Washington University in St. Louis (WU)
My research focuses on inflammasome signaling and how its dysregulation drives tissue damage in autoinflammatory and inflammatory bone diseases, particularly Neonatal-Onset Multisystem Inflammatory Disease (NOMID), the most severe form of Cryopyrin-Associated Periodic Syndromes (CAPS). In NOMID, gain-of-function mutations in NLRP3 cause constitutive inflammasome activation and pyroptosis, leading to progressive organ and skeletal damage. In parallel, I study Staphylococcus aureus osteomyelitis, where bacterial persistence in bone triggers chronic immune activation and disrupts bone remodeling. Using cellular and in vivo models, I define how inflammasome activation in osteoclast-lineage cells regulates inflammation, cell death, and pathological bone resorption. By linking inflammasome signaling to cytoskeletal dynamics and calcium flux, I aim to uncover mechanisms coupling immune activation to structural damage and translate these insights into therapies that preserve bone integrity and improve outcomes in CAPS and inflammatory bone disease.