Professor Elizabeth M. Nolan is the recipient of the 2016 Eli Lily Award in Biological Chemistry in recognition of her contributions to metal homeostasis and human innate immunity. Her research program is motivated by the global public health problems of infectious disease and antibiotic resistance, and affords paradigms for the discovery and elucidation of new bioinorganic chemistry, advancing fundamental understanding of human innate immunity and microbial pathogenesis, and providing new molecules with potential therapeutic application. Her recent initiatives focus on deciphering the biochemical and biophysical properties of biomolecules employed by the human host and colonizing microbe at mucosal surfaces and sites of infection. Metal ions are essential nutrients for all organisms, and one strategy the human innate immune system employs to prevent microbial colonization involves the deployment of metal-chelating proteins that sequester nutrient metals (e.g. manganese, iron, zinc) from invading microbes in the extracellular space. Her laboratory has illuminated the bioinorganic chemistry of human calprotectin, an abundant neutrophil protein that sequesters first-row transition metals at sites of infection. Her group recently discovered that human calprotectin sequesters ferrous iron at an unusual hexahistidine site, which expands the biological coordination chemistry of non-heme iron. Her laboratory also pursues biochemical and biophysical studies of two cysteine-rich defensin peptides, human α-defensin 5 and 6, that are abundant in the human small intestine and contribute to intestinal homeostasis. Towards the discovery and development of new strategies to treat infectious disease, her group studies the chemistry and biology of siderophores, small-molecule iron chelators that are biosynthesized by bacteria seeking to replicate in iron-limited environments. Her research focuses on employing native siderophore scaffolds in targeted antibiotic delivery, and on identifying new strategies to block siderophore-mediated iron acquisition by bacterial pathogens.