About this Research Topic
As microglia-independent neuropathic pain has been increasingly observed, emerging evidence supports that reciprocal interactions between tissue macrophages and nociceptors can either promote or attenuate both evoked and spontaneous neuropathic pain behaviors. Moreover, it has been reported that macrophages modulate cutaneous sensory neurons and alter acute nociceptive thresholds. Thus, a better understanding of the underlying pathways in both microglia and macrophages, will provide new information concerning the mechanism through which nerve injury contributes to the transition from acute to persistent neuropathic pain. Targeting the neuroinflammation through modulating microglia and tissue macrophages could be of therapeutic benefit in treating refractory inflammatory and neuropathic pain condition.
This Research Topic accepts Original Research, Systematic Review, Methods, Review and Mini-Review, Clinical Trial, Perspective, General Commentary, Opinion. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
• Contribution of microglia in acute and chronic pain
• Contribution of tissue macrophages in acute and chronic pain
• Interaction between microglia and tissue macrophages with neurons in acute and chronic pain
• Mechanisms of microglia and/or tissue macrophage proliferation
• Transcriptomic and proteinomic profiling on microglia and/or tissue macrophage after peripheral nerve injury
• Contribution of microglia and tissue macrophages in clinical pain patients
• Neuroimaging study of microglia and tissue macrophages in preclinical and clinical pain
The Topic Editors declare no competing interests with regard to the Research Topic subject.
Keywords: Microglia, macrophage, pain, neuropathic, inflammatory, DRG, spinal cord, sensory neuron
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