Impact of selenium on gut inflammation
Open Access
- Author:
- Fraker, John Hunter
- Area of Honors:
- Immunology and Infectious Disease
- Degree:
- Bachelor of Science
- Document Type:
- Thesis
- Thesis Supervisors:
- Dr. Kumble Sandeep Prabhu, Thesis Supervisor
Dr. Pamela A. Hankey-Giblin, Thesis Honors Advisor - Keywords:
- ulcerative colitis
inflammatory bowel disease
selenium
gut microbiota
inflammation - Abstract:
- Ulcerative colitis (UC) is a chronic condition that causes inflammation in the colon. Because there are only temporary solutions to UC, there is a significant interest within the biomedical community to discover preventive as well as permanent treatment measures for it. During an inflammatory response in the gastrointestinal tract, the composition of the microbiota has been shown to change, subsequently creating an environment where pathogenic microbes can colonize and increase the probability of a relapse. Due to its role in mitigating inflammation and affecting immune cell function, the micronutrient selenium offers a potential solution for managing the dysregulated immune response seen in inflammatory bowel disease (IBD). This dissertation examines several experiments involving gut inflammation and the ability of selenium in modulating inflammation at several levels in mice on respective selenium diets that are deficient (<0.01 ppm selenium), adequate (0.08 ppm selenium), or supplemented (0.4 ppm selenium). The effects of selenium on bacterial growth in vitro, bacterial virulence in vivo, and microbiota composition in a chemical (dextran sodium sulfate, DSS)-induced colitis murine model will be investigated. These studies are based on the hypothesis that mice on selenium supplemented diets will have minimal changes in their microbiota composition and will resolve the inflammatory condition faster than mice placed on selenium deficient or selenium adequate diets. If successful, these experiments could provide further insight into preventive and maintenance treatments in patients affected by IBD.