Social-evaluative threat and proinflammatory cytokine regulation: an experimental laboratory investigation.
Social-evaluative threat and proinflammatory cytokine regulation: an experimental laboratory investigation.
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DOI：
10.1111/j.1467-9280.2009.02437.x
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发表时间：
2009-10
影响因子：
8.2
通讯作者：
Kemeny ME
中科院分区：
文献类型：
--
作者：
Dickerson SS;Gable SL;Irwin MR;Aziz N;Kemeny ME
这项研究通过实验测试了以社会评估性威胁(SET)为特征的压力源是否会导致促炎细胞因子活性的增加并改变这种反应的调节。这一假说部分源于对非人类动物对社会威胁的免疫反应的研究。健康的女性参与者被指派在有或没有评价性听众(分别为组和非组)的情况下进行演讲和数学任务。根据假设，促炎细胞因子肿瘤坏死因子-α(肿瘤坏死因子-α)的刺激产生在SET条件下从基线到应激后增加，但在非SET条件下没有变化。此外，肿瘤坏死因子-α产量的增加与参与者对被评估的认知评估有关。此外，糖皮质激素关闭炎症反应的能力在设定的条件下降低。这些发现强调了社会评估的重要性，因为它是一种能够引发促炎细胞因子活动并改变其调节的威胁。
This study experimentally tested whether a stressor characterized by social-evaluative threat (SET), a context in which the self can be judged negatively by others, would elicit increases in proinflammatory cytokine activity and alter the regulation of this response. This hypothesis was derived in part from research on immunological responses to social threat in nonhuman animals. Healthy female participants were assigned to perform a speech and a math task in the presence or absence of an evaluative audience (SET or non-SET, respectively). As hypothesized, stimulated production of the proinflammatory cytokine tumor necrosis factor-α (TNF-α) increased from baseline to poststressor in the SET condition, but was unchanged in the non-SET condition. Further, the increases in TNF-α production correlated with participants’ cognitive appraisals of being evaluated. Additionally, the ability of glucocorticoids to shut down the inflammatory response was decreased in the SET condition. These findings underscore the importance of social evaluation as a threat capable of eliciting proinflammatory cytokine activity and altering its regulation.
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影响因子：
4.2
作者：
Dickerson, Sally S.;Mycek, Peggy J.;Zaldivar, Frank
通讯作者：
Zaldivar, Frank
影响因子：
5.9
作者：
Harris, TB;Ferrucci, L;Wallace, R
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3.2
作者：
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HELLHAMMER, DH
影响因子：
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作者：
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通讯作者：
Kirschbaum, C
影响因子：
3.3
作者：
Gruenewald, TL;Kemeny, ME;Fahey, JL
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Fahey, JL