不良研究所

The main stream of our research program is to investigate the immune etiology of chronic pain by exploring the interactions between injured neurons and their surrounding glia/immune cells and the impact of glial activation in pain behaviour. Chronic pain is a sensory disorder resulting from infection, injury, cancer or some metabolic/neurodegenerative diseases, which has an enormous negative impact on the quality of life of individuals affected by this problem. While for decades, a neuron-centric view has predominated to explain the pathophysiology of chronic pain, recent work has uncovered extensive neuroimmune interactions as substrates. Interactions between the immune and nervous systems occur at multiple levels, where different types of glia/immune cells and immune-derived substances are implicated at different stages of the pathogenesis. We have identified that chemokine MCP-1, released by damaged neurons is a trigger in inducing spinal microglial activation which is necessary for the development of hypersensitivity (J Neurochem, J of Neuroscience). Our results also demonstrated that spinal microglial activation induced by peripheral nerve injury is not just a property of those cells that already existed in the spinal cord, there include populations of cells coming from proliferation and recruitment of blood-born macrophages (J of Neuroscience, Pain). By using well established animal models of chronic pain, molecular, neuroanatomical and behaviroal approaches, we are currently focusing on:

1) Characterizing the phenotypes of CNS glial cells or peripheral immune cells in the circumstance of inflammation, nerve injury and chronic neurodegenerative diseases, and the correlation with pain behaviour

2) Examining the impact of neuron-glia, neuron-immune interaction in the pathogenesis of chronic pain

3) Developing new therapeutic strategy by targeting both spinal glial cells and bone marrow derived macrophages for an effective pain relief.

In addition to our activities in pain research, we are also interested in exploring the impact of normal aging on glial cell biology. We want to understand aging dependent glial degeneration and the impacts of glial senescence on neuronal functions.
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