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

Griffis C.A.a · Irwin M.R.b · Martinez-Maza O.c · Doering L.a · Nyamathi A.a · Kaufman R.d · Elashoff D.a · Aziz N.e · Compton P.a
aSchool of Nursing, bCousins Center for Psychoneuroimmunology, and Departments of cMicrobiology, Immunology & Molecular Genetics, dAnesthesiology, and ePathology and Laboratory Medicine, University of California at Los Angeles, Los Angeles, Calif., USA Neuroimmunomodulation 2007;14:224–228 (DOI:10.1159/000112046)


Background/Aims: 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. Methods: 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. Results: 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. Conclusion: 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.


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