Lyle L Moldawer, PhD

Dr. Moldawer is currently a professor in the department of surgery at the University of Florida College of Medicine. He is the former Robert H and Kathleen M Axline Endowed Research Professor in the UF College of Medicine. He is currently the Director of the Sepsis and Critical Illness Research Center, and emeritus director of the Laboratory of Inflammation Biology and Surgical Science. He has been on the UF College of Medicine faculty since 1993. Prior to that, he was on the faculty of the Weil College of Medicine at Cornell University where he joined the faculty in 1987, rising to the rank of Associate Professor of Surgery, and Cell Biology. He completed his Ph.D. degree from the Medical Faculty of Gotesborgs Universitet, Gotesborg, SWEDEN in 1986 (academic year 1987).

For the past 30 years, Dr. Moldawer has been conducting inflammation research, and exploring the inflammatory response to trauma, sepsis and burn injury. Funded continuously by the NIH (R01) since 1988, Dr. Moldawer is a past NIH MERIT Award recipient, and has been the past chairman of the Surgery, Anesthesiology and Trauma Study Section at CSR/NIH. Since 1986, Dr. Moldawer was one of the first to describe the “cytokine storm” and first report the plasma appearance of several inflammatory mediators in human disease, including IL-6, sTNFRI, sTNFRII, IL-1ra and sIL1RII. In 2011, as a member of the Glue Grant, he was one of the first to describe the human host response to severe trauma and burns as a “genomic storm”, demonstrating in the blood leukocyte that 70% of the leukocyte transcriptome changed in response to trauma. Over the past ten years, he has branched out examining the communication between innate and adaptive immunity in the septic and traumatized young adult and the aged.

Dr. Moldawer was one of the first to argue that dysregulated ‘emergency myelopoiesis’ contributes to the loss of protective immunity in these at-risk populations. In 2007, he was the first to demonstrate the expansion of an immature myeloid population, designated myeloid-derived suppressor cells (MDSC), in severe sepsis, and postulated that they contributed to post-sepsis, post-trauma immune suppression. He and Dr. Efron confirmed these findings in humans in 2016.

In 2012, Dr. Moldawer, in collaboration with Dr. Frederick Moore, described a new syndrome, entitled PICS (a persistent inflammatory/immune-suppressive catabolic state) in severe sepsis and trauma. The syndrome has become the predominant phenotype of severely traumatized sepsis and trauma patients who survive their initial event. Dr. Moldawer’s current research interest is focused on the underlying mechanisms that drive chronic critical illness in patients who have severe trauma or sepsis. Specifically, he is focused on the myelopoietic dyscrasia that results in a preferential myelopoiesis and the dramatic increase in “pathologically-activated myeloid cells”, myeloid-derived suppressor cells (MDSC).

In 2016, Dr. Moldawer and Dr. Frederick A. Moore established the University-recognized “Sepsis and Critical Illness Research Center” (SCIRC). SCIRC is focused on the mechanisms of chronic inflammation and immunosuppression that result from severe sepsis and trauma, especially in the aged. It is focused on ‘induced-frailty’ as a long-term outcome in patients with severe sepsis and trauma.

In July, 2019, Dr. Moldawer voluntarily resigned his endowed chair, his vice chair of the department of surgery, and his vice chair of the UF IACUC (as well as all other college of medicine responsibilities). He turned over the directorship of the Laboratory of Inflammation Biology and Surgical Science to Dr. Efron. His only University responsibility (0.9 FTE) is research and T32 training, and his primary focus is the mechanistic clinical studies in severe sepsis and trauma. He continues to oversee his T32 that he has had for 24 years (T32 GM008721, Molecular Biology and Gene Therapy in Burns and Trauma), the training of surgical residents in research. In addition, Dr. Moldawer serves on the executive committee and internal advisory committee for a new T32 (PARADIGM T32 HG008958-01A1) training program in genomics and genetics. The program is focused on providing clinical doctorates (M.D., Pharm.D.) with an intense two year training into the future of genetic and genomic analyses in the diagnosis and therapeutic interventions in hospitalized patients. To date, three surgical residents have enrolled in the program, and one has completed his tenure.

In 2021, Dr. Moldawer was awarded a new 5 year RM1 Program award focused on the pathological activation of myelopoiesis in severe trauma and sepsis (RM1 GM139690,Dysfunctional Myelopoiesis and Myeloid-Derived Suppressor Cells in Sepsis Pathobiology). The study is focused on understanding the immunological endotype that drives the clinical phenotype of ‘chronic critical illness’ in survivors of severe blunt trauma and sepsis. The overarching hypothesis is that dyscratic myelopoiesis and dysfunctional myeloid pathological activation drives this immunological endotype of persistent inflammation, immunosuppression and protein catabolism (PICS) similar to that seen in advanced cancers, autoimmune disease and chronic organ dysfunction, including chronic renal and obstructive pulmonary disease and congestive heart failure.

• Critical care monitoring
• Inflammation biology
• Innate immunity
• Neonatal Sepsis
• Sepsis
• Trauma and Shock

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