Increasing CD11c+ microglia cells facilitates the resolution of neuropathic pain behavior

Abstract

Neuropathic pain is a pathological pain state caused by a lesion or disease affecting the somatosensory system. Because existing analgesics often do not work, the development of new drugs for neuropathic pain is needed. A mouse model of neuropathic pain in which the fourth lumbar spinal nerve is transected (SpNT: spinal nerve transection) shows pain behavior that is resolved spontaneously. Recently, we found that a CD11c+ microglia subset emerged in the spinal cord after SpNT is necessary for the pain resolution. However, the role of CD11c+ microglia in other neuropathic pain models remains to be determined, especially in spared nerve injury (SNI) model that does not exhibit the spontaneous resolution of pain behavior. In this study, we found the number of CD11c+ microglia in the spinal cord was lower in the SNI model than the SpNT model, suggesting that prolonged behavioral pain hypersensitivity in the SNI model may be related to an impaired emergence of CD11c+ microglia. In addition, increasing the number of CD11c+ microglia by a cytokine administrated exogenously facilitated the resolution of pain behavior in both models. The alleviating effect was abolished by depletion of spinal CD11c+ microglia. Thus, increasing CD11c+ microglia or augmenting their function could be a new therapeutic strategy for neuropathic pain.