Chronic pain is a leading cause of disability, its treatment is challenging, and its burden is increasing. Our research is focused on neuropathic pain, a particularly debilitating form of chronic pain caused by a lesion or disease affecting the somatosensory nervous system. Specifically, our work has demonstrated that there is a complex interplay between immune responses and sensory pathways and that chronic pain following nervous system damage results from a neuroimmune imbalance leading to chronic neuroinflammation and long-lasting neuropathic pain. Thus, boosting anti-inflammatory responses, such as expanding populations of immunoregulatory immune cells, or administering anti-inflammatory mediators, at the site of nervous system injury may be beneficial in neuropathic pain.
The principal aim of our research is to understand the relationship between the nervous system and the immune system, with particular emphasis on how immune cells and their mediators affect neuropathic pain, and to assess immunotherapeutic approaches. This knowledge can then be used for identifying target molecules or cells for therapeutic purposes in reducing chronic pain.
We use in vitro and in vivo models of neuropathic pain to investigate the neuroimmune crosstalk in the injured nervous system. Animal models include peripheral nerve injury, chemotherapy-induced peripheral neuropathy, and an autoimmune disease of the central nervous system (experimental autoimmune encephalomyelitis, EAE; a model of multiple sclerosis). In vitro models include primary cultures of dorsal root ganglia sensory neurons, microglia and regulatory T cells.