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Borna  Mehrad
Degree(s): MD
Graduate School: University of Nottingham, United Kingdom
Primary Appointment: Professor, Medicine, Pulmonary and Critical Care Medicine
Research Interests:
Pulmonary anti-microbial host defense
Email Address: mehrad@virginia.edu
Biomedical Sciences Graduate Program(s)
  • Biomedical Sciences Graduate Programs
    • Research Description

    Our lab is interested in the innate defenses of the lung against inhaled microorganisms. The gas exchange surface of the the lung represents a huge interface between the body and the environment, and it is constantly barraged by microorganisms that are inhaled or aspirated. We have evolved a complex and highly effective set of defenses that kill the vast majority of microorganisms quickly once they arrive on this surface. Our lab studies these innate immune mechanisms in the context of mouse models, in response to two commonly inhaled pathogens: the mould, Aspergillus fumigatus, and the Gram negative bacterium, Klebsiella pneumoniae.

    A. fumigatus is the most common cause of invasive aspergillosis, a severe infection in immunocompromised hosts. Allergic airwayresponses to the same organism can cause illness in immunocompetent individuals. Much of our work in invasive aspergillosis has focused  on the role of a lymphocytes subset, natural killer cells.  Specifically, we are examining the  mechanisms of influx, activation,  and anti-microbial effector  functions of NK cells in this infection.

    K. pneumoniae is a frequent cause of Gram negative bacterial pneumonia, a serious infection in hospitalized patients. In the context of this infection, we have found a genetic locus that confers a marked resistance to this infection in a mouse model of this infection. We are in the process of defining the mechanism of protection that this locus confers.

    Selected Publications
  • Park SJ, Burdick MD, Brix WK, Stoler MH, Askew DS, Strieter RM, Mehrad B. 2010. Neutropenia enhances lung dendritic cell recruitment in response to an opportunistic mold via a cytokine-to-chemokine positive feedback loop. J Immunol. 185;6190-7.
  • Strieter RM, Keeley EC, Hughes MA, Burdick MD, Mehrad B. 2009. The role of circulating mesenchymal progenitor cells (fibrocytes) in the pathogenesis of pulmonary fibrosis. J Leukoc Biol 86(5):1111-8.
  • Mehrad B, Burdick MD, Strieter RM. 2009. Fibrocyte CXCR4 regulation as a therapeutic target in pulmonary fibrosis. Int J Biochem Cell Biol 41(8-9):1708-18.
  • Park SJ, Hughes MA, Burdick MD, Strieter RM, Mehrad B. 2009. Early NK cell-derived interferon gamma is essential to host defense in neutropenic invasive aspergillosis. J Immunol 182(7):4306-12.
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