Hughes Martina M, Connor Thomas J, Harkin Andrew
Neuroimmunology Research Group, Department of Physiology, School of Medicine & Trinity College Institute of Neuroscience (Drs Hughes and Connor), and Neuropsychopharmacology Research Group, School of Pharmacy and Pharmaceutical Sciences & Trinity College Institute of Neuroscience, Trinity College, Dublin, Ireland (Dr Harkin).
Int J Neuropsychopharmacol. 2016 Jun;19(6). doi: 10.1093/ijnp/pyw001. Epub 2016 Jan 16.
Major depression is a serious psychiatric disorder; however, the precise biological basis of depression still remains elusive. A large body of evidence implicates a dysregulated endocrine and inflammatory response system in the pathogenesis of depression. Despite this, given the heterogeneity of depression, not all depressed patients exhibit dysregulation of the inflammatory and endocrine systems. Evidence suggests that inflammation is associated with depression in certain subgroups of patients and that those who have experienced stressful life events such as childhood trauma or bereavement may be at greater risk of developing depression. Consequently, prolonged exposure to stress is thought to be a key trigger for the onset of a depressive episode. This review assesses the relationship between stress and the immune system, with a particular interest in the mechanisms by which stress impacts immune function, and how altered immune functioning, in turn, may lead to a feed forward cascade of multiple systems dysregulation and the subsequent manifestation of depressive symptomology. The identification of stress-related immune markers and potential avenues for advances in therapeutic intervention is vital. Changes in specific biological markers may be used to characterize or differentiate depressive subtypes or specific symptoms and may predict treatment response, in turn facilitating a more effective, targeted, and fast-acting approach to treatment.
重度抑郁症是一种严重的精神疾病；然而，抑郁症确切的生物学基础仍然难以捉摸。大量证据表明，内分泌和炎症反应系统失调与抑郁症的发病机制有关。尽管如此，鉴于抑郁症的异质性，并非所有抑郁症患者都表现出炎症和内分泌系统失调。有证据表明，炎症在某些患者亚组中与抑郁症有关，并且那些经历过童年创伤或丧亲之痛等应激性生活事件的人可能患抑郁症的风险更高。因此，长期暴露于压力被认为是抑郁发作的关键触发因素。本综述评估了压力与免疫系统之间的关系，特别关注压力影响免疫功能的机制，以及免疫功能改变如何反过来导致多个系统失调的前馈级联反应和随后抑郁症状的表现。识别与压力相关的免疫标志物以及治疗干预的潜在进展途径至关重要。特定生物标志物的变化可用于表征或区分抑郁亚型或特定症状，并可预测治疗反应，进而促进更有效、有针对性和速效的治疗方法。
