Acute Painful Stress and Inflammatory Mediator Production

作者：Griffis Charles A^*; Breen Elizabeth Crabb; Compton Peggy; Goldberg Alyssa; Witarama Tuff; Kotlerman Jenny; Irwin Michael R

来源：Neuroimmunomodulation, 2013, 20(3): 127-133.

DOI：10.1159/000346199

• Cellular adhesion molecules
• Cytokines
• Neurohormonal response
• Neuroimmunity
• Pain
• Stress

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-1 RA 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.

• 出版日期2013