Pain regulation by non-neuronal cells and inflammation.
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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.
Published Version (Please cite this version)10.1126/science.aaf8924
Publication InfoJi, 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.
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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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