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Chemokines are central to the innate immune response following tissue damage, injury and some diseases. There is also growing evidence that disease-associated or injury-induced functional expression of chemokines/receptors in both neural and nonneural elements of the nervous system play crucial roles in the pathophysiology of chronic pain. Evidence of chemokine contribution to chronic pain includes the upregulation of monocyte hemoattractant protein-1 (MCP1/CCL2) and its respective receptor, CCR2. Increased signaling by stromal-derived factor-1 (SDF1/CXCL12) and its receptor, CXCR4, has also been shown to contribute to Nucleoside Reverse Transcriptase Inhibitor (NRTI-) and HIV1-related pain behavior. Most recently, opioidinduced hyperalgesia appears to be modulated by increased neuronal CXCL12/CXCR4 signaling. Taken together, upregulation of chemokine/receptor signaling may be a mechanism that directly and/or indirectly contributes to the development and maintenance of chronic pain syndromes and these molecular molecules may represent novel targets for therapeutic intervention in sustained pain states.

Hosted By: Dr. Ling Cao