Abstract:
: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 α 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.
journal_name
Painjournal_title
Painauthors
Kallenborn-Gerhardt W,Hohmann SW,Syhr KM,Schröder K,Sisignano M,Weigert A,Lorenz JE,Lu R,Brüne B,Brandes RP,Geisslinger G,Schmidtko Adoi
10.1016/j.pain.2014.08.013subject
Has Abstractpub_date
2014-10-01 00:00:00pages
2161-70issue
10eissn
0304-3959issn
1872-6623pii
S0304-3959(14)00372-8journal_volume
155pub_type
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