Journal
PAIN
Volume 155, Issue 10, Pages 2161-2170Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/j.pain.2014.08.013
Keywords
Neuropathic pain; Peripheral nerve injury; Reactive oxygen species; Dorsal root ganglion; Knockout mice
Categories
Funding
- Deutsche Forschungsgemeinschaft [Sonderforschungsbereich 815-A1, A14]
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Emerging lines of evidence indicate that production of reactive oxygen species (ROS) at distinct sites of the nociceptive system contributes to the processing of neuropathic pain. However, the mechanisms underlying ROS production during neuropathic pain processing are not fully understood. We here detected the ROS-generating nicotinamide adenine dinucleotide phosphate oxidase isoform Nox2 in macrophages of dorsal root ganglia (DRG) in mice. In response to peripheral nerve injury, Nox2-positive macrophages were recruited to DRG, and ROS production was increased in a Nox2-dependent manner. Nox2-deficient mice displayed reduced neuropathic pain behavior after peripheral nerve injury, whereas their immediate responses to noxious stimuli were normal. Moreover, injury-induced upregulation of tumor necrosis factor a was absent, and activating transcription factor 3 induction was reduced in DRG of Nox2-deficient mice, suggesting an attenuated macrophage-neuron signaling. These data suggest that Nox2-dependent ROS production in macrophages recruited to DRG contributes to neuropathic pain hypersensitivity, underlining the observation that Nox-derived ROS exert specific functions during the processing of pain. (C) 2014 International Association for the Study of Pain. Published by Elsevier B. V. All rights reserved.
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