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NameEmailPhD ProgramResearch InterestPublications
Rosenthal, Adam
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Microbiology & Immunology

RESEARCH INTEREST
Bacteriology, Molecular Biology, Pathogenesis & Infection, Systems Biology

Our lab uses a systems biology approach to study phenotypic heterogeneity in bacteria. We develop tools that quantify single cell bacterial transcription. We then compare dynamic measurements during vegetative growth and infection to identify regulators of gene expression and mechanisms that bacteria use to coordinate community organization. With this data we want to understand the role of heterogeneity and noise in infectious disease.

Walls, Alex

EMAIL

PHD PROGRAM

RESEARCH INTEREST
Bacteriology, Molecular Biology, Pathogenesis & Infection

Puller, Gabby

EMAIL

PHD PROGRAM

RESEARCH INTEREST
Bacteriology, Biochemistry, Molecular Biology

Miller, Sarah

EMAIL

PHD PROGRAM

RESEARCH INTEREST
Bacteriology, Pathology, Toxicology

Thurlow, Lance

EMAIL
PUBLICATIONS

PHD PROGRAM
Microbiology & Immunology

RESEARCH INTEREST
Bacteriology, Cell Signaling, Immunology, Metabolism, Pathogenesis & Infection

By 2035, more than 500 million people worldwide will be diagnosed with diabetes. Individuals with diabetes are prone to frequent and invasive infections that commonly manifest as skin and soft tissue infections (SSTIs). Staphylococcus aureus is the most commonly isolated pathogen from diabetic SSTI. S. aureus is a problematic pathogen that is responsible for tens of thousands of invasive infections and deaths annually in the US. Most S. aureus infections manifest as skin and soft tissue infections (SSTIs) that are usually self-resolving. However, in patients with comorbidities, particularly diabetes, S. aureus SSTIs can disseminate resulting in systemic disease including osteomyelitis, endocarditis and sepsis. The goal of my research is to understand the complex interactions between bacterial pathogens and the host innate immune response with focus on S. aureus and invasive infections associated with diabetes. My research is roughly divided into two project areas in order to understand the contributions of the pathogen and the host response to invasive infections associated with diabetes. Project 1: Defining mechanisms of immune suppression in diabetic infections. Project 2: Determine the role of bacterial metabolism in virulence potential and pathogenesis.

Azcarate-Peril, M. Andrea
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Nutrition

RESEARCH INTEREST
Bacteriology, Bioinformatics, Genomics, Molecular Biology, Systems Biology

We are interested in determining the mechanisms involved in the beneficial modulation of the gut microbiota by prebiotics (functional foods that stimulate growth of gut native beneficial bacteria) and probiotics (live bacteria that benefit their host). Specifically, we aim to develop prebiotic and probiotic interventions as alternatives to traditional treatments for microbiota-health related conditions, and to advance microbiota-based health surveillance methods.

Goldman, William
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Microbiology & Immunology

RESEARCH INTEREST
Bacteriology, Biochemistry, Genetics, Immunology, Pathogenesis & Infection

Successful respiratory pathogens must be able to respond swiftly to a wide array of sophisticated defense mechanisms in the mammalian lung.  In histoplasmosis, macrophages — a first line of defense in the lower respiratory tract — are effectively parasitized by Histoplasma capsulatum.  We are studying this process by focusing on virulence factors produced as this “dimorphic” fungus undergoes a temperature-triggered conversion from a saprophytic mold form to a parasitic yeast form.  Yersinia pestis also displays two temperature-regulated lifestyles, depending on whether it is colonizing a flea or mammalian host.  Inhalation by humans leads to a rapid and overwhelming disease, and we are trying to understand the development of pneumonic plague by studying genes that are activated during the stages of pulmonary colonization.

Duncan, Alex
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Pharmacology

RESEARCH INTEREST
Bacteriology, Biochemistry, Cell Signaling, Immunology, Pathogenesis & Infection

My lab studies a recently identified pathogen-sensing signaling complex known as the inflammasome. The inflammasome is responsible for the proteolytic maturation of some cytokines and induces a novel necrotic cell death program. We have found that critical virulence factors from certain pathogens are able to activate NLRP3-mediated signaling, suggesting these pathogens may exploit this host signaling system in order to promote infections.  Our lab has active research projects in several areas relating to inflammasome signaling ranging from understanding basic molecular mechanisms of the pathway to studying the role of the system in animal models of infectious diseases.

de Silva, Aravinda
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Microbiology & Immunology

RESEARCH INTEREST
Bacteriology, Cell Biology, Immunology, Molecular Biology, Pathogenesis & Infection

We study Borrelia burgdorferi (the agent of Lyme disease) as a model for understanding arthropod vector-borne disease transmission. We also study the epidemiology and pathogenesis of dengue viruses associated with hemorrhagic disease.

Cotter, Peggy
WEBSITE
EMAIL
PUBLICATIONS

PHD PROGRAM
Microbiology & Immunology

RESEARCH INTEREST
Bacteriology, Biochemistry, Genetics, Molecular Biology, Pathogenesis & Infection

Dr. Cotter’s research is aimed at understanding molecular mechanisms of bacterial pathogenesis. Using Bordetella species as models, her group is studying the role of virulence gene regulation in respiratory pathogenesis, how virulence factors activate and suppress inflammation in the respiratory tract, and how proteins of the Two Partner Secretion pathway family are secreted to the bacterial surface and into the extracellular environment. A second major project is focused on Burkholderia pseudomallei, an emerging infectious disease and potential biothreat agent. This research is aimed at understanding the role of autotransporter proteins in the ability of this organism to cause disease via the respiratory route.