Acute painful stress and inflammatory mediator production.
|Title||Acute painful stress and inflammatory mediator production.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Griffis CA, Breen ECrabb, Compton P, Goldberg A, Witarama T, Kotlerman J, Irwin MR|
|Keywords||Adolescent, Adult, Blood Pressure, Enzyme-Linked Immunosorbent Assay, Female, Heart Rate, Humans, Inflammation Mediators, Male, Pain, Pain Measurement, Pressure, Stress, Psychological, Young Adult|
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.
|PubMed Central ID||PMC3932154|
|Grant List||5P AG028748 / AG / NIA NIH HHS / United States |
M01 RR000865 / RR / NCRR NIH HHS / United States
M01-RR00865 / RR / NCRR NIH HHS / United States
P30 AG028748 / AG / NIA NIH HHS / United States
R03 NR009106 / NR / NINR NIH HHS / United States
R03 NR009106-01A1 / NR / NINR NIH HHS / United States