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. In an article published in Science on Nov. 4, Ru-Rong Ji, along with graduate student Alexander Chamessian and Dr. Yu Qiu Zhang from the Institute of Brain Science in Shanghai, review how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain. Recent studies also suggest bacterial infections regulate pain through direct actions on sensory neurons, and specific receptors are present in nociceptors to detect danger signals from infections. They also discuss new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.
Monday, November 7, 2016