Pain regulation by non-neuronal cells and inflammation.
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2016-11-04
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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.
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Ji, Ru-Rong, Alexander Chamessian and Yu-Qiu Zhang (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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Ru-Rong Ji
I have been doing neuroscience and pain research for over 25 years in multiple academic institutes, including Duke University (2012-current), Harvard Medical School (1998-2012), Johns Hopkins Medical School, Karolinska Institute, and Peking University. The long-term goal of my lab is to identify molecular and cellular mechanisms that underlie the induction and resolution of pathological pain and develop novel pain therapeutics that can target these mechanisms, with specific focus on neuroimmune interactions. We are interested in the following scientific questions. (1) How does inflammation induce and resolve pain via immune cell interaction with primary sensory neurons? (2) How does neuroinflammation drive chronic pain via activation of glial cells in the CNS (microglia and astrocytes) and PNS (satellite glial cells) and regulation of sensory neuron plasticity (peripheral sensitization) and spinal cord synaptic plasticity (central sensitization)? (3) How do specialized pro-resolution mediators (SPMs, e.g., resolvins, protectins, and maresins) control pain via GPCR signaling? (4) How do immunotherapies through the PD-L1/PD-1 and STING/IFN pathways regulate pain, cognition, and neuronal activities? (5) How do secreted miRNAs regulate pain and itch via direct activation of surface receptors and ion channels? (6) How do nerve terminals interact with cancers in chronic pain and itch? (7) How do Toll-like receptors (TLR) in primary sensory neurons sense danger signals and regulate pain and itch? (8) How do regenerative approaches such as autologous conditioned serum (ACS) and bone marrow stromal cells (MSCs) produce long-term pain relief via secreting anti-inflammatory factors and exosomes? We employ a multidisciplinary approach that covers in vitro, ex vivo, and in vivo studies for animal behaviors, electrophysiology, molecular biology, cell biology, and transgenic animals. We have identified numerous therapeutic targets and filed many patents for translational studies. As the Director of the Center for Translational Pain Medicine (CTPM) and a highly cited researcher (Cross Field, Clarivate), I have both administrative and scientific leadership for successful completion of many research projects.
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