Peggy Compton1, Charles Griffis2, Elizabeth Crabb Breen3, Matthew Torrington4, Ryan Sadakane3, Eshetu Tefera5, Michael R Irwin3. 1. Department of Nursing, School of Nursing and Health Studies, Georgetown University, Washington, DC. 2. Department of Anesthesiology, University of California, Los Angeles, Los Angeles, California. 3. Cousins Center for Psychoneuroimmunology, Semel Institute for Neurosciences, University of California, Los Angeles, Los Angeles, California. 4. Department of Family Medicine, University of California, Los Angeles, Los Angeles, California. 5. Department of Biostatistics and Epidemiology, MedStar Health Research Institute, Columbia, Maryland.
Abstract
OBJECTIVE: 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). DESIGN: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. SETTING: University General Clinical Research Center. PARTICIPANTS: Twenty-one (11 female) healthy controls. INTERVENTIONS: Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained. MAIN OUTCOME MEASURES: Intracellular levels of activated NF-κB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes. RESULTS: 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. CONCLUSIONS: The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses.
RCT Entities:
OBJECTIVE: 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). DESIGN: 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. SETTING: University General Clinical Research Center. PARTICIPANTS: Twenty-one (11 female) healthy controls. INTERVENTIONS: Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained. MAIN OUTCOME MEASURES: Intracellular levels of activated NF-κB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes. RESULTS: 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. CONCLUSIONS: The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses.
Authors: J P Zacny; M A McKay; A Y Toledano; S Marks; C J Young; P A Klock; J L Apfelbaum Journal: Drug Alcohol Depend Date: 1996-10 Impact factor: 4.492
Authors: Burel R Goodin; Noel B Quinn; Christopher D King; Gayle G Page; Jennifer A Haythornthwaite; Robert R Edwards; Laura Stapleton; Lynanne McGuire Journal: Psychophysiology Date: 2011-09-06 Impact factor: 4.016
Authors: David J Miklowitz; Larissa C Portnoff; Casey C Armstrong; Danielle Keenan-Miller; Elizabeth C Breen; Keely A Muscatell; Naomi I Eisenberger; Michael R Irwin Journal: Psychiatry Res Date: 2016-05-07 Impact factor: 3.222