Post doc research associate Washington University in St. Louis ST LOUIS, Missouri, United States
Stress is a key factor in migraine chronification, often triggering transitions from acute to chronic pain via neuroimmune mechanisms. Using a mouse model, we investigated the effects of low-dose interleukin-2 (LD-IL-2) on stress-induced mechanical hypersensitivity. Repetitive restraint stress induced acute and chronic hypersensitivity in female mice. Behavioral assays confirmed hypersensitivity following stress and exposure to pain triggers like BLS and SNP. LD-IL-2 (administered post-stress) accelerated recovery of mechanical thresholds and prevented sensitization upon re-exposure to triggers. These effects were observed with both early and delayed IL-2 treatment. Findings highlight LD-IL-2's potential to modulate neuroimmune responses, reduce pain sensitization, and support its use in managing stress-triggered migraine and chronic pain conditions.
Learning Objectives:
Upon completion, participant will be able to describe that repetitive restraint stress induces acute and chronic mechanical hypersensitivity in facial in mice, modeling stress-triggered migraine.
Upon completion, participant will be able to discuss that migraine-related triggers such as bright light stress (BLS) and sodium nitroprusside (SNP), contribute to hyperalgesic priming following stress.
Upon completion, participant will be able to summarize the effects of low-dose IL-2 administration — both early and delayed — in preventing and reversing pain sensitization in stress-induced migraine models.
