TNFα were associated with melancholia, while both PICs were associated with CF. Melancholia-group membership was predicted by the HDRS and neopterin, and CF group membership by age, the FF score and serum TNFα. Discussion: Depression and melancholia are accompanied by CMI activation, suggesting that neopterin plays a role in their pathophysiology, e.g. through activation of oxidative and nitrosative stress and apoptosis pathways. The intertwined CMI and inflammatory responses are potentially associated with the onset of depression and with the melancholic and CF symptoms of depression. Exposure to previous depressive episodes may magnify the size of CMI and PIC responses, possibly increasing the likelihood of new depressive episodes. CMI activation and inflammation may contribute to the staging or recurrence of depression.
机译:背景:抑郁症的特征在于激活细胞介导的免疫(CMI),包括增加新蝶呤的水平,以及增加促炎细胞因子(PIC),例如白介素-1(IL-1)和肿瘤坏死因子-α(TNFα)。 。这些PIC可能会导致抑郁,忧郁和慢性疲劳(CF)症状。方法:我们检查了抑郁亚组的血清新蝶呤和血浆PIC水平与抑郁亚型以及抑郁的忧郁和CF症状的关系。参加者有85名抑郁症患者和26名正常对照者。抑郁症的严重程度通过汉密尔顿抑郁量表(HDRS)进行评估,而CF的严重程度通过纤维肌痛和慢性疲劳综合症(FF)量表进行评估。结果:抑郁症患者,尤其是忧郁症患者的血清新蝶呤明显升高。血清新蝶呤,血浆PICs与以前的抑郁发作次数之间呈正相关。新蝶呤和TNFα与忧郁症相关,而两个PIC与CF相关。通过HDRS和新蝶呤预测忧郁症成员身份,根据年龄,FF评分和血清TNFα预测CF成员身份。讨论:抑郁症和忧郁症伴有CMI激活,提示新蝶呤在其病理生理中起着重要作用,例如通过激活氧化,亚硝化应激和细胞凋亡途径。相互交织的CMI和炎症反应可能与抑郁症的发作以及抑郁症的忧郁和CF症状有关。接触先前的抑郁发作可能会放大CMI和PIC反应的大小,可能会增加新的抑郁发作的可能性。 CMI激活和炎症可能有助于抑郁症的分期或复发。

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