Department of Psychology, University of California, Los Angeles, CA 90095-1563, USA.
Brain Behav Immun. 2010 May;24(4):558-63. doi: 10.1016/j.bbi.2009.12.009. Epub 2010 Jan 4.
Although research has established links between feelings of social isolation and inflammation, the direction of these effects is unclear. Based on the role that proinflammatory cytokines play in initiating "sickness behavior," which includes symptoms such as social withdrawal, it is possible that inflammatory processes heighten feelings of 'social disconnection.' Here, we examined whether exposure to an inflammatory challenge increased self-reported feelings of social disconnection. In addition, because both inflammatory processes and feelings of social disconnection contribute to depressive symptoms, we also explored whether increases in feelings of social disconnection played a role in the link between inflammation and depressed mood. Participants were randomly assigned to either receive endotoxin, an inflammatory challenge, or placebo. Proinflammatory cytokines (IL-6, TNF-alpha) were collected at baseline and then hourly for 6h. Participants completed self-reports of sickness symptoms ("fatigue"), social disconnection ("I feel disconnected from others"), and depressed mood ("unhappy") hourly. Results revealed that endotoxin led to significant increases (from baseline) in IL-6 and TNF-alpha levels as well as feelings of social disconnection and depressed mood. Moreover, controlling for increases in social disconnection eliminated the relationship between exposure to inflammatory challenge and depressed mood. This study demonstrates that inflammation can have social psychological consequences, which may play a role in cytokine-related depressive symptoms.
尽管研究已经确立了社交孤立感和炎症之间的联系,但这些影响的方向尚不清楚。基于促炎细胞因子在引发“疾病行为”(包括社交退缩等症状)中的作用,炎症过程可能会加剧“社交脱节”的感觉。在这里,我们研究了炎症挑战是否会增加自我报告的社交脱节感。此外,由于炎症过程和社交脱节感都会导致抑郁症状,我们还探讨了社交脱节感的增加是否在炎症与抑郁情绪之间的联系中起作用。参与者被随机分配接受内毒素(一种炎症挑战)或安慰剂。在基线和 6 小时内每小时收集促炎细胞因子(IL-6、TNF-α)。参与者每小时完成关于疾病症状(“疲劳”)、社交脱节(“我感到与他人脱节”)和抑郁情绪(“不快乐”)的自我报告。结果表明,内毒素导致 IL-6 和 TNF-α水平以及社交脱节感和抑郁情绪显著增加(与基线相比)。此外,控制社交脱节感的增加消除了炎症挑战暴露与抑郁情绪之间的关系。这项研究表明,炎症可能会产生社会心理后果,这可能在细胞因子相关的抑郁症状中起作用。