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Peter Larson, BS

Predoctoral Associate

Farmington, CT

Engineering the human skin microbiome to treat diseases and prevent infections.

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Contact me at: 207-288-6000

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Contact Peter Larson, BS

About Peter Larson, BS

I've brought my background in synthetic biology to the Oh Lab with the aspiration to leverage the human microbiome (the bacteria, fungi, viruses, and other microbes that live on us) to promote health, prevent infections, and treat diseases. Here I have been engineering Staphylococcus epidermidis, a ubiquitous skin commensal, to detect and kill pathogens, as well as secrete therapeutics. Additionally, I have been conducting a sizable clinical metagenome study investigating the relationship between aging, health, and the microbiome. This study should help us understand how we can leverage the microbiome to promote healthy aging, combat chronic illnesses, and prevent infections commonly acquired by older adults in healthcare settings. Finally, I have been exploring the use of human skin explants and stem cell derived skin “organoids” to model human skin microbiome interactions. This will allow us and others to test engineered skin microbiome therapeutics, and better identify mechanisms by which the skin microbiome modulates health and disease.

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Education and experience

Education

UConn Health
MD/PhD Candidate
Adv: Julia Oh
2015-Present

University of Connecticut College of Agriculture, Health, and Natural Resources
B.S. Pathobiology
Adv: Paulo Verardi
2011-2015

University of Connecticut College of Liberal Arts and Sciences
B.S. Molecular and Cell Biology
2011-2015

Experience

Oh Lab, The Jackson Laboratory for Genomic Medicine
Graduate Assistant
2015-Present

Verardi Lab, University of Connecticut
Undergraduate Researcher
2011-2015

St. Vincent's Hospital, Bridgeport, CT
Research Associate
2012

Harbor River Watch, Earthplace, Wilton, CT
Intern
2009-2011

Selected Publications

Highlighted Abstract

Vancomycin-resistant Enterococcus (VRE) are highly antibiotic-resistant and readily transmissible pathogens that cause severe infections in hospitalized patients. We discovered that lithocholic acid (LCA), a secondary bile acid prevalent in the cecum and colon of mice and humans, impairs separation of growing VRE diplococci, causing the formation of long chains and increased biofilm formation. Divalent cations reversed this LCA-induced switch to chaining and biofilm formation. Experimental evolution in the presence of LCA yielded mutations in the essential two-component kinase yycG/walK and three-component response regulator liaR that locked VRE in diplococcal mode, impaired biofilm formation, and increased susceptibility to the antibiotic daptomycin. These mutant VRE strains were deficient in host colonization because of their inability to compete with intestinal microbiota. This morphotype switch presents a potential non-bactericidal therapeutic target that may help clear VRE from the intestines of dominated patients, as occurs frequently during hematopoietic stem cell transplantation.

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