Opioid treatment of experimental pain activates nuclear factor-κB.

Objective: To determine the independent and combined effects of pain and opioids on the activation of an early marker of inflammation, nuclear factor- κ B (NF- κ B). Design: NF- κ B activation was compared within-subjects following four randomly ordered experimental sessions of opioid-only (intravenous fentanyl 1 μg/kg), pain-only (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-kB analysis were obtained. Main outcome measures: Intracellular levels of activated NF- κ B, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes. Results: Neither pain nor opioid administration alone effected NF- κ B levels in cell populations; however, the combination of treatments induced significant increases of NF- κ B 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.