Journal
NEURON
Volume 110, Issue 4, Pages 613-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2021.11.020
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Funding
- European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant [642720, 814244]
- Netherlands Organization for Scientific Research (NWO) [863.14.016, 821.02.025, 016.VENI.192.053, NWO Vici 918.15.608, Vici 865.14.004]
- Life Sciences Seed grant of the University Utrecht
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The resolution of inflammatory pain is actively controlled by macrophages through the transfer of mitochondria to sensory neurons. This process requires the expression of CD200R on macrophages and the non-canonical CD200R ligand iSec1 on sensory neurons.
The current paradigm is that inflammatory pain passively resolves following the cessation of inflammation. Yet, in a substantial proportion of patients with inflammatory diseases, resolution of inflammation is not sufficient to resolve pain, resulting in chronic pain. Mechanistic insight into how inflammatory pain is resolved is lacking. Here, we show that macrophages actively control resolution of inflammatory pain remotely from the site of inflammation by transferring mitochondria to sensory neurons. During resolution of inflammatory pain in mice, M2-like macrophages infiltrate the dorsal root ganglia that contain the somata of sensory neurons, concurrent with the recovery of oxidative phosphorylation in sensory neurons. The resolution of pain and the transfer of mitochondria requires expression of CD200 receptor (CD200R) on macrophages and the non canonical CD200R-ligand iSec1 on sensory neurons. Our data reveal a novel mechanism for active resolution of inflammatory pain.
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