THE EFFECT OF PAIN ON LEUKOCYTE CAM EXPRESSION

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. SPECIFIC AIMS Although functional in the case of acute inflammation, we posit that the immune response induced by the potent and unique stressor of pain has important health implications for those patients with chronic inflammatory diseases, including atherosclerosis, inflammatory bowel disease, and rheumatoid arthritis. Understanding how pain may contribute to the pathology and symptomatology of such diseases is clearly an area worthy of nursing investigation. To this end, the specific aims of this preliminary work are to: 1 Via a formal pilot study, describe and compare the particular immune and inflammatory system responses (including changes in catecholamines, cytokines, and cellular adhesion molecules) in healthy male and female controls to experimental pain stress conditions. 2. Develop a new line of investigation for the principal investigator, who will expand her expertise in pain physiology to include the effects of pain on immune and inflammatory parameters, via multidisciplinary collaboration with nationally-recognized neurophysiologists and immunologists. The proposed pilot study will test the novel idea that pain, as a unique stressor, has detrimental effects via inflammatory processes via its effect on increasing CAM levels. Study hypotheses are based upon a stress framework, in which pain is conceptualized as both a psychological (affective) stressor and a uniquely nociceptive (neural-sensory) stressor, the effects of which are evident in adrenergic markers, cytokine production, and ultimately CAM levels.