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Controlling neuropathic pain by adeno-associated virus driven production of the anti-inflammatory cytokine, interleukin-10

Erin D Milligan1, Evan M Sloane1, Stephen J Langer2, Pedro E Cruz3, Marucia Chacur1, Leah Spataro1, Julie Wieseler-Frank1, Sayamwong E Hammack1, Steven F Maier1, Terence R Flotte3, John R Forsayeth4, Leslie A Leinwand2, Raymond Chavez4 and Linda R Watkins1*

Author Affiliations

1 Department of Psychology & the Center for Neuroscience, University of CO at Boulder, Boulder, CO 80309 USA

2 Department of Molecular, Cellular & Developmental Biology, University of CO at Boulder, Boulder, CO 80309 USA

3 Genetics Institute, the Powell Gene Therapy Center & Department of Pediatrics, University of FL at Gainesville, Gainesville, FL 32610 USA

4 Avigen, Inc., Alameda, CA 94502 USA

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Molecular Pain 2005, 1:9  doi:10.1186/1744-8069-1-9

Published: 25 February 2005

Abstract

Despite 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.