Pain regulation by non-neuronal cells and inflammation.
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.
Type
Journal articlePermalink
https://hdl.handle.net/10161/13677Published Version (Please cite this version)
10.1126/science.aaf8924Publication Info
Ji, Ru-Rong; Chamessian, Alexander; & Zhang, Yu-Qiu (2016). Pain regulation by non-neuronal cells and inflammation. Science, 354(6312). pp. 572-577. 10.1126/science.aaf8924. Retrieved from https://hdl.handle.net/10161/13677.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Ru-Rong Ji
Distinguished Professor of Anesthesiology, in the School of Medicine
Chronic pain is a major health problem in the US, affecting 100 million Americans.
The long-term goal of the lab is to identify molecular and cellular mechanisms that
underlie the genesis of chronic pain and, furthermore, to develop novel pain therapeutics
that can target these mechanisms. We are interested in the following questions. (1)
How do neuroinflammation and activation of glial cells (microglia and astrocytes)
regulate pain and spinal cord synaptic plasticity via neuro-glia

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