Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress.
Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress.
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DOI：
10.3389/fnbeh.2018.00240
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发表时间：
2018
影响因子：
3
通讯作者：
Wood SK
中科院分区：
文献类型：
--
作者：
Finnell JE;Wood SK
人们已经充分认识到，暴露在压力下会导致抑郁症等心理社会障碍的发作。虽然目前有许多抗抑郁治疗，尽管产生立即的神经化学变化，但它们需要连续使用数周才能显示出抗抑郁疗效。此外，高达30%的患者对典型的抗抑郁药没有反应，这表明我们对压力诱导的抑郁症的病理生理学的理解仍然有限。近年来，炎症已成为抑郁症研究的一个主要焦点，因为一些临床和临床前研究表明，外周和中枢炎症介质，包括白细胞介素（IL）-1β，在抑郁症患者中升高。此外，已经表明，炎症，特别是神经炎症可能是应激诱导的抑郁症的出现的直接和直接的联系，这是由于促炎细胞因子引起的广泛的神经和神经胶质作用。重要的是，炎症反应的个体差异可以进一步解释为什么某些个体对压力后果表现出不同的易感性。在这篇综述文章中，我们讨论了个体差异的来源，如年龄，性别和应对机制，这些可能是压力诱导的神经免疫因子的明显变化的来源，并强调了易感个体夸大神经炎症的推定来源。此外，我们回顾了目前的文献，具体的神经和神经胶质细胞的机制，包括线粒体功能，氧化应激和谷氨酸兴奋性毒性的机制，调节应激和炎症。总之，本综述的动力是更好地了解炎症细胞因子和趋化因子调控的机制，这些因子能够促进易感个体出现抑郁样行为。
It has been well recognized that exposure to stress can lead to the onset of psychosocial disorders such as depression. While there are a number of antidepressant therapies currently available and despite producing immediate neurochemical alterations, they require weeks of continuous use in order to exhibit antidepressant efficacy. Moreover, up to 30% of patients do not respond to typical antidepressants, suggesting that our understanding of the pathophysiology underlying stress-induced depression is still limited. In recent years inflammation has become a major focus in the study of depression as several clinical and preclinical studies have demonstrated that peripheral and central inflammatory mediators, including interleukin (IL)-1β, are elevated in depressed patients. Moreover, it has been suggested that inflammation and particularly neuroinflammation may be a direct and immediate link in the emergence of stress-induced depression due to the broad neural and glial effects that are elicited by proinflammatory cytokines. Importantly, individual differences in inflammatory reactivity may further explain why certain individuals exhibit differing susceptibility to the consequences of stress. In this review article, we discuss sources of individual differences such as age, sex and coping mechanisms that are likely sources of distinct changes in stress-induced neuroimmune factors and highlight putative sources of exaggerated neuroinflammation in susceptible individuals. Furthermore, we review the current literature of specific neural and glial mechanisms that are regulated by stress and inflammation including mitochondrial function, oxidative stress and mechanisms of glutamate excitotoxicity. Taken together, the impetus for this review is to move towards a better understanding of mechanisms regulated by inflammatory cytokines and chemokines that are capable of contributing to the emergence of depressive-like behaviors in susceptible individuals.
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影响因子：
5
作者：
Allen AP;Kennedy PJ;Dockray S;Cryan JF;Dinan TG;Clarke G
通讯作者：
Clarke G
影响因子：
2.6
作者：
Armagan, Guliz;Kanit, Lutfiye;Yalcin, Ayfer
通讯作者：
Yalcin, Ayfer
影响因子：
4.7
作者：
Barger, Steven W.;Goodwin, Mary E.;Beggs, Marjorie L.
通讯作者：
Beggs, Marjorie L.
影响因子：
10.6
作者：
Berman, RM;Cappiello, A;Krystal, JH
通讯作者：
Krystal, JH
影响因子：
5.3
作者：
Brites D;Fernandes A
通讯作者：
Fernandes A