In the Rathmell lab I study immunometabolism in the context of anti-tumor immunotherapy. Specifically, I am investigating metabolic programs that may be targeted to enhance CD8+ T cell function in the tumor microenvironment.

During my thesis studies, I am looking forward to exploring the antagonistic link between two secreted Helicobacter pylori virulence factors, CagA and VacA, and the way that they are able to manipulate host cell functions, such as metabolism and mounting immune responses.

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The gastrointestinal tract is host to a dense microbial community, known as the gut microbiota, which is dominated by bacteria belonging to the phyla Bacteroidetes (class Bacteroidia) and Firmicutes (class Clostridia). Disruption of the delicate balance between the 'good' and 'bad' bacteria of the gut microbiota (dysbiosis) has been linked to various non-communicable diseases, including inflammatory bowel disease (IBD). My graduate research focuses on understanding how early life exposure to detrimental factors can affect the gut microbiota and increases predisposition for the development of intestinal disease later on in life.

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I am studying the metabolic interactions of pathogenic Enterobacteriaceae and the gut microbiota. I am especially interested in the production and utilization of short chain fatty acids (SCFAs) and amino acids.

In the Skaar lab, I'm interested in using advanced analytical technologies to answer questions related to the struggle for nutrient metals during bacterial infections.

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I am a graduate student in the Microbe-Host Interactions graduate program in the Pathology, Microbiology, and Immunology Department. My research focuses on innate host defense and inflammation during sepsis. My focus is on the tumor suppressor protein, phosphatase and tensin homolog (PTEN), which can modulate mitochondrial and cellular metabolism, as well as cellular effector functions via the PI3K/Akt/mTORC1 pathways in macrophages. We aim to unveil a new regulatory axis involving different processes (phosphatase activation, bacterial killing, inflammasome activation, along with fatty acid generation and oxidation) that regulate homeostatic events and, when alternated, leads to an exaggerated inflammatory response that culminates in organ damage and mortality