Chloe C Boyle1, Kate R Kuhlman2, Larissa N Dooley3, Marcie D Haydon4, Theodore F Robles4, Yuen-Siang Ang5, Diego A Pizzagalli5, Julienne E Bower6. 1. Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Behavior, University of California, Los Angeles, CA, 90095, United States. Electronic address: ccboyle@ucla.edu. 2. Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Behavior, University of California, Los Angeles, CA, 90095, United States; School of Social Ecology, University of California, Irvine, CA, 92497, United States. 3. See Change Institute, Los Angeles, CA, United States. 4. Department of Psychology, University of California, Los Angeles, CA, 90095, United States. 5. Department of Psychiatry and McLean Hospital, Harvard Medical School, Belmont, MA, 02478, United States. 6. Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Behavior, University of California, Los Angeles, CA, 90095, United States; Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, 90095, United States; Department of Psychology, University of California, Los Angeles, CA, 90095, United States.
Abstract
BACKGROUND: Alterations in reward processing are a central feature of depression and may be influenced by inflammation. Indeed, inflammation is associated with deficits in reward-related processes in animal models and with dysregulation in reward-related neural circuitry in humans. However, the downstream behavioral manifestations of such impairments are rarely examined in humans. METHODS: The influenza vaccination was used to elicit a mild inflammatory response in 41 healthy young adults (age range: 18-22, 30 female). Participants provided blood samples and completed behavioral measures of three key aspects of reward-reward motivation, reward learning, and reward sensitivity-before and 1 day after receiving the influenza vaccine. RESULTS: The influenza vaccine led to mild but significant increases in circulating levels of the pro-inflammatory cytokine interleukin-6 (IL-6) (p < .001). Consistent with hypotheses, increases in IL-6 predicted lower reward motivation (p = .029). However, contrary to hypotheses, increases in IL-6 predicted increased performance on a reward learning task (p = .043) and were not associated with changes in reward sensitivity (p's > .288). CONCLUSIONS: These findings contribute to an emerging literature on the nuanced associations between inflammation and reward and demonstrate that even mild alterations in inflammation are associated with multiple facets of reward processing.
BACKGROUND: Alterations in reward processing are a central feature of depression and may be influenced by inflammation. Indeed, inflammation is associated with deficits in reward-related processes in animal models and with dysregulation in reward-related neural circuitry in humans. However, the downstream behavioral manifestations of such impairments are rarely examined in humans. METHODS: The influenza vaccination was used to elicit a mild inflammatory response in 41 healthy young adults (age range: 18-22, 30 female). Participants provided blood samples and completed behavioral measures of three key aspects of reward-reward motivation, reward learning, and reward sensitivity-before and 1 day after receiving the influenza vaccine. RESULTS: The influenza vaccine led to mild but significant increases in circulating levels of the pro-inflammatory cytokine interleukin-6 (IL-6) (p < .001). Consistent with hypotheses, increases in IL-6 predicted lower reward motivation (p = .029). However, contrary to hypotheses, increases in IL-6 predicted increased performance on a reward learning task (p = .043) and were not associated with changes in reward sensitivity (p's > .288). CONCLUSIONS: These findings contribute to an emerging literature on the nuanced associations between inflammation and reward and demonstrate that even mild alterations in inflammation are associated with multiple facets of reward processing.
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