Keita Kohno

Neuropathic pain is often caused by injury and diseases that affect the somatosensory system. Although pain development has been well studied, pain recovery mechanisms remain largely unknown. Here, we found that CD11c-expressing spinal microglia appear after the development of behavioral pain hypersensitivity following nerve injury. Nerve-injured mice with spinal CD11c⁺ microglial depletion failed to recover spontaneously from this hypersensitivity. CD11c⁺ microglia express

Pain plays an indispensable role as an alarm system to protect us from dangers or injuries. However, neuropathic pain, a debilitating pain condition caused by damage to the nervous system, persists for a long period even in the absence of dangerous stimuli or after injuries have healed. In this condition, pain becomes a disease itself rather than the alarm system and is often resistant to currently available medications. A growing body of evidence indicates that microglia, a type of macrophages

Neuropathic pain, a highly debilitating chronic pain following nerve damage, is a reflection of the aberrant functioning of a pathologically altered nervous system. Previous studies have implicated activated microglia in the spinal dorsal horn (SDH) as key cellular intermediaries in neuropathic pain. Microgliosis is among the dramatic cellular alterations that occur in the SDH in models of neuropathic pain established by peripheral nerve injury (PNI), but detailed characterization of SDH microgl

Neuropathic pain arises from injury or disease to the sensory nervous system and is characterized by intense pain that is disproportionate to the stimulus. However, effective treatments remain limited, highlighting an urgent need for novel therapeutic approaches. Over the past two decades, studies have revealed that microglia-resident macrophages in the central nervous system-play an essential role in the development of neuropathic pain. In the dorsal horn of the spinal cord, microglia respond t

Neuropathic pain, a debilitating chronic pain condition, is a major clinical challenge. The pleiotropic cytokine interleukin-4 (IL-4) has been shown to suppress neuropathic pain in rodent models, but its underlying mechanism remains unclear. Here, we show that intrathecal administration of IL-4 to mice with spinal nerve transection (SpNT) increased the number of CD11c⁺ microglia (a microglia subset important for pain remission) in the spinal dorsal horn (SDH) and that this effect of I

Abstract Neuropathic pain, a debilitating chronic pain condition, is a major clinical challenge. The pleiotropic cytokine interleukin-4 (IL-4) has been shown to suppress neuropathic pain in rodent models, but its underlying mechanism remains unclear. Here, we show that intrathecal administration of IL-4 to mice with spinal nerve transection (SpNT) increased the number of CD11c + microglia (a microglia subset important for pain remission) in the spinal dorsal horn (SDH) and that this effect of IL

Neuropathic pain is a highly debilitating chronic pain condition occurring after insult in the nervous system. Peripheral nerve injury (PNI) is used as a rodent model of neuropathic pain and causes activation of spinal cord microglia, resident immune cells in the central nervous system. Accumulating evidence indicates that microglia activated in the spinal dorsal horn are critical elements for neuropathic pain development. However, the role of microglia in a later phase of neuropathic pain remai

Abstract Neuropathic pain, a debilitating chronic pain condition, is a major clinical challenge. The pleiotropic cytokine interleukin-4 (IL-4) has been shown to suppress neuropathic pain in rodent models, but its underlying mechanism remains unclear. Here, we show that intrathecal administration of IL-4 to mice with spinal nerve transection (SpNT) increased the number of CD11c+ microglia (a microglia subset important for pain remission) in the spinal dorsal horn (SDH) and that this effect of IL-

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 th

Neuropathic pain, a debilitating chronic pain condition, is a major clinical challenge. The pleiotropic cytokine interleukin-4 (IL-4) has been shown to suppress neuropathic pain in rodent models, but its underlying mechanism remains unclear. Here, we show that intrathecal administration of IL-4 to mice with spinal nerve transection (SpNT) increased the number of CD11c+ microglia (a microglia subset important for pain remission) in the spinal dorsal horn (SDH) and that this effect of IL-4 was ess

Neuropathic pain, a debilitating chronic pain condition, is a major clinical challenge. The pleiotropic cytokine interleukin-4 (IL-4) has been shown to suppress neuropathic pain in rodent models, but its underlying mechanism remains unclear. Here, we show that intrathecal administration of IL-4 to mice with spinal nerve transection (SpNT) increased the number of CD11c + microglia (a microglia subset important for pain remission) in the spinal dorsal horn (SDH) and that this effect of IL-4 was es

Neuropathic pain, a debilitating chronic pain condition, is a major clinical challenge. The pleiotropic cytokine interleukin-4 (IL-4) has been shown to suppress neuropathic pain in rodent models, but its underlying mechanism remains unclear. Here, we show that intrathecal administration of IL-4 to mice with spinal nerve transection (SpNT) increased the number of CD11c+ microglia (a microglia subset important for pain remission) in the spinal dorsal horn (SDH) and that this effect of IL-4 was ess