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Acute Painful Stress and Inflammatory Mediator Production

Griffis C.A.a · Crabb Breen E.b · Compton P.e · Goldberg A.b · Witarama T.b · Kotlerman J.d · Irwin M.R.b–d
aUCLA Department of Anesthesiology, bUCLA Cousins Center for Psychoneuroimmunology, cSemel Institute for Neuroscience and Department of Psychiatry and Biobehavioral Sciences, dDavid Geffen School of Medicine at UCLA, and eUCLA School of Nursing, Los Angeles, Calif., USA Neuroimmunomodulation 2013;20:127–133 (DOI:10.1159/000346199)


Background: Proinflammatory pathways may be activated under conditions of painful stress, which is hypothesized to worsen the experience of pain and place medically vulnerable populations at risk for increased morbidity. Objectives: To evaluate the effects of pain and subjective pain-related stress on proinflammatory activity. Methods: A total of 19 healthy control subjects underwent a single standard cold-pressor pain test (CPT) and a no-pain control condition. Indicators of pain and stress were measured and related to inflammatory immune responses [CD8+ cells expressing the integrin molecule CD11a (CD811a), interleukin (IL)-1 receptor agonist (IL-1RA), and IL-6] immediately following the painful stimulus and compared to responses under no-pain conditions. Heart rate and mean arterial pressure were measured as indicators of sympathetic stimulation. Results: CPT was clearly painful and generated an activation of the sympathetic nervous system. CD811a increased in both conditions, but with no statistically significantly greater increase following CPT (p < 0.06). IL-1RA demonstrated a non-statistically significant increase following CPT (p < 0.07). The change in IL-6 following CPT differed significantly from the response seen in the control condition (p < 0.02). Conclusions: These findings suggest that CP acute pain may affect proinflammatory pathways, possibly through mechanisms related to adrenergic activation.


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