Pain-Related Activation of Leukocyte Cellular Adhesion Molecules: Preliminary Findings

School of Nursing, University of California at Los Angeles, Los Angeles, CA 90095-1702, USA.
NeuroImmunoModulation (Impact Factor: 1.88). 02/2007; 14(5):224-8. DOI: 10.1159/000112046
Source: PubMed


Acute adrenergic stressors have been found to activate neuroendocrine pathways that can alter leukocyte migration and activity. Leukocyte migration is known to affect the pathophysiology of inflammatory disease processes. This study examined the effects of acute experimental pain on catecholamine and cortisol levels and leukocyte expression of cellular adhesion molecules.
Healthy subjects (n = 10) underwent 45 min of acute experimental pain using earlobe electrical stimulation. Measures included sensory and affective pain responses, perceived stress, circulating levels of catecholamines, cortisol, and expression of integrin (CD11a+) cellular adhesion molecules on leukocyte subsets. Data were collected at baseline, after 22.5 and 45 min of pain, and 180 min after pain cessation.
Experimental pain acutely increased circulating levels of epinephrine, along with increases in the number of CD8+CD11a+ leukocytes and the density of CD11a molecules on CD8+ cells. Positive correlations were found between pain and stress scores, and the number of CD8+CD11a+ leukocytes.
Acute pain induces elevated cellular adhesion molecule expression on leukocytes, which has possible implications for increasing leukocyte infiltration and disease exacerbation in patient populations with inflammatory syndromes.

Download full-text


Available from: Michael R Irwin,
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To assess experimental pain sensitivity and compare the inflammatory response to pain in 26 osteoarthritis (OA) patients and 33 age- and sex-matched controls from the general population in order to examine the nature of the association between pain and inflammation in OA. The participants underwent psychophysical pain testing to assess pain sensitivity in response to heat, cold, and mechanical stimuli. Blood samples were taken at baseline and at 4 time points after testing to determine the effect of acute pain on C-reactive protein (CRP), interleukin-6 (IL-6), IL-1β, and tumor necrosis factor α levels. OA patients had lower pressure pain thresholds (P ≤ 0.003) and higher heat pain ratings (P ≤ 0.04) than controls across multiple body sites. OA patients had higher CRP levels than controls (P = 0.007). CRP levels did not change in response to pain testing. Although not statistically significant, OA patients tended to have higher IL-6 levels than controls (P = 0.12). IL-6 levels increased after pain testing in OA patients and controls (P < 0.0001), but the amount of increase was not different between the 2 groups. Among OA patients, heightened pain sensitivity was associated with elevated CRP and IL-6 levels (P ≤ 0.05). Compared with controls, OA patients are more sensitive to experimental pain at multiple body sites. IL-6 levels in OA patients and controls exhibited reactivity to acute painful stimuli, increasing at similar rates after psychophysical pain testing.
    01/2010; 63(3):320-7. DOI:10.1002/acr.20373
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    NeuroImmunoModulation 02/2013; 20(3):127-133. DOI:10.1159/000346199 · 1.88 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To determine the independent and combined effects of pain and opioids on the activation of an early marker of inflammation, nuclear factor-κB (NF-κB). NF-κB activation was compared within-subjects following four randomly ordered experimental sessions of opioid-only (intravenous fentanyl 1 μg/kg), painonly (cold-pressor), opioid + pain, and a resting condition. University General Clinical Research Center. Twenty-one (11 female) healthy controls. Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained. Intracellular levels of activated NF-κB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes. Neither pain nor opioid administration alone effected NF-κB levels in cell populations; however, the combination of treatments induced significant increases of NF-κB in stimulated peripheral blood mononuclear cell, lymphocytes, and monocytes. The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses.
    Journal of opioid management 03/2015; 11(2):115-25. DOI:10.5055/jom.2015.0261