title: Opioid treatment of experimental pain activates nuclear factor-κB.
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).
  
  
  METHODS
  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.
  
  
  METHODS
  University General Clinical Research Center.
  
  
  METHODS
  Twenty-one (11 female) healthy controls.
  
  
  METHODS
  Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained.
  
  
  METHODS
  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.affiliation: Department of Nursing, School of Nursing and Health Studies, Georgetown University, Washington, DC.
authors.forename: Peggy
authors.initials: P
authors.lastname: Compton
authors.affiliation: Department of Anesthesiology, University of California, Los Angeles, Los Angeles, California.
authors.forename: Charles
authors.initials: C
authors.lastname: Griffis
authors.affiliation: Cousins Center for Psychoneuroimmunology, Semel Institute for Neurosciences, University of California, Los Angeles, Los Angeles, California.
authors.forename: Elizabeth Crabb
authors.initials: EC
authors.lastname: Breen
authors.affiliation: Department of Family Medicine, University of California, Los Angeles, Los Angeles, California.
authors.forename: Matthew
authors.initials: M
authors.lastname: Torrington
authors.affiliation: Cousins Center for Psychoneuroimmunology, Semel Institute for Neurosciences, University of California, Los Angeles, Los Angeles, California.
authors.forename: Ryan
authors.initials: R
authors.lastname: Sadakane
authors.affiliation: Department of Biostatistics and Epidemiology, MedStar Health Research Institute, Columbia, Maryland.
authors.forename: Eshetu
authors.initials: E
authors.lastname: Tefera
authors.affiliation: Cousins Center for Psychoneuroimmunology, Semel Institute for Neurosciences, University of California, Los Angeles, Los Angeles, California.
authors.forename: Michael R
authors.initials: MR
authors.lastname: Irwin
mesh_terms: D000328:Adult; D005260:Female; D006801:Humans; D008297:Male; D000701:Analgesics, Opioid / Q000627:therapeutic use; D005283:Fentanyl / Q000627:therapeutic use; D005500:Follow-Up Studies; D064368:Healthy Volunteers; D007275:Injections, Intravenous; D009000:Monocytes / Q000187:drug effects; D016328:NF-kappa B / Q000097:blood; D010146:Pain / Q000097:blood / Q000188:drug therapy; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000701:Analgesics, Opioid; D005283:Fentanyl; D016328:NF-kappa B