Our lab is interested in the mechanisms of pain in autoimmune diseases and how interactions between innate immune cells, adaptive immune cells, satellite glia and sensory neurons drive pain. We currently have two main research focuses. First, autoantibodies may underlie a subset of fibromyalgia, but why the autoantibodies develop in the first place is unclear. We are investigating the hypothesis that fibromyalgia autoantibodies develop through molecular mimicry with dysregulated gut microbiota. Second, we are investigating how extracellular matrix remodelling in the dorsal root ganglia regulates nociceptor sensitivity in chemotherapy-induced peripheral neuropathy and other chronic pain conditions. We use a combination of animal models, human samples, and human clinical data and leverage techniques like animal behaviour, tissue-clearing immunofluorescent staining, machine vision-aided image analysis, cell culture and flow cytometry.
Caption for image:
A and B) Collagen I (magenta) is found throughout the dorsal root ganglia and between each neuron (green) and a 3D reconstruction of an iDisco cleared DRG (B) suggests that collagen I is a major structural component of the dorsal root ganglia ECM. Fluorescent in situ hybridization (FISH) shows that Col1a1 is primarily expressed by cells that are likely specialized fibroblasts and not neurons, satellite glia cells (GS+) or macrophages (Cx3cr1-expressing).