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Stefanie N Vogel

Stefanie N Vogel Ph.D.

Academic Title: Professor
Primary Appointment: Microbiology and Immunology
Secondary Appointments: Medicine
Location: HH 310
Phone: (410) 706-4838 (office)
Phone: (410) 706-4716 (lab)
Fax: (410) 706-8607

Research Interests:

The innate immune system provides a first line of defense against microbial infection and prepares the host for the induction of an antigen-specific, adaptive immune response. Central to the ability of the phagocytic leukocytes of the immune system to recognize and respond to bacteria and viruses are evolutionarily conserved "pattern recognition receptors" that sense foreign pathogens and enable the phagocytic cell to engulf the microbes or to release inflammatory mediators that facilitate clearance of organisms. Dr. Vogel's research is focused on the capacity of macrophages to respond to bacterial products such as the endotoxic lipopolysaccharide (LPS) of Gram negative bacteria. Their studies on the role of Toll-like receptors (TLRs) in this process has led to the dissection of intracellular signaling pathways that define TLR responses to different pathogens, suggesting that these receptors have evolved to enable the host to respond appropriately to specific pathogens. Recently, their work led to the identification of a novel immunodeficiency mediated by a complex mutation within a key enzyme of the TLR signaling pathway in a patient that presented with severe, repeated bacterial infections. 

In addition to examining the expression of a variety of proinflammatory genes as a consequence of exposure of macrophages to LPS and other bacterial and viral products, the Vogel laboratory is also actively studying mechanisms by which the inflammatory response to infection is controlled. Specifically, they have utilized a paradigm of in vitro and in vivo "endotoxin tolerance" in which macrophages or mice exposed to a relatively low dose of LPS become transiently refractory to subsequent challenge to a variety of TLR agonists. An analysis of the effects of tolerance on kinase and DNA binding activities of signaling components involved in TLR signaling pathways have been examined systemmatically by her group, in addition to studies that demonstrate dysregulated interactions among intracellular proteins required for this activation. The Vogel laboratory combines a unique collection of molecular, genetic, and biochemical approaches to tackle these sorts of questions. Dr. Vogel has only been at UMB for just over two years, but has had 22 years of experience with graduate students at Uniformed Services University of the Health Sciences, Bethesda, MD, where she contributed to a training grant and successfully mentored 6 Ph.D. students and one M.S. student during her 22 year tenure there.


S. Divanovic, S. F. Atabani, R. Madan, A. Trompette, S. Recking, D. T. Golenbock, R. W. Finberg, A. Tarakhovsky, S. N. Vogel, Y. Belkaid, E. A. Kurt-Jones, and C. L. Karp. Negative regulation of TLR4 signaling by RP105. Nature Immunol. 6: 571-578 (2005).

A. Lentschat, H. Karahashi, K. S. Michelsen, L. Thomas, W. Zhang, S. N. Vogel, and M. Arditi. Mastoparan, a G protein agonist peptide, differentially modulates TLR4- and TLR2-mediated signaling in human endothelial cells and murine macrophages J. Immunol. 174: 4252-4261 (2005).

A. E. Medvedev, K. Thomas, A. Awomoyi, D. B. Kuhns, J. I. Gallin, X. Li, and S. N. Vogel. Expression of IL-1 Receptor-Associated Kinase-4 (IRAK-4) mutations identified in a patient with recurrent bacterial infections alters IRAK-4 interactions with signaling components of the IL-1 receptor complex. J. Immunol. 174:

J. Y. Richardson, M. G. Ottolini, L. Pletneva, M. Boukhvalova, S. Zhang, S. N. Vogel, G. A. Prince, and J. C. G. Blanco. Respiratory syncytial virus(RSV) infection induces cyclooxygenase 2 (COX-2) - a potential target

V. Toshchakov, S. Basu, M. J. Fenton, and S. N. Vogel. Differential involvement of BB-loops of TIR domain-containing adapter proteins in Toll-like receptor (TLR) 4- versus TLR2-mediated signal transduction.

S. N. Vogel, K. A. Fitzgerald, and M. J. Fenton. Differential adapter utilization by Toll-like receptors (TLRs) mediates TLR-specific patterns of gene expression. Molecular Interventions 3: 466-477 (2003).

A. E. Medvedev, A. Lentschat, D. B. Kuhns, J. C. G. Blanco, C. Salkoswski, S. Zhang, M. Arditi, J. I. Gallin, and S. N. Vogel. Distinct mutations in IRAK-4 confer hyporesponsiveness to lipopolysaccharide and Interleukin-1 in a patient with recurrent bacterial infections. J. Exp. Med. 198: 521-531 (2003).

Qureshi, N., P.-Y. Perera, G. Splitter, D. C. Morrison, and S. N. Vogel. The proteosome as a LPS-binding protein in macrophages: Toxic lipopolysaccharide activates the proteosome complex. J. Immunol. 171: 1515-1525 (2003).

Y. Chen, J. M. Hallenbeck, D. Bol, K. Thomas, and S. N. Vogel. Overexpression of MCP-1 in the brain exacerbates ischemic brain injury and is associated with recruitment of monocytic cells. J. Cerebral Blood Flow and Metabolism 23: 748-455 (2003).

M. Martin, R. E. Schifferle, N. Cuesta, S. N. Vogel, J. Katz, and S. M. Michalek. Role of the PI3 kinase-Akt pathway in the regulation of IL-10 and IL-12 by Porphyromonas gingivalis lipopolysaccharide. J. Immunol. 171:717-725 (2003).

X. Zhou, J. A. Gir¿¿A. G. Torres, J. A. Crawford, E. Negrete, S. N. Vogel, and J. B. Kaper. Flagellin of enteropathogenic Escherichia coli stimulates Interleukin-8 production in T84 cells. Infect. Immun. 71: 2120-2129 (2003).

N. Cuesta, C. A. Salkowski, K. E. Thomas, and S. N. Vogel. Regulation of LPS Sensitivity by Interferon Regulatory Factor-2. J. Immunol. 170: 5739-5747 (2003).

V. Toshchakov, B. W. Jones, A. Lentschat, A. Silva, P.-Y. Perera, K. Thomas, M. J. Cody, S. Zhang, B. W. G. Williams, J. Major, T. A. Hamilton, M. J. Fenton, and S. N. Vogel. TLR2 and TLR4 agonists stimulate unique repertoires of host resistance genes in murine macrophages: Interferon-¿-dependent signaling in TLR4-mediated responses. J. Endotoxin Res. 9: 169-175 (2003).

A. E. Medvedev and S. N. Vogel. Overexpression of CD14, TLR4, and MD-2 in HEK 293 cells does not prevent induction of in vitro endotoxin tolerance. J. Endotoxin Res. 9: 60-64 (2003).

M. Dobrovolskaia, A. E. Medvedev, K. E. Thomas, N. Cuesta, V. Toshchakov, T. Ren, M. J. Cody, S.M. Michalek, N. R. Rice, and S. N. Vogel. Induction of in vitro reprogramming by TLR2 and TLR4 agonists in murine macrophages: effects of TLR "homotolerance" versus "heterotolerance" on NF-¿B signaling pathway components. J. Immunol. 170: 508-519 (2003).

V. Toshchakov, B. W. Jones, P.-Y. Perera, K. Thomas, M. J. Cody, S. Zhang, B. W. G. Williams, J. Major, T. A. Hamilton, M. J. Fenton, and S.N. Vogel. Differential STAT1 phosphorylation secondary to IFN-¿ production mediates the distinct pattern of macrophage gene expression observed in response to TLR4 and TLR2 agonists. Nature Immunol 3: 392-398 (2002).