Editors' ChoicePain

Feeling No (Chronic) Pain

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Science's STKE  08 Jul 2003:
Vol. 2003, Issue 190, pp. tw258-TW258
DOI: 10.1126/stke.2003.190.tw258

Abbadie et al. investigated the role of chemotactic chemokine receptor 2 (CCR2) in pain and discovered evidence implicating this receptor in chronic neuropathic pain. Chronic neuropathic pain, a condition that can have substantial effects on quality of life and may interfere with common activities of daily living, can be difficult to treat and remains poorly understood. Abbadie et al. compared the responses of wild-type mice and mutant mice lacking CCR2, which mediates the chemotactic response of monocytes to the inflammatory chemokine monocyte attractant protein-1 (MCP-1), in several models of pain. After injury to the sciatic nerve, the mutant mice lacked a behavioral response associated with chronic neuropathic pain. In wild-type mice, nerve injury led to increased levels of CCR2 in the sciatic nerve and dorsal root ganglia. In addition, numerous CCR2-immunoreactive macrophages were identified in the sciatic nerve and CCR2-immunoreactive microglia were observed in the spinal cord. The CCR2 knockout mice had fewer astrocytes in the dorsal horn of the spinal cord after nerve injury than did wild-type mice, and their microglia showed lower levels of p38 mitogen-activated protein kinase. Both of these observations are indicative of reduced glial activation. CCR2's role in chronic neuropathic pain could lead to new therapies for this condition.

C. Abbadie, J. A. Lindia, A. M. Cumiskey, L. B. Peterson, J. S. Mudgett, E. K. Bayne, J. A. DeMartino, D. E. MacIntyre, M. J. Forrest, Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2. Proc. Natl. Acad. Sci. U.S.A. 100, 7947-7952 (2003). [Abstract] [Full Text]

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