Dr. Malcangio will discuss how neuron-derived miRNAs regulate macrophage phenotype in neuropathic pain. She will also provide evidence that macrophages communicate with sensory neurons via miR-containing EV release and contribute to nociceptive mechanisms under neuropathic conditions. Dr Malcangio will illustrate mechanisms and pathways that can be targeted to promote a shift in macrophage phenotype from pro-nociceptive (M1) to anti-nociceptive (M2) and promote resolution of pain.  She will present evidence that delivery of miRNA antagomirs encapsulated in nanoparticles constitutes a novel strategy to maintain polarization of DRG macrophages at M2-like state and attenuate neuropathic pain. Specifically, in neuropathic pain conditions, on one hand the transfer of miR-21containing extracellular vehicles (EVs) from sensory-neuron is associated with via activation of pro-inflammatory pathways in macrophages. On the other hand, M1-like macrophages release EV containing miR-155 which are taken up by sensory neurons and influence neuronal activity.