Polymorphonuclear neutrophils (PMNs) are the most abundant leukocyte subset in human blood and bone marrow. Since their discovery at the end of the 19th century, PMNs have been viewed as short-lived cells solely dedicated to the task of phagocytosis. Contradicting this view, two new PMN fates were uncovered recently. One is NETosis, a rapid death modality associated with the release of bacteriostatic neutrophil extracellular traps (NETs). Another PMN fate recently discovered by our group is adaptive reprogramming, which depends on the ability of human blood PMNs to undergo rapid conditioning within injured tissues, leading them to become anabolic and extend their survival to perform an array of new effector and regulatory functions. The Tirouvanziam lab at Emory focuses on three fundamental questions: 1. What are the immunological and metabolic checkpoints in human PMN fate? 2. What determines PMN fate in a diseased environment? 3. Can we intervene to selectively modulate PMN fate for therapeutic benefit in intractable human diseases such as cystic fibrosis, chronic obstructive pulmonary disease, and severe athma?