"I applied to the USP scholars program because it was an opportunity to become more involved with research and provided a means of funding my own project. This year, I hope to learn how to become a research scientist, knowing not only how to do the techniques, but also understanding why certain procedures are done and when each is necessary. My goal this year is to become proficient and self sufficient in the laboratory and to gain a strong respect for research and all it encompasses."
My primary academic interest is medicine: I am currently applying to medical schools for the coming year. My research interests are in immunology.
Academic and Other Awards
- University Scholars Program Scholarship (2011-2012)
- Anderson Scholar (2010)
- Dean's List (2008-2010)
- President's Honor Roll (2009-2010)
- Phi Kappa Phi (2010
- Intramural Sports
- National Equestrian
I have volunteered at the Emergency Department and the Radiology Department in Shands, at a summer horse camp for kids as a camp counselor, at a therapeutic riding center (Horses Helping People), at an after school program through Afterschool Gators,and at local elementary schools teaching students science experiments (Chemistry Outreach Program).
Hobbies and Interests
- Riding and showing Arabian horses, hanging out with friends, soccer, basketball, and flag football.
TLR Signaling in the Innate Immune Response to Neonatal Sepsis
Toll like receptors (TLRs) play a role in the innate immune response to infection and inflammation. TLRs recognize bacterial and viral products and utilize the signaling adaptor proteins known as myeloid differentiation factor 88 (MyD88) and toll-interleukin 1 receptor domain (TIR)-containing adaptor molecule-1 (TRIF-1) for downstream signaling. These pathways result in the production of various chemokines and cytokines responsible for innate immune effector cell function, and directing the adaptive immune response. Chemokines are intermediates in innate immune signaling. The chemokine interferonγ-inducible protein 10 (CXCL10) is an early diagnostic marker for bacterial infection in preterm infants. Previous research has demonstrated that CXCL10 is critical for the recruitment of neutrophils in adult bacterial peritonitis and that lipopolysaccharide (LPS) pretreatment of neonatal mice improves outcome during experimentally-induced sepsis by increasing neutrophil recruitment and reactive oxygen species production. However, the role of CXCL10 during TLR agonist adjuvant protection and recruitment of innate immunity during neonatal sepsis is unknown. Our hypothesis is that the neonate has greater risk to sepsis-induced mortality because of increased dependence on their innate immune system, which differs from young adults. We believe that these differences in their response to sepsis are due in part to differences in TLR adaptor signaling in the early innate immune response. We propose that TRIF signaling leading to downstream CXCL10 production is abnormal in neonates, and that neonate survival to sepsis is adversely affected this. One million infants die each year from sepsis or severe infection, with highest mortality rates in very low birth weight infants. The goal of this research is to discover novel therapeutics that will enhance the survival of these particularly susceptible children. The aim is to provide a better understanding of the neonatal response during sepsis and to elucidate possible pathways that may be used to improve neonatal immunity to sepsis.