Award: Arthritis and Related Autoimmune Disease Research Grant
Biography: Dr. Adam Dourson is a translational neuroscientist at Washington University in St. Louis dedicated to bridging clinical observation and mechanistic science to address the complexities of chronic pain. His research investigates how peripheral immune and endocrine interactions with sensory neurons drive pain pathology, primarily within the dorsal root ganglion (DRG). By integrating patient data, sequencing, and human tissue samples, he’s established a “reverse-translation” pipeline where clinical insights directly inform mechanistic studies.
A central focus of Dr. Dourson’s work involves elucidating the distinctions between painful and non-painful juvenile idiopathic arthritis (JIA). Specifically investigating age-dependent differences in nociceptive pathways and biochemical factors in synovial fluid to understand why some pediatric patients experience pain while others do not. This methodology utilizes patient reports and biological samples to identify candidate mechanisms for rigorous validation through precise genetic, molecular, and electrophysiological tools. Additionally, he applies a similar workflow to endometriosis, combining clinical pain phenotyping with molecular analysis of surgical samples to identify and test therapeutic targets in animal models and on human tissues, including DRG neurons.
By characterizing human tissues and validating findings through surgical and behavioral techniques in mice, his research creates a holistic picture of the mechanisms driving pain. This comprehensive framework ensures that scientific discovery remains anchored in human pathology. Ultimately, he aims to uncover the underlying biology of sensory neuron sensitization to facilitate the development of targeted, evidence-based therapeutic strategies for individuals living with chronic pain.
Research Summary: Children are not simply small adults. Many biological systems continue to develop after birth, meaning that diseases and treatments can affect children differently than adults. As a result, childhood diseases require separate study to develop effective therapies. This is especially true for juvenile idiopathic arthritis (JIA), a chronic inflammatory disease that causes joint swelling and stiffness in children. In JIA, inflammation within the joint produces signaling molecules in patient’s synovial fluid (SF), which surrounds the joint. These molecules interact with nearby nerves and contribute to pain. However, not all children with JIA experience pain. Our work has focused on understanding why. We identified a key difference between children with JIA who report pain and those who do not. Interleukin-10 (IL-10), a molecule known to reduce pain and inflammation and shown to be particularly effective in early life, was present in the SF of children without pain but absent in those who reported pain. To test whether this difference is meaningful, we examined how SF from these two patient groups affects pain and nerve activity. When SF from children with pain was injected into the knee of animals, it caused pain-like sensitivity and activated neurons. In contrast, SF from children without pain did not produce pain-like sensitivity and made neurons less sensitive than normal. This proposal will test whether IL-10 directly causes these protective effects, define the broader inflammatory profiles associated with pain and no pain, and validate these findings using human sensory neurons.