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The artists
Skylar Cuevas
In January of 2020, I began working with Dr. Oliver in the ArtLab program pursing my interest in the intersection of art and science. I decided to become apart of the AiR Program in order to broaden my experience and work with a lab to create artworks for their research.
Paired to work with Dr. Byndloss and her lab, I was challenged with creating pieces representing the lab's research on non-communicable diseases. A highlight of the lab's research focuses on inflammation-induced gut dysbiosis due to microbial imbalance. These two cover pieces were created to depict Dr. Byndloss's two abstracts on S. Typhimurium expansion and the license of Escherichia coli choline catabolism as a result of a high fat diet.
The purpose of these pieces is to produce a simple visual for those to reference when interpreting Dr. Byndloss's abstracts. With that in mind, the pieces are less abstract in an artistic sense and more straightforward in regard to labeling chemical structures and visualizing their location in the mechanism (represented metaphorically in the piece on S. Typhimurium) and body.
The Mariana Byndloss Lab
In high-income countries, the leading causes of death are non-communicable diseases, such as Inflammatory Bowel Disease (IBD), cancer and cardiovascular disease. An important feature of most non-communicable diseases is inflammation-induced gut dysbiosis characterized by a shift in the microbial community structure from obligate to facultative anaerobes such as Proteobacteria. This microbial imbalance can contribute to disease pathogenesis due to either a microbiota-derived metabolite being depleted or produced at a harmful concentration. However, little is known about the mechanism by which inflammation mediates changes in the host physiology to induce disruption of the microbial ecosystem in our large intestine leading to disease.
Our group uses a multidisciplinary approach combining microbiology, molecular biology, cell biology, immunology and pathology to try to understand how inflammation-dependent changes in gut epithelial metabolism can result in gut dysbiosis and increased risk to non- communicable disease. Specifically, we used a variety of mouse models, including diet-induced-obesity, chemical-induced colitis, infectious gastroenteritis (Salmonella enterica serovar Typhiumurium), and germ-free animals with the goal to identify metabolic pathways in the gut bacteria and in the host response to microbiota-induced metabolites that will aid in prevention of human disease.
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