• Erin D Milligan, Evan M Sloane, Stephen J Langer, Pedro E Cruz, Marucia Chacur, Leah Spataro, Julie Wieseler-Frank, Sayamwong E Hammack, Steven F Maier, Terence R Flotte, John R Forsayeth, Leslie A Leinwand, Raymond Chavez, and Linda R Watkins.
• Department of Psychology & the Center for Neuroscience, University of CO at Boulder, Boulder, CO 80309 USA. emilligan@psych.Colorado.edu
• Mol Pain. 2005 Feb 25; 1: 9.

AbstractDespite many decades of drug development, effective therapies for neuropathic pain remain elusive. The recent recognition of spinal cord glia and glial pro-inflammatory cytokines as important contributors to neuropathic pain suggests an alternative therapeutic strategy; that is, targeting glial activation or its downstream consequences. While several glial-selective drugs have been successful in controlling neuropathic pain in animal models, none are optimal for human use. Thus the aim of the present studies was to explore a novel approach for controlling neuropathic pain. Here, an adeno-associated viral (serotype II; AAV2) vector was created that encodes the anti-inflammatory cytokine, interleukin-10 (IL-10). This anti-inflammatory cytokine is known to suppress the production of pro-inflammatory cytokines. Upon intrathecal administration, this novel AAV2-IL-10 vector was successful in transiently preventing and reversing neuropathic pain. Intrathecal administration of an AAV2 vector encoding beta-galactosidase revealed that AAV2 preferentially infects meningeal cells surrounding the CSF space. Taken together, these data provide initial support that intrathecal gene therapy to drive the production of IL-10 may prove to be an efficacious treatment for neuropathic pain.

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