Inflammation-Induced Depressed Mood: The Role of Social Neurocognitive Mechanisms

炎症引起的抑郁情绪：社会神经认知机制的作用

基本信息

批准号：
8429495
负责人：
Naomi Ilana Eisenberger
金额：
$ 39.49万
依托单位：
UNIVERSITY OF CALIFORNIA LOS ANGELES
依托单位国家：
美国
项目类别：
财政年份：
2010
资助国家：
美国
起止时间：
2010-07-01 至 2016-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8429495
关键词：
Accounting Affective Anterior Behavioral Blood Coupled Cytokine Gene Data Depressed mood Depressive disorder Disease Distress Dorsal Endotoxins Exposure to Fatigue Feeling Female Functional Magnetic Resonance Imaging General Population Genes Genetic Polymorphism Happiness Hour Human Immune Individual Individual Differences Inflammation Inflammatory Insula of Reil Interleukin-6 Link Loneliness Measures Mediating Mental Depression Methodology Monitor Moods National Institute of Mental Health Neurocognitive Opioid Opioid Receptor Outcome Participant Pathway interactions Patient Self-Report Patients Placebos Play Prevalence Process Randomized Research Role Sampling Sleep Sleeplessness Social Change Social Perception Social isolation Social support Testing Time Variant Ventral Striatum Withdrawal Work base cingulate cortex cytokine depressive symptoms experience indexing innovation insight interest neuroimaging novel programs psychologic public health relevance relating to nervous system response reward processing social

项目摘要

DESCRIPTION (provided by applicant): This application is submitted to the NIMH DATR Mood/Sleep Research Program A2-AID. Depressive disorders occur at a high rate in patients with inflammatory disorders, with a point prevalence of 15-29%, which is two to three times greater than that observed in the general population. Substantial evidence has shown that inflammation and increases in proinflammatory cytokine activity play a critical role in the onset and perpetuation of depression and depressive symptoms (e.g. insomnia, fatigue) in those who are co-morbid for inflammatory disorders (Miller et al., 2009). Consistent with this, experimental work has shown that an inflammatory challenge can increase depressed mood in an otherwise healthy sample (Reichenberg et al., 2001). Based on these findings, there has been a growing interest in whether inflammatory processes can contribute to depression in a causal manner and how these effects might occur. Given the observation that inflammatory processes trigger social withdrawal (Dantzer, 2001; Hart, 1988), coupled with evidence that feelings of 'social disconnection' play a critical role in the onset and perpetuation of (non-inflammatory forms of) depression (Heinrich & Gullone, 2006), it is surprising that the social psychological consequences of inflammation and their contribution to depression have not been more fully explored. Here, we suggest that inflammation may increase feelings of social disconnection and that these social psychological changes may be an important contributor to inflammation-associated depression. Indeed, preliminary data demonstrated that an experimentally-induced inflammatory challenge (endotoxin) led to increases in self-reported feelings of social disconnection (e.g., "I feel disconnected from others") in addition to increases in depressed mood (Eisenberger et al., 2009b). Aside from these findings, however, there are no studies that have explored the effect of inflammatory processes on social experience in humans. The over- arching objective of this proposal is to explore the experiential and neural correlates of inflammatory- induced changes in social experience (e.g., feelings of social disconnection), which may provide a critical missing link in understanding the relationship between inflammation and depression. Participants (n=100) will be randomly assigned to receive either endotoxin or placebo and will then be monitored for the next six hours. Blood draws to assess cytokine levels as well as self-reported feelings of social disconnection and depressed mood will be collected hourly. In addition, at the time of peak cytokine response, participants will complete a neuroimaging session to examine the effect of inflammatory challenge on neural sensitivity to social rejection and social acceptance. It is hypothesized that endotoxin will increase feelings of social disconnection over time, and that the underlying neural sensitivities that give rise to these feelings (e.g., increased neural sensitivity to social rejection; decreased neural sensitivity to social acceptance) will contribute to inflammatory-induced depressed mood.

