University of North Carolina at Chapel Hill Graduate School
Doi
Abstract
In the United States and globally, rates of obesity have greatly increased and prevalence is continuing to grow. As of 2014, 35.0% of adult males and 40.4% of adult females in the U.S. were obese, according to the National Health and Nutrition Examination Survey (NHANES).1 Previous research in the Beck lab has demonstrated that vaccinated obese individuals have twice the likelihood of developing influenza or “flu-like-illness” when compared to healthy weight individuals, despite antibody levels above the threshold of protection.2 This is concerning because the influenza vaccination is the single most effective method of protection. What is not understood is the mechanisms underlying this difference in obese individuals. Previous work in the Beck Lab has found that antibody response is not significantly different between obese and lean individuals 30 days post vaccination, but falters between that time and one-year post vaccination. We have also found that there is a difference in the metabolism and function of T cells in the response to the influenza vaccination. With the goal of discovering new research directions that might aid in the discovery of molecular mechanisms underlying this phenomenon, I conducted a study using a bioinformatics approach to analyze the gut microbiota as a potential mediator. Strong preliminary evidence was found linking BMI, Firmicutes, and the antibody response to the 2014-2015 TIV immunization.Master of Scienc
