Crosstalk between endocannabinoid and immune systems: a potential dysregulation in depression?
Crosstalk between endocannabinoid and immune systems: a potential dysregulation in depression?
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DOI：
10.1007/s00213-015-4105-9
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发表时间：
2016-05
影响因子：
3.4
通讯作者：
Zunszain PA
中科院分区：
文献类型：
--
作者：
Boorman E;Zajkowska Z;Ahmed R;Pariante CM;Zunszain PA
内源性大麻素系统(ECB)是一种内源性脂质信号系统，在抑郁症中似乎存在调节失调。内源性大麻素(ECB)作为有效的免疫调节剂的作用，以及对抑郁症慢性低度炎症特征的累积支持，提出了一个令人信服的假说，即在抑郁症中，它们之间的相互交流存在根本损害。我们的目标是回顾以前关于免疫系统和欧洲央行系统与抑郁症之间的个体关联的文献。它将聚焦于欧洲央行和免疫系统之间相互干扰的外围和核心机制。我们将在抑郁症的背景下讨论这场相声中潜在的失调。调查主要报告，抑郁症患者的欧洲央行系统活动不足，炎性标志物增加。研究结果描绘了一种多方面的沟通，免疫活性细胞和欧洲央行相关细胞都可以影响周围和中枢神经系统中对方活动的抑制和增强。欧洲央行系统的失调，如抑郁症所见，似乎与中枢和外周炎症介质的浓度有关，这些炎症介质与这种疾病的病理生理有关。欧洲央行和免疫系统已经分别与抑郁症的发病机制联系在一起并牵涉其中。这两个系统都严格控制着对方的活动。因此，这种串扰中的调节失调有可能影响这种神经精神疾病的发生和维持。然而，很少有研究同时研究这两个系统和抑郁症。这篇综述强调了在抑郁症的病因学中考虑欧洲央行-免疫联合作用的必要性。
The endocannabinoid (eCB) system, an endogenous lipid signaling system, appears to be dysregulated in depression. The role of endocannabinoids (eCBs) as potent immunomodulators, together with the accumulating support for a chronic low-grade inflammatory profile in depression, suggests a compelling hypothesis for a fundamental impairment in their intercommunication, in depression. We aim to review previous literature on individual associations between the immune and eCB systems and depression. It will focus on peripheral and central mechanisms of crosstalk between the eCB and immune systems. A potential dysregulation in this crosstalk will be discussed in the context of depression. Investigations largely report a hypoactivity of the eCB system and increased inflammatory markers in individuals with depression. Findings depict a multifaceted communication whereby immunocompetent and eCB-related cells can both influence the suppression and enhancement of the other’s activity in both the periphery and central nervous system. A dysregulation of the eCB system, as seen in depression, appears to be associated with central and peripheral concentrations of inflammatory agents implicated in the pathophysiology of this illness. The eCB and immune systems have been individually associated with and implicated in pathogenic mechanisms of depression. Both systems tightly regulate the other’s activity. As such, a dysregulation in this crosstalk has potential to influence the onset and maintenance of this neuropsychiatric illness. However, few studies have investigated both systems and depression conjointly. This review highlights the demand to consider joint eCB-immune interactions in the pathoetiology of depression.