Chemokines, chemokine receptors and pain.
Many patients suffer from neuropathic pain as a result of injury to the peripheral nervous system (e.g. post-herpetic neuralgia or diabetic neuropathy) or to the central nervous system (e.g. spinal cord injury or stroke). The most distinctive symptom of neuropathic pain is allodynia, whereby normally non-painful stimuli, such as light touch, become painful. Traditionally, inflammatory and neuropathic pain syndromes have been considered distinct entities; however, recent evidence belies this strict dichotomy. Nerve damage can stimulate macrophage infiltration and increase the number of activated T cells. Under these conditions, neuroinflammatory and immune responses contribute as much to the development and maintenance of pain as the initial damage itself. Recently, studies using animal models have shown that upregulation of chemokines is one of the mechanisms underlying the development and maintenance of chronic pain.[1]References
- Chemokines, chemokine receptors and pain. Abbadie, C. Trends Immunol. (2005) [Pubmed]
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