描述（由申请人提供）：此申请已提交给NIMH DATR情绪/睡眠研究计划A2-AID。炎症性疾病患者的抑郁症以高率发生，患病率为15-29％，比普通人群中观察到的抑郁症患病率为15-29％。大量证据表明，炎症和促炎性细胞因子活性的增加在抑郁症的发作和永久性和抑郁症状（例如失眠症，疲劳）中起着至关重要的作用（Miller等人，2009年）。与此一致，实验性工作表明，炎症挑战可以增加原本健康的样本中的情绪抑郁（Reichenberg等，2001）。基于这些发现，人们对炎症过程是否可以以因果关系以及如何发生这些影响来促进抑郁症的兴趣越来越大。考虑到炎症过程引发社会撤离的观察（Dantzer，2001; Hart，1988），再加上证据表明，“社会脱节”的感觉在（Heinrich＆Gullone，2006年）的抑郁症（非炎症形式）（非炎症形式）（非炎症形式）中起着至关重要的作用，令人惊讶的是，这是更多的社会心理抑制作用，并没有促进抑郁症的贡献。在这里，我们建议炎症可能会增加社会脱节的感觉，而这些社会心理变化可能是导致炎症相关抑郁症的重要促进者。的确，初步数据表明，除了情绪抑郁症的情绪增加外（Eisenberger等人，2009b）之外，除了增加抑郁症的情绪外，还导致自我报告的社会脱节感觉增加了自我报告的社会脱节感觉（例如，“我感到与他人脱节”）。但是，除了这些发现之外，没有研究探讨炎症过程对人类社会经验的影响。该提议的过度拱形目标是探索炎症引起的社会经验变化（例如，社会脱节的感觉）的体验和神经相关性，这可能在理解炎症与抑郁症之间的关系方面提供了严重的缺失联系。参与者（n = 100）将随机分配以接收内毒素或安慰剂，然后在接下来的六个小时内进行监视。抽血以评估细胞因子水平以及每小时会收集自我报告的社会脱节和情绪低落的感觉。此外，在峰值细胞因子反应时，参与者将完成神经影像学会议，以研究炎症挑战对神经敏感性对社会拒绝和社会接受的影响。假设内毒素会随着时间的流逝增加社会脱节的感觉，并且产生这些感觉的潜在神经敏感性（例如，对社会拒绝的神经敏感性提高；对社会接受的神经敏感性降低）将导致炎症引起的抑郁情绪。

项目成果

期刊论文数量（9）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

An empirical review of the neural underpinnings of receiving and giving social support: implications for health.

DOI：
10.1097/psy.0b013e31829de2e7
发表时间：
2013-07
期刊：
Psychosomatic medicine
影响因子：
3.3
作者：
Eisenberger NI
通讯作者：
Eisenberger NI

Ventromedial prefrontal cortex activity differentiates sick from healthy faces: Associations with inflammatory responses and disease avoidance motivation.

腹内侧前额叶皮层活动区分病人和健康的面孔：与炎症反应和疾病回避动机的关联。

DOI：
10.1016/j.bbi.2021.11.011
发表时间：
2022
期刊：
Brain, behavior, and immunity
影响因子：
0
作者：
Leschak,CarrianneJ;Hornstein,EricaA;ByrneHaltom,KateE;Johnson,KerriL;Breen,ElizabethC;Irwin,MichaelR;Eisenberger,NaomiI
通讯作者：
Eisenberger,NaomiI

Effects of inflammation on social processes and implications for health.

DOI：
10.1111/nyas.13864
发表时间：
2018-09
期刊：
Annals of the New York Academy of Sciences
影响因子：
5.2
作者：
Moieni M;Eisenberger NI
通讯作者：
Eisenberger NI

Frontostriatal functional connectivity underlies self-enhancement during social evaluation.

DOI：
10.1093/scan/nsab139
发表时间：
2022-08-01
期刊：
SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
影响因子：
4.2
作者：
Parrish, Michael H.;Dutcher, Janine M.;Muscatell, Keely A.;Inagaki, Tristen K.;Moieni, Mona;Irwin, Michael R.;Eisenberger, Naomi, I
通讯作者：
Eisenberger, Naomi, I

Social ties and health: a social neuroscience perspective.