Lyle Moldawer, Ph.D.


PO Box 100019
Gainesville, FL 32610-0001


1986 Ph.D. (Dr. Med. Sci.), University of Gothenberg, Gothenburg, Sweden, in Experimental Medicine

Academic Appointments

  • 2014- Robert H. and Kathleen M. Axline Basic Science Research Professor of Surgery
  • 2014- Adjunct Professor, Department of Pathology, Immunology and Laboratory Medicine
  • 2014-2016- University of Florida Research Foundation Professor
  • 2004- present Vice Chairman of Research, University of Florida, College of Medicine, Gainesville, Florida
  • 1996 – present Professor of Surgery, University of Florida College of Medicine, Gainesville, Florida
  • 1994 – 1996 Associate Professor of Surgery (with tenure)University of Florida College of Medicine,Gainesville, Florida
  • 1993 – 1996 Associate Professor of Surgery, University of Florida College of Medicine, Gainesville, Florida
  • 1991 – 1993 Associate Professor of Cell Biology and Anatomy,Cornell University Medical College, New York, New York
  • 1991 – 1993 Associate Professor of Surgery, Cornell University Medical College, New York, New York
  • 1988 – 1991 Assistant Professor of Cell Biology and Anatomy, Cornell University Medical College, New York, New York
  • 1987 – 1991 Assistant Professor of Surgery, Cornell University Medical College, New York, New York
  • 1985 – 1987 Visiting Scientist, Department of Surgery I, Sahlgrenska sjukhuset,S-41345 Goteborg, Sweden

Contributions to Science

1. First to Describe the Inflammatory Cytokine Response to Severe Sepsis, Burns and Endotoxicosis. While working in the laboratories of Dr. Stephen Lowry and Anthony Cerami at Cornell Medical College and Rockefeller University between 1987-1994, Dr. Moldawer and his collaborators made significant contributions to our understanding of the ‘cytokine storm’. Dr. Moldawer and the laboratory were the first to describe the plasma appearance of IL-6, soluble TNF receptors, sIL-1RII, and IL-1ra, and were the first to show that soluble TNF receptors and IL-1ra could be used to block excessive TNF and IL-1 production during sepsis.

  • Fong, Y., Moldawer , L.L., Marano, M., Wei, H., Tatter, S.B., Clarick, R.H., Santhanam, U., May, L.T., Sehgal, P.B., Lowry, S.F. Endotoxemia elicits increased circulating beta2-IFN/IL-6 in man. J Immun 142:2321-2324, 1989. (cited 340 times).
  • Van Zee, K.J., Kohno, T., Fischer, E., Rock, C.S., Moldawer , L.L., Lowry, S.F. TNF soluble receptors circulate during experimental and clinical inflammation and can protect against excessive TNF alpha in vitro and in vivo. Proc Natl Acad of Sci U S A 89:4845-4849, 1992. (cited 710 times)
  • Pruitt, J.H., Welborn, M.B., Edwards, P.D., Harward, T.R.S., Seeger, J.W., Martin, T.D., Smith, C.S., Kenney, J.A., Wesdorp, R.I.C., Meijer, S., Cuesta,M.A., Abouhanze, A., Copeland, E.M., Giri, J., Sims, J.E., Moldawer , L.L., Oldenburg, H.S.A. Increased soluble interleukin-1 type II receptor concentrations in post-operative patients and in patients with sepsis syndrome. Blood 87:3282-3288, 1996.
  • Fischer, E., Poutsiaka, D.D., Van Zee, K.J., Marano, M.A., Rock, C.S., Kenney, J.S., Dinarello, C.A., Lowry, S.F., Moldawer , L.L. Interleukin-1 receptor antagonist circulates in experimental inflammation and in human disease. Blood 79:2196-2200, 1992.
  • Fischer, E., Marano, M.A., Van Zee, K.J., Rock, C.S., Hawes, A.S., Thompson, W.A., DeForge, L., Kenney, J.S., Remick, D.G., Bloedow, D.C., Thompson, R.C., Lowry, S.F., Moldawer , L.L. Interleukin-1 receptor blockade improves survival and hemodynamic performance in Escherichia coli septic shock, but fails to alter host responses to sublethal endotoxemia. J Clin Invest 89:1551-1557, 1992. (cited 275 times).

2.  First to Describe the Role That Proinflammatory Cytokines Like IL-1, TNF and IL-6 Produced During Inflammation can Contribute to Cachexia. Dr. Moldawer’s Ph.D. thesis conducted with Kent Lundholm in Göteborg, Sweden, focused on the role of inflammatory cytokines in cancer cachexia. Since leaving Sweden and moving to New York and then Gainesville, Dr. Moldawer continued to pursue the investigation of how cytokines regulate skeletal muscle protein balance. Dr. Moldawer was the first to show that in acute models of inflammation, IL-1 and not TNF was responsible for the loss of skeletal muscle protein (Gershenwald, PNAS). Subsequent studies revealed that it was the IL-1-induced production of IL-6 that was responsible for both the skeletal muscle wasting and the hepatic acute phase protein response.

