Julie Wieseler-Frank

TL;DR: Results suggest that IL-1 and fractalkine are endogenous regulators of morphine analgesia and are involved in the increases in pain sensitivity that occur after chronic opiates.

TL;DR: The potential implications of such glial regulation of pain and opioid actions are vast, suggestive that targeting glia and their proinflammatory products may provide a novel and effective therapy for controlling clinical pain syndromes and increasing the clinical utility of analgesic drugs.

TL;DR: Glia are described as newly recognized mediators of exaggerated pain, and as new therapeutic targets for pathological pain, which are likely to play significant roles in other behavioral phenomena.

TL;DR: IL‐10 gene therapy both prevented and reversed thermal hyperalgesia and mechanical allodynia, without affecting basal responses to thermal or mechanical stimuli, and support that this gene therapy approach provides an alternative to neuronally focused drug and gene therapies for clinical pain control.

TL;DR: The role of proinflammatory cytokines in experimental models of prolonged pain states is discussed andGene therapy to augment the endogenous anti-inflammatory cytokine, interleukin-10, is one of the more promising therapies currently under study.