My research is in the area of pulmonary molecular and cell biology as it relates to acute lung injury (ALI) and the mechanisms of sepsis. As an internationally recognized investigator in the area of lipid metabolism and ubiquitin-mediated proteolysis, I focus on mechanisms of inflammatory lung injury. My laboratory discovered a new model of innate immunity that led to the synthesis of a first-in-class genus of ubiquitin E3 ligase (F box) inhibitors that modulate proteolysis thereby inhibiting inflammation in preclinical models of ALI and multi-organ failure. This work moved through the FDA milestone pipeline with an IND for first-in-human studies with eventual therapeutic application for subjects with respiratory illness. A second, more untapped area of interest is based on the laboratory’s discovery that the mitochondrial-specific lipid, cardiolipin, is a unique cellular damage signal and important mediator of pneumonia. Our lab uncovered a new paradigm for pneumonia. Pneumonia patients had increased levels of a toxin, cardiolipin, which reproduces this disorder when given to mice. From clues in a rare disease, we uncovered that a pump normally removes cardiolipin from lung fluid but is degraded in pneumonia. This work is ongoing and could lead to non-antibiotic therapies in this illness.