Date of Award

Summer 8-12-2022

Level of Access Assigned by Author

Open-Access Thesis

Degree Name

Master of Science (MS)

Department

Food Science and Human Nutrition

Advisor

Sue L. Ishaq

Second Committee Member

Yanyan Li

Third Committee Member

Dorothy Klimis-Zacas

Additional Committee Members

Jennifer Perry

Tao Zhang

Abstract

Inflammatory Bowel Diseases (IBD) are chronic, reoccurring, and debilitating conditions characterized by inflammation in the gastrointestinal tract, some of which can lead to more systemic complications and can include autoimmune dysfunction, a change in the taxonomic and functional structure of microbial communities in the gut, and complicated burdens in a person’s daily life. Like many diseases based in chronic inflammation, research on IBD has pointed towards a multifactorial origin involving factors of the host’s lifestyle, immune system, associated microbial communities, and environmental conditions. Too often, research focuses on just one aspect of IBD or uses one model with a narrow scope, that may result in unanticipated microbial changes, or that are not representative of genetic factors. This is reflected in the absence of genetic models in biochemical-centric research focused on the role of broccoli-metabolite sulforaphane (SFN) in preventing and treating IBD. To be an accurate reflection of IBD, research studies should expand their scope, for example by addressing the concepts of biogeographic specificity of both nutrient absorption and microbial community dynamics, or by using multiple research tools to better mimic the multiple presentations of IBD.

To date, no previous SFN or broccoli diet studies have used the IL-10-ko mouse model. With our study, we sought to cover this research gap by, first, proofing broccoli dietary measures in IL-10-ko mice that have a Crohn’s disease-like presentation of inflammation. We fed IL-10-ko mice either a broccoli diet or a control diet, initiated inflammation, and assessed that inflammation using bodyweight gain, a disease activity index score, and immunohistology. All three of the parameters measured showed a consistent and marked reduction of inflammation in mice that were fed a broccoli diet. To assess the performance of this study, we also compared the bodyweight results of our novel IL-10-ko model to the results of an established dextran sulfate sodium (DSS) model of IBD. As expected, the broccoli diet prevented inflammation in the DSS model when compared to control diet fed mice. Excitingly, the IL-10 model had a much more pronounced effect on bodyweight gain, suggesting IL-10-ko mice may be an excellent environment for studying broccoli diet and SFN interactions with gut microbes.

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