  • Gershenwald, J.E., Fong, Y., Fahey, T.J. III, Calvano, S.E., Chizzonite, R., Kilian, P.L., Lowry, S.F., Moldawer , L.L. Interleukin-1 receptor blockade attenuates the host inflammatory response. Proc Natl Acad Sci U S A 87:4966-4970, 1990. (cited 239 times).
  • Oldenburg, H.S.A., Van Zee, K.J., Lazarus, D.D., Rogy, M.A., Keeler, B.P., Thompson, W.A., Chizzonite, R.A., Lowry, S.F., Moldawer , L.L. Cachexia and the acute-phase protein response in inflammation are regulated by interleukin-6. Eur J Immunol 23:1889-1894, 1993.
  • Oldenburg, H.S.A., Pruitt, J.H., Lazarus, D.D., Rogy, M.A., Chizzonite, R., Lowry, S.F., Moldawer , L.L. Interleukin 1 binding to its type I, but not type II receptor, modulates the in vivo acute phase response. Cytokine 7; 6: 510-516, 1995.
  • Labow, M., Shuster, D., Zetterstrom, M., Nunes, P., Terry R., Cullinan, E.B., Bartfai, T., Solorzano, C., Moldawer, L.L., Chizzonite, R., McIntyre, K.W. Absence of IL-1 signaling and reduced inflammatory response in IL-1 type I receptor-deficient mice. J Immunol, 159(5):2452-2461, 1997. (cited 225 times)

3. First to Describe the ‘Genomic Storm’ in Human Total and Enriched Leukocyte Populations After Trauma, Burns and Leukocytosis. In 2001, Dr. Moldawer joined the Inflammation and Host Response to Injury Consortium (Glue Grant) as a Steering Committee member and Core Director. The goal of the Program was to describe in its entirety the genome-wide response to trauma, burns and endotoxicosis, and to relate those changes to clinical outcomes. The concept then and now is that by understanding how the leukocyte (PMN, monocyte and lymphocyte) genomic response differs in patients who survive or expire from their trauma or burn could not only lead to novel diagnostics but also novel therapeutic approaches.

  • Calvano, S.E., Xiao, W., Richards, D.R., Felciano, R.M., Baker, H.V., Cho, R.J., Chen, R.O., Brownstein, B.H., Cobb, J.P., Tschoeke, S.K., Miller-Graziano, C., Moldawer, L.L., Mindrinos, M.N., Davis, R.W., Tompkins, R.G., Lowry, S.F., Bankey, P.E., Billiar, T.R., Camp, D.G., Casella, G., Chaudry, I.H., Choudhry, M.A., Cooper, C., De, A., Elson, C., Freeman, B., Gamelli, R.L., Campbell-Finnerty, C., Gibran, N.S., Hayden, D.L., Harbrecht, B.G., Herndon, D.N., Horton, J.W., Hubbard, W.J., Hunt, J.L., Johnson, J., Klein, M.B., Lederer, J.A., Logvinenko, T., Maier, R.V., Mannick, J.A., Mason, P.H., McKinley, B.A., Minei, J.P., Moore, E.E., Moore, F.A., O’keefe, G.E., Rahme, L.G., Remick, D.G., Schoenfeld, D.A., Schwacha, M.G., Shapiro, M.B., Silver, G.M., Smith, R.D., Storey, J.D., Toner, M., Warren, H.S., West, M.A. Nature. 2005 Dec 1;438(7068):696 (cited 785 times).

  • Laudanski, K., Miller-Graziano, C., Xiao, W., Mindrinos, M.N., Richards, D.R., De, A., Moldawer, L.L., Maier, R.V., Bankey, P., Baker, H.V., Brownstein, B.H., Cobb, J.P., Calvano, S.E., Davis, R.W., Tompkins, R.G. Cell-specific expression and pathway analyses reveal alterations in trauma-related human T cell and monocyte pathways. Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15564-9.

