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Address: D154 MTF
Phone: (319) 335-4285
Mentor: Lee-Ann Allen, PhD
Undergraduate Institution: Minnesota State University, Mankato
Francisella tularensis is a Gram-negative, facultative intracellular organism and the etiologic agent of the disease tularemia. The pathogenicity of F. tularensis is dependent on its ability to modulate the host immune responses, and survive and replicate within host cells. F. tularensis infects many cell types, including polymorphonuclear leukocytes (PMN; neutrophils). Neutrophils are an important component of the innate immune system as they are the most abundant leukocyte in circulation and are the first to arrive at the site of infection. Neutrophils are short-lived cells as they undergo constitutive, spontaneous apoptosis. Some intracellular pathogens, including Neisseria gonorrhoeae and Chlamydia pneumoniae, inhibit neutrophil apoptosis to allow for intracellular survival and growth. Our lab recently demonstrated that F. tularensis prolongs human neutrophil lifespan by inhibiting the major apoptotic pathways. The factors that function in prolonging neutrophil lifespan remain undefined. In addition, direct contact between F. tularensis and neutrophils is not essential for the survival of infected neutrophils suggesting that a secreted bacterial factor may contribute to this effect. The primary goal of my research is to identify the factor(s) responsible for prolonging human neutrophil lifespan following infection with F. tularensis and further characterize the mechanism by which this prolongation occurs to gain insight into the mechanism(s) by which F. tularensis manipulates the host immune response in order to cause disease.
Bryant K.A., L.C. Kinkead, M.A. Larson, S.H. Hinrichs, and P.D. Fey. 2010. Genetic analysis of the Staphylococcus epidermidis macromolecular synthesis operon: Serp1129 is an ATP binding protein and sigA transcription is regulated by both sA- and sB- dependent promoters. BMC Microbiology 10(8).
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