Medical Professor and Chair
Dr. Sanna M. Goyert is Professor and Chair of the Department of Pathobiology at the Sophie Davis School of Biomedical Education. Previously she was an Associate Professor of Medicine and Pathology at New York University School of Medicine and Director of the Laboratory of Innate Immunity at the Feinstein Institute for Medical Research at North Shore-LIJ Health Systems in Manhasset, New York.
She is an internationally renowned scientist studying innate immune mechanisms of defense against bacterial pathogens. Dr. Goyert has published more than 100 research papers and book chapters and is a former recipient of the prestigious Stohlman Scholars award from the Leukemia Society of America. She has been continuously funded by the National Institutes of Health (NIH) for the past 24 years. Her most notable accomplishment is the identification of a human gene known as CD14 that plays a prominent role in a disease called septic shock that kills more than 500,000 Americans annually. Dr. Goyert's seminal work showed that mice genetically engineered to lack the CD14 gene are resistant to septic shock caused by E. coli. Dr. Goyert holds two major patents associated with her work on innate immunity that are currently licensed to several companies aiming to further the therapeutic potential of these discoveries. Dr. Goyert's current work focuses on the host's response to pathogens and includes studies aimed at the identification of additional genes and molecules that regulate the innate immune response by bacteria expressing specific virulence factors.
Ph.D., 1983, New York University
B.S., 1968, University of Cincinnati
Dr. Goyert studies innate immunity and the host's defense against bacterial pathogens. She has identified a protein expressed on the surface of monocytes/macrophages (CD14) that serves as a receptor for a toxin (lipopolysaccharide, LPS) in Gram-negative bacteria and is currently developing animal models to study the importance of this receptor in regulating the host's response to severe infection with live bacteria. Surprisingly, the absence of CD14 is protective in severe infection.
Her current goal is to identify the protective mechanisms that operate in the absence of CD14 and to develop reagents that can amplify such pathways to override the deleterious responses that occur in the presence of CD14. For these studies, Dr. Goyert's lab uses a variety of techniques that include real-time PCR, flow cytometry, analysis of chemokines/cytokines by ELISA, microscopy, immunohistochemistry, and in vivo animal models of infection.
Additional studies in Dr. Goyert's lab include comparison of primate (human, chimpanzee, baboon) responses to bacteria/bacterial products. Most recently, her lab has identified a new pathway for chemokine induction that leads to early neutrophil recruitment, bacterial killing and clearance in severe infection in the absence of CD14. Such efficient bacterial killing and clearance alleviates bacterial dissemination and its deleterious consequences and allows survival of the host. Dr. Goyert believes that identifying components of this pathway will allow identification of agents that can specifically activate this CD14-independent pathway in normal animals and promote
Brinkworth, JF, EA Pechenkina, J Silver, and SM Goyert. 2012. Innate immune responses to TLR2 and TLR4 agonists differ between baboons, chimpanzees and humans. Journal of Medical Primatology 41: 388-393.
Metkar, S, KS Kim, J Silver, and SM Goyert. 2012. Differential expression of CD14-dependent and independent pathways for chemokine induction regulates neutrophil trafficking in infection. J. Leukocyte Biology 92: 389-396.
Metkar, S., S. Awasthi, E. Denamur, K. S. Kim, S. C. Gangloff, S. Teichberg, A. Haziot, J. Silver, and S. M. Goyert. 2007. Role of CD14 in responses to clinical isolates of Escherichia coli: effects of K1 capsule expression. Infect Immun. 75:5415-5424.
Haziot, A., N. Hijiya, S. C. Gangloff, J. Silver, and S. M. Goyert. 2001. Induction of a novel mechanism of accelerated bacterial clearance by lipopolysaccharide in CD14-deficient and Toll-like receptor 4-deficient mice. J Immunol 166:1075-1078.
Haziot, A., E. Ferrero, F. Kontgen, N. Hijiya, S. Yamamoto, J. Silver, C. L. Stewart, and S. M. Goyert. 1996. Resistance to endotoxin shock and reduced dissemination of gram-negative bacteria in CD14-deficient mice. Immunity 4:407-414.
Ferrero, E., D. Jiao, B. Z. Tsuberi, L. Tesio, G. W. Rong, A. Haziot, and S. M. Goyert. 1993. Transgenic mice expressing human CD14 are hypersensitive to lipopolysaccharide. Proc Natl Acad Sci U S A 90:2380-2384.
Ferrero, E., C. L. Hsieh, U. Francke, and S. M. Goyert. 1990. CD14 is a member of the family of leucine-rich proteins and is encoded by a gene syntenic with multiple receptor genes. J Immunol 145:331-336.
Goyert, S. M., E. Ferrero, W. J. Rettig, A. K. Yenamandra, F. Obata, and M. M. Le Beau. 1988. The CD14 monocyte differentiation antigen maps to a region encoding growth factors and receptors. Science 239:497-500.
Ferrero, E., and S. M. Goyert. 1988. Nucleotide sequence of the gene encoding the monocyte differentiation antigen, CD14. Nucleic Acids Res 16:4173.