  • Seok J., Warren H.S., Cuenca A.G., Mindrinos M.N., Baker H.V., Xu W., Richards D.R., McDonald-Smith G.P., Gao H., Hennessy L., Finnerty C.C., Lopez C.M., Honari S., Moore E.E., Minei J.P., Cuschieri J., Bankey P.E., Johnson J.L., Sperry J., Nathens A.B., Billiar T.R., West M.A., Jeschke M.G., Klein M.B., Gamelli R.L., Gibran N.S., Brownstein B.H., Miller-Graziano C., Calvano S.E., Mason P.H., Cobb J.P., Rahme L.G., Lowry S.F., Maier R.V., Moldawer L.L., Herndon D.N., Davis R.W., Xiao W., Tompkins R.G.; Inflammation and Host Response to Injury, Large Scale Collaborative Research Program. Genomic responses in mouse models poorly mimic human inflammatory diseases. Proc Natl Acad Sci U S A. 2013 Feb 26;110(9):3507-12. (cited 523 times)

  • Gentile L.F., Nacionales D.C., Lopez M.C., Vanzant E., Cuenca A., Cuenca A.G., Ungaro R., Baslanti T.O., McKinley B.A., Bihorac A., Cuschieri J., Maier R.V., Moore F.A., Leeuwenburgh C., Baker H.V., Moldawer L.L., Efron P.A. A Better Understanding of Why Murine Models of Trauma Do Not Recapitulate the Human Syndrome. Crit Care Med. 2014; 42(6):1406-13.

  • Cuenca A.G., Gentile L.F., Lopez M.C., Ungaro R., Liu H., Xiao W., Seok J., Mindrinos M.N., Ang D., Baslanti T.O., Bihorac A., Efron P.A., Cuschieri J., Warren H.S., Tompkins R.G., Maier R.V., Baker H.V., Moldawer L.L.; Inflammation and Host Response to Injury Collaborative Research Program. Development of a genomic metric that can be rapidly used to predict clinical outcome in severely injured trauma patients. Crit Care Med. 2013 May;41(5):1175-85. 

4. First to Describe the Expansion of MDSCs after Sepsis and their Contribution to the Development of a Persistent inflammatory/Immunosuppressive and Catabolic Syndrome (PICS). In 2012, Drs. Moldawer and Frederick A. Moore first proposed that with earlier diagnoses and more standardized supportive therapy, severe sepsis was no longer ending in MOF and early hospital death, but a new phenotype of post-sepsis patients is presenting with prolonged hospitalizations and chronic critical illness. We have more recently proposed that this chronic critical illness and PICS is secondary to the expansion of myeloid derived suppressor cells, a novel population of immature myeloid cells that we first described in 2007 which is responsible for both the chronic inflammation and immunosuppression.

  • Delano, M.J., Scumpia, P.O., Weinstein, J.S., Coco, D., Nagaraj, S., Kelly-Scumpia, K.M., O’malley, K.A., Wynn, J.L., Antonenko, S., Al-Quran, S.Z., Swan, R., Chung, C.S., Atkinson, M.A., Ramphal, R., Gabrilovich, D.I., Reeves, W.H., Ayala, A., Phillips, J., Laface, D., Heyworth, P.G., Clare-Salzler, M., Moldawer, L.L. MyD88-dependent expansion of an immature GR-1+CD11b+ population induces T cell suppression and Th2 polarization in sepsis. J Exp Med. 2007 Jun 11;204(6):1463-74. (cited 244 times)
  • Cuenca, A.G., Delano, M.J., Kelly-Scumpia, K.M., Moreno, C., Scumpia, P.O., Laface, D.M., Heyworth, P.G., Efron, P.A., Moldawer, L.L. A paradoxical role for myeloid-derived suppressor cells in sepsis and trauma. Mol Med. 2011 Mar-Apr;17 (3-4):281-92.
  • Gentile L.F., Cuenca A.G., Efron P.A., Ang D., Bihorac A., McKinley B.A., Moldawer L.L., Moore F.A. Persistent inflammation and immunosuppression: a common syndrome and new horizon for surgical intensive care. J Trauma Acute Care Surg. 2012 Jun;72(6):1491-501.
  • Vanzant E.L., Lopez C.M., Ozrazgat-Baslanti T., Ungaro R., Davis R., Cuenca A.G., Gentile L.F., Nacionales D.C., Cuenca A.L., Bihorac A., Leeuwenburgh C., Lanz J., Baker H.V., McKinley B., Moldawer L.L., Moore F.A., Efron P.A. Persistent inflammation, immunosuppression, and catabolism syndrome after severe blunt trauma. J Trauma Acute Care Surg. 2014 Jan;76(1):21-30.
  • HotchkissS., Moldawer L.L. Parallels between cancer and infectious disease. N Engl J Med. 2014 Jul 24;371(4):380-3.

5. Development of Novel Strategies to Prevent Sepsis in the Neonate.  We have documented as has others that the two highest cohorts of patients at risk of developing sepsis, and have the highest mortality rates are the very old and the very young. Premature infants are at elevated risk of developing both early and late sepsis, as well as necrotizing enterocolitis.

