Enhanced microglia reactivity contributes to persistent pain in several preclinical pain models, including peripheral and spinal injury, peripheral inflammation, bone cancer pain, and colitis.7, 8, 9, 10, 11 During active colitis, activated microglia produce a large panel of proinflammatory mediators including interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), and brain-derived neurotrophic factor (BDNF), which contribute to neuronal sensitization.11, 12, 13 However, microglial activation persists during the recovery phase of colitis in which animals experience VHS.14 This evidence concerns the gene IL1B and colitis.