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October 23, 2009

Social-Evaluative Threat and Proinflammatory Cytokine Regulation: An Experimental Laboratory Investigation

Sally S. Dickerson 1 , Shelly L. Gable 2 , Michael R. Irwin 3 , Najib Aziz 4 , and Margaret E. Kemeny 5
  1 Department of Psychology and Social Behavior, University of California, Irvine;   2 Department of Psychology, University of California, Santa Barbara;   3 Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience, David Geffen School of Medicine, University of California, Los Angeles;   4 Department of Pathology and Laboratory Medicine, University of California, Los Angeles; and   5 Department of Psychiatry, University of California, San Francisco
 Address correspondence to Sally S. Dickerson, Department of Psychology and Social Behavior, University of California, Irvine, 3340 Social Ecology II, Irvine, CA 92697-7085, e-mail: sdickers@uci.edu.
Copyright © 2009 Association for Psychological Science

ABSTRACT

ABSTRACT—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.

via www3.interscience.wiley.com

 

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