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Science. 2016 Nov 4;354(6312):572-577.

Pain regulation by non-neuronal cells and inflammation.

Author information

1
Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA. ru-rong.ji@duke.edu.
2
Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.
3
Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA.
4
Institute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.

Abstract

Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous system. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain. We review how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain. Recent studies also suggest that bacterial infections regulate pain through direct actions on sensory neurons, and specific receptors are present in nociceptors to detect danger signals from infections. We also discuss new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.

PMID:
27811267
PMCID:
PMC5488328
DOI:
10.1126/science.aaf8924
[Indexed for MEDLINE]
Free PMC Article

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