Opioid treatment of experimental pain activates nuclear factor-κB.

Abstract

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). 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. University General Clinical Research Center. Twenty-one (11 female) healthy controls. Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained. Intracellular levels of activated NF-κB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes. 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. The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses.