To unravel how pain is initiated, sustained, and resolved, we developed advanced in vitro models of neuro-immune interactions. We employ cell lines models, murine primary sensory neurons and human induced pluripotent stem cell (hiPSC)-derived neurons in mono- and co-culture systems with immune cells. We aim to study how inflammatory signals, chemotherapeutics, and metabolic stressors alter neuronal excitability, immune phenotype and mitochondrial functions. By combining functional readouts such as calcium imaging, multi-electrode array electrophysiology, and live-cell imaging, we try to dissect the cellular mechanisms that drive pain and its resolution.