UCLA

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.