Stacey D. Gilk, PhD
Assistant Professor of Microbiology & Immunology
Dr. Gilk received her B.S. in Biology from the University of Notre Dame in 1998 and a PhD from the University of Vermont in 2004, where she studied host cell invasion by the obligate intracellular parasite Toxoplasma gondii. Following a postdoctoral fellowship at the University of North Carolina, Chapel Hill on the role of lipids during Toxoplasma infection, Dr. Gilk did a postdoctoral fellowship at Rocky Mountain Labs, National Institutes of Health on the role of lipids during infection by Coxiella burnetii. Dr. Gilk joined IUSM in 2013 as an Assistant Professor. Her primary interest in how obligate intracellular pathogens subvert host cell lipids and lipid signaling during infection. Her lab currently focuses on discovering why Coxiella is exquisitely sensitive to cellular cholesterol levels.
Elevated Cholesterol in the Coxiella burnetii Intracellular Niche Is Bacteriolytic. mBio Mulye M; Samanta D; Winfree S; Heinzen RA; Gilk SD; 2017 Feb 28
Interactions between the Coxiella burnetii parasitophorous vacuole and the endoplasmic reticulum involve the host protein ORP1L. Cellular microbiology. Justis AV; Hansen B; Beare PA; King KB; Heinzen RA; Gilk SD; 2016 Jun 26
Bacterial colonization of host cells in the absence of cholesterol. PLoS pathogens. Gilk SD; Cockrell DC; Luterbach C; Hansen B; Knodler LA; Ibarra JA; Steele-Mortimer O; Heinzen RA; 2013 Jan 24
The Gilk Lab studies manipulation of host cell lipids and lipid signaling by the intracellular bacterial pathogen Coxiella burnetii.
Coxiella causes human Q fever, where acute disease generally presents as a debilitating flu-like illness, while chronic Q fever manifests as a life-threatening endocarditis. During infection, Coxiella targets macrophages and survives in a unique, lysosomal-like compartment termed the parasitophorous vacuole (PV). Formation of the PV is essential for bacterial survival, yet we know little about PV biogenesis and maintenance. We are especially interested in how cholesterol and other lipids contribute to PV formation and the unique properties of the PV membrane.
We use a combination of cell biology, biochemistry, and molecular biology to address the role of cholesterol in Coxiella-host cell interactions. Using a novel cholesterol-free tissue culture system, we discovered that Coxiella is in fact sensitive to increasing host cholesterol levels, and elevated cholesterol increases the PV pH and kills the bacteria. We hypothesize that Coxiella manipulates host cholesterol metabolism and trafficking to support intracellular growth. We are elucidating both bacterial and host factors involved in cholesterol homeostasis during Coxiella infection, with the goal of identifying new targets for therapeutic intervention.
Interactions between the Coxiella burnetii parasitophorous vacuole and the endoplasmic reticulum involve the host protein ORP1L.
Comparative genomics reveal extensive transposon-mediated genomic plasticity and diversity among potential effector proteins within the genus Coxiella.
Desc: 2016 Outstanding Postdoc Mentor
Desc: Elwert Award in Medicine