Macrophages transfer mitochondria to sensory neurons to resolve inflammatory pain
Inflammatory pain and hyperalgesia are considered functional features of an immune response, intended to protect tissue from further damage. At the affected site, immune cells and inflammatory mediators activate sensory neurons, resulting in pain signalling. The general consensus asserts that this pain passively resolves following cessation of the inflammatory stimulus. However, in many patients with chronic inflammatory diseases (such as rheumatoid arthritis and inflammatory bowel disease), resolution of inflammation does not translate to cessation of pain. This subsequently leads to chronic pain, where pain signals remain active for weeks to years, severely impacting a patient’s quality of life. The mechanism by which inflammatory pain is successfully resolved remains poorly understood.