  • Wynn, J.L., Scumpia, P.O., Winfield, R.D., Delano, M.J., Kelly-Scumpia, K., Barker, T., Ungaro, R., Levy, O., Moldawer, L.L. Defective innate immunity predisposes murine neonates to poor sepsis outcome but is reversed by TLR agonists. Blood. 2008 Sep 1;112(5):1750-8.
  • Cuenca, A.G., Wynn, J.L., Kelly-Scumpia, K.M., Scumpia, P.O., Vila, L., Delano, M.J., Mathews, C.E, Wallet, S.M., Reeves, W.H., Behrns, K.E., Nacionales, D.C., Efron, P.A., Kunkel, S.L., Moldawer, L.L. Critical role for CXC ligand 10/CXC receptor 3 signaling in the murine neonatal response to sepsis. Infect Immun. 2011 Jul;79(7):2746-54.
  • GentileF., Nacionales D.C., Lopez M.C., Vanzant E., Cuenca A., Cuenca A.G., Ungaro R., Szpila B.E., Larson S., Joseph A., Moore F.A., Leeuwenburgh C., Baker H.V., Moldawer L.L., Efron P.A.. Protective immunity and defects in the neonatal and elderly immune response to sepsis. J Immunol 2014 Apr 1;192(7):3156-65.
  • Cuenca A.G., Joiner D.N., Gentile L.F., Cuenca A.L., Wynn J.L., Kelly-Scumpia K.M., Scumpia P.O., Behrns K.E., Efron P.A., Nacionales D., Lui C., Wallet S.M., Reeves W.H., Mathews C.E., Moldawer L.L. TRIF-dependent innate immune activation is critical for survival to neonatal gram-negative sepsis. J Immunol 2015 Feb 1;194(3):1169-77.
  • Gentile L.F., Cuenca A.L., Cuenca A.G., Nacionales D.C., Ungaro R., Efron P.A., Moldawer L.L., Larson S.D. Improved Emergency Myelopoiesis and Survival in Neonatal Sepsis by Caspase-1/11 Ablation. Immunol 2015 Feb 12. [Epub ahead of print]
  • WynnJ.L., Wilson C.S., Hawiger J., Scumpia P.O., Marshall A.F., Liu J.H., Zharkikh I., Wong H.R., Lahni P., Benjamin J.T., Plosa E.J., Weitkamp J.H., Sherwood E.R,. Moldawer L.L., Ungaro R., Baker H.V., Lopez M.C., McElroy S.J., Colliou N., Mohamadzadeh M., Moore D.J..Targeting IL-17A attenuates neonatal sepsis mortality induced by IL-18. Proc Natl Acad Sci U S A. 2016 May 10;113(19):E2627-35. Epub 2016 Apr 25. 

View a complete list of Dr. Moldawer’s published work in MyBibliography (409 pubs., h-factor = 89 Google Scholar, cited 27,547 times).   


Dr. Moldawer has received independent funding from the National Institutes of Health (NIH) continuously since 1988. In 1998, Dr. Moldawer received the prestigious Merit Award from the National Institute of General Medical Sciences, extending his current NIH support through the year 2006. Dr. Moldawer is the principal investigator on a training grant from the NIH to prepare surgical residents in training with a two year research experience in molecular biology and gene therapy. Dr. Moldawer is one of only a small number of Ph.D.’s in the country who holds the academic rank of Full Professor in a Department of Surgery. Since 1988, Dr. Moldawer has trained 28 surgical residents in research methodologies (19 at the University of Florida). Sixteen of these surgical residents have continued in academic training programs, and eight are currently on the faculty of colleges of medicine.

He is currently one of the principal investigators for an NIH-funded P50 center grant for the UF Sepsis and Critical Illness Research Center to study the persistent inflammation, immunosuppression and catabolism syndrome (PICS) following sepsis in surgical intensive care unit patients.

General information

Dr. Moldawer serves on numerous federal government public advisory groups, including:

  • Ad Hoc Member, several Special Emphasis Panels CSR, NIAID, NIGMS, NIDDK and NHLBI 2009-2016
  • Ad Hoc Member, Integrative Clinical Endocrinology and Reproductive Sciences Study Section, 2010, 2011
  • Ad Hoc Member, NIGMS Program Project and Center Grant Special Emphasis Panel, 2010, 2016
  • Regular Member, Surgery Anesthesiology and Trauma Study Section, 2004-2009, Chairperson, 2007-2009
  • Ad Hoc Member, Surgery B Study Section, Veterans Affairs Scientific Review Group, 2004-2005
  • Regular Member, Metabolic Pathology Study Section, DRG, 1